"The Doctor is In"

Your Heart Health: 13 Numbers Everyone Should Know

2011-02-12T18:33:00.000-08:00

1. Alcohol intake

Those fond of tipple may be dismayed, but the science on alcohol as an agent to promote heart health is just not definitive. "If you have heart disease, alcohol plays no role in your medicine cabinet; if [you do] not, alcohol is not the right way to reduce your risk," says Jonathan Whiteson, director of the Cardiovascular Rehabilitation Program at New York University Langone Medical Center. Some research has suggested that drinking red wine may increase one's HDL, or "good" cholesterol, but Whiteson notes that the boost is minimal. "Exercise [offers] a better increase in HDL," he says.

While he's not against a drink in a social setting, it's certainly not something folks—especially those with heart disease—should engage in with the idea that it will offer a heart benefit, says Whiteson. In fact, medications' effectiveness can be either hampered or heightened by alcohol, sometimes to a dangerous extent. (Common herbal supplements can interact with heart drugs, too). And drinking too much can lead to high blood pressure or increased blood levels of triglycerides, a type of fat.

Bottom line: The American Heart Association suggests that otherwise healthy individuals who drink should do so in moderation. That is defined as one to two drinks per day for men and one drink per day for women. And be careful with that pour: The AHA defines a drink as one 12-ounce beer, a 4 ounce glass of wine, 1.5 ounce of 80-proof spirits, or 1 ounce of 100-proof spirits.

2. Salt intake

Some experts say that the pervasive use of sodium in the America diet is wreaking havoc on our cardiovascular systems. "Sodium causes retention of fluid within the circulation, and if you're sodium-sensitive, it expands your blood volume and can contribute to high blood pressure, stroke, and other heart disease," explains Clyde Yancy, medical director of the Baylor Heart and Vascular Institute at Baylor University Medical Center in Dallas and spokesman for the American Heart Association.

A report in the New England Journal of Medicine suggested that if Americans reduced daily salt intake by 3 grams, we could significantly lower the annual number of new cases of coronary heart disease (by between 60,000 and 120,000), stroke (by 32,000 to 66,000), heart attack (by 54,000 to 99,000), and even the number of deaths from any cause (by 44,000 to 92,000). The paper's authors noted previous research that showed the average American man consumes 10.4 grams of salt daily, while the average American woman gets 7.3 grams.

Bottom line: The AHA recommends Americans limit salt intake to 1.5 grams daily. Be wary: Sodium creeps in via unexpected sources, and it's not so much the salt shaker on our table that's to blame. Research suggests we get as much as 80 percent of our daily salt intake from processed foods.

3. Sugar intake

It's not just the savory flavors that'll get you; sweets, too, can ultimately become a cause for concern, says the American Heart Association. Like salt, sugar creeps into the processed foods that make up much of the American diet, and sweetened beverages—soda, juices, and sports drinks—are especially loaded with the stuff. Here's some disturbing math for you: A 12-ounce can of soda has about 8 teaspoons (or 33 grams) of added sugars, totaling about 130 calories. (A gram of sugar translates into 4 calories.)

A can of Coke or Pepsi, then, basically takes you to the AHA's new upper limit on the recommended amount of added sugar Americans should ingest on a daily basis. The association's primary concern is the number of excess calories that added sugars sneak into our diets and pile onto our waistlines, which can contribute to metabolic changes that increase the chances of developing a host of diseases.

Bottom line: According to the AHA, women should get no more than 100 calories per day of added sugars and men should stop at 150 calories per day.

4. Resting heart rate

How hard does your heart have to work—and how fast does it have to pump—to get oxygen-rich blood throughout your body? A lower number suggests your cardiovascular system is more efficient at doing this. Thus, a highly trained athlete can have a resting heart rate in the 40s, says Whiteson.

And while the research is still emerging on what one's resting heart rate predicts about heart disease risk, a picture is beginning to take shape. "There is certain evidence to support [the idea that] a higher resting heart rate is associated with heart disease," especially ischemic heart disease, he says, which involves reduced blood flow (and oxygen) getting to heart arteries and the heart muscle. This effect seems to be more pronounced in women than in men, but a study in the Journal of Epidemiology and Community Health suggested that in women up to the age of 70, every 10-beats-per-minute increase in resting heart rate boosted the risk of dying from ischemic heart disease by 18 percent. In men, the risk was increased by 10 percent for every extra 10 beats per minute, and age didn't have an impact. The study also found that women who got high levels of physical activity were able to reduce their risk of death considerably, compared with those who did little or no activity. The same effect was not found in men, but the researchers suggest the results may have been skewed because men tend to overestimate how much exercise they get.

Bottom line: A normal resting heart rate is between 60 and 100 beats per minute. Check yours by finding your wrist's pulse, counting the beats in a 15-second period, then multiplying by four.

5. Hours of sleep per night

An overcaffeinated America seems to perpetually crave more shut-eye. And evidence is cropping up to suggest that a poor night's sleep is not only felt the next day but could have implications for one's heart over the long term. It is well established that sleep apnea, which results in numerous interruptions to breathing while asleep, is associated with stroke and coronary artery disease.

The reason is not clear, says Whiteson, but it's been hypothesized that people with disrupted sleep breathing have higher blood pressure overall because they don't get the restorative sleep that normally allows blood pressure to go down and gives the cardiovascular system a break during slumber. And a study in the Journal of the American Medical Association showed that middle-aged people who got five hours of shut-eye or less a night had a greater risk of developing coronary artery disease than those who got eight hours. The clue was the beginnings of calcium buildup in their arteries, found by CT scanning long before the disease process would normally be picked up.

Bottom line: Get eight hours of sleep per night. Making it happen isn't easy, we know.

6. Exercise

You've heard it a thousand times over, and the message stays the same: Regular, heart-thumping exercise offers a multitude of health benefits, particularly for cardiovascular fitness. Perhaps clinicians (and health writers) keep bashing us over the head with that fact because of the eye-popping number of American adults who reported getting zero vigorous activity in a 2008 Centers of Disease Control and Prevention survey: 59 percent.

Bottom line: For a clean bill of health, the major health associations (including the AHA and the American College of Sports Medicine) suggest a minimum of 150 minutes of moderate-intensity physical activity each week—say, brisk walking that boosts your heart rate. This translates into 30 minutes of exercise on five days of the week. Twice-weekly strength training of eight to 10 exercises, up to 12 reps each, is also on their to-do list.

Whiteson at NYU Langone Medical Center suggests that those who don't have heart disease should bump that recommendation up to 60 minutes a day, five days a week of vigorous activity, where you're breathing pretty heavily and sweating. But he offers a concession: "You can break it up" into, say, three 20-minute sessions per day, since "the effect of aerobic exercise is cumulative." He also thinks those without heart disease should do strength training thrice weekly. Individuals with heart disease should always discuss a new exercise regimen with a doctor first, he says.

7. Cigarettes

A 2009 study of Norwegians found that heavy smokers—those who puff at least 20 cigarettes per day—were 2.5 times more likely to die over a 30-year period than nonsmokers. But the cardiovascular risks associated with smoking aren't just seen in chain smokers.

The more nuanced message that doesn't always get across is the risk that the occasional smoker is exposed to. Even 10 minutes of secondhand smoke exposure may affect cardiovascular function. Just because you might not smoke a pack a day or even a week doesn't mean you're in the clear. "There is no safe level of exposure" to tobacco smoke, says Yancy.

Bottom line To protect against heart disease (not to mention cancer, stroke, and reproductive problems), the goal is to smoke exactly zero cigarettes.

8. Blood sugar

Over time, high blood sugar levels associated with diabetes can damage nerves and blood vessels. This can spur the buildup of fat on blood vessel walls, which can impede blood flow and promote atherosclerosis. Having diabetes increases one's risk of cardiovascular disease considerably. Three quarters of those with diabetes die of heart or blood vessel disease.

Your body's ability to use glucose (blood sugar) properly can be tested by getting a fasting blood glucose test, which is a snapshot of your blood sugar at the time, or by getting a hemoglobin A1C test, which measures overall blood glucose over the previous three months. Both can be insightful. "There is data to suggest that there is a significant decrease in the risk of heart and vascular disease with every 1 percent reduction in hemoglobin A1C," says Whiteson.

Bottom line: The more controlled, the better. The normal range for a fasting blood glucose test is typically less than 100 milligrams per deciliter; prediabetes is indicated by a level between 100 and 125 mg/dL and diabetes by a reading of 126 mg/dL or above. A normal hemoglobin A1C level is below 6 percent, and those with diabetes should aim to keep it under 7 percent.

9. C-reactive protein

Inflammation is a process our body uses to fight off an assault, like a cold or injury, in order to heal. But over the long term, chronic inflammation plays a detrimental role to health because the nasty byproducts—inflammatory molecules like cytokines—are believed to be part of several disease processes, including atherosclerosis, obesity, and Alzheimer's disease. In the realm of heart disease, much ado has been made of c-reactive protein, a marker for one's level of inflammation that can be picked up through a blood test called hs-CRP, for high-sensitivity c-reactive protein.

Who should get the test, and what are doctors to do with the results? Those are matters of considerable debate. "We can't treat high [c-reactive protein]," says Whiteson. It's an indicator of potential heart trouble, but medicine doesn't have the tools, via medications or procedures, to bring an elevated c-reactive protein down to normal. It is possible, however, to directly treat other critical risk factors like high blood pressure and high cholesterol. Doing so can bring down the risk of future cardiac events and death. A landmark study from late 2008 found that subjects who did not have heart disease and had normal cholesterol and who took statins had a lower risk of heart attack and stroke and also had fewer angioplasties and bypass surgeries over the course of the study, compared with the group who took a placebo. But too many questions remain about the study to make a blanket statement that folks should be taking statins more liberally.

Bottom line: According to the American Heart Association, a hs-CRP measure of 1 mg/L means you are at low risk of developing cardiovascular disease, a measure between 1 and 3 mg/L means you are at average risk, and levels above 3 mg/L means your risk is high. Getting the test may be helpful, says Yancy, if you are at intermediate risk for heart disease based on other risk factors and your doctors would like another data point to determine treatment. But "there is no need to check CRP if a person already has high risk or truly is in the healthy bracket," he says.

10. Waist circumference

While not a direct measure of heart disease, a high waist circumference tracks with increased risk for high blood pressure, high cholesterol, and diabetes—all of which have a direct impact on heart health. And the bigger the belly, the heavier one tends to be. Obesity, of course, is a well-known risk factor for a range of diseases, including heart disease.

Importantly, a higher waist circumference indicates distribution of fat around the abdomen and packing fat around vital organs, which research has indicated is more dangerous than carrying weight in the thighs or buttocks. Be sure you're measuring properly. The correct waist circumference measurement is taken by wrapping a measuring tape around the natural waist at the belly button, not around the hips.

Bottom line: Men should have a waist circumference of less than 40 inches. The figure for women is less than 35 inches.

11. Body mass index

Your weight matters, but it has to be considered in the context of how tall you are. Body mass index takes the two numbers into account. Like waist circumference, BMI is an indirect measure of risk, but a higher measure correlates with greater risk. The catch, however, is that it is not always entirely accurate. A person in excellent condition who has a lot of muscle mass may have a high BMI.

Too much excess weight is associated with diabetes, heart disease and stroke, some cancers, sleep apnea, osteoarthritis, fatty liver disease, and complications in pregnancy.

Bottom line: People with BMIs less than 18.5 are underweight. Target BMI range is between 18.5 and 24.9. Overweight is considered between 25 and 30, and a BMI above 30 puts you in the obese category.

12. Blood pressure

This one is critical to heart health. According to the National Heart Lung and Blood Institute, 1 in 3 Americans have high blood pressure. When a nurse wraps the cuff around your arm, she's taking a reading of the force on the walls of your arteries, which is subject to fluctuating pressure as the heart beats to push blood through your body. The trouble is, high blood pressure doesn't have any telltale symptoms, so a person might be living with hypertension unknowingly. Over the long haul, elevated blood pressure can damage organs and fuel a cascade of problems.

Action to lower blood pressure can include medications, but diet and exercise can really beat those numbers back into submission. The DASH diet (Dietary Approaches to Stop Hypertension)—high in veggies, fruit, fish, and whole grains but low in red meat fat and sugar—has been shown to lower blood pressure significantly. And research has suggested that the DASH diet packs an especially powerful wallop when people simultaneously work to reduce salt intake, a known blood pressure booster.

Bottom line: "The only number that really matters is 120 over 80," which is the cutoff for a normal blood pressure reading, says Yancy. The more one's blood pressure surpasses that level, the more damage to the vascular system, heart, and kidneys. The top number is called systolic blood pressure and is the measure of pressure while the heart beats. The bottom number is called diastolic and is the measure of pressure between heart beats. A reading above 120/80 but below 140/90 is considered prehypertension; anything above that is high blood pressure. Both require attention and steps to bring the blood pressure back under control.

13. Cholesterol

Your cholesterol level is a measure of the fats circulating in your bloodstream. With out-of-whack cholesterol levels comes greater risk for coronary artery disease and stroke. Reducing saturated fat, trans fat, cholesterol, and total fat can help bring down your cholesterol level. And exercise, says Whiteson, "is one pill that treats all ills. It can touch all risk factors for heart disease," including reducing weight, reducing stress, improving blood sugar profiles, bringing down high blood pressure, and lowering total cholesterol, lowering LDL (the "bad" cholesterol), increasing HDL (the "good" cholesterol), and lowering triglycerides, a type of fat in the blood.

Bottom line: You're aiming for total cholesterol below 200 mg/DL; above 240 mg/DL puts you at twice the risk of coronary artery disease as a person within the normal range. HDL should be above 40 mg/DL for men and above 50 mg/DL for women (women tend to have higher HDL before menopause); above 60 mg/DL is categorized as protective to your heart. LDL ideally should be below 100 mg/DL, though up to 129 mg/DL is near optimal. High LDL is considered 160 mg/DL or above. Triglycerides should be below 150 mg/DL; a measure above 200 mg/DL is considered high.

Article from Sarah Baldauf, USNews.com

2010 AHA Guidelines: The ABCs of CPR Rearranged to "CAB"

2010-10-22T17:54:00.000-07:00

October 20, 2010 — Chest compressions should be the first step in addressing cardiac arrest. Therefore, the American Heart Association (AHA) now recommends that the A-B-Cs (Airway-Breathing-Compressions) of cardiorespiratory resuscitation (CPR) be changed to C-A-B (Compressions-Airway-Breathing).

The changes were documented in the 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care, published in the November 2 supplemental issue of Circulation: Journal of the American Heart Association, and represent an update to previous guidelines issued in 2005.

"The 2010 AHA Guidelines for CPR and ECC [Emergency Cardiovascular Care] are based on the most current and comprehensive review of resuscitation literature ever published," note the authors in the executive summary. The new research includes information from "356 resuscitation experts from 29 countries who reviewed, analyzed, evaluated, debated, and discussed research and hypotheses through in-person meetings, teleconferences, and online sessions ('webinars') during the 36-month period before the 2010 Consensus Conference."

According to the AHA, chest compressions should be started immediately on anyone who is unresponsive and is not breathing normally. Oxygen will be present in the lungs and bloodstream within the first few minutes, so initiating chest compressions first will facilitate distribution of that oxygen into the brain and heart sooner; starting with "A" rather than "C" adds another 30 critical seconds.

"For more than 40 years, CPR training has emphasized the ABCs of CPR, which instructed people to open a victim's airway by tilting their head back, pinching the nose and breathing into the victim's mouth, and only then giving chest compressions," noted Michael R. Sayre, MD, coauthor and chairman of the AHA's Emergency Cardiovascular Care Committee, in an AHA written release. "This approach was causing significant delays in starting chest compressions, which are essential for keeping oxygen-rich blood circulating through the body," he added.

The new guidelines also recommend that during CPR, rescuers increase the speed of chest compressions to a rate of at least 100 times a minute. In addition, compressions should be made more deeply into the chest, to a depth of at least 2 inches in adults and children and 1.5 inches in infants.

Persons performing CPR should also avoid leaning on the chest so that it can return to its starting position, and compression should be continued as long as possible without the use of excessive ventilation.

9-1-1 centers are now directed to deliver instructions assertively so that chest compressions can be started when cardiac arrest is suspected.

The new guidelines also recommend more strongly that dispatchers instruct untrained lay rescuers to provide Hands-Only CPR (chest compression only) for adults who are unresponsive, with no breathing or no normal breathing.

Other Key Recommendations

Other key recommendations for healthcare professionals performing CPR include the following:

    * Effective teamwork techniques should be learned and practiced regularly.
    * Quantitative waveform capnography, used to measure carbon dioxide output, should be used to confirm intubation and monitor CPR quality.
    * Therapeutic hypothermia should be part of an overall interdisciplinary system of care after resuscitation from cardiac arrest.
    * Atropine is no longer recommended for routine use in managing and treating pulseless electrical activity or asystole.

Pediatric advanced life support guidelines emphasize organizing care around 2-minute periods of continuous CPR. The new guidelines also discuss resuscitation of infants and children with various congenital heart diseases and pulmonary hypertension.

Toothbrushing Less Than Twice a Day Linked to Increased Cardiovascular Risk

2010-06-20T08:08:00.000-07:00

June 7, 2010 — Individuals who do not brush their teeth twice a day have an increased risk of heart disease, a new study shows.

The study was published online May 27, 2010 in BMJ; corresponding author is Prof Richard Watt (University College London, UK).

The researchers note that while it has been established that inflammation in the body (including mouth and gums) plays an important role in the buildup of atherosclerosis, this is the first study to investigate whether the number of times individuals brush their teeth has any bearing on the risk of developing heart disease.

They analyzed data from more than 11 000 adults who took part in the Scottish Health Survey, in which individuals were asked about lifestyle behaviors such as smoking, physical activity, and oral health routines. Questions asked included how often they visited the dentist and how often they brushed their teeth (twice a day, once a day, or less than once a day). Information was also collated on medical history and family history of heart disease and blood pressure. Blood samples were taken from a subgroup of participants and tested for C-reactive protein (CRP) and fibrinogen levels. The data gathered from the interviews were linked to hospital admissions and deaths.

Results showed generally good oral hygiene practices, with 62% of participants saying they visited the dentist every six months and 71% reporting that they brushed their teeth twice a day. After adjustment for established risk factors, it was found that participants who reported less frequent toothbrushing had an increased risk of heart disease compared with people who brushed their teeth twice a day. Participants who had poor oral hygiene also had increased levels of CRP and fibrinogen.

Hazard Ratio for Cardiovascular Events (Fatal and Nonfatal) Relative to How Often Teeth Are Brushed Each Day
Frequency of toothbrushing HR* (95% CI)
Twice a day 1.0
Once a day 1.3 (1.0–1.5)
Less than once a day 1.7 (1.3–2.3)
p for trend 0.001

*Adjusted for age, sex, socioeconomic group, smoking, physical activity, visits to dentist, body-mass index, family history of cardiovascular disease, hypertension, and diabetes

The researchers say: "To the best of our knowledge, this is the first study to show an association between a single-item self-reported measure of toothbrushing and incident cardiovascular disease in a large representative sample of adults without overt cardiovascular disease."

They add: "Our study suggests a possible role of poor oral hygiene in the risk of cardiovascular disease via systemic inflammation. Raised inflammatory and homoeostatic responses as well as lipid metabolism disturbance caused by periodontal infection might be possible pathways underlying the observed association between periodontal disease and the increased risk for cardiovascular disease."

But they note that further studies are needed to confirm whether the observed association between oral health behavior and cardiovascular disease is in fact causal or merely a risk marker.

References

1. de Oliveira C, Watt R, and Hamer M. Toothbrushing, inflammation, and risk of cardiovascular disease: Results from Scottish Health Survey. BMJ 2010; DOI:10.1136/bmj.c2451. Available at: http://www.bmj.com.

Additional Information

Information about oral hygiene and cardiovascular risk is available online on the National Institute of Dental and Craniofacial Research Web site
Clinical Context

Systemic inflammation plays a role in cardiovascular events, and a previous study by Danesh and colleagues, which was published in the July 22, 2000, issue of the BMJ, found that certain serum markers of inflammation were independent predictors of the risk for coronary heart disease events. Specifically, CRP and serum amyloid A protein were significantly associated with the risk for nonfatal myocardial infarction or coronary heart disease death, even after a multivariate analysis. The serum white blood cell count and albumin levels were not significantly associated with coronary heart disease risk.

Periodontal disease is associated with a moderate systemic inflammatory response. The current study explores the relationship between oral hygiene behavior and inflammatory response as well as the risk for cardiovascular disease.
Study Highlights

* Data were drawn from the Scottish Health Survey administered in 1995, 1998, and 2003. The survey is a broad questionnaire of health behaviors and outcomes among adults 35 years and older.
* Participants who were edentulous (no natural teeth) or had existing cardiovascular disease were excluded from the current analysis.
* Researchers of the current study specifically examined oral hygiene behaviors and their relationship to a composite of cardiovascular diagnoses, which were derived from hospital discharge and death certificate databases. These diagnoses included myocardial infarction, coronary artery bypass surgery, percutaneous coronary angioplasty, stroke, and heart failure.
* The main study outcome was adjusted to account for other cardiovascular risk factors.
* Researchers also examined the relationship between oral hygiene and 2 serum markers of systemic inflammation: CRP and fibrinogen.
* 11,869 individuals provided study data. The mean age was 50 years old, and 46.1% of participants were men.
* 62% of participants reported visiting a dentist at least every 6 months, and 71% said they brushed their teeth twice a day.
* Participants who brushed their teeth less than twice a day were more likely to be older and have a higher number of cardiovascular risk factors.
* There were 555 cardiovascular events during an average of 8.1 years of follow-up.
* Compared with participants who brushed their teeth twice daily, individuals who brushed less often than once a day experienced a significant multivariate hazard ratio of 1.7 for cardiovascular events. The adjusted hazard ratio among patients who brushed once a day was 1.3, a result of borderline significance.
* The risk for cardiovascular disease related to poor oral hygiene was similar among men and women, and it also did not differ by age or smoking status.
* Mean levels of CRP among participants who brushed twice daily, once daily, and less than once daily were 3.07, 3.51, and 4.18 mg/L, respectively. The respective fibrinogen levels were 2.86, 2.95, and 2.98 mg/L.
* Further analyses indicated that these markers of systemic inflammation at least partly mediated the risk for cardiovascular events associated with poor oral hygiene.

Clinical Implications

* A previous study found that serum levels of CRP and amyloid A protein, but not the white blood cell count or albumin level, were positively and independently associated with the risk for coronary heart disease events.
* The current study suggests that toothbrushing less than twice daily might independently increase serum markers of systemic inflammation as well as the risk for cardiovascular disease.

From Heartwire CME © 2010 Medscape, LLC

Super Foods for Men and Women

2010-05-17T16:13:00.000-07:00

Guess what? You have different nutritional needs than the opposite sex. Discover the best foods for you both.

One in five women have a history of painful urinary tract infections. "I had three in one year," says Patty Buxton*, a Colorado middle-school teacher. Reading that cranberry juice may help prevent these infections, Buxton went on a regimen a year ago, and since then she's been infection-free. She thinks cranberry juice did the trick.

Cranberry juice isn't the only food that offers protection from specific illnesses. Here's a list of disease-fighting foods for men and women.

Foods for Men

1. Tomato Sauce.
Men who eat a lot of tomatoes, tomato sauce, or pizza smothered with the stuff may be giving themselves a hedge against prostate cancer. So say researchers at Harvard, who studied the eating habits of more than 47,000 male health professionals. They found that men who ate tomato sauce two to four times per week had a 35 percent lower risk of developing prostate cancer than men who ate none. A carotenoid called lycopene, which tomatoes contain in abundance, appeared to be responsible. But scientists were puzzled: tomato juice didn't seem to have a protective effect. Other research showed why. For best absorption, lycopene should be cooked with some kind of fat. So pizza may be just what the doctor ordered.

2. Oysters.
Myth has it that oysters are the food of love. Science may agree. Just two to three oysters deliver a full day's supply of zinc, a mineral critical for normal functioning of the male reproductive system. Scientists are divided over reports that sperm counts have declined over the last 50 years and that environmental factors are to blame. Nutritional deficiencies do seem to be the cause of certain cases of low testosterone. Getting adequate zinc is sometimes the answer (11 mg per day is recommended for men; more than 40 mg can pose risks). In one trial, 22 men with low testosterone levels and sperm counts were given zinc every day for 45 to 50 days. Testosterone levels and sperm counts rose.

3. Broccoli.
A recent Harvard study finds that cruciferous vegetables, like broccoli, may protect against bladder cancer. It's one of the most common cancers in this country, and affects two to three times as many men as women. Scientists analyzed the diets of nearly 50,000 men and discovered that those who ate five servings or more per week of cruciferous veggies were half as likely to develop bladder cancer over a ten-year period as men who rarely ate them. And broccoli and cabbage were singled out as the most protective foods.

4. Peanut Butter.
If you want a healthy heart, spread your morning toast with peanut butter. Heart disease is the leading killer of men and women, but men fall victim at an earlier age. Researchers from Pennsylvania State University compared the cholesterol-lowering effect of the American Heart Association's Step II Diet with a higher-fat diet based on peanuts. The AHA plan included more carbohydrates. The peanut regimen was 36 percent fat. After 24 days both diets lowered "bad" LDL cholesterol. But the peanut plan also caused a drop in blood fats called triglycerides and did not decrease HDL, the "good" cholesterol. The AHA diet raised levels of triglycerides and lowered levels of HDL.

"Peanut butter is a little higher in fat," says Penny Kris-Etherton, Ph.D., the lead author of the Penn State study. "But it's the type that's good for you -- monounsaturated fat." Researchers have predicted that the peanut diet could reduce heart-disease risk even more than could the AHA diet. Just don't go nutty plastering on the tasty spread, since it is high in calories.

5. Watermelon.
Until the age of 55, more men suffer from high blood pressure than do women. Research suggests that foods rich in potassium can reduce the risk of high blood pressure and stroke. The evidence is so convincing that the Food and Drug Administration recently allowed food labels to bear a health claim about the connection between potassium-rich foods and blood pressure. "There isn't a dietary requirement for potassium," says Kathleen Cappellano, nutrition-information manager at Tufts University in Boston. "But a good goal is about 2000 milligrams or more a day." Watermelon, a rich source of this mineral, has more potassium -- 664 mg -- in one large slice than the amount found in a banana or a cup of orange juice. So cut yourself another slice and enjoy the taste of summer.

Foods for Women

1. Papaya.
This tropical fruit packs about twice the vitamin C of an orange. Add it to your arsenal against gallbladder disease, which afflicts twice as many women as men.

After analyzing the blood of over 13,000 people, scientists from the University of California, San Francisco, found that women who had lower levels of vitamin C were more likely to have gallbladder illnesses. One medium papaya (about ten ounces), with its 188 mg of vitamin C and a mere 119 calories, is a refreshing source of the vitamin. The once exotic fruit now can be found in most supermarkets.

2. Flaxseed.
Bakers use this nutty-flavored seed mainly to add flavor and fiber. But scientists see the tiny reddish-brown seed, rich in estrogenlike compounds called lignans, as a potential weapon against breast cancer. An exciting report at last year's San Antonio Breast Cancer Symposium showed that adding flaxseed to the diet of women with breast cancer effectively slowed tumor growth. You can flavor your muffins with flaxseed, but the easiest way to get the beneficial lignans is to sprinkle a few tablespoons of ground flaxseed on your morning cereal. Look for the seeds in health food stores or in supermarkets on the flour aisle. They're easy to grind in a blender or coffee grinder. But get seeds -- there are no lignans in the oil.

3. Tofu.
Foods high in soy protein can lower cholesterol and may minimize menopausal hot flashes and strengthen bone. Isoflavones, plant chemicals in soybeans that have a structure similar to estrogen, may be the reason. Though animal studies form the bulk of the evidence, a human study found that 90 mg of isoflavones was beneficial to bone (specifically the spine). And two other studies suggest that 50 to 76 mg of isoflavones a day may offer some relief from hot flashes. A half-cup of tofu contains about 25 to 35 mg of isoflavones.

4. Buffalo Meat.
Due largely to menstruation, women tend to be anemic more than men. And low iron levels in blood can cause severe fatigue. To get a good dose of iron, try bison. Bison, or buffalo, meat is lean and has what diet-conscious women want -- lots of iron and less fat than most cuts of beef. "The iron content is about 3 milligrams in a 3 1/2-ounce uncooked portion," says Marty Marchello, Ph.D., at North Dakota State University. "That portion contains less than 3 grams of fat." Buffalo meat can help boost energy and lower weight. And you don't have to have a home on the range to get some bison anymore. You can pick it up at many supermarkets across the United States, or through mail order or on the Internet.

5. Collard Greens.
This humble vegetable may help fight osteoporosis, which afflicts many women late in life. In addition to getting adequate amounts of calcium and vitamin D, some studies suggest that vitamin K may have a bone-protective effect as well. Based on data from one of the largest studies of women, the Nurses' Health Study, researchers discovered that women who ate enough vitamin K-rich foods (at least 109 micrograms of the vitamin daily) were 30 percent less likely to suffer a hip fracture during ten years of follow-up than women who ate less. Researchers point out that dark-green leafy vegetables -- Brussels sprouts, spinach, broccoli -- are all good sources of the vitamin. But collard greens, with about 375 micrograms per half-cup, are among the best.

There you have it: five great foods for women and for men that can keep both of you well fed and healthy too.

By Maureen Callahan of Yahoo Shine

New Physicians at Increased Risk for Depression During Internship

2010-04-09T16:19:00.000-07:00

From the Arch Gen Psychiatry. Published online April 5, 2010.

April 7, 2010 — The percentage of new clinicians who develop depressive symptoms increases significantly during medical internship, new research suggests.

A large prospective study showed a marked increase in depressive symptoms among new clinicians — from 3.9% at baseline to an average of 25.7% (P < .001) during internship — as reflected by increases in the 9-item Patient Health Questionnaire (PHQ-9).

Srijan Sen, MD, PhD, University of Michigan, Ann Arbor, and colleagues also found that 41.8% of participants met criteria for major depression at one or more quarterly assessments.

On stepwise linear regression analysis, neuroticism (P < .001), personal history of depression (P < .001), lower baseline depressive symptoms (P < .001), female sex (P = .03), US medical education (P = .005), and a difficult early family environment (P = .04) significantly correlated with a change in depressive symptoms.

"When myself and coinvestigator Constance Guille were interns 4 years ago, we noticed that people who were well adjusted and happy a few months before were having trouble sleeping and problems with their relationships and just struggling to adjust, so it struck us that these problems were very common during internship," Dr. Sen told Medscape Psychiatry.

"And while I think internship will always be a stressful time, there are things that we may be able to do to make it better for interns, including working fewer hours and using electronic records to reduce the risk of errors and making sure interns have some resources in place before they become depressed to reduce the effects of stress," he added.

The study was published online April 5 in the Archives of General Psychiatry.

No Link to Medical Specialty or Age

For the study, investigators recruited a total 1271 interns entering traditional and primary care internal medicine, general surgery, pediatrics, obstetrics-gynecology, and psychiatry residency programs during the 2007-2008 and 2008-2009 academic years. Depressive symptoms were measured using the depression module of the PHQ-9, where the total score ranges from 0 to 27. The PHQ-9 scores of 10 to 14 correspond to moderate depression, scores between 15 and 19 to moderately severe depression, and scores of 20 or greater to severe depression.

Mean PHQ-9 scores increased significantly from 2.38 at baseline to 6.70 at 3 months, 6.48 at 9 months, and 6.26 at 12 months (all P < .001 vs baseline). The percentage of subjects meeting criteria for moderately severe depression increased from 0.7% at baseline to 6.6%, 6.2%, 7.8%, and 7.6% at 3-, 6-, 9-, and 12-month points of the internship, respectively, the investigators add.

Similarly, the percentage of interns who met criteria for severe depression increased from 0% at baseline to 2.3%, 1.6%, 1.8%, and 0.8% at 3, 6, 9, and 12 months of internship, respectively. Investigators also assessed factors during internship that were associated with a change in depressive symptoms.

The 3 key variables that were associated with a significant increase in the risk for depressive symptoms were work hours (P < .001), reported medical errors (P < .001), and noninternship stressful life events (P < .001).

Interestingly, medical specialty and age were not associated with the development of depression.

5-HTTLPR Moderates Stress and Depression Response

Investigators also used internship as a model to explore the relationship between a serotonin transporter promoter polymorphism and stress in the development of depression.

"We found evidence that this variant moderates the response to stress in European American subjects, with subjects carrying at least one low-functioning 5-HTTLPR allele reporting a 43% greater increase in depressive symptoms than subjects with two low-functioning alleles," the study authors write.

European American participants with 2 high-functioning 5-HTTLPR alleles who met criteria for depression increased from 5.1% before internship to 36.2% at its highest during internship. Investigators also found that the association between 5-HTTLPR and the development of depressive symptoms under stress was moderated by neuroticism and work hours, although not with medical errors or stressful life events.

"Medical internship provided us with the unique situation where we know that a group of people currently under low stress will enter a period of high stress, and we showed that 5-HTTLPR had no effect on depression under the low stress conditions but was strongly associated with depression under high stress," Dr. Sen told Medscape Psychiatry. "So in my view, this provides strong evidence that 5-HTTLPR moderates the relationship between stress and depression, [although] the effect of this one genetic variant is relatively small compared with other factors, such as work hours, gender, and prior history of depression."

Stressful Experience

Gregory Dalack, MD, University of Michigan, Ann Arbor, agreed that internship is clearly a stressful experience, "as all of us who went through it know."

"Nevertheless," he said, "depressive symptoms detected in this cohort of interns were self-reported, which is different than detecting symptoms with a clinical diagnosis, because with a clinical diagnosis, physicians can rule out ongoing substance abuse problems or other medical conditions that may be contributing to symptoms such as sleep disturbances, which on self-reported questionnaires may be mistakenly attributed to depression."

Dr. Dalack also noted that a number of organizations have already put forward suggestions that are intended to reduce stress among interns, including limitations of hours worked. Currently, interns are still allowed to work 80 hours per week.

"They are following these recommendations prospectively to make sure hospitals are putting systems in place so that residents are not overworked, and while there may be transgressions from the rules under some circumstances, there is a higher level of scrutiny now in place to make sure people stay within those limits so as to reduce interns’ fatigue and depression and maintain a high level of quality care for patients," he said.

The study was supported by a Donaghue Foundation Clinical and Community Grant, an American Psychiatric Association Substance Abuse and Mental Health Services Administration grant, a Veterans Administration Research Enhancement Award Program award, and an American Foundation for Suicide Prevention Young Investigator grant.

Soft Drink Consumption Linked to Pancreatic Cancer

2010-02-27T18:54:00.000-08:00

February 16, 2010 — The regular consumption of sugar-laden soft drinks could boost a person's risk of developing pancreatic cancer. The results of a new study found that individuals who consumed 2 or more soft drinks per week had an 87% increased risk for pancreatic cancer, compared with those who did not.

Even after taking factors such as smoking, caloric intake, and type 2 diabetes mellitus into account, the authors found that consuming soft drinks might play an independent role in the development of pancreatic cancer.

The finding is reported in the February issue of Cancer Epidemiology, Biomarkers & Prevention.

Both soft drinks and fruit juices have a high glycemic load relative to other foods and drinks, and it has been hypothesized that both are risk factors for pancreatic cancer. The high levels of sugar can increase levels of insulin in the body, and this can contribute to pancreatic cancer cell growth, the researchers explain.

Association Not Seen With Fruit Juice

However, this study did not find an association between consumption of juice and an increased risk for pancreatic cancer.

"There are several plausible explanations why fruit juice was not significantly associated with pancreatic cancer," said first author Noel Mueller, MPH, a research associate at Georgetown University Medical Center in Washington, DC.

One reason is that the finding was based on a relatively small number of cases, so there might have been too few cases to detect an effect with fruit juice, he explained. Another is that there are differences between soft drinks and fruit juice — fruit juice is lower in sugar, includes many nutrients, and is typically served in smaller portion sizes.

A third explanation is that fruit juice intake is associated with healthier lifestyle characteristics than soft drink intake, he said.

The consumption of soft drinks coincided with a number of other unhealthy lifestyle characteristics, making it somewhat difficult to separate smoking, caloric intake, body weight, and type 2 diabetes mellitus from soft drink consumption. "But the findings from our study suggest that soft drinks may play an independent role in the development of pancreatic cancer," Mr. Mueller told Medscape Oncology.

"The influence of soft drink intake on the risk of pancreatic cancer remained virtually unchanged after adjustment for smoking status, energy intake, body weight, and type 2 diabetes mellitus," he added.

Results Statistically Significant for Soft Drinks

The current study examined the association between the consumption of soft drinks and juice and the risk for pancreatic cancer among Chinese people residing in Singapore. The data came from the Singapore Chinese Health Study (n = 60,524), and information regarding the consumption of soft drinks, juice, and other dietary items, along with lifestyle factors and environmental exposures, was collected at recruitment to the study. The participants were followed for up to 14 years.

At the start of the study, 9.7% of the participants consumed at least 2 soft drinks per week and 10.2% consumed at least 2 servings of juice per week. The authors note that, compared with those who did not consume soft drinks, those who consumed 2 or more soft drinks per week were younger, were more likely to be men, and were more likely to smoke cigarettes. They also had higher levels of education, alcohol consumption, and total energy intake; lower levels of physical activity; and consumed more total carbohydrates, fat, added sugar, and red meat.

Individuals who reported consuming 2 or more juice drinks a week had lifestyle and dietary habits that were similar to those who consumed soft drinks. However, there was no association between juice intake and cigarette smoking, and body mass index (BMI) was comparable across different categories of soft drink and juice consumption.

At 14 years and a cumulative 648,387 person-years of follow-up, 140 incident pancreatic cancers developed in people who were cancer free at baseline. After adjustment for confounders such as BMI, type 2 diabetes mellitus, and fruit juice intake, the authors found that those consuming 2 or more soft drinks per week experienced a statistically significant increased risk for pancreatic cancer (hazard ratio [HR], 1.87; 95% confidence interval [CI], 1.10 - 3.15).

Although people who consumed 2 or more juice drinks a week had an increased risk for pancreatic cancer of approximately 30%, elevated HR was not statistically significant after adjustment for variables.

However, in an age-adjusted analysis, smoking was also a risk factor. After excluding former smokers, the authors found that current smokers had a 49% increased risk for pancreatic cancer, compared with never smokers (HR, 1.49; 95% CI, 0.98 - 2.27). This risk factor remained unaffected after adjustment for diabetes and BMI.

Can Be Extrapolated to United States and Europe

Singapore is a highly industrialized nation with lifestyle and nutritional patterns reminiscent of many westernized countries. In that sense, these findings could be extrapolated to the United States and Europe, explained Mr. Mueller. Soft drinks are the leading source of added sugar in the American diet, the authors note.

"However, there are inherent differences between Singaporean Chinese and Caucasians, which is why one must be cautious when generalizing these results to the United States and Europe," he said. "But it is important to note that other studies in Caucasian populations have suggested that soft drink intake may increase risk for pancreatic cancer."

Because pancreatic cancer is a relatively rare disease, the number of cases in this study was relatively small, the authors point out. This limited the statistical power of the study. Another limitation was the inability to collect repeated dietary measurements during the course of the study; therefore, they could not account for changes in consumption of soft drinks and juices.

However, this study adds to the evidence that soft drink consumption plays a role in the development of pancreatic cancer, they conclude, and that "clinical studies examining biomarkers for glycemia and insulinemia and taking a mechanistic approach to the question of soft drink consumption and pancreatic cancer are warranted."

There is "still much to understand on the link between sugar-sweetened beverages and pancreatic cancer," the authors write.

The study was supported by a grant from the National Cancer Institute. The researchers have disclosed no relevant financial relationships.

Chocolate Linked to Lower Stroke and Stroke Mortality Risk

2010-02-19T22:51:00.000-08:00

February 12, 2010 — Just in time for Valentine's Day, a new systematic review from Canadian researchers suggests higher chocolate consumption may be associated with a lower risk for incident stroke and stroke-related mortality.

Results of 2 prospective cohort studies showed, respectively, a 22% reduction in stroke risk for those who had 1 serving of chocolate per week and a 46% reduction in stroke mortality from weekly consumption of flavonoids in 50 g of chocolate vs no consumption. A third study showed no association between chocolate intake and stroke or death.
However, the number of studies looking at this relationship was small, senior author Gustavo Saposnik, MD, from St. Michael's Hospital and the University of Toronto, Canada, told Medscape Neurology. "We need more prospective studies that specifically identify the type of chocolate and the amount, including the amount of flavonoids included in the composition of the chocolate, to make more valid conclusions," he said.
The results were released February 11 in advance of their planned presentation at the upcoming American Academy of Neurology 62nd Annual Meeting in April. The abstract will post to http://www.aan.com on February 17.

Varying Effects
Chocolate contains cocoa butter, flavonoids, carbohydrates, and vitamins. Previous studies, most of them epidemiological, have shown varying effects of chocolate consumption on the risk for cardiovascular disease, the researchers, with first author Sarah Sahib, BScCA, from McMaster University in Hamilton, Ontario, Canada, write. "Less is known about the risk of stroke in association with flavonoid intake," they note.
To examine this association, the authors carried out a systematic review of studies published between 2001 and 2009, using search terms including flavonoids, flavanols, isoflavones, and anthocyanidins, as well as stroke and mortality.

"We found 88 publications, among them 3 prospective studies, and another retrospective study providing some information on the effect of chocolate consumption on the incident risk of stroke," Dr. Saposnik said. "Two of these studies show a reduction in the incident risk of stroke, and the other 2 didn't show any substantial difference."

For example, of the 3 prospective studies, 1 found no association between flavonoid intake and the risk for stroke or death when 3% of catechin intake came from chocolate (relative risk [RR], 0.92; 95% confidence interval [CI], 0.51 - 1.68).

However, a second study found a reduction in incident stroke for chocolate consumption once per week vs no consumption (RR, 0.78; 95% CI, 0.65 - 0.94).

The third study looked at the association between flavonoid intake and stroke mortality and found a suggestion of protection against stroke mortality from 50 g of chocolate (hazard ratio, 0.54; 95% CI, 0.30 - 0.96).

The authors conclude that further prospective studies are needed "to assess whether the benefit of chocolate-based flavonoid consumption truly lowers stroke risk, or whether the apparent benefit is biased by a healthy user effect."

Investigation a Challenge
However, although more data on this link would be helpful, Dr. Saposnik pointed to several challenges to doing these kinds of studies. First, it is important to document the actual content of flavonoids or other substances thought to be active in the chocolate being consumed.
"There are some studies that compare the content of flavonoids for different food elements and antioxidant capacity," he said. Dark chocolate is one with the highest flavonoids and procyanidins, which have been associated with lower cardiovascular risk, and in addition, dark chocolate has the highest antioxidant capacity.
Still, there are varying types of chocolate, and the amounts that are required to affect stroke risk may bring a load of sugar and fats that may work counter to the beneficial effects. "50g of chocolate per day is a significant amount," Dr. Saposnik notes.

Finally, large longitudinal studies are also expensive, and funding for them scarce, which may explain why much of the evidence is coming from epidemiologic studies, he added. One alternative may be to conduct smaller studies, looking the effects of consuming controlled amounts of chocolate on some intermediate biomarker of stroke risk.

The study received no commercial support. The authors have disclosed no relevant financial relationships.

American Academy of Neurology 62nd Annual Meeting. April 10-17, 2010. Published online February 11, 2009.

American Diabetes Association Revises Diabetes Guidelines

2010-01-02T15:09:00.000-08:00

December 29, 2009 — The American Diabetes Association (ADA) revised clinical practice recommendations for diabetes diagnosis promote hemoglobin A1c (A1c) as a faster, easier diagnostic test that could help reduce the number of undiagnosed patients and better identify patients with prediabetes. The new recommendations are published December 29 in the January supplement of Diabetes Care.

"We believe that use of the A1c, because it doesn't require fasting, will encourage more people to get tested for type 2 diabetes and help further reduce the number of people who are undiagnosed but living with this chronic and potentially life-threatening disease," Richard M. Bergenstal, MD, ADA president-elect of medicine & science, said in a news release. "Additionally, early detection can make an enormous difference in a person's quality of life. Unlike many chronic diseases, type 2 diabetes actually can be prevented, as long as lifestyle changes are made while blood glucose levels are still in the pre-diabetes range."

The A1c test, which measures average blood glucose levels for a period of up to 3 months, was previously used only to evaluate diabetic control with time. An A1c level of approximately 5% indicates the absence of diabetes, and according to the revised evidence-based guidelines, an A1c score of 5.7% to 6.4% indicates prediabetes, and an A1c level of 6.5% or higher indicates the presence of diabetes.

For optimal diabetic control, the recommended ADA target for most people with diabetes is an A1c level no greater than 7%. It is hoped that achieving this target would help prevent serious diabetes-related complications including nephropathy, neuropathy, retinopathy, and gum disease.

Unlike fasting plasma glucose testing and the oral glucose tolerance test, A1c testing does not require overnight fasting. Compliance with screening may therefore be improved through use of the A1c test, which can be determined from a single nonfasting blood sample.

Recommendation Changes for 2010
Specific changes in the 2010 Clinical Practice Recommendations are as follows:

A section on diabetes related to cystic fibrosis has been added to "Standards of Medical Care in Diabetes." New evidence has shown that early diagnosis of cystic fibrosis-related diabetes and aggressive treatment with insulin have narrowed the gap in mortality between patients with cystic fibrosis with and without diabetes and have eliminated the sex difference in mortality rates. New recommendations for the clinical management of cystic fibrosis-related diabetes, based on a 2009 consensus conference, will be published in 2010 in a consensus report.
Revision of the section "Diagnosis of Diabetes" now includes the use of the A1c level for diabetes diagnosis, with a cutoff point of 6.5%.
The section formerly named "Diagnosis of Pre-diabetes" is now named "Categories of Increased Risk for Diabetes." Categories suggesting an increased risk for future diabetes now include an A1c range of 5.7% to 6.4%, as well as impaired fasting glucose and impaired glucose tolerance levels.
Revisions to the section "Detection and Diagnosis of GDM [Gestational Diabetes Mellitus]" now include a discussion of possible future changes in this diagnosis, according to international consensus. Screening recommendations for gestational diabetes are to use risk factor analysis and an oral glucose tolerance test, if appropriate. Women diagnosed with gestational diabetes should be screened for diabetes 6 to 12 weeks postpartum and should have subsequent screening for the development of diabetes or prediabetes.
Extensive revisions to the section "Diabetes Self-Management Education" are based on new evidence. Goals of diabetes self-management education are to improve adherence to standard of care, to educate patients regarding appropriate glycemic targets, and to increase the percentage of patients achieving target A1c levels.
Extensive revisions to the section "Antiplatelet Agents" now reflect evidence from recent trials suggesting that in moderate- or low-risk patients, aspirin is of questionable benefit for primary prevention of cardiovascular disease. The revised recommendation is to consider aspirin treatment as a primary prevention strategy in patients with diabetes who are at increased cardiovascular risk, defined as a 10-year risk greater than 10%. Patients at increased cardiovascular risk include men older than 50 years or women older than 60 years with at least 1 additional major risk factor.
Fundus photography may be used as a screening strategy for retinopathy, as described in the section "Retinopathy Screening and Treatment." However, although high-quality fundus photographs detect most clinically significant diabetic retinopathy, they should not act as a substitute for an initial and dilated comprehensive eye examination. Retinal examinations should be carried out annually or at least every 2 to 3 years among low-risk patients with normal eye examination results in the past.
Extensive revisions to the section "Diabetes Care in the Hospital" now question the benefit of very tight glycemic control goals in critically ill patients, based on new evidence.
Extensive revisions to the section "Strategies for Improving Diabetes Care" are based on newer evidence. Successful strategies to improve diabetes care, which have resulted in improved process measures such as measurement of A1c levels, lipid levels, and blood pressure, include the following:
- Delivery of diabetes self-management education.
- Adoption of practice guidelines developed with participation of healthcare professionals and having them readily accessible at the point of service.
- Use of checklists mirroring guidelines, which help improve adherence to standards of care.
- Systems changes, including providing automated reminders to healthcare professionals and patients and audit and feedback of process and outcome data to providers.
- Quality improvement programs, in which continuous quality improvement or other cycles of analysis and intervention are combined with provider performance data.
- Practice changes, which may include access to point-of-care A1c testing, scheduling planned diabetes visits, and clustering dedicated diabetes visits into specific times.
- Tracking systems with either an electronic medical record or patient registry to improve adherence to standards of care.
- Availability of case or (preferably) care management services using nurses, pharmacists, and other nonphysician healthcare professionals following detailed algorithms under physician supervision.

"The most successful practices have an institutional priority for quality of care, involve all of the staff in their initiatives, redesign their delivery system, activate and educate their patients, and use electronic health record tools," the guidelines authors conclude. "It is clear that optimal diabetes management requires an organized, systematic approach and involvement of a coordinated team of dedicated health care professionals working in an environment where quality care is a priority."

Source: Medscape.com

Mummies and Heart Disease

2009-12-03T07:38:00.000-08:00

Now this article got my attention. Don't blame everything to the fast foods...

November 23, 2009 (Orlando, Florida) — Checking in on some very old patients with cutting-edge computed tomographic (CT) technology reveals that atherosclerosis might not necessarily be a disease caused by a modern lifestyle. Imaging scans of Egyptian mummies, including some 3500 years old, reveals evidence of atherosclerosis, report researchers.

"There were parts of the cardiovascular system [amazingly] intact," said researcher Dr Randall Thompson (University of Missouri-Kansas City School of Medicine). "We found that on CT scan, atherosclerosis, the disease that we deal so much with, looks surprisingly like it does in our modern-day patients."

Presenting their findings here at the American Heart Association 2009 Scientific Sessions last week, Thompson, along with coinvestigator Dr Sam Wann (Wisconsin Heart Hospital, Milwaukee), said the mummies included in the study all had high social status and many served in the court of the Pharaoh or as priests or priestesses. He added that the group had not expected to see any signs of cardiovascular disease because atherosclerosis is traditionally thought of as a disease caused by an unhealthy fast-food diet, smoking, and lack of exercise. This study, however, suggests the need to look beyond traditional risk factors.

"It looks like people 3000 years ago had the propensity, at least under the circumstances of living in the King's court, to develop this disease," said Wann.

The Mummy and the Skeptical Cardiologist

During a media briefing at the AHA last week, researchers said that the study began when Dr Gregory Thomas (University of California, Irvine), another member of the team, was touring the Museum of Egyptian Antiquities in Cairo last year and came upon Pharaoh Merenptah (c. 1213-1203 BCE). Information on the Pharaoh's nameplate stated that he died at approximately age 60 and was afflicted with atherosclerosis. Skeptical that someone who lived so long ago would have atherosclerosis, American and Egyptian researchers initiated the study to determine if the diagnosis was correct and, if it was, to determine how common atherosclerosis was in a small sample of ancient Egyptians.

Working with Dr Adel Allam (Al Azhar Medical School, Cairo, Egypt) and Dr Michael Miyamoto (University of California, San Diego), as well as with archeologists and mummy experts, in February 2009, the researchers scanned 22 mummies, the oldest of which was 3500 years old. The coronary, aortic, and peripheral vasculature was identified in 16 of the specimens. Definite or probable atherosclerosis was present in nine of the 16 mummies, but among those who were 45 years or older when they died, atherosclerosis was present in 87%.

The most ancient mummy with evidence of atherosclerosis was Lady Rai, a nursemaid to Queen Amrose Nefertari. Lady Rai died in 1530 BCE at an estimated age of 30 to 40 years; she had definite disease in her aortic arch.

At the AHA last week, Thompson and Wann noted that members of the Egyptian upper classes were meat eaters, and their diets would have included cattle, geese, and ducks. Lack of refrigeration, however, meant that many of these meats would have been heavily salted to prevent spoiling, and this might have led some individuals to develop high blood pressure. Although the exact reasons for the calcified build-up in the arteries is unknown, researchers said the results challenge the view that atherosclerosis is a disease of modern humans.

"This disease has been around since the time of Moses; it's as old as the Pyramids," said Thompson.

The report is also published in the November 18, 2009 issue of the Journal of the American Medical Association.

Live life long and healthy!!

2009-11-04T15:25:00.000-08:00

A forwarded email which I think has medical merit.

The top five cancer-causing foods are:

1. Hot dogs
Because they are high in nitrates, the Cancer Prevention Coalition advises that children eat no more than 12 hot dogs a month. If you can't live without hot dogs, buy those made without sodium nitrate.

2. Processed meats and bacon
Also high in the same sodium nitrates found in hot dogs, bacon, and other processed meats raise the risk of heart disease. The saturated fat in bacon also contributes to cancer.

3. Doughnuts
Doughnuts are cancer-causing double trouble. First, they are made with white flour, sugar, and hydrogenated oils, then fried at high temperatures. Doughnuts, says Adams , may be the worst food you can possibly eat to raise your risk of cancer.

4. French fries
Like doughnuts, French fries are made with hydrogenated oils and then fried at high temperatures. They also contain cancer- causing acryl amides which occur during the frying process. They should be called cancer fries, not French fries, said Adams .

5. Chips, crackers, and cookies
All are usually made with white flour and sugar. Even the ones whose labels claim to be free of trans-fats generally contain small amounts of trans-fats.

BRAIN DAMAGING HABITS

1. No Breakfast
People who do not take breakfast are going to have a lower blood sugar level.
This leads to an insufficient supply of nutrients to the brain causing brain degeneration.

2. Overeating
It causes hardening of the brain arteries, leading to a decrease in mental power.

3. Smoking
It causes multiple brain shrinkage and may lead to Alzheimer disease.

4. High Sugar consumption
Too much sugar will interrupt the absorption of proteins and nutrients causing malnutrition and may interfere with brain development.

5. Air Pollution
The brain is the largest oxygen consumer in our body. Inhaling polluted air decreases the supply of oxygen to the brain, bringing about a decrease in brain efficiency.

6. Sleep Deprivation
Sleep allows our brain to rest. Long term deprivation from sleep will accelerate the death of brain cells.
7. Head covered while sleeping
Sleeping with the head covered increases the concentration of carbon dioxide and decrease concentration of oxygen that may lead to brain damaging effects.

8. Working your brain during illness
Working hard or studying with sickness may lead to a decrease in effectiveness of the brain as well as damage the brain.

9. Lacking in stimulating thoughts
Thinking is the best way to train our brain, lacking in brain stimulation thoughts may cause brain shrinkage.

10. Talking Rarely
Intellectual conversations will promote the efficiency of the brain

------------------------------ ------------------------------ -------------------------------

The main causes of liver damage are:

1. Sleeping too late and waking up too late are main cause.
2. Not urinating in the morning.
3. Too much eating.
4. Skipping breakfast.
5. Consuming too much medication.
6. Consuming too much preservatives, additives, food coloring, and artificial sweetener.
7. Consuming unhealthy cooking oil. As much as possible reduce cooking oil use when frying, which includes even the best cooking oils like olive oil. Do not consume fried foods when you are tired, except if the body is very fit.
8. Consuming raw (overly done) foods also add to the burden of liver.
Veggies should be eaten raw or cooked 3-5 parts. Fried veggies should be finished in one sitting, do not store.

We should prevent this without necessarily spending more. We just have to adopt a good daily lifestyle and eating habits. Maintaining good eating habits and time condition are very important for our bodies to absorb and get rid of unnecessary chemicals according to 'schedule.'

DO TAKE CARE ABOUT YOUR HEALTH.................

New Joint Statement Streamlines Definition of Metabolic Syndrome

2009-10-30T05:07:00.000-07:00

From Heartwire CME

October 12, 2009 — A new joint statement from a number of professional organizations has identified specific criteria for the clinical diagnosis of the metabolic syndrome, tightening up the definition, which previously differed from one organization to the next [1].
The statement, published online October 5, 2009, in Circulation, includes the participation of the International Diabetes Federation (IDF), the National Heart, Lung, and Blood Institute (NHLBI), the World Heart Federation, the International Atherosclerosis Society, and the American Heart Association (AHA) and is an attempt to eliminate some of the confusion regarding how to identify patients with the syndrome.
"This paper represents an attempt to make the definition global," Dr Robert Eckel (University of Colorado, Denver), one of the authors of the new report, told heartwire . "The IDF definition and the [National Cholesterol Education Program Adult Treatment Panel] ATP III definition have been the two that have been utilized most frequently, and now the different organizations--the IDF, the International Atherosclerosis Society, the NHLBI, and the AHA--have all signed on to a single definition. I think that's a step forward in terms of not continuing to confuse people who are working in this field."
Specifically, the new metabolic-syndrome definition streamlines previous differences related to abdominal obesity as defined by measurements in waist circumference. Substantial disparities existed between the previous IDF and the ATP III definitions of what constituted an excessively large waist circumference, by as much as 8 cm between the two groups, but these have been amended. Now, the criteria for elevated waist circumference are based on population- and country-specific definitions, which, although streamlined, do leave some work to be done, said Eckel.
"The problem that still exists is that regional differences around the world may be substantial in terms of what waist circumference confers additional risk for heart disease and diabetes," he said. "The new definition relies on different geographic regions, or different countries, to drill down into their own databases in terms of relating waist circumference to risk." Eckel noted that the IDF previously considered elevations in waist circumference mandatory when defining metabolic syndrome, although the ATP III did not. Now, waist circumference is just one of five criteria that physicians can use when diagnosing the metabolic syndrome. Patients with three of the five criteria--including elevated waist circumference, elevated triglycerides, reduced high-density lipoprotein (HDL)-cholesterol levels, elevated blood pressure, and elevated fasting-glucose levels--are considered to have the syndrome.

Criteria for Clinical Diagnosis of the Metabolic Syndrome

Measure	Categorical cut points
Elevated waist circumference	Population- and country-specific definitions
Elevated triglycerides (drug treatment for elevated triglycerides is an alternate indicator)	>150 mg/dL
Reduced HDL cholesterol (drug treatment for reduced HDL cholesterol is an alternate indicator)	<40 mg/dL for males and <50 mg/dL for females
Elevated blood pressure (drug treatment for elevated blood pressure is an alternate indicator)	Systolic >130 mm Hg and/or diastolic >85 mm Hg
Elevated fasting glucose (drug treatment for elevated glucose is an alternate indicator)	>100 mg/dL

Notably absent from the joint statement is the American Diabetes Association. As reported by heartwire , there are unresolved scientific issues between the ADA and other associations, including the AHA, regarding the metabolic syndrome. Specifically, the ADA, as well as the European Association for the Study of Diabetes (EASD), objected to the manner in which the metabolic syndrome was characterized as a risk factor for heart disease or diabetes, arguing that there was no need to diagnose a patient with the syndrome because emphasis should be placed on aggressively treating the individual risk factors. In 2005, the ADA and EASD issued their own joint statement calling for a critical appraisal of the metabolic syndrome, its designation as a syndrome, and its clinical utility.
To heartwire , Eckel said the IDF, AHA, NHLBI, and others began working on the new metabolic syndrome definition in 2008 and that they simply went ahead without ADA participation. He stressed the metabolic syndrome is not a disease but simply a clustering of risk factors. The original intention of identifying the syndrome was simply to draw clinicians' and the public's attention to the importance of a high-quality lifestyle, and the metabolic syndrome is never meant to be used as a predictor of heart disease or diabetes risk.

Clinical Context

The metabolic syndrome has received significant attention because of its role in disease. In general, patients with this syndrome exhibit a proinflammatory state, and, in addition to high serum levels of triglycerides and low levels of high-density lipoprotein cholesterol, they tend to have high levels of apolipoprotein B and elevations in small low-density lipoprotein particles. All of these factors contribute to doubling the risk for incident cardiovascular disease within 5 to 10 years as well as a 5-fold increase in the risk for incident type 2 diabetes.
Despite the importance of the metabolic syndrome as a risk marker, there remains disagreement regarding the best way to define it. The current scientific statement attempts to clarify the definition of metabolic syndrome and identifies possible future refinements to this definition.

Study Highlights

The primary factors used to define the metabolic syndrome have been atherogenic dyslipidemia, elevated blood pressure, and elevated blood glucose levels.
Whereas some criteria for metabolic syndrome excluded patients with existing type 2 diabetes, current recommendations do not.
The most significant controversy regarding the definition of the metabolic syndrome has been the inclusion of abdominal obesity. It has been required in some recommendations to diagnose the metabolic syndrome, whereas it has served as a nonintegral variable in the diagnosis in other algorithms.
Moreover, the definition of abdominal obesity is challenging. Predictive values for various levels of abdominal obesity for cardiovascular disease and diabetes may differ. Different health systems may define abdominal obesity based on more strict or loose criteria to satisfy pragmatic public health or economic concerns.
Most important, the waist circumference threshold for abdominal obesity varies according to sex and ethnic group. For example, the World Health Organization cutoff values for abdominal obesity for Caucasians are 94 cm or more and 80 cm or more for men and women, respectively. Their respective cutoff values for Asian men and women are 90 cm and 80 cm, and the Japanese Obesity Society defines its respective cutoff values at 85 cm and 90 cm.
The population-specific method of defining abdominal obesity is also limited by a lack of information from large regions, including the Middle East and Africa.
At the same time, the use of common diagnostic thresholds across international borders and types of patients will make the diagnosis of metabolic syndrome easier to understand and treat.
Using recommendations from the different organizations, the authors of the current scientific statement therefore recommend 5 specific criteria and categorical cutoff points to diagnose metabolic syndrome. Patients with at least 3 of these 5 criteria may be considered to have the diagnosis. The criteria are as follows:
- Elevated triglyceride levels or drug treatment of these elevated levels (≥ 150 mg/dL [≥ 1.7 mmol/L])
- Reduced HDL cholesterol levels or drug treatment of these reduced levels (< 40 mg/dL [1.0 mmol/L] in men; < 50 mg/dL [1.3 mmol/L] in women)
- Elevated blood pressure or treatment of hypertension (systolic 130 mm Hg and/or diastolic ≥ 85 mm Hg)
- Elevated fasting glucose levels or treatment with antihyperglycemic medications (≥ 100 mg/dL)
- Elevated waist circumference (population- and country-specific definitions)
New data should emerge, which may help to determine a standard definition for elevated waist circumference, and additional meetings between lead organizations will focus on the development of a single set of diagnostic criteria for metabolic syndrome.

Clinical Implications

The metabolic syndrome is associated with high levels of apolipoprotein B and increases in small low-density lipoprotein particles as well as a 2-fold increase in the risk for incident cardiovascular disease and a 5-fold increase in the risk for incident type 2 diabetes.
The current international guidelines set cutoff points for 4 of the 5 criteria that contribute to the diagnosis of metabolic syndrome, but the variability of waist circumference based on sex and race makes a uniform definition for abdominal obesity difficult.

An Overview of the Expanded Definition and Classification of Hypertension Part 5/5

2009-10-28T07:16:00.000-07:00

Strategies for and the Clinical Implications of Treating Patients Along a Continuum of Global Cardiovascular Risk

The paradigm shift in viewing elevated BP as a marker for hypertension and hypertension as a progressive CVD syndrome has important implications for treating patients in the clinical setting. The risk-based approach proposed by the HWG will lead to reclassifying patients who were previously designated prehypertensive (based on JNC 7 criteria) to either HWG normal or stage 1 hypertension.^[4] In terms of treatment, lowering BP remains an important goal of antihypertensive therapy, yet ultimately the overarching objective is to prevent CV complications.^[9] Treatment of other CV risk factors is therefore equally important. Moreover, CV risk factors, including elevated BP, are not only precipitators, but also continuous pathogenic components at every stage of progression of CVD.^[9] Clinical strategies, therefore, need to focus on detecting and treating patients at risk at every stage along the continuum, from preventing target-organ damage and interrupting CVD progression in patients with early-stage hypertension, to making aggressive efforts to slow further disease progression and avoid CV events in patients with late-stage hypertension.
Evidence for the benefit of antihypertensive treatment in early-stage hypertension (HWG stage 1 or JNC 7 prehypertension category) has only recently become available. The Trial of Preventing Hypertension (TROPHY) study has shown that antihypertensive therapy may help prevent the development of elevated BP levels among individuals with BP lower than 140/90 mm Hg who are at high risk for frank hypertension (due to the presence of multiple CV risk factors).^[17] In line with the HWG paradigm, patients in this study had high-normal SBP/DBP levels of 130-139/85-89 mm Hg at baseline, yet had a strikingly high rate of CV risk factors other than elevated BP.^[17] Among the TROPHY patients, 96% had at least 1 additional CV risk factor, includingvarious measures of dyslipidemia, insulin resistance, and obesity, as well as elevatedhematocrit and heart rate; 81% had 2 or more additional risk factors; and33% had 4 or more additional risk factors. The most prevalent risk factor in thecohort as being overweight.^[2,17] Patients were randomized to receive treatment with the angiotensin receptor blocker candesartan or placebo for 2 years, followed by an additional 2 years of placebo-only therapy; all patients were instructed to make changes in lifestyle to reduce BP throughout the trial.^[17] After 2 years, hypertension haddeveloped in 154 patients in the placebo group and 53 patients in the angiotensin receptor blockergroup, representing a significant 63% relative risk reduction with pharmacotherapy (P < .001). After 4 years, hypertension had developed in 240 patients assigned to placeboand 208 patients assigned to active treatment (relative risk reduction, 15.6%;P < .007). Serious adverse events occurred in 3.5% of patients who received active treatment and in 5.9% of those who received placebo. As the authors noted, the absolute difference between active treatment and placebo at 2 years in TROPHY, 26.8%, is much higher than the 8% absolute difference observed in the Trials of Hypertension Prevention,^[18] the only trial of lifestyle modification with a similar duration, suggesting that drug therapy plus lifestyle modification is more effective than lifestyle modification alone in early hypertension.^[17]
The benefit of treatment with antihypertensive agents in patients classified as normotensive by conventional standards also is supported by the Perindopril Protection Against Recurrent Stroke Study (PROGRESS).^[19] In this study, antihypertensive treatment in subjects without elevated BP (mean BP, 136/79 mm Hg) but with a history of target-organ damage -- in this case, a history of transient ischemic attacks or stroke -- was associated with a significant 27% reduction in the relative risk for stroke compared with placebo (P < .01), similar to the 32% reduction observed in patients designated as hypertensive.^[19] Moreover, intensive BP reduction with combination therapy was associated with better outcomes than less-intensive BP reduction with single-agent therapy, regardless of hypertension status. Because individuals similar to those considered normotensive in PROGRESS would be classified as having stage 2 hypertension (based on the presence of target-organ damage) in the HWG paradigm, results of this study highlight the importance of considering comprehensive risk factor assessment, including the presence of target-organ damage, when defining and staging patients with hypertension.
Whether all individuals with early-stage hypertension, as defined by the HWG, should be treated with antihypertensive therapy requires further study. As the group emphasized in their 2005 report, characterizing hypertension as a complex CV disorder associated with, but not exclusively defined by, high BP is best viewed as a transitional strategy that is intended to generate further clinical research into improved strategies for detecting, treating, and possibly preventing the disease.^[4]

Summary

The key points advanced by the HWG in their updated hypertension position paper are that BP serves as a biomarker for the disease hypertension and, as such, elevated BP is not synonymous with hypertension. Some individuals may exhibit elevated BP in the absence of hypertension, whereas other individuals with the same levels of BP might be classified into different stages of hypertension.^[6] Therefore, for purposes of calculating total CV risk and staging patients as normal or hypertensive, BP should be evaluated in the context of other CV risk factors and disease markers. Ultimately, it is hoped that the risk-based approach to defining and staging hypertension, as proposed by the HWG, will lead to earlier identification of individuals with hypertensive CVD. Preliminary data, such as that described by the TROPHY Investigators, suggest that lowering BP with pharmacologic therapy can prevent or delay the progression of hypertensive CVD even at early stages (ie, HWG stage 1 hypertension/JNC 7 prehypertension). Additional research is necessary to confirm these findings and identify cost-effective methods to detect and measure early CVD markers in clinical practice.

An Overview of the Expanded Definition and Classification of Hypertension Part 4/5

2009-10-25T07:13:00.000-07:00

Clinical Characteristics and Practical Implications of the Proposed Hypertension Categories

A practical clinical interpretation of the revised hypertension categories is shown in Table 6.
Table 6. Clinical Characterization, BP Patterns, and Practical Implications of the Hypertension Algorithm

Hypertension Category	Clinical Characterization	BP Pattern	Practical Implications
Normal	Optimal BP levels	Resting BP levels usually < 120/80 mm Hg	Includes some patients identified as having prehypertension (based on JNC 7 criteria)
Normal	No identifiable early markers of CVD	Occasional BP elevations, even to ≥ 140/90 mm Hg, may occur
Stage 1	Early CVD markers present	BP levels > 115/75 mm Hg	Earliest identifiable stage of hypertensive disease
	Frequently 1 or more CVD risk factors present	BP may be frankly elevated, particularly with environmental stress	Includes individuals with prehypertension (based on JNC 7 criteria) who also have CVD risk factors or early disease markers
	No evidence of target-organ damage
Stage 2	Diffuse disease markers present OR evidence (limited) of early target-organ damage	Sustained resting BP frequently ≥ 140/90 mm Hg, with much higher elevations induced by physiologic or psychologic stressors	Equivalent to JNC 7 stage 1 hypertension
			Indicates progressive disease
			Risk factors, if not attenuated, continue to contribute to progressive target-organ disease
Stage 3	Overt CVD present	Sustained resting BP levels ≥ 140/90 mm Hg usual (untreated or inadequately treated)	Equivalent to JNC 7 stage 2 hypertension
Stage 3		Marked BP elevations to levels > 160/100 mm Hg not uncommon (untreated or inadequately treated)	Includes all individuals with clinical evidence of overt target-organ damage or CVD, or who have sustained a CVD event, regardless of BP levels

BP = blood pressure; CVD = cardiovascular disease; JNC 7 = Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure
In the algorithm, individuals with optimal levels of BP and no identifiable early markers of CVD are categorized as normal. These individuals usually have resting BP levels of 120/80 mm Hg or lower, but BP may be elevated occasionally, even to levels of 140/90 mm Hg or higher.^[6] Given the limits of clinic BP measurements, home BP determinations or 24-hour ambulatory BP recordings may be helpful in identifying patients with more than occasional BP elevations, who may be categorized more appropriately as having stage 1 hypertension.^[16]Because the HWG algorithm does not recognize a prehypertension category, some individuals designated as having prehypertension according to the JNC 7 classification may be considered normal in the paradigm.
The earliest identifiable stage of hypertensive disease, stage 1 hypertension, is characterized by the presence of early CVD markers. Although BP levels are higher than 115/75 mm Hg and may be frankly elevated in patients at this stage, abnormal BP patterns -- including loss of nocturnal dipping, exaggerated responses to exercise or mental stress, and widened pulse pressure -- may provide clearer evidence of the presence of early hypertensive disease.^[4] Although patients should have more than 1 CV risk factor to be included in this category, they should not have any evidence of target-organ damage.
In contrast to stage 1, stage 2 hypertension is characterized by diffuse disease markers and evidence of progressive disease as a consequence of persistent functional and structural changes in BP control mechanisms and in the heart and vasculature. Although patients at this stage frequently have sustained elevations in resting BP levels of 140/90 mm Hg or higher -- with much higher elevations induced by physiologic or psychologic stress -- it is important to recognize that any individual with numerous disease markers or limited evidence of early target-organ damage, such as left ventricular hypertrophy, fits into this category, regardless of BP levels. Methods of detecting or measuring some of the early target-organ damage characteristic of this stage of hypertension are currently limited to specialized or research settings, and further evaluation is needed to determine their potential utility and cost-effectiveness in clinical settings.^[6] Nonetheless, aggressive management of CV risk factors that are identified in patients at this stage may help attenuate the progression of target-organ damage.
Finally, stage 3 hypertension is an advanced stage of the hypertensive continuum, characterized by the presence of overt CVD. Overt hypertensive target-organ disease is often pervasive, and CVD events may have already occurred. If inadequately treated or left untreated, individuals at this stage usually have sustained resting BP levels of 140/90 mm Hg or higher, although marked elevations to levels higher than 160/100 mm Hg are not uncommon.^[6] Regardless of BP levels, however, all individuals with clinical evidence of overt target-organ damage or CVD, as well as those who have already sustained CVD events, are included in this category. Reaching this phase means that damage to target organs, as well as overt cardiorenal disease, has already occurred. As a consequence, CV risk factor modification and treatment of target-organ disease and all identified CVD should be vigorous and sustained.[6

An Overview of the Expanded Definition and Classification of Hypertension Part 3/5

2009-10-22T06:58:00.000-07:00

The+Interrelationship+of+High+Blood+Pressure+and+Other+Cardiovascular+Risk+Factors%0D%0A%0D%0AAnother+key+principle+endorsed+by+the+HWG+is+that+of+the+interrelationship+between+elevated+BP+and+other+CV+risk+factors.+Even+in+patients+with+frank+elevations+in+BP%2C+risk+stratification+based+on+BP+levels+alone+often+underestimates+CV+risk.+This+is+because+above-optimal+BP+levels+rarely+occur+in+isolation%2C+and+patients+seen+in+clinical+practice+frequently+have+multiple+CVD+markers+or+risk+factors+%28eg%2C+overweight%2C+insulin+resistance%2C+dyslipidemia%29+that+point+to+greater+overall+risk.%5B1%2C9-13%5D+What+is+particularly+significant%2C+from+the+perspective+of+defining+hypertension+beyond+BP+thresholds%2C+is+that+many+of+these+disease+processes+are+intimately+interrelated+and+interact+via+common+pathobiologic+processes+involving+oxidative+stress+and+endothelial+dysfunction+%28Figure%29.%5B14%5D+Moreover%2C+the+presence+of+risk+factors+and+disease+markers+defines+the+earliest+stage+in+this+CVD+continuum%2C+well+before+overt+CVD+and+target-organ+damage+can+be+measured+in+the+clinic.%5B14%5D+From+this+perspective%2C+above-optimal+BP+%28a+risk+factor%29+is+not+necessarily+synonymous+with+hypertension+%28a+disease+representative+of+progressive+CVD+and+tissue+injury%29.%5B6%5D+%0D%0A%0D%0AAnother+consequence+of+the+CV+and+renal+pathophysiologic+continuum+is+that+the+complex+interplay+of+risk+factors+and+disease+markers+frequently+may+manifest+as+a+dramatically+higher+CV+risk+than+would+be+expected%2C+based+on+thresholds+for+each+individual+risk+factor+alone.+This+is+highlighted+by+the+particularly+deleterious+condition+known+as+the+cardiometabolic+syndrome%2C+in+which+individual+risk+factors+combine+to+increase+CV+risk+synergistically%2C+rather+than+additively.%5B12%2C15%5D+Ultimately%2C+a+more+clinically+meaningful+assessment+of+CV+risk+can+be+obtained+by+global+assessment+of+a+patient%27s+risk%2C+rather+than+focusing+solely+on+whether+a+patient+has+crossed+a+particular+BP+threshold.%0D%0A%0D%0ATaken+together%2C+this+evidence+suggests+that+it+may+be+more+useful+to+view+BP+as+1%2C+but+not+the+only%2C+biomarker+for+the+disease+hypertension%2C+and+to+view+above-optimal+levels+of+BP+in+an+individual+patient+as+those+that%2C+when+sustained%2C+cause+damage+to+the+vasculature.%5B6%5D+This+forms+the+basis+of+the+revised+definition+of+hypertension%2C+as+shown+in+Table+1.%0D%0A%0D%0A%3Cb%3ETable+1.+Revised+Definition+of+Hypertension+From+Hypertension+Writing+Group+2009%3C%2Fb%3E%0D%0A%E2%80%A2+Hypertension+is+a+progressive+CV+syndrome+arising+from+complex+and+interrelated+etiologies%0D%0A%E2%80%A2+Early+markers+of+the+syndrome+are+often+present+before+BP+elevation+is+sustained%3B+therefore%2C+hypertension+cannot+be+classified+solely+by+discreet+BP+thresholds%0D%0A%E2%80%A2+Progression+is+strongly+associated+with+functional+and+structural+cardiac+and+vascular+abnormalities+that+damage+the+heart%2C+kidneys%2C+brain%2C+vasculature%2C+and+other+organs%2C+and+lead+to+premature+morbidity+and+death%0D%0A%E2%80%A2+Reduction+of+elevated+BP+generally+confers+a+reduction+in+the+risk+for+CV+events.+Note+that+HWG+separates+elevated+BP+%28one+manifestation+of+the+disease%29+from+hypertension+%28the+disease%29%0D%0A%0D%0ABP+%3D+blood+pressure%3B+CV+%3D+cardiovascular%0D%0AFrom+Giles+T%2C+et+al.%5B6%5D+%0D%0A%0D%0ABecause+hypertension+is+defined+by+as+%22a+progressive+cardiovascular+syndrome%2C%22+it+is+clinically+helpful+to+categorize%2C+or+stage%2C+patients+%28Table+2%29%2C+with+each+stage+characterized+by+the+cumulative+presence+or+absence+of+markers+of+hypertensive+CVD+and+evidence+of+target-organ+damage.+This+provides+a+snapshot+of+the+extent+to+which+the+disease+has+advanced+at+a+particular+time.%5B6%5D%0D%0A%0D%0A%3Cb%3ETable+2.+Revised+Definition+and+Classification+of+Hypertension+From+Hypertension+Writing+Group+2009%3C%2Fb%3E+++++++++++++++++++++++++%0D%0A%3Ctable+border%3D%221%22+cellpadding%3D%223%22+cellspacing%3D%221%22%3E%3Ctbody%3E%0D%0A%3Ctr+valign%3D%22top%22%3E+++++++++++++++++++++++++++++++++++++%3Ctd%3E%3Cb%3EClassification%3C%2Fb%3E+++++++++++++++++++++++++++++++++++++%0D%0A%3C%2Ftd%3E++++++++++++++++++++++++++++++++++++++%3Ctd%3E%3Cb%3ENormal%3C%2Fb%3E+++++++++++++++++++++++++++++++++++++%0D%0A%3C%2Ftd%3E++++++++++++++++++++++++++++++++++++++%3Ctd%3E%3Cb%3EStage+1+Hypertension%3C%2Fb%3E+++++++++++++++++++++++++++++++++++++%0D%0A%3C%2Ftd%3E++++++++++++++++++++++++++++++++++++++%3Ctd%3E%3Cb%3EStage+2+Hypertension%3C%2Fb%3E+++++++++++++++++++++++++++++++++++++%0D%0A%3C%2Ftd%3E++++++++++++++++++++++++++++++++++++++%3Ctd%3E%3Cb%3EStage+3+Hypertension%3C%2Fb%3E+++++++++++++++++++++++++++++++++++++%0D%0A%3C%2Ftd%3E++++++++++++++++++++++++++++++++++%3C%2Ftr%3E%0D%0A%3Ctr+valign%3D%22top%22%3E+++++++++++++++++++++++++++++++++++++%3Ctd%3EDescriptive+category%0D%0A%3C%2Ftd%3E++++++++++++++++++++++++++++++++++++++%3Ctd+align%3D%22center%22%3ENormal+BP+or+rare+BP+elevations%0D%0AAND%0D%0Ano+identifiable+CVD%0D%0A%3C%2Ftd%3E++++++++++++++++++++++++++++++++++++++%3Ctd+align%3D%22center%22%3EOccasional+or+intermittent+BP+elevations%0D%0AOR%0D%0Aearly+CVD%0D%0A%3C%2Ftd%3E++++++++++++++++++++++++++++++++++++++%3Ctd+align%3D%22center%22%3ESustained+BP+elevations%0D%0AOR%0D%0Aprogressive+CVD%0D%0A%3C%2Ftd%3E++++++++++++++++++++++++++++++++++++++%3Ctd+align%3D%22center%22%3EMarked+and+sustained+BP+elevations%0D%0AOR%0D%0Aadvanced+CVD%0D%0A%3C%2Ftd%3E++++++++++++++++++++++++++++++++++%3C%2Ftr%3E%0D%0A%3Ctr+valign%3D%22top%22%3E+++++++++++++++++++++++++++++++++++++%3Ctd%3ECardiovascular+risk+factors+%0D%0A%28see+Table+3%29%0D%0A%3C%2Ftd%3E++++++++++++++++++++++++++++++++++++++%3Ctd+align%3D%22center%22%3ENone+or+few%0D%0A%3C%2Ftd%3E++++++++++++++++++++++++++++++++++++++%3Ctd+align%3D%22center%22%3ESeveral+risk+factors+present%0D%0A%3C%2Ftd%3E++++++++++++++++++++++++++++++++++++++%3Ctd+align%3D%22center%22%3EMany+risk+factors+present%0D%0A%3C%2Ftd%3E++++++++++++++++++++++++++++++++++++++%3Ctd+align%3D%22center%22%3EMany+risk+factors+present%0D%0A%3C%2Ftd%3E++++++++++++++++++++++++++++++++++%3C%2Ftr%3E%0D%0A%3Ctr+valign%3D%22top%22%3E+++++++++++++++++++++++++++++++++++++%3Ctd%3EEarly+disease+markers+++++++++++++%0D%0A%28see+Table+4%29%0D%0A%3C%2Ftd%3E++++++++++++++++++++++++++++++++++++++%3Ctd+align%3D%22center%22%3ENone%0D%0A%3C%2Ftd%3E++++++++++++++++++++++++++++++++++++++%3Ctd+align%3D%22center%22%3EUsually+present%0D%0A%3C%2Ftd%3E++++++++++++++++++++++++++++++++++++++%3Ctd+align%3D%22center%22%3EOvertly+present%0D%0A%3C%2Ftd%3E++++++++++++++++++++++++++++++++++++++%3Ctd+align%3D%22center%22%3EOvertly+present+with+progression%0D%0A%3C%2Ftd%3E++++++++++++++++++++++++++++++++++%3C%2Ftr%3E%0D%0A%3Ctr+valign%3D%22top%22%3E+++++++++++++++++++++++++++++++++++++%3Ctd%3ETarget-organ+disease+%0D%0A%28see+Table+5%29%0D%0A%3C%2Ftd%3E++++++++++++++++++++++++++++++++++++++%3Ctd+align%3D%22center%22%3ENone%0D%0A%3C%2Ftd%3E++++++++++++++++++++++++++++++++++++++%3Ctd+align%3D%22center%22%3ENone%0D%0A%3C%2Ftd%3E++++++++++++++++++++++++++++++++++++++%3Ctd+align%3D%22center%22%3EEarly+signs+present%0D%0A%3C%2Ftd%3E++++++++++++++++++++++++++++++++++++++%3Ctd+align%3D%22center%22%3EOvertly+present+with+or+without+CVD+events%0D%0A%3C%2Ftd%3E++++++++++++++++++++++++++++++++++%3C%2Ftr%3E%0D%0A%3C%2Ftbody%3E+++++++++++++++++++++++++%3C%2Ftable%3E%0D%0A%3Ci%3EBP+%3D+blood+pressure%3B+CVD+%3D+cardiovascular+disease%3C%2Fi%3E+++++++++++++++++++++++++++++%0D%0AFrom+Giles+T%2C+et+al.%3Csup%3E%3Ca+href%3D%22javascript%3Anewshowcontent%28%27active%27%2C%27references%27%29%3B%22%3E%5B6%5D%3C%2Fa%3E%3C%2Fsup%3E%0D%0A%0D%0AIn+the+broadest+sense%2C+individuals+are+classified+as+either+normal+or+hypertensive+based+on+their+CV+status+%28ie%2C+the+absence+or+presence+of+identifiable+CVD%29%2C+regardless+of+their+BP+pattern.+The+stages+within+the+hypertension+category+are+further+refined%2C+based+on+BP+patterns+or+the+extent+of+CVD+%28early%2C+advanced%2C+or+progressive%29.+Each+hypertension+stage+is+further+characterized+by+the+cumulative+presence+or+absence+of+risk+factors+for+CVD+%28Table+3%29%3Bmarkers+of+hypertensive+CVD%2C+such+as+microalbuminuria+or+mild+left+ventricular+hypertrophy+%28Table+4%29%3B+and+evidence+of+target-organ+damage%2C+such+as+frank+albuminuria+or+moderate-to-severe+left+ventricular+hypertrophy+%28Table+5%29.%3Csup%3E%3Ca+href%3D%22javascript%3Anewshowcontent%28%27active%27%2C%27references%27%29%3B%22%3E%5B6%5D%3C%2Fa%3E%3C%2Fsup%3E+The+occurrence+of+a+major+cardiac+event+clearly+places+the+progression+of+hypertensive+CVD+at+a+more+advanced+stage.%3Csup%3E%3Ca+href%3D%22javascript%3Anewshowcontent%28%27active%27%2C%27references%27%29%3B%22%3E%5B6%5D%3C%2Fa%3E%3C%2Fsup%3E%0D%0A%0D%0A%3Cb%3ETable+3.+Cardiovascular+Risk+Factors%3C%2Fb%3E+++++++++++++++++++++++++%0D%0A%3Ctable+border%3D%221%22+cellpadding%3D%223%22+cellspacing%3D%221%22%3E%3Ctbody%3E%0D%0A%3Ctr+valign%3D%22top%22%3E+++++++++++++++++++++++++++++++++++++%3Ctd%3EIncreasing+age%0D%0A%3C%2Ftd%3E++++++++++++++++++++++++++++++++++%3C%2Ftr%3E%0D%0A%3Ctr+valign%3D%22top%22%3E+++++++++++++++++++++++++++++++++++++%3Ctd%3EElevated+BP%3Csup%3Ea%3C%2Fsup%3E+++++++++++++++++++++++++++++++++++++%0D%0A%3C%2Ftd%3E++++++++++++++++++++++++++++++++++%3C%2Ftr%3E%0D%0A%3Ctr+valign%3D%22top%22%3E+++++++++++++++++++++++++++++++++++++%3Ctd%3EHigh+heart+rate%0D%0A%3C%2Ftd%3E++++++++++++++++++++++++++++++++++%3C%2Ftr%3E%0D%0A%3Ctr+valign%3D%22top%22%3E+++++++++++++++++++++++++++++++++++++%3Ctd%3EOverweight%2Fobesity%0D%0A%3C%2Ftd%3E++++++++++++++++++++++++++++++++++%3C%2Ftr%3E%0D%0A%3Ctr+valign%3D%22top%22%3E+++++++++++++++++++++++++++++++++++++%3Ctd%3E%26nbsp%3B%26nbsp%3B%26nbsp%3B+%E2%88%92+Increased+BMI%0D%0A%3C%2Ftd%3E++++++++++++++++++++++++++++++++++%3C%2Ftr%3E%0D%0A%3Ctr+valign%3D%22top%22%3E+++++++++++++++++++++++++++++++++++++%3Ctd%3E%26nbsp%3B%26nbsp%3B%26nbsp%3B+%E2%88%92+Central+obesity%0D%0A%3C%2Ftd%3E++++++++++++++++++++++++++++++++++%3C%2Ftr%3E%0D%0A%3Ctr+valign%3D%22top%22%3E+++++++++++++++++++++++++++++++++++++%3Ctd%3E%26nbsp%3B%26nbsp%3B%26nbsp%3B+%E2%88%92+Increased+abdominal+circumference%0D%0A%3C%2Ftd%3E++++++++++++++++++++++++++++++++++%3C%2Ftr%3E%0D%0A%3Ctr+valign%3D%22top%22%3E+++++++++++++++++++++++++++++++++++++%3Ctd%3E%26nbsp%3B%26nbsp%3B%26nbsp%3B+%E2%88%92+Increased+abdominal+adiposity+%28waist-to-hip+ratio%29%3Csup%3Ea%3C%2Fsup%3E+++++++++++++++++++++++++++++++++++++%0D%0A%3C%2Ftd%3E++++++++++++++++++++++++++++++++++%3C%2Ftr%3E%0D%0A%3Ctr+valign%3D%22top%22%3E+++++++++++++++++++++++++++++++++++++%3Ctd%3EDyslipidemia%0D%0A%3C%2Ftd%3E++++++++++++++++++++++++++++++++++%3C%2Ftr%3E%0D%0A%3Ctr+valign%3D%22top%22%3E+++++++++++++++++++++++++++++++++++++%3Ctd%3E%26nbsp%3B%26nbsp%3B%26nbsp%3B+%E2%88%92+Elevated+LDL+or+non-HDL%3Csup%3Eb%3C%2Fsup%3E+cholesterol%0D%0A%3C%2Ftd%3E++++++++++++++++++++++++++++++++++%3C%2Ftr%3E%0D%0A%3Ctr+valign%3D%22top%22%3E+++++++++++++++++++++++++++++++++++++%3Ctd%3E%26nbsp%3B%26nbsp%3B%26nbsp%3B+%E2%88%92+Low+HDL+cholesterol%3Csup%3Ea%3C%2Fsup%3E+++++++++++++++++++++++++++++++++++++%0D%0A%3C%2Ftd%3E++++++++++++++++++++++++++++++++++%3C%2Ftr%3E%0D%0A%3Ctr+valign%3D%22top%22%3E+++++++++++++++++++++++++++++++++++++%3Ctd%3E%26nbsp%3B%26nbsp%3B%26nbsp%3B+%E2%88%92+Elevated+triglycerides%3Csup%3Ea%3C%2Fsup%3E+++++++++++++++++++++++++++++++++++++%0D%0A%3C%2Ftd%3E++++++++++++++++++++++++++++++++++%3C%2Ftr%3E%0D%0A%3Ctr+valign%3D%22top%22%3E+++++++++++++++++++++++++++++++++++++%3Ctd%3EElevated+blood+glucose%2C+insulin+resistance%2C+or+diabetes+mellitus%3Csup%3Ea%3C%2Fsup%3E+++++++++++++++++++++++++++++++++++++%0D%0A%3C%2Ftd%3E++++++++++++++++++++++++++++++++++%3C%2Ftr%3E%0D%0A%3Ctr+valign%3D%22top%22%3E+++++++++++++++++++++++++++++++++++++%3Ctd%3EChronic+kidney+disease%0D%0A%3C%2Ftd%3E++++++++++++++++++++++++++++++++++%3C%2Ftr%3E%0D%0A%3Ctr+valign%3D%22top%22%3E+++++++++++++++++++++++++++++++++++++%3Ctd%3ESmoking%0D%0A%3C%2Ftd%3E++++++++++++++++++++++++++++++++++%3C%2Ftr%3E%0D%0A%3Ctr+valign%3D%22top%22%3E+++++++++++++++++++++++++++++++++++++%3Ctd%3EFamily+history+of+premature+CVD+%28age+%26lt%3B+50+yr+in+men%2C+%2C+%%3B+60+yr+in+women%29%0D%0A%3C%2Ftd%3E++++++++++++++++++++++++++++++++++%3C%2Ftr%3E%0D%0A%3Ctr+valign%3D%22top%22%3E+++++++++++++++++++++++++++++++++++++%3Ctd%3ESedentary+lifestyle%0D%0A%3C%2Ftd%3E++++++++++++++++++++++++++++++++++%3C%2Ftr%3E%0D%0A%3Ctr+valign%3D%22top%22%3E+++++++++++++++++++++++++++++++++++++%3Ctd%3EPsychosocial+stressors%0D%0A%3C%2Ftd%3E++++++++++++++++++++++++++++++++++%3C%2Ftr%3E%0D%0A%3Ctr+valign%3D%22top%22%3E+++++++++++++++++++++++++++++++++++++%3Ctd%3EElevated+hs-CRP%0D%0A%3C%2Ftd%3E++++++++++++++++++++++++++++++++++%3C%2Ftr%3E%0D%0A%3C%2Ftbody%3E+++++++++++++++++++++++++%3C%2Ftable%3E%0D%0A%3Ci%3EBMI+%3D+body+mass+index%3B+BP+%3D+blood+pressure%3B+CVD+%3D+cardiovascular+disease%3B+HDL+%3D+high-density+lipoprotein%3B+hs-CRP+%3D+high-sensitivity+C-reactive+protein%3B+LDL+%3D+low-density+lipoprotein+%3C%2Fi%3E+++++++++++++++++++++++++++++%0D%0A%3Csup%3Ea%3C%2Fsup%3EComponents+of+the+metabolic+syndrome%0D%0A%3Csup%3Eb%3C%2Fsup%3ENon-HDL+cholesterol+%3D+total+cholesterol+minus+HDL+cholesterol%0D%0A%3Cb%3ETable+4.+Early+Markers+of+Hypertensive+Cardiovascular+Disease%3C%2Fb%3E+++++++++++++++++++++++++%0D%0A%3Ctable+border%3D%221%22+cellpadding%3D%223%22+cellspacing%3D%221%22%3E%3Ctbody%3E%0D%0A%3Ctr+valign%3D%22top%22%3E+++++++++++++++++++++++++++++++++++++%3Ctd%3E%3Cb%3ESystem%3C%2Fb%3E+++++++++++++++++++++++++++++++++++++%0D%0A%3C%2Ftd%3E++++++++++++++++++++++++++++++++++++++%3Ctd%3E%3Cb%3EPhysiologic+Alteration%3C%2Fb%3E+++++++++++++++++++++++++++++++++++++%0D%0A%3C%2Ftd%3E++++++++++++++++++++++++++++++++++%3C%2Ftr%3E%0D%0A%3Ctr+valign%3D%22top%22%3E+++++++++++++++++++++++++++++++++++++%3Ctd+rowspan%3D%225%22%3EBlood+pressure%0D%0A%3C%2Ftd%3E++++++++++++++++++++++++++++++++++%3C%2Ftr%3E%0D%0A%3Ctr+valign%3D%22top%22%3E+++++++++++++++++++++++++++++++++++++%3Ctd%3ELoss+of+nocturnal+BP+dipping%0D%0A%3C%2Ftd%3E++++++++++++++++++++++++++++++++++%3C%2Ftr%3E%0D%0A%3Ctr+valign%3D%22top%22%3E+++++++++++++++++++++++++++++++++++++%3Ctd%3EExaggerated+BP+responses+to+exercise+or+mental+stress%0D%0A%3C%2Ftd%3E++++++++++++++++++++++++++++++++++%3C%2Ftr%3E%0D%0A%3Ctr+valign%3D%22top%22%3E+++++++++++++++++++++++++++++++++++++%3Ctd%3ESalt+sensitivity%0D%0A%3C%2Ftd%3E++++++++++++++++++++++++++++++++++%3C%2Ftr%3E%0D%0A%3Ctr+valign%3D%22top%22%3E+++++++++++++++++++++++++++++++++++++%3Ctd%3EWidened+pulse+pressure%0D%0A%3C%2Ftd%3E++++++++++++++++++++++++++++++++++%3C%2Ftr%3E%0D%0A%3Ctr+valign%3D%22top%22%3E+++++++++++++++++++++++++++++++++++++%3Ctd+rowspan%3D%225%22%3ECardiac%0D%0A%3C%2Ftd%3E++++++++++++++++++++++++++++++++++%3C%2Ftr%3E%0D%0A%3Ctr+valign%3D%22top%22%3E+++++++++++++++++++++++++++++++++++++%3Ctd%3ELeft+ventricular+hypertrophy+%28mild%29%0D%0A%3C%2Ftd%3E++++++++++++++++++++++++++++++++++%3C%2Ftr%3E%0D%0A%3Ctr+valign%3D%22top%22%3E+++++++++++++++++++++++++++++++++++++%3Ctd%3EIncreased+atrial+filling+pressure%0D%0A%3C%2Ftd%3E++++++++++++++++++++++++++++++++++%3C%2Ftr%3E%0D%0A%3Ctr+valign%3D%22top%22%3E+++++++++++++++++++++++++++++++++++++%3Ctd%3EDecreased+diastolic+relaxation%0D%0A%3C%2Ftd%3E++++++++++++++++++++++++++++++++++%3C%2Ftr%3E%0D%0A%3Ctr+valign%3D%22top%22%3E+++++++++++++++++++++++++++++++++++++%3Ctd%3EIncreased+natriuretic+peptide%0D%0A%3C%2Ftd%3E++++++++++++++++++++++++++++++++++%3C%2Ftr%3E%0D%0A%3Ctr+valign%3D%22top%22%3E+++++++++++++++++++++++++++++++++++++%3Ctd+rowspan%3D%223%22%3ERenal%0D%0A%3C%2Ftd%3E++++++++++++++++++++++++++++++++++%3C%2Ftr%3E%0D%0A%3Ctr+valign%3D%22top%22%3E+++++++++++++++++++++++++++++++++++++%3Ctd%3EMicroalbuminuria+%28urinary+albumin+excretion+of+30-300+mg%2Fday%29%3Csup%3Ea%3C%2Fsup%3E+++++++++++++++++++++++++++++++++++++%0D%0A%3C%2Ftd%3E++++++++++++++++++++++++++++++++++%3C%2Ftr%3E%0D%0A%3Ctr+valign%3D%22top%22%3E+++++++++++++++++++++++++++++++++++++%3Ctd%3EReduced+estimated+GFR+%2860-90+mL%2Fmin%29%0D%0A%3C%2Ftd%3E++++++++++++++++++++++++++++++++++%3C%2Ftr%3E%0D%0A%3Ctr+valign%3D%22top%22%3E%3C%2Ftr%3E%0D%0A%3Ctr+valign%3D%22top%22%3E+++++++++++++++++++++++++++++++++++++%3Ctd+rowspan%3D%226%22%3ECerebrovascular%0D%0A%3C%2Ftd%3E++++++++++++++++++++++++++++++++++%3C%2Ftr%3E%0D%0A%3Ctr+valign%3D%22top%22%3E+++++++++++++++++++++++++++++++++++++%3Ctd%3EStroke%0D%0A%3C%2Ftd%3E++++++++++++++++++++++++++++++++++%3C%2Ftr%3E%0D%0A%3Ctr+valign%3D%22top%22%3E+++++++++++++++++++++++++++++++++++++%3Ctd%3ETransient+ischemic+attack%0D%0A%3C%2Ftd%3E++++++++++++++++++++++++++++++++++%3C%2Ftr%3E%0D%0A%3Ctr+valign%3D%22top%22%3E+++++++++++++++++++++++++++++++++++++%3Ctd%3EDecreased+cognitive+function%0D%0A%3C%2Ftd%3E++++++++++++++++++++++++++++++++++%3C%2Ftr%3E%0D%0A%3Ctr+valign%3D%22top%22%3E+++++++++++++++++++++++++++++++++++++%3Ctd%3EDementia%0D%0A%3C%2Ftd%3E++++++++++++++++++++++++++++++++++%3C%2Ftr%3E%0D%0A%3Ctr+valign%3D%22top%22%3E+++++++++++++++++++++++++++++++++++++%3Ctd%3ELoss+of+vision%0D%0A%3C%2Ftd%3E++++++++++++++++++++++++++++++++++%3C%2Ftr%3E%0D%0A%3C%2Ftbody%3E+++++++++++++++++++++++++%3C%2Ftable%3E%0D%0A%3Ci%3EBP+%3D+blood+pressure%3B+GFR+%3D+glomerular+filtration+rate%3C%2Fi%3E+++++++++++++++++++++++++++++%0D%0A%3Csup%3Ea%3C%2Fsup%3EAlso+a+marker+of+microcirculatory+disease%0D%0A%3Cb%3ETable+5.+Hypertensive+Target-Organ+Damage+and+Overt+Cardiovascular+Disease%3C%2Fb%3E+++++++++++++++++++++++++%0D%0A%3Ctable+border%3D%221%22+cellpadding%3D%223%22+cellspacing%3D%221%22%3E%3Ctbody%3E%0D%0A%3Ctr+valign%3D%22top%22%3E+++++++++++++++++++++++++++++++++++++%3Ctd%3E%3Cb%3ESystem%3C%2Fb%3E+++++++++++++++++++++++++++++++++++++%0D%0A%3C%2Ftd%3E++++++++++++++++++++++++++++++++++++++%3Ctd%3E%3Cb%3EEvidence+of+Target-organ+Damage+and+Cardiovascular+Disease%3C%2Fb%3E+++++++++++++++++++++++++++++++++++++%0D%0A%3C%2Ftd%3E++++++++++++++++++++++++++++++++++%3C%2Ftr%3E%0D%0A%3Ctr+valign%3D%22top%22%3E+++++++++++++++++++++++++++++++++++++%3Ctd+rowspan%3D%227%22%3ECardiac%0D%0A%3C%2Ftd%3E++++++++++++++++++++++++++++++++++%3C%2Ftr%3E%0D%0A%3Ctr+valign%3D%22top%22%3E+++++++++++++++++++++++++++++++++++++%3Ctd%3ELeft+ventricular+hypertrophy+%28moderate+to+severe%29%0D%0A%3C%2Ftd%3E++++++++++++++++++++++++++++++++++%3C%2Ftr%3E%0D%0A%3Ctr+valign%3D%22top%22%3E+++++++++++++++++++++++++++++++++++++%3Ctd%3ESystolic+or+diastolic+cardiac+dysfunction%0D%0A%3C%2Ftd%3E++++++++++++++++++++++++++++++++++%3C%2Ftr%3E%0D%0A%3Ctr+valign%3D%22top%22%3E+++++++++++++++++++++++++++++++++++++%3Ctd%3ESymptomatic+heart+failure%0D%0A%3C%2Ftd%3E++++++++++++++++++++++++++++++++++%3C%2Ftr%3E%0D%0A%3Ctr+valign%3D%22top%22%3E+++++++++++++++++++++++++++++++++++++%3Ctd%3EMyocardial+infarction%0D%0A%3C%2Ftd%3E++++++++++++++++++++++++++++++++++%3C%2Ftr%3E%0D%0A%3Ctr+valign%3D%22top%22%3E+++++++++++++++++++++++++++++++++++++%3Ctd%3EAngina+pectoris%0D%0A%3C%2Ftd%3E++++++++++++++++++++++++++++++++++%3C%2Ftr%3E%0D%0A%3Ctr+valign%3D%22top%22%3E+++++++++++++++++++++++++++++++++++++%3Ctd%3EIschemic+heart+disease+or+prior+revascularization%0D%0A%3C%2Ftd%3E++++++++++++++++++++++++++++++++++%3C%2Ftr%3E%0D%0A%3Ctr+valign%3D%22top%22%3E+++++++++++++++++++++++++++++++++++++%3Ctd+rowspan%3D%224%22%3EVascular%0D%0A%3C%2Ftd%3E++++++++++++++++++++++++++++++++++%3C%2Ftr%3E%0D%0A%3Ctr+valign%3D%22top%22%3E+++++++++++++++++++++++++++++++++++++%3Ctd%3EPeripheral+arterial+disease%0D%0A%3C%2Ftd%3E++++++++++++++++++++++++++++++++++%3C%2Ftr%3E%0D%0A%3Ctr+valign%3D%22top%22%3E+++++++++++++++++++++++++++++++++++++%3Ctd%3ECarotid+arterial+disease%0D%0A%3C%2Ftd%3E++++++++++++++++++++++++++++++++++%3C%2Ftr%3E%0D%0A%3Ctr+valign%3D%22top%22%3E+++++++++++++++++++++++++++++++++++++%3Ctd%3EAortic+aneurysm%0D%0A%3C%2Ftd%3E++++++++++++++++++++++++++++++++++%3C%2Ftr%3E%0D%0A%3Ctr+valign%3D%22top%22%3E+++++++++++++++++++++++++++++++++++++%3Ctd+rowspan%3D%223%22%3ERenal%0D%0A%3C%2Ftd%3E++++++++++++++++++++++++++++++++++%3C%2Ftr%3E%0D%0A%3Ctr+valign%3D%22top%22%3E+++++++++++++++++++++++++++++++++++++%3Ctd%3EAlbuminuria+%28urinary+albumin+excretion+%26gt%3B+300+mg%2Fday%29%0D%0A%3C%2Ftd%3E++++++++++++++++++++++++++++++++++%3C%2Ftr%3E%0D%0A%3Ctr+valign%3D%22top%22%3E+++++++++++++++++++++++++++++++++++++%3Ctd%3EChronic+kidney+disease+%28estimated+GFR+%26lt%3B+60+mL%2Fmin%29+or+ESRD%0D%0A%3C%2Ftd%3E++++++++++++++++++++++++++++++++++%3C%2Ftr%3E%0D%0A%3Ctr+valign%3D%22top%22%3E%3C%2Ftr%3E%0D%0A%3Ctr+valign%3D%22top%22%3E+++++++++++++++++++++++++++++++++++++%3Ctd+rowspan%3D%226%22%3ECerebrovascular%0D%0A%3C%2Ftd%3E++++++++++++++++++++++++++++++++++%3C%2Ftr%3E%0D%0A%3Ctr+valign%3D%22top%22%3E+++++++++++++++++++++++++++++++++++++%3Ctd%3EStroke%0D%0A%3C%2Ftd%3E++++++++++++++++++++++++++++++++++%3C%2Ftr%3E%0D%0A%3Ctr+valign%3D%22top%22%3E+++++++++++++++++++++++++++++++++++++%3Ctd%3ETransient+ischemic+attack%0D%0A%3C%2Ftd%3E++++++++++++++++++++++++++++++++++%3C%2Ftr%3E%0D%0A%3Ctr+valign%3D%22top%22%3E+++++++++++++++++++++++++++++++++++++%3Ctd%3EDecreased+cognitive+function%0D%0A%3C%2Ftd%3E++++++++++++++++++++++++++++++++++%3C%2Ftr%3E%0D%0A%3Ctr+valign%3D%22top%22%3E+++++++++++++++++++++++++++++++++++++%3Ctd%3EDementia%0D%0A%3C%2Ftd%3E++++++++++++++++++++++++++++++++++%3C%2Ftr%3E%0D%0A%3Ctr+valign%3D%22top%22%3E+++++++++++++++++++++++++++++++++++++%3Ctd%3ELoss+of+vision%0D%0A%3C%2Ftd%3E++++++++++++++++++++++++++++++++++%3C%2Ftr%3E%0D%0A%3C%2Ftbody%3E+++++++++++++++++++++++++%3C%2Ftable%3E%0D%0A%3Ci%3EESRD+%3D+end-stage+renal+disease%3B+GFR+%3D+glomerular+filtration+rate+%3C%2Fi%3E%0D%0A

An Overview of the Expanded Definition and Classification of Hypertension Part 2/5

2009-10-19T06:55:00.000-07:00

Blood Pressure as a Biomarker for Hypertension

The concept of elevated BP as a disease marker for hypertension, rather than its cause, is supported by multiple lines of evidence suggesting that the risk for renovascular and CV sequelae may be higher than expected in the presence of normal or near-normal BP in some patients, or, conversely, lower than expected in the presence of above-normal BP in others. This view is based, in part, on the physiologically dynamic nature of BP, in which tissue perfusion is matched with metabolic demands in a complex, ever-changing manner that depends on the coordinated activity of numerous mechanisms involved in hemostasis, including the sympathetic nervous system, the renin-angiotensin system, and the vasodilatory system (eg, prostaglandins and nitric oxide).[4] According to this perspective, optimal BP can vary among individuals and within the same person, depending on hemodynamic circumstances. Sporadic BP elevations may occur in individuals who have no evidence of early CVD.[2] Conversely, because adverse CV and renal outcomes increase across all BP values, hypertension-related morbidity and mortality can occur even at BP levels considered normal by conventional standards. The significant proportions of myocardial infarctions and strokes that occur in patients who have only slight BP elevation, or even normal BP, adds weight to this argument.[7]

Perhaps the most convincing evidence against using BP thresholds to define hypertension is that there is no threshold of BP above 115/70 mm Hg that identifies CV risk -- that is, risk is linear and doubles for each 20/10 mm Hg increase in BP.[2] As a consequence of the dynamic nature of BP, it may be more clinically relevant to use BP patterns, rather than discrete BP thresholds as measured in the clinic, when assessing CV risk in an individual patient. Thus, the HWG places particular attention on ambulatory BP and the contribution of systolic BP (SBP) and pulse pressure (the difference between SBP and diastolic BP [DBP]) to risk, because these are widely considered to be more accurate markers of CV risk than is office DBP, particularly in older patients.[5,8]

An Overview of the Expanded Definition and Classification of Hypertension Part 1/5

2009-10-16T06:51:00.000-07:00

For the medical colleagues out there very aching to know all about the NEW JNC 8, these next few posts in the following days are for you..

Introduction

As epidemiologic and clinical data regarding the relationship between blood pressure (BP) and the risk for cardiovascular disease (CVD) have accumulated, a pronounced shift has taken place in how the disease of hypertension is viewed and defined. Cardiovascular (CV) risk has been found to be elevated at BP levels previously considered normal; in some cases, sporadic elevations in BP levels may be physiologically benign and not associated with additional CVD risk.[1-3] As a consequence, many hypertension experts consider elevated BP at its core a disease marker, rather than a cause of hypertension. Moreover, elevated BP, as 1 marker of CVD, frequently coexists with other equally compelling disease markers.[2] Elevated BP should not, therefore, be viewed or treated in isolation, but considered in the context of whole patient care, which takes into account the presence of other risk factors and disease markers for CVD to achieve a more comprehensive, or global, assessment of CV risk.

With these points in mind, in 2005, the Hypertension Writing Group (HWG), a national group of hypertension specialists, proposed a new definition of hypertension as "a progressive cardiovascular syndrome, the early markers of which may be present even before BP elevations are observed."[4] The stated goal of the new definition was to identify individuals at risk for CVD at an earlier point in the disease process, as well as to avoid labeling persons as hypertensive who are at low risk for CVD.[4] Viewed from this perspective, the HWG believed that threshold-based classification systems of hypertension, such as that endorsed in the Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure (JNC 7),[5] while serving as tools to identify patients across a broad range of CVD risk, may lead to underestimation or overestimation of clinical risk within individual patients. In either case, the presence or absence of other disease markers or risk factors, the coexistence of target-organ damage, or both can be used to risk-stratify patients with hypertension more accurately.

To simplify risk stratification and align it more closely with clinical practice, the HWG proposed classifying all patients as either normal or hypertensive (eliminating the prehypertension category proposed in JNC 7), with hypertension classified into stage 1, stage 2, or stage 3.[4] Because the CV syndrome represented by hypertension may be present even when BP falls within the normal category by conventional standards, the risk categories created by the HWG focus not on BP levels per se, but on the presence of deleterious BP patterns or the presence of CVD. Stages of hypertension are further categorized based on the presence of risk factors for early, advanced, or progressive CVD, as well as by other CVD markers (classified as BP, cardiac, vascular, renal, and retinal changes) and target-organ damage (classified as cardiac, vascular, renal, and cerebrovascular).[4]

Beyond the goal of providing a more clinically relevant assessment of global CV risk in clinical practice, this paradigm shift served to focus attention on the enormous unmet need regarding prevention and optimal treatment of hypertension across a spectrum of fields, from basic research and drug development to patient education and clinical management.[4] Two critical areas of research in particular -- the development of specific and sensitive cost-effective tests that can detect early CVD markers in the clinical setting, and the development of strategies to slow or prevent the onset of target-organ damage or overt CVD by treating early vascular derangements -- may benefit from being examined within the context of the categories for hypertension.

Recently, the HWG further refined and updated the definition and classification of hypertension.[6] This article reviews the revised definition and classification scheme and the implications for clinical practice. As the authors stressed, however, while definitions of disease are useful for detection, management, research, and education, definitions alone do not constitute recommendations for treatment. In the latter case, the initiation of treatment should be individualized and guided by CV risk, rather than BP thresholds.[1]

Warfarin Use in Patients With End-Stage Renal Disease May Increase Stroke Risk

2009-10-13T00:54:00.000-07:00

If you happen to be taking coumadin and had been told that you also have kidney disease, this should be read...

September 3, 2009 — Use of warfarin as chemoprophylaxis in patients with atrial fibrillation and end-stage renal disease (ESRD) may paradoxically increase stroke risk, according to the results of a cohort study reported in the August 27 Online First issue of the Journal of the American Society of Nephrology.

"Use of warfarin, clopidogrel, or aspirin associates with mortality among patients with ESRD, but the risk-benefit ratio may depend on underlying comorbidities," write Kevin E. Chan, MD, from Fresenius Medical Care NA in Waltham, Massachusetts, and colleagues. "We previously reported a significant excess mortality associated with anticoagulation and/or antiplatelet use in a large, heterogeneous population of incident hemodialysis (HD) patients."

The purpose of this follow-up study was to evaluate the potential risk-benefit ratio of warfarin, clopidogrel, and aspirin specifically in dialysis patients with coexisting atrial fibrillation. The investigators looked at the association between these medications and new stroke, mortality, and hospitalization in a retrospective cohort of 1671 patients with preexisting atrial fibrillation who were receiving hemodialysis. Average follow-up of patient outcomes was 1.6 years from the time dialysis was started.

Patients receiving warfarin therapy had a significantly increased risk for new stroke vs patients not taking warfarin (hazard ratio [HR], 1.93; 95% confidence interval [CI], 1.29 - 2.90). Risk for new stroke was not associated with clopidogrel or aspirin use.

There appeared to be a dose-response relationship between the degree of anticoagulation and new stroke in patients receiving warfarin, based on an analysis using international normnormed ratio (INR; P = .02 for trend). Compared with nonusers of warfarin, those users who had no INR monitoring in the first 90 days of dialysis had the highest risk for stroke (HR, 2.79; 95% CI, 1.65 - 4.70). Use of warfarin was not statistically significantly associated with any increases in all-cause mortality or hospitalization rates.

"Warfarin use among patients with both ESRD and atrial fibrillation associates with an increased risk for stroke," the study authors write. "The risk is greatest in warfarin users who do not receive in-facility INR monitoring."

Limitations of this study include retrospective design, potential misclassification bias, confounding by indication, survivorship bias, ascertainment bias, and selection bias from missing data.

"Before definitive conclusions can be drawn, large, prospective, randomized, controlled trials are required," the study authors conclude. "Until then, physicians should be cognizant of the possible risks associated with warfarin use for atrial fibrillation in patients with ESRD, with careful evaluation of the risks and benefits of intervention at the individual patient level. Close monitoring of the degree of anticoagulation (INR) in patients who are on warfarin would also be a reasonable recommendation to minimize the risk for hemorrhagic complications."

Music Therapy Lowers Blood Pressure and Reduces Reinfarction Rates in ACS

2009-10-09T07:10:00.000-07:00

Some article to back up old anti stress therapy for the one with sick heart...

September 4, 2009 (Barcelona, Spain) – Music might be good for the soul, but a study presented this week suggests it could also be associated with more tangible cardiovascular benefits.

Researchers here at the European Society of Cardiology 2009 Congress showed that music therapy reduced blood pressure, heart rate, and patient anxiety and had a significant effect on future events, including reinfarction and sudden death, in acute coronary syndrome patients who underwent revascularization.

Speaking with heartwire , lead investigator Dr Predrag Mitrovic (University of Belgrade, Serbia) said previous studies have shown that music therapy can have positive effects on the heart, namely by decreasing sympathetic nervous activity. Other reports, including a study reported previously by heartwire , have shown that the positive emotions aroused by happy, joyful music can have favorable effects on the endothelium.

In this study, Mitrovic and colleagues provide data on their seven-year experience with using music therapy in patients with acute coronary syndrome who had undergone revascularization. In total, 740 patients between April 1990 and January 2009 were included in the analysis, with 370 patients receiving two sessions of music therapy for 12 minutes daily and 370 patients not listening to music.

During the seven-year follow-up period, patients who listened to music had less anxiety, although the score did not reach statistical significance, and statistically significant reductions in systolic and diastolic blood pressures and heart rate. Patients who listened to music also had significantly less angina, less heart failure, and lower rates of reinfarction, sudden death, and revascularization.

Mitrovic said the music preferred by patients is typically classical but that they are not always up front, at least at first, about their musical preferences. "A lot of patients don't want to tell us the truth about the type of music they like," said Mitrovic. "Some of them like national music, and they don't like to tell us about it. But if we give them the wrong type of music, it might have a negative effect."

The group hopes to publish the study shortly, but in the meantime it recommends music therapy in acute coronary syndrome patients who have undergone revascularization as an inexpensive means to lower the stress and emotional disturbance they might feel worrying about a second event.

Role of the A1c Assay in the Diagnosis of Diabetes (part 1)

2009-09-29T10:01:00.000-07:00

Abstract

An International Expert Committee with members appointed by the American Diabetes Association, the European Association for the Study of Diabetes, and the International Diabetes Federation was convened in 2008 to consider the current and future means of diagnosing diabetes in nonpregnant individuals. The report of the International Expert Committee represents the consensus view of its members and not necessarily the view of the organizations that appointed them. The International Expert Committee hopes that its report will serve as a stimulus to the international community and professional organizations to consider the use of the A1C assay for the diagnosis of diabetes.

Introduction

Diabetes is a disease characterized by abnormal metabolism, most notably hyperglycemia, and an associated heightened risk for relatively specific long-term complications affecting the eyes, kidney, and nervous system. Although diabetes also substantially increases the risk for cardiovascular disease, cardiovascular disease is not specific to diabetes and the risk for cardiovascular disease has not been incorporated into previous definitions or classifications of diabetes or of subdiabetic hyperglycemia.

Can the A1C Test Be Used to Diagnose Diabetes?

If chronic hyperglycemia sufficient to cause diabetes-specific complications is the hallmark of diabetes, common sense would dictate that laboratory measures that capture long-term glycemic exposure should provide a better marker for the presence and severity of the disease than single measures of glucose concentration. Observational studies that have assessed glycemia with measures that capture longer-term exposure (i.e., A1C) or with single or longitudinal measurements of glucose levels have consistently demonstrated a strong correlation between retinopathy and A1C[24-26] but a less consistent relationship with fasting glucose levels.[27] In one study that measured both FPG and A1C, there was a stronger correlation between A1C and retinopathy than between fasting glucose levels and retinopathy.[25] The correlation between A1C levels and complications has also been shown in the setting of controlled clinical trials in type 1[28] and type 2[29] diabetes, and these findings have been used to establish the widely accepted A1C treatment goals for diabetes care.[30]

All of these observations suggest that a reliable measure of chronic glycemic levels such as A1C, which captures the degree of glucose exposure over time[31,32] and which is related more intimately to the risk of complications than single or episodic measures of glucose levels, may serve as a better biochemical marker of diabetes and should be considered a diagnostic tool. Although the 1997 expert committee report considered this option, it recommended against using A1C values for diagnosis in part because of the lack of assay standardization.[17] The 2003 follow-up report noted that, while the National Glycohemoglobin Standardization Program [33] had succeeded in standardizing the vast majority of assays used in the U.S., the use of A1C for diagnosis still had "disadvantages," and it reaffirmed the previous recommendation that A1C not be used to diagnose diabetes.[21]

An updated examination of the laboratory measurements of glucose and A1C by the current International Expert Committee indicates that with advances in instrumentation and standardization, the accuracy and precision of A1C assays at least match those of glucose assays. The measurement of glucose itself is less accurate and precise than most clinicians realize.[34] A recent analysis of the performance of a variety of clinical laboratory instruments and methods that measure glucose revealed that 41% of instruments have a significant bias from the reference method that would result in potential misclassification of >12% of patients.[35] There are also potential preanalytic errors owing to sample handling and the well-recognized lability of glucose in the collection tube at room temperature.[36,37] Even when whole blood samples are collected in sodium fluoride to inhibit in vitro glycolysis, storage at room temperature for as little as 1 to 4 h before analysis may result in decreases in glucose levels by 3-10 mg/dl in nondiabetic individuals.[36-39]

By contrast, A1C values are relatively stable after collection,[40] and the recent introduction of a new reference method to calibrate all A1C assay instruments should further improve A1C assay standardization in most of the world.[41-43] In addition, between- and within-subject coefficients of variation have been shown to be substantially lower for A1C than for glucose measurements.[44] The variability of A1C values is also considerably less than that of FPG levels, with day-to-day within-person variance of <2% for A1C but 12-15% for FPG.[45-47] The convenience for the patient and ease of sample collection for A1C testing (which can be obtained at any time, requires no patient preparation, and is relatively stable at room temperature) compared with that of FPG testing (which requires a timed sample after at least an 8-h fast and which is unstable at room temperature) support using the A1C assay to diagnose diabetes.

In summary, compared with the measurement of glucose, the A1C assay is at least as good at defining the level of hyperglycemia at which retinopathy prevalence increases; has appreciably superior technical attributes, including less preanalytic instability and less biologic variability; and is more clinically convenient. A1C is a more stable biological index than FPG, as would be expected with a measure of chronic glycemia levels compared with glucose concentrations that are known to fluctuate within and between days ( Table 1 ).

Table 1. Advantages of A1C Testing Compared With FPG or 2HPG for the Diagnosis of Diabetes

* Standardized and aligned to the DCCT/UKPDS; measurement of glucose is less well standardized
* Better index of overall glycemic exposure and risk for long-term complications
* Substantially less biologic variability
* Substantially less preanalytic instability
* No need for fasting or timed samples
* Relatively unaffected by acute (e.g., stress or illness related) perturbations in glucose levels
* Currently used to guide management and adjust therapy

CDC Guidelines for Use of Influenza A (H1N1) 2009 Monovalent Vaccine

2009-09-26T08:31:00.000-07:00

August 27, 2009 — The US Centers for Disease Control and Prevention's (CDC's) Advisory Committee on Immunization Practices (ACIP) has issued guidelines regarding the use of vaccine against infection with novel influenza A (H1N1) virus. The new recommendations were posted online August 21 in the Morbidity and Mortality Weekly Report.

"Because novel influenza A (H1N1) virus is continuing to cause illness in the United States and worldwide, the primary focus of vaccination efforts should be to vaccinate as many persons as possible in the recommended target groups as quickly as possible once vaccine becomes available," write Anne Schuchat, MD, and colleagues from the National Center for Immunization and Respiratory Diseases, CDC.

H1N1 Vaccine Use

"As vaccine availability increases, additional groups are recommended for vaccination.... These recommendations are intended to provide vaccination programs and providers with information to assist in planning and to alert providers and the public about target groups comprising an estimated 159 million persons who are recommended to be first to receive influenza A (H1N1) 2009 monovalent vaccine," write Dr. Schuchat and colleagues.

To assess which population groups should first be targeted for vaccination, the ACIP reviewed epidemiologic and clinical data on July 29, 2009. The ACIP also evaluated the projected supply likely to be available when the vaccine first becomes available, as well as the anticipated increase in vaccine availability during the following 6 months. By mid-October 2009, it is anticipated that licensed H1N1 vaccine will be available.

The guidelines recommend that vaccination efforts begin as soon as the vaccine is available. In accordance with state and local conditions, state and local health officials and vaccination providers should make decisions concerning vaccine administration and distribution.

Vaccination and healthcare providers should be vigilant about following announcements and other information forthcoming from state and local health departments and the CDC regarding vaccination against H1N1 virus infection. The CDC's influenza Web site and state and local health departments may provide additional information.

ACIP H1N1 Vaccine Recommendations

Key points of the ACIP recommendations include the following 3 items.

* First, 5 general population groups that should be targeted as an initial focus of vaccination efforts are pregnant women, household contacts or caregivers for infants younger than 6 months (such as parents, siblings, and daycare providers), healthcare and emergency medical services personnel, children and young adults 6 months to 24 years of age, and persons aged 25 to 64 years who are at greater risk for influenza-related complications because of underlying medical conditions. These medical conditions increasing risk for influenza-related complications include chronic pulmonary conditions, including asthma; cardiovascular conditions except for hypertension; renal, hepatic, cognitive, neurologic/neuromuscular, hematologic, or metabolic disorders, including diabetes mellitus; and immunosuppression caused by medications or by human immunodeficiency virus.
* Second, if initial vaccine availability is insufficient to meet demand, priority is established for a subset of persons within the initial target groups. These persons who are to receive priority for vaccination (order of target groups does not indicate priority) include pregnant women, household contacts or caregivers for infants younger than 6 months, healthcare and emergency medical services personnel in direct contact with patients or infectious material, children 6 months to 4 years of age, and children and adolescents aged 5 to 18 years who are at greater risk for influenza-related complications because of underlying medical conditions.
* Third, as vaccine availability increases, other adult population groups should receive H1N1 vaccine in accordance with the guidelines recommendations.

In addition, ACIP made additional recommendations concerning the use of influenza A (H1N1) 2009 monovalent vaccine, as follows:

* The number of doses of vaccine needed for immunization against H1N1 has not been determined. Vaccine should not be stockpiled for patients who already have received 1 dose but might require a second dose, because vaccine availability is expected to increase over time.
* If different anatomic sites are used, inactivated vaccines against seasonal and H1N1 viruses may be administered simultaneously. However, ACIP does not recommend simultaneous administration of live, attenuated vaccines against seasonal and H1N1 virus.
* All persons, including those older than 65 years of age, who are currently recommended for seasonal influenza vaccine should receive the seasonal vaccine as soon as it is available. Recommendations for use of the 2009 to 2010 seasonal influenza vaccine were previously published.

"The guiding principle of these recommendations is to vaccinate as many persons as possible as quickly as possible," the guidelines authors state."ACIP will review new epidemiologic and clinical data as they become available and might revise these recommendations."

Morb Mortal Wkly Rep. Published online August 21, 2009.

WHO Guidelines for Antiviral Treatment for H1N1 and Other Influenza

2009-09-26T08:24:00.000-07:00

August 25, 2009 — The World Health Organization (WHO) has issued guidelines for antiviral treatment for novel influenza A (H1N1) and other influenza. The purpose of the new recommendations, which were posted online August 20, is to provide a basis for advice to clinicians regarding the use of the currently available antivirals for patients presenting with illness caused by influenza virus infection, as well as considerations regarding potential use of these antiviral medications for chemoprophylaxis.

On the basis of a review of data collected with previously circulating strains, and treatment of human H5N1 influenza virus infections, the new guidelines expand on recommendations published in May 2009, titled ʺClinical management of human infection with new influenza A (H1N1) virus: Initial guidance." These new guidelines do not change recommendations in the WHO rapid advice guidelines on pharmacological management of humans infected with highly pathogenic avian influenza A (H5N1) virus.

"In April 2009, the [WHO] received reports of sustained person to person infections with [H1N1] virus in Mexico and the United States," write Edgar Bautista, from Médico Neumólogo Intensivista, Jefe de UCI-INER in Mexico, and colleagues. "Subsequent international spread led WHO to declare on 11 June 2009 that the first influenza pandemic in 41 years had occurred. This 2009 pandemic H1N1 influenza virus has now spread worldwide, with confirmed cases of pandemic H1N1 virus infection reported in more than 100 countries in all 6 WHO regions[, which] has led to the need to add to the existing guidance on the use of antivirals."

The new recommendations highlight oseltamivir and zanamivir, which are neuraminidase inhibitors, and amantadine and rimantadine, which are M2 inhibitors. Suggestions are also provided regarding the use of some other potential pharmacological treatments, such as ribavirin, interferons, immunoglobulins, and corticosteroids.

Management of patients with pandemic influenza (H1N1) 2009 virus infection is the primary focus of the statement, although it also includes guidance regarding the use of the antivirals for treatment of other seasonal influenza virus strains, as well as for infections resulting from novel influenza A virus strains.

The guidelines urge country and local public health authorities to issue local recommendations for clinicians periodically, based on epidemiological and antiviral susceptibility data on the locally circulating influenza strains. As the prevalence and severity of the current pandemic evolves, WHO anticipates that additional data will be forthcoming that may require revision of the current recommendations. WHO therefore plans to review the guidance no later than September 2009 to determine whether modifications to the recommendations are needed.

Recommendations for Antiviral Treatment of H1N1

For patients with confirmed or strongly suspected infection with influenza pandemic (H1N1) 2009, when antiviral medications for influenza are available, specific recommendations regarding use of antivirals for treatment of pandemic (H1N1) 2009 influenza virus infection are as follows:

* Oseltamivir should be prescribed, and treatment started as soon as possible, for patients with severe or progressive clinical illness (strong recommendation, low-quality evidence). Depending on clinical response, higher doses of up to 150 mg twice daily and longer duration of treatment may be indicated. This recommendation is intended for all patient groups, including pregnant women, neonates, and children younger than 5 years of age.
* Zanamivir is indicated for patients with severe or progressive clinical illness when oseltamivir is not available or not possible to use, or when the virus is resistant to oseltamivir but known or likely to be susceptible to zanamivir (strong recommendation, very low quality evidence).
* Antiviral treatment is not required in patients not in at-risk groups who have uncomplicated illness caused by confirmed or strongly suspected influenza virus infection (weak recommendation, low-quality evidence). Patients considered to be at risk are infants and children younger than 5 years of age; adults older than 65 years of age; nursing home residents; pregnant women; patients with chronic comorbid disease including cardiovascular, respiratory, or liver disease and diabetes; and immunosuppressed patients because of malignancy, HIV infection, or other diseases.
* Oseltamivir or zanamivir treatment should be started as soon as possible after the onset of illness in patients in at-risk groups who have uncomplicated illness caused by influenza virus infection (strong recommendation, very low quality evidence).

Recommendations for Chemoprophylaxis of H1N1

Specific recommendations regarding the use of antivirals for chemoprophylaxis of pandemic (H1N1) 2009 influenza virus infection are as follows:

* When risk for human-to-human transmission of influenza is high or low, and the probability of complications of infection is high, either because of the influenza strain or because of the baseline risk of the exposed group, use of oseltamivir or zanamivir may be considered as postexposure chemoprophylaxis for the affected community or group, for individuals in at-risk groups, or for healthcare workers (weak recommendation, moderate-quality evidence).
* Individuals in at-risk groups or healthcare personnel need not be offered antiviral chemoprophylaxis if the likelihood of complications of infection is low. This recommendation should be applied independent of risk for human-to-human transmission (weak recommendation, low-quality evidence).

For treatment of mild to moderate uncomplicated clinical presentation of infection with multiple cocirculating influenza A subtypes or viruses with different antiviral susceptibilities, patients in at-risk groups should be treated with zanamivir or oseltamivir plus M2 inhibitor (noting that amantadine should not be used in pregnant women). Otherwise-healthy patients with this presentation need not be treated.

When the clinical presentation of infection with multiple cocirculating influenza A subtypes or viruses with different antiviral susceptibilities is severe or progressive, all patients should be treated with oseltamivir plus M2 inhibitor, or zanamivir.

For treatment of mild to moderate uncomplicated clinical presentation of infection with sporadic zoonotic influenza A viruses including H5N1, the at-risk population should be treated with oseltamivir or zanamivir, and the otherwise-healthy population with oseltamivir. All patients, regardless of risk status, with severe or progressive presentation of infection with sporadic zoonotic influenza A viruses including H5N1 should be treated with oseltamivir plus an M2 inhibitor.

WHO Rapid Advice Guidelines on Pharmacological Management of Influenza Virus. Published online August 20, 2009.

Interim Guidance on Antiviral Recommendations for Patients with Novel Influenza A (H1N1) Virus Infection and Their Close Contacts

2009-05-09T23:13:00.000-07:00

Objective: To provide updated interim guidance on the use of antiviral agents for treatment and chemoprophylaxis of novel influenza (H1N1) virus infection, and assist clinicians in prioritizing use of antivirals for treatment or chemoprophylaxis of patients at higher risk for influenza-related complications. Additional revisions to these recommendations for antiviral treatment should be expected as the epidemiology and clinical presentation of novel influenza A (H1N1) virus infection is better understood. This guidance can be adapted according to local epidemiologic data and antiviral supply considerations.

High-risk groups: A person who is at high-risk for complications of novel influenza (H1N1) virus infection is defined as the same for seasonal influenza at this time. As more epidemiologic and clinical data become available, these risk groups might be revised.

Children younger than 5 years old. The risk for severe complications from seasonal influenza is highest among children younger than 2 years old.
Adults 65 years of age and older.
Persons with the following conditions:

Chronic pulmonary (including asthma), cardiovascular (except hypertension), renal, hepatic, hematological (including sickle cell disease), neurologic, neuromuscular, or metabolic disorders (including diabetes mellitus);
Immunosuppression, including that caused by medications or by HIV;
Pregnant women;
Persons younger than 19 years of age who are receiving long-term aspirin therapy;
Residents of nursing homes and other chronic-care facilities.

Transmission: Transmission of novel influenza A (H1N1) is being studied as part of the ongoing outbreak investigation, but limited data available indicate that this virus is likely transmitted in ways similar to other influenza viruses. Seasonal human influenza viruses are thought to be transmitted between persons primarily through large-particle respiratory droplet transmission (e.g., when an infected person coughs or sneezes near a susceptible person). Transmission via these large-particle droplets requires close contact between source and recipient persons because droplets do not remain suspended in the air and generally travel only a short distance (<>

Close contact, for the purposes of this document, is defined as having cared for or lived with a person who is a confirmed, probable or suspected case of novel influenza A (H1N1), or having been in a setting where there was a high likelihood of contact with respiratory droplets and/or body fluids of such a person. Examples of close contact include kissing or embracing, sharing eating or drinking utensils, physical examination, or any other contact between persons likely to result in exposure to respiratory droplets. Close contact typically does not include activities such as walking by an infected person or sitting across from a symptomatic patient in a waiting room or office.

Special Considerations for Children
Aspirin or aspirin-containing products (e.g. bismuth subsalicylate – Pepto Bismol) should not be administered to any confirmed or suspected ill case of novel influenza H1N1 virus infection aged 18 years old and younger due to the risk of Reye syndrome. For relief of fever, other anti-pyretic medications such as acetaminophen or non- steroidal anti-inflammatory drugs are recommended.

Children younger than 4 years of age should not be given over-the-counter cold medications without first speaking with a healthcare provider.

Antiviral Resistance

This novel (H1N1) influenza virus is sensitive (susceptible) to the neuraminidase inhibitor antiviral medications, zanamivir and oseltamivir. It is resistant to the adamantane antiviral medications, amantadine and rimantadine.

Antiviral Treatment for Novel (H1N1) Influenza

For antiviral treatment of novel influenza (H1N1) virus infection, either oseltamivir or zanamivir are recommended. Recommendations for use of antivirals may change as data on antiviral effectiveness, clinical spectrum of illness, adverse events from antiviral use, and antiviral susceptibility data become available.

Clinical judgment is an important factor in treatment decisions. Persons with suspected novel H1N1 influenza who present with an uncomplicated febrile illness typically do not require treatment unless they are at higher risk for influenza complications, and in areas with limited antiviral mediation availability, local public health authorities might provide additional guidance about prioritizing treatment within groups at higher risk for infection.

Treatment is recommended for:

All hospitalized patients with confirmed, probable or suspected novel influenza (H1N1).
Patients who are at higher risk for seasonal influenza complications (see above).

If a patient is not in a high-risk group or is not hospitalized, healthcare providers should use clinical judgment to guide treatment decisions, and when evaluating children should be aware that the risk for severe complications from seasonal influenza among children younger than 5 years old is highest among children younger than 2 years old. Many patients who have had novel influenza (H1N1) virus infection, but who are not in a high-risk group have had a self-limited respiratory illness similar to typical seasonal influenza. For most of these patients, the benefits of using antivirals may be modest. Therefore, testing, treatment and chemoprophylaxis efforts should be directed primarily at persons who are hospitalized or at higher risk for influenza complications.

Once the decision to administer antiviral treatment is made, treatment with zanamivir or oseltamivir should be initiated as soon as possible after the onset of symptoms. Evidence for benefits from antiviral treatment in studies of seasonal influenza is strongest when treatment is started within 48 hours of illness onset. However, some studies of oseltamivir treatment of hospitalized patients with seasonal influenza have indicated benefit, including reductions in mortality or duration of hospitalization even for patients whose treatment was started more than 48 hours after illness onset. Recommended duration of treatment is five days. Antiviral doses recommended for treatment of novel H1N1 influenza virus infection in adults or children 1 year of age or older are the same as those recommended for seasonal influenza .

Oseltamivir use for children <1>

Note: Areas that continue to have seasonal influenza activity, especially those with circulation of oseltamivir-resistant seasonal human influenza A (H1N1) viruses, might prefer to use either zanamivir or a combination of oseltamivir and rimantadine or amantadine to provide adequate empiric treatment or chemoprophylaxis for patients who might have seasonal human influenza A (H1N1) virus infection.

Antiviral Chemoprophylaxis for Novel (H1N1) Influenza

For antiviral chemoprophylaxis of novel (H1N1) influenza virus infection, either oseltamivir or zanamivir are recommended (Table 1). Duration of antiviral chemoprophylaxis post-exposure is 10 days after the last known exposure to novel (H1N1) influenza. The indication for post-exposure chemoprophylaxis is based upon close contact with a person who is a confirmed, probable or suspected case of novel influenza A (H1N1) virus infection during the infectious period of the case. The infectious period for persons infected with the novel influenza A (H1N1) virus is assumed to be similar to that observed in studies of seasonal influenza. With seasonal influenza, studies have shown that people may be able to transmit infection beginning one day before they develop symptoms to up to 7 days after they get sick. Children, especially younger children, might potentially be infectious for longer periods. However, for this guidance, the infectious period is defined as one day before until 7 days after the case’s onset of illness. If the contact occurred with a case whose illness started more than 7 days before contact with the person under consideration for antivirals, then chemoprophylaxis is not necessary. For pre-exposure chemoprophylaxis, antiviral medications should be given during the potential exposure period and continued for 10 days after the last known exposure to a person with novel (H1N1) influenza virus infection during the cases infectious period. Oseltamivir can also be used for chemoprophylaxis under the EUA for children less than 1 year of age (see Children Under 1 Year of Age).

Post exposure antiviral chemoprophylaxis with either oseltamivir or zanamivir can be considered for the following:

Close contacts of cases (confirmed, probable, or suspected) who are at high-risk for complications of influenza
Health care personnel, public health workers, or first responders who haves had a recognized, unprotected close contact exposure to a person with novel (H1N1) influenza virus infection (confirmed, probable, or suspected) during that person’s infectious period. Information on appropriate personal protective equipment is available at: Interim Guidance for Infection Control for Care of Patients with Confirmed or Suspected Swine Influenza A (H1N1) Virus Infection in a Healthcare Setting and might be updated frequently as additional information on transmission becomes available.

Pre-exposure antiviral chemoprophylaxis should only be used in limited circumstances, and in consultation with local medical or public health authorities. Certain persons at ongoing occupational risk for exposure who are also at higher risk for complications of influenza (e.g., health care personnel, public health workers, or first responders who are working in communities with influenza A H1N1 outbreaks) should carefully follow guidelines for appropriate personal protective equipment or consider temporary reassignment.

Antiviral Use for Control of Novel H1N1 Influenza Outbreaks

Use of antiviral drugs for treatment and chemoprophylaxis of influenza has been a cornerstone for the control of seasonal influenza outbreaks in nursing homes and other long term care facilities.

At this time, no outbreaks of novel influenza A (H1N1) have been reported in such settings. However, if such outbreaks were to occur, it is recommended that ill patients be treated with oseltamivir or zanamivir and that chemoprophylaxis with either oseltamivir or zanamivir be started as early as possible to reduce the spread of the virus as is recommended for seasonal influenza outbreaks in such settings.

Chemoprophylaxis should be administered to all non-ill residents and should continue for a minimum of 2 weeks. If surveillance indicates that new cases continue to occur, chemoprophylaxis should be continued until approximately 7 days after illness onset in the last patient. In addition to antiviral medications, other outbreak-control measures include appropriate infection control, establishing cohorts of patients with confirmed or suspected influenza, restricting staff movement between wards or buildings, and restricting contact between ill staff or visitors and patients, and active surveillance for new cases. Medical directors of long-term care facilities should review their plans for outbreak control of influenza.

In addition to use in nursing homes, antiviral chemoprophylaxis also can be considered for controlling influenza outbreaks in other closed or semiclosed settings (e.g., correctional facilities, or other settings in which persons live in close proximity.

Table 1. Antiviral medication dosing recommendations for treatment or chemoprophylaxis of novel influenza A (H1N1) infection. (Table extracted from IDSA guidelines for seasonal influenza .)
Agent, group		Treatment	Chemoprophylaxis
Oseltamivir
Adults		75-mg capsule twice per day for 5 days	75-mg capsule once per day
Children ≥ 12 months	15 kg or less	60 mg per day divided into 2 doses	30 mg once per day
	15-23 kg	90 mg per day divided into 2 doses	45 mg once per day
	24-40 kg	120 mg per day divided into 2 doses	60 mg once per day
	>40 kg	150 mg per day divided into 2 doses	75 mg once per day
Zanamivir
Adults		Two 5-mg inhalations (10 mg total) twice per day	Two 5-mg inhalations (10 mg total) once per day
Children		Two 5-mg inhalations (10 mg total) twice per day (age, 7 years or older)	Two 5-mg inhalations (10 mg total) once per day (age, 5 years or older)

General Info on the H1N1 (swine) flu virus

2009-05-06T07:16:00.000-07:00

What is H1N1 (swine flu)?
H1N1 (referred to as “swine flu” early on) is a new influenza virus causing illness in people. This new virus was first detected in people in the United States in April 2009. Other countries, including Mexico and Canada, have reported people sick with this new virus. This virus is spreading from person-to-person, probably in much the same way that regular seasonal influenza viruses spread.

Why is this new H1N1 virus sometimes called “swine flu”?
This virus was originally referred to as “swine flu” because laboratory testing showed that many of the genes in this new virus were very similar to influenza viruses that normally occur in pigs in North America. But further study has shown that this new virus is very different from what normally circulates in North American pigs. It has two genes from flu viruses that normally circulate in pigs in Europe and Asia and avian genes and human genes. Scientists call this a “quadruple reassortant” virus.

Are there human infections with this H1N1 virus in the U.S.?
Yes. Cases of human infection with this H1N1 influenza virus were first confirmed in the U.S. in Southern California and near Guadalupe County, Texas. The outbreak intensified rapidly from that time and more and more states have been reporting cases of illness from this virus. CDC and local and state health agencies are working together to investigate this situation.

Is this new H1N1 virus contagious?
CDC has determined that this new H1N1 virus is contagious and is spreading from human to human. However, at this time, it is not known how easily the virus spreads between people.

What are the signs and symptoms of this virus in people?
The symptoms of this new H1N1 flu virus in people are similar to the symptoms of seasonal flu and include fever, cough, sore throat, runny or stuffy nose, body aches, headache, chills and fatigue. A significant number of people who have been infected with this virus also have reported diarrhea and vomiting. Also, like seasonal flu, severe illnesses and death has occurred as a result of illness associated with this virus.

How severe is illness associated with this new H1N1 virus?
It’s not known at this time how severe this virus will be in the general population. CDC is studying the medical histories of people who have been infected with this virus to determine whether some people may be at greater risk from infection, serious illness or hospitalization from the virus. In seasonal flu, there are certain people that are at higher risk of serious flu-related complications. This includes people 65 years and older, children younger than five years old, pregnant women, and people of any age with chronic medical conditions. It’s unknown at this time whether certain groups of people are at greater risk of serious flu-related complications from infection with this new virus. CDC also is conducting laboratory studies to see if certain people might have natural immunity to this virus, depending on their age.

How does this new H1N1 virus spread?
Spread of this H1N1 virus is thought to be happening in the same way that seasonal flu spreads. Flu viruses are spread mainly from person to person through coughing or sneezing by people with influenza. Sometimes people may become infected by touching something with flu viruses on it and then touching their mouth or nose.

How long can an infected person spread this virus to others?
At the current time, CDC believes that this virus has the same properties in terms of spread as seasonal flu viruses. With seasonal flu, studies have shown that people may be contagious from one day before they develop symptoms to up to 7 days after they get sick. Children, especially younger children, might potentially be contagious for longer periods. CDC is studying the virus and its capabilities to try to learn more and will provide more information as it becomes available.

Exposures Not Thought to Spread New H1N1 Flu

Can I get infected with this new H1N1 virus from eating or preparing pork?
No. H1N1 viruses are not spread by food. You cannot get this new HIN1 virus from eating pork or pork products. Eating properly handled and cooked pork products is safe.

Is there a risk from drinking water?
Tap water that has been treated by conventional disinfection processes does not likely pose a risk for transmission of influenza viruses. Current drinking water treatment regulations provide a high degree of protection from viruses. No research has been completed on the susceptibility of the novel H1N1 flu virus to conventional drinking water treatment processes. However, recent studies have demonstrated that free chlorine levels typically used in drinking water treatment are adequate to inactivate highly pathogenic H5N1 avian influenza. It is likely that other influenza viruses such as novel H1N1 would also be similarly inactivated by chlorination. To date, there have been no documented human cases of influenza caused by exposure to influenza-contaminated drinking water.

Can the new H1N1 flu virus be spread through water in swimming pools, spas, water parks, interactive fountains, and other treated recreational water venues?
Influenza viruses infect the human upper respiratory tract. There has never been a documented case of influenza virus infection associated with water exposure. Recreational water that has been treated at CDC recommended disinfectant levels does not likely pose a risk for transmission of influenza viruses. No research has been completed on the susceptibility of the H1N1 influenza virus to chlorine and other disinfectants used in swimming pools, spas, water parks, interactive fountains, and other treated recreational venues. However, recent studies have demonstrated that free chlorine levels recommended by CDC (1–3 parts per million [ppm or mg/L] for pools and 2–5 ppm for spas) are adequate to disinfect avian influenza A (H5N1) virus. It is likely that other influenza viruses such as novel H1N1 virus would also be similarly disinfected by chlorine.

Can H1N1 influenza virus be spread at recreational water venues outside of the water?
Yes, recreational water venues are no different than any other group setting. The spread of this novel H1N1 flu is thought to be happening in the same way that seasonal flu spreads. Flu viruses are spread mainly from person to person through coughing or sneezing of people with influenza. Sometimes people may become infected by touching something with flu viruses on it and then touching their mouth or nose.

Prevention & Treatment

What can I do to protect myself from getting sick?
There is no vaccine available right now to protect against this new H1N1 virus. There are everyday actions that can help prevent the spread of germs that cause respiratory illnesses like influenza.

Take these everyday steps to protect your health:

Cover your nose and mouth with a tissue when you cough or sneeze. Throw the tissue in the trash after you use it.
Wash your hands often with soap and water, especially after you cough or sneeze. Alcohol-based hand cleaners are also effective.
Avoid touching your eyes, nose or mouth. Germs spread this way.
Try to avoid close contact with sick people.
Stay home if you are sick for 7 days after your symptoms begin or until you have been symptom-free for 24 hours, whichever is longer. This is to keep from infecting others and spreading the virus further.

Other important actions that you can take are:

Follow public health advice regarding school closures, avoiding crowds and other social distancing measures.
Be prepared in case you get sick and need to stay home for a week or so; a supply of over-the-counter medicines, alcohol-based hand rubs, tissues and other related items might could be useful and help avoid the need to make trips out in public while you are sick and contagious.

What is the best way to keep from spreading the virus through coughing or sneezing?
If you are sick, limit your contact with other people as much as possible. If you are sick, stay home for 7 days after your symptoms begin or until you have been symptom-free for 24 hours, whichever is longer. Cover your mouth and nose with a tissue when coughing or sneezing. Put your used tissue in the waste basket. Then, clean your hands, and do so every time you cough or sneeze.

What is the best technique for washing my hands to avoid getting the flu?
Washing your hands often will help protect you from germs. Wash with soap and water or clean with alcohol-based hand cleaner. CDC recommends that when you wash your hands -- with soap and warm water -- that you wash for 15 to 20 seconds. When soap and water are not available, alcohol-based disposable hand wipes or gel sanitizers may be used. You can find them in most supermarkets and drugstores. If using gel, rub your hands until the gel is dry. The gel doesn't need water to work; the alcohol in it kills the germs on your hands.

What should I do if I get sick?
If you live in areas where people have been identified with new H1N1 flu and become ill with influenza-like symptoms, including fever, body aches, runny or stuffy nose, sore throat, nausea, or vomiting or diarrhea, you should stay home and avoid contact with other people, except to seek medical care.

If you have severe illness or you are at high risk for flu complications, contact your health care provider or seek medical care. Your health care provider will determine whether flu testing or treatment is needed

If you become ill and experience any of the following warning signs, seek emergency medical care.

In children emergency warning signs that need urgent medical attention include:

Fast breathing or trouble breathing
Bluish or gray skin color
Not drinking enough fluids
Severe or persistent vomiting
Not waking up or not interacting
Being so irritable that the child does not want to be held
Flu-like symptoms improve but then return with fever and worse cough

In adults, emergency warning signs that need urgent medical attention include:

Difficulty breathing or shortness of breath
Pain or pressure in the chest or abdomen
Sudden dizziness
Confusion
Severe or persistent vomiting
Flu-like symptoms improve but then return with fever and worse cough

Are there medicines to treat infection with this new virus?
Yes. CDC recommends the use of oseltamivir or zanamivir for the treatment and/or prevention of infection with the new H1N1 flu virus. Antiviral drugs are prescription medicines (pills, liquid or an inhaler) that fight against the flu by keeping flu viruses from reproducing in your body. If you get sick, antiviral drugs can make your illness milder and make you feel better faster. They may also prevent serious flu complications. During the current outbreak, the priority use for influenza antiviral drugs during is to treat severe influenza illness.

Contamination & Cleaning

How long can influenza virus remain viable on objects (such as books and doorknobs)?
Studies have shown that influenza virus can survive on environmental surfaces and can infect a person for up to 2-8 hours after being deposited on the surface.

What kills influenza virus?
Influenza virus is destroyed by heat (167-212°F [75-100°C]). In addition, several chemical germicides, including chlorine, hydrogen peroxide, detergents (soap), iodophors (iodine-based antiseptics), and alcohols are effective against human influenza viruses if used in proper concentration for a sufficient length of time. For example, wipes or gels with alcohol in them can be used to clean hands. The gels should be rubbed into hands until they are dry.

What surfaces are most likely to be sources of contamination?
Germs can be spread when a person touches something that is contaminated with germs and then touches his or her eyes, nose, or mouth. Droplets from a cough or sneeze of an infected person move through the air. Germs can be spread when a person touches respiratory droplets from another person on a surface like a desk, for example, and then touches their own eyes, mouth or nose before washing their hands.

How should waste disposal be handled to prevent the spread of influenza virus?
To prevent the spread of influenza virus, it is recommended that tissues and other disposable items used by an infected person be thrown in the trash. Additionally, persons should wash their hands with soap and water after touching used tissues and similar waste.

What household cleaning should be done to prevent the spread of influenza virus?
To prevent the spread of influenza virus it is important to keep surfaces (especially bedside tables, surfaces in the bathroom, kitchen counters and toys for children) clean by wiping them down with a household disinfectant according to directions on the product label.

How should linens, eating utensils and dishes of persons infected with influenza virus be handled?
Linens, eating utensils, and dishes belonging to those who are sick do not need to be cleaned separately, but importantly these items should not be shared without washing thoroughly first.
Linens (such as bed sheets and towels) should be washed by using household laundry soap and tumbled dry on a hot setting. Individuals should avoid “hugging” laundry prior to washing it to prevent contaminating themselves. Individuals should wash their hands with soap and water or alcohol-based hand rub immediately after handling dirty laundry.

Eating utensils should be washed either in a dishwasher or by hand with water and soap.

Response & Investigation

What is CDC doing in response to the outbreak?
CDC or the Center for Disease Control has implemented its emergency response. The agency’s goals are to reduce transmission and illness severity, and provide information to help health care providers, public health officials and the public address the challenges posed by the new virus. CDC continues to issue new interim guidance for clinicians and public health professionals. In addition, CDC’s Division of the Strategic National Stockpile (SNS) continues to send antiviral drugs, personal protective equipment, and respiratory protection devices to all 50 states and U.S. territories to help them respond to the outbreak.

What epidemiological investigations are taking place in response to the recent outbreak?
CDC works very closely with state and local officials in areas where human cases of new H1N1 flu infections have been identified. In California and Texas, where EpiAid teams have been deployed, many epidemiological activities are taking place or planned including:

Active surveillance in the counties where infections in humans have been identified;
Studies of health care workers who were exposed to patients infected with the virus to see if they became infected;
Studies of households and other contacts of people who were confirmed to have been infected to see if they became infected;
Study of a public high school where three confirmed human cases of H1N1 flu occurred to see if anyone became infected and how much contact they had with a confirmed case; and
Study to see how long a person with the virus infection sheds the virus.

KEEP POSTED FOR MORE INFO re: H1N1 virus
Source: CDC

GINA clinical based management of Asthma

2009-04-18T08:28:00.001-07:00

Treatment

The following treatments are usually administered concurrently to achieve the most rapid resolution of the exacerbation.

Oxygen. To achieve arterial oxygen saturation of a 90% (a 95% in children), oxygen should be administered by nasal cannulae, by mask, or rarely by head box in some infants. PaCO2 may worsen in some patients on 100 percent oxygen, especially those with more severe airflow

Obstruction. Oxygen therapy should be titrated against pulse oximetry to maintain a satisfactory oxygen saturation.

Rapid-acting inhaled ß2–agonists. Rapid-acting inhaled beta2-agonists should be administered at regular intervals. Although most rapid-acting beta2-agonists have a short duration of effect, the long-acting bronchodilator formoterol, which has both a rapid onset of action and a long duration of effect, has been shown to be equally effective without increasing side effects, though it is considerably more expensive.

The importance of this feature of formoterol is that it provides support and reassurance regarding the use of a combination of formoterol and budesonide early in asthma exacerbations. A modestly greater bronchodilator effect has been shown with levabuterol compared to racemic albuterol in both adults and children with an asthma exacerbation. In a large study of acute asthma in children and in adults not previously treated with glucocorticosteroid, levabuterol

treatment resulted in lower hospitalization rates compared to racemic albuterol treatment, but in children the length of hospital stay was no different.

Studies of intermittent versus continuous nebulized shortacting beta2-agonists in acute asthma provide conflicting results. In a systematic review of six studies, there were no significant differences in bronchodilator effect or hospital admissions between the two treatments. In

patients who require hospitalization, one study found that intermittent on-demand therapy led to a significantly shorter hospital stay, fewer nebulizations, and fewer palpitations when compared with intermittent therapy given every 4 hours. A reasonable approach to inhaled therapy

in exacerbations, therefore, would be the initial use of continuous therapy, followed by intermittent on-demand therapy for hospitalized patients. There is no evidence to support the routine use of intravenous beta2-agonists in patients with severe asthma exacerbations.

Epinephrine. A subcutaneous or intramuscular injection of epinephrine (adrenaline) may be indicated for acute treatment of anaphylaxis and angioedema, but is not routinely indicated during asthma exacerbations.

Additional bronchodilators.

Ipratropium bromide. A combination of nebulized beta2- agonist with an anticholinergic (ipratropium bromide) may produce better bronchodilation than either drug alone and should be administered before methylxanthines are considered. Combination beta2- agonist/anticholinergic therapy is associated with lower hospitalization rates and greater improvement in PEF and FEV1. Similar data have been reported in the pediatric literature . However, once children with asthma are hospitalized following intensive emergency department treatment, the addition of nebulized ipratropium bromide to nebulized beta2-agonist and systemic glucocorticosteroids appears to confer no extra benefit.

Theophylline. In view of the effectiveness and relative safety of rapid-acting beta2-agonists, theophylline has a minimal role in the management of acute asthma. Its use is associated with severe and potentially fatal side effects, particularly in those on long-term therapy with

sustained-release theophylline, and their bronchodilator effect is less than that of beta2-agonists. The benefit asadd-on treatment in adults with severe asthma exacerbations has not been demonstrated. However, in one study of children with near-fatal asthma, intravenous

theophylline provided additional benefit to patients also receiving an aggressive regimen of inhaled and intravenous beta2-agonists, inhaled ipatropium bromide, and intravenous systemic glucocorticosteroids.

Systemic glucocorticosteroids. Systemic glucocorticosteroids speed resolution of xacerbations and should be utilized in the all but the mildest exacerbations, especially if:

• The initial rapid-acting inhaled beta2-agonist therapy fails to achieve lasting improvement

• The exacerbation develops even though the patient was already taking oral glucocorticosteroids

• Previous exacerbations required oral glucocorticosteroids.

Oral glucocorticosteroids are usually as effective as those administered intravenously and are preferred because this route of delivery is less invasive and less expensive.

If vomiting has occurred shortly after administration of oral glucocorticosteroids, then an equivalent dose should be re-administered intravenously. In patients discharged from the emergency department, intramuscular administration may be helpful, especially if there are concerns about compliance with oral therapy. Oral glucocorticosteroids require at least 4 hours to produce clinical improvement.

Daily doses of systemic glucocorticosteroids equivalent to 60-80 mg methylprednisolone as a single dose, or 300-400 mg hydrocortisone in divided doses, are adequate for hospitalized patients, and 40 mg methylprednisolone or 200 mg hydrocortisone is probably adequate in most

cases. An oral glucocorticosteroid dose of 1 mg/kg daily is adequate for treatment of exacer-bations in children with mild persistent asthma. A 7-day course in adults has been found to be as effective as a 14-day course, and a 3- to 5-day course in children is usually considered appro-priate. Current evidence suggests that there is no benefit to tapering the dose of oral glucocorticosteroids, either in the short-term or over several weeks.

Inhaled glucocorticosteroids. Inhaled glucocorticosteroids are effective as part of therapy for asthma exacerbations. In one study, the combination of high-dose inhaled glucocorticosteroids and salbutamol in acute asthma provided greater bronchodilation than salbutamol alone, and conferred greater benefit than the addition of systemic glucocorticosteroids across all parameters, including hospitalizations, especially for patients with more severe attacks. Inhaled glucocorticosteroids can be as effective as oral glucocorticosteroids at preventing relapses. Patients discharged from the emergency department on prednisone and inhaled budesonide have a lower rate of relapse than

those on prednisone alone. A high-dose of inhaled glucocorticosteroid (2.4 mg budesonide daily in

four divided doses) achieves a relapse rate similar to 40 mg oral prednisone daily.

Cost is a significant factor in the use of such high-doses of inhaled glucocorticosteroids, and further studies are required to document their potential benefits, especially cost effectiveness, in acute asthma.

Magnesium. Intravenous magnesium sulphate (usually given as a single 2 g infusion over 20 minutes) is not recommended for routine use in asthma exacerbations, but can help reduce hospital admission rates in certain patients, including adults with FEV1 25-30% predicted at presentation, adults and children who fail to respond to initial treatment, and children whose FEV1 fails to improve

above 60% predicted after 1 hour of care. Nebulized salbutamol administered in isotonic magnesium sulfate provides greater benefit than if it is delivered in normal saline. Intravenous magnesium sulphate has not been studied in young children.

Helium oxygen therapy. A systematic survey of studies that have evaluated the effect of a combination of helium and oxygen, compared to helium alone, suggests there is no routine role for this intervention. It might be considered for patients who do not respond to standard therapy.

Leukotriene modifiers. There is little data to suggest a role for leukotriene modifiers in acute asthma.

Sedatives. Sedation should be strictly avoided during exacerbations of asthma because of the respiratory depressant effect of anxiolytic and hypnotic drugs. An association between the use of these drugs and avoidable asthma deaths has been demonstrated.

The foregoing are just the regimens listed (as recommended by GINA or the Global Initiative for Asthma), Global Strategy for Asthma Management and Prevention 2008 report.

For the whole report and comprehensive guideline ebook, visit http://www.ginasthma.com/index.asp?l1=1&l2=0

Herbs and Nutrients for Asthma

2009-04-16T04:21:00.000-07:00

The following are the nutrients, herbs, and other recommendations beneficial to thwart atherosclerosis:

NUTRIENTS

Supplement	Suggested Dosage	Comments
*Essential*
Pantothenic acid (Vit B₆)	50 mg 3x a day	The anti stress vitamin
Quercitin-C from Ecological Formulas plus bromelain	500 mg 3x a day 100 mg 3x a day	Powerful immunostimulants. Antihistamine effect
Vitamin C with bioflavonoids	1500 mg 3x a day (avoid high doses when with kidney stones)	Needed to protect lung tissue and keep down infection. Also increases air flow and fights inflammation
Zinc lozenges	Do not take over 100 mg daily	Can shorten an attack or halt one before it becomes severe.
*Very Important*
Betaine HCl with pepsin	As directed on label, or as prescribed	Combats malabsorption problems
Coenzyme Q	100 mg daily	Has the ability to counter histamine
Magnesium plus calcium	750 mg daily 1500 mg daily	May stop the acute asthmatic episode by increasing the vital capacity of the lungs. Has a dilating effect on the bronchial muscles. Use chelate forms
Multivitamin and mineral complex with Selenium Vitamin B12	As directed on the label 200 mcg daily 2000 mcg daily	Necessary for enhanced immune function. Use a high potency formula. Destroys radicals from air pollutants

Herbs

Lobelia extract is helpful during an asthma attack attack; it is a bronchial soothing muscle relaxant and expectorant. Do not take long term.

Boswellia, an Indian herb (also known as frankincense), in studies was shown to reduce the number of asthma attacks.

Mullein oil is said to be a powerful remedy for bronchial congestion. The oil stops cough, unclogs bronchial tubes, and helps clear up asthma attacks. Users say that when they take it in tea or fruit juice, the effect is almost immediate.

Proponents of the East Indian mind-body-earth philosophy called Ayurveda recommend the following herbs for people with asthma: vasaka (Adhatoda vasica) relieves cough, bronchitis, and other asthmatic symptoms; boswellia (Boswellia serrata), to relieve pain or inflammation; and tylophora (Tylophora indica) for respiratory relief.

Other herbs beneficial for asthma include Echinacea, licorice root, and slippery elm bark tablets. Licorice root, ginger root, and elderberry open up the respiratory tract.

Caution: Do not take Echinacea if you have an autoiimune disorder. Do not use licorice on a daily basis for more than seven days in a row, and avoid it completely if you have high blood pressure.

Recommendations:

Homeopathic use of belladonna have been shown to relax the bronchioles in the lungs which alleviates the wheezing symptoms in an asthma attack.

Eat a diet consisting primarily of fresh fruits and vegetables, oatmeal, brown rice, and whole grains. The diet should be relatively high in protein, low in carbohydrate, and contain no sugar.

Include garlic and oinions in your diet. These food contain quercatin and mustard oils, which have been shown to inhibit an enzyme that aids in releasing inflammatory chemicals.

Avoid gas-producing foods, such as beans, brassicas ( broccoli, cauliflower, and cabbage) and large amounts of bran. Gas can aggravate an asthmatic condition by putting pressure in the diaphragm.

Do not eat ice cream or drink extremely cold liquids. Cold can shock the bronchial tubes into spasms.

Use a juice fast, a fast using distilled water or lemon juice or a combination of both for three days each month to help rid the body of toxins and mucus.

Eat lightly- a large meal can cause shortness of breath by making the stomach put pressure on the diaphragm

Practice methods to relieve stress as they can trigger an attack.

In the next article, we would deal with clinical (hospital based) regimens on the management of asthma.

On Asthma

2009-04-13T08:47:00.000-07:00

Asthma is a lung disease that causes obstruction of the airways. It is an overreaction of the body’s immune system usually caused by exposure to an allergen, a substance that the body perceives as foreign and dangerous.

During an asthma attack, spasms in the muscles surrounding the bronchi (small airways in the lungs) constrict, impeding the outward passage of air. Asthma sufferers often describe this plight as “starving for air”. Typical symptoms of an asthma attack are coughing, wheezing, a feeling of tightness in the chest, and difficulty breathing. An attack can last for a few minutes or several hours.

The spasms characterizing an acute attack are not the cause of the disorder, but a result of chronic inflammation and hypersensitivity of the airways to certain stimuli. An attack can be triggered if a susceptible individual is exposed to an allergen, but irritants, infection, stress, exercise, use of aspirin, ibuprofen, naproxen, or other NSAIDs – or even rapid changes in weather and humidity- can trigger an attack.

Common asthma provoking allergens include animal dander, cockroach allergens, pollens, mold, pet dander, chemicals, drugs, dust mites, environmental pollutants, feathers, food additives ( such as monosodium glutamate, sulfites such as sodium metabisulfite), sea food, dairy products, nuts, yeast-based food, fumes, mold, and tobacco smoke.

Factors that can trigger non allergic asthma include adrenal disorders, anxiety, temperature changes, exercise, extremes of dryness or humidity, fear, laughing, low blood sugar, and stress. A respiratory infection like bronchitis is the most common provoker. Whatever the particular instigator, the bronchial tubes swell and become plugged with mucus. This inflammation further irritates the airways, resulting in even greater sensitivity. The attacks become more frequent and the inflammation more severe.

Asthma epidemics related to atmospheric contamination – situations in which dust and chemical particles are abundant, especially in enclosed environments- are well known. Occupational exposure to certain substances, such as urethrane and polyurethrane, used in the adhesives and plastic industry, along with rubber epoxy resins from paint, textile cleaner’s fumes, dry cleaning chemicals, and others also may be major risk factors.

Asthma symptoms may resemble those of other diseases, such as emphysema, bronchitis, heart burn, and lower respiratory infections.

Common signs and symptoms of asthma include: recurrent wheezing, coughing, trouble breathing, chest tightness, symptoms that occur or worsen at night, symptoms that are triggered by cold air, exercise or exposure to allergens.

Wheezing — high-pitched whistling sounds when you breathe out — is one of the main signs of asthma and indicates obstructed airways.

Although your symptoms, medical history and physical examination may suggest that you have asthma, lung (pulmonary) function tests may be needed to confirm an asthma diagnosis. Lung function tests may include one or more of the following tests:

a. Spirometry

This noninvasive test measures how well you breathe. During spirometry, you take deep breaths and forcefully exhale into a hose connected to a machine called a spirometer. Spirometry testing reveals two measurements that are important in diagnosing asthma:

Forced vital capacity (FVC), which is the maximum amount of air you can inhale and exhale.

Forced expiratory volume (FEV-1), which is the maximum amount of air you can exhale in one second.

The two measurements are compared. If certain key measurements are below normal for a person your age, it may be a sign that your airways are obstructed. Your doctor may ask you to inhale a bronchodilator drug used in asthma treatment to open obstructed air passages and then try the test again. If your measurements improve significantly, it's likely that you have asthma. Your doctor may still suspect that you have asthma even if your initial spirometry measurements are normal. If so, you may need additional tests.

b. Challenge test

During this test, your doctor deliberately tries to trigger airway obstruction and asthma symptoms by having you inhale an airway-constricting substance or take several breaths of cold air. If you appear to have exercise-induced asthma, you may be asked to do vigorous physical activity to trigger symptoms.

After triggering your symptoms, you retake the spirometry test. If your spirometry measurements are still normal, it's likely that you don't have asthma. But if your measurements have fallen significantly, it may mean you have asthma.

On Wednesday, April 15, we'll deal with nutrients, herbs, and other traditional approaches in the management of asthma.

Medical Guidelines vs Atherosclerosis

2009-04-11T08:51:00.000-07:00

The following is the secondary prevention from progressive atherosclerosis for patients with coronary and other vascular diseases as released by the American Heart Association and American College of Cardiology in 2006

Intervention Recommendations With Class of Recommendation and Level of Evidence

SMOKING:

Goal: Complete cessation. No exposure to environmental tobacco smoke.

• Ask about tobacco use status at every visit.

• Advise every tobacco user to quit.

• Assess the tobacco user’s willingness to quit.

• Assist by counseling and developing a plan for quitting.

• Arrange follow-up, referral to special programs, or pharmacotherapy (including nicotine replacement and bupropion).

• Urge avoidance of exposure to environmental tobacco smoke at work and home.

BLOOD PRESSURE CONTROL:

<140/90>
For all patients: Initiate or maintain lifestyle modification—weight control; increased physical activity; alcohol moderation; sodium reduction; and emphasis on increased consumption of fresh fruits, vegetables, and low-fat dairy products.

For patients with blood pressure 140/90 mm Hg (or 130/80 mm Hg for individuals with chronic kidney disease or diabetes):

As tolerated, add blood pressure medication, treating initially with ß-blockers and/or ACE inhibitors, with addition of other drugs such as thiazides as needed to achieve goal blood pressure.

LIPID MANAGEMENT:

Goal: LDL-C <100> 200 mg/dL, non-HDL-C should be <130>

For all patients:

• Start dietary therapy. Reduce intake of saturated fats (to <7%>trans-fatty acids, and cholesterol (to <200>

• Adding plant stanol/sterols (2 g/d) and viscous fiber (>10 g/d) will further lower LDL-C.

• Promote daily physical activity and weight management.

• Encourage increased consumption of omega-3 fatty acids in the form of fish or in capsule form (1 g/d) for risk reduction. For treatment of elevated triglycerides, higher doses are usually necessary for risk reduction. Usefulness/ efficacy on this is less well established by evidence/opinion.

For lipid management:

Assess fasting lipid profile in all patients, and within 24 hours of hospitalization for those with an acute cardiovascular or coronary event. For hospitalized patients, initiate lipid-lowering medication as recommended below before discharge according to the following schedule:

• LDL-C should be <100>and

• Further reduction of LDL-C to <70>

• If baseline LDL-C is 100 mg/dL, initiate LDL-lowering drug therapy.

• If on-treatment LDL-C is 100 mg/dL, intensify LDL-lowering drug therapy (may require LDL-lowering drug combination.

• If baseline LDL-C is 70 to 100 mg/dL, it is reasonable to treat to LDL-C <70>

• If triglycerides are 200 to 499 mg/dL, non-HDL-C should be <130>and

• Further reduction of non-HDL-C to <100>

• Therapeutic options to reduce non-HDL-C are:

More intense LDL-C–lowering therapy , or

Niacin (after LDL-C–lowering therapy) , or

Fibrate therapy (after LDL-C–lowering therapy)

• If triglycerides are 500 mg/dL, therapeutic options to prevent pancreatitis are fibrate or niacin before LDL-lowering therapy; and treat LDL-C to goal after triglyceride-lowering therapy. Achieve non-HDL-C <130>

PHYSICAL ACTIVITY:

Goal: 30 minutes, 7 days per week (minimum 5 days per week)

• For all patients, assess risk with a physical activity history and/or an exercise test, to guide prescription.

• For all patients, encourage 30 to 60 minutes of moderate-intensity aerobic activity, such as brisk walking, on most, preferably all, days of the week, supplemented by an increase in daily lifestyle activities (eg, walking breaks at work, gardening, household work).

• Encourage resistance training 2 days per week.

• Advise medically supervised programs for high-risk patients (eg, recent acute coronary syndrome or revascularization, heart failure).

WEIGHT MANAGEMENT:

Goal: Body mass index: 18.5 to 24.9 kg/m² and

Waist circumference: men <40>

• Assess body mass index and/or waist circumference on each visit and consistently encourage weight maintenance/reduction through an appropriate balance of physical activity, caloric intake, and formal behavioral programs when indicated to maintain/achieve a body mass index between 18.5 and 24.9 kg/m².

• If waist circumference (measured horizontally at the iliac crest) is 35 inches in women and 40 inches in men, initiate lifestyle changes and consider treatment strategies for metabolic syndrome as indicated.

• The initial goal of weight loss therapy should be to reduce body weight by approximately 10% from baseline. With success, further weight loss can be attempted if indicated through further assessment.

DIABETES MANAGEMENT:

Goal: HbA_1c <7%

• Initiate lifestyle and pharmacotherapy to achieve near-normal HbA_1c.

• Begin vigorous modification of other risk factors (eg, physical activity, weight management, blood pressure control, and cholesterol management as recommended above).

• Coordinate diabetic care with patient’s primary care physician or endocrinologist.

ANTIPLATELET AGENTS/ ANTICOAGULANTS:

• Start aspirin 75 to 162 mg/d and continue indefinitely in all patients unless contraindicated.

For patients undergoing coronary artery bypass grafting, aspirin should be started within 48 hours after surgery to reduce saphenous vein graft closure. Dosing regimens ranging from 100 to 325 mg/d appear to be efficacious. Doses higher than 162 mg/d can be continued for up to 1 year.

• Start and continue clopidogrel 75 mg/d in combination with aspirin for up to 12 months in patients after acute coronary syndrome or percutaneous coronary intervention with stent placement (1 month for bare metal stent, 3 months for sirolimus-eluting stent, and 6 months for paclitaxel-eluting stent).

Patients who have undergone percutaneous coronary intervention with stent placement should initially receive higher-dose aspirin at 325 mg/d for 1 month for bare metal stent, 3 months for sirolimus-eluting stent, and 6 months for paclitaxel-eluting stent.

• Manage warfarin to INR of 2.0 to 3.0 for paroxysmal or chronic atrial fibrillation or flutter, and in post–myocardial infarction patients when clinically indicated (eg, atrial fibrillation, left ventricular thrombus).

• Use of warfarin in conjunction with aspirin and/or clopidogrel is associated with increased risk of bleeding and should be monitored closely.

RENIN-ANGIOTENSIN-ALDOSTERONE SYSTEM BLOCKERS:

ACE inhibitors:

• Start and continue indefinitely in all patients with left ventricular ejection fraction 40% and in those with hypertension, diabetes, or chronic kidney disease, unless contraindicated.

• Consider for all other patients.

• Among lower-risk patients with normal left ventricular ejection fraction in whom cardiovascular risk factors are well controlled and revascularization has been performed, use of ACE inhibitors may be considered optional.

Angiotensin receptor blockers:

• Use in patients who are intolerant of ACE inhibitors and have heart failure or have had a myocardial infarction with left ventricular ejection fraction 40%.

• Consider in other patients who are ACE inhibitor intolerant.

• Consider use in combination with ACE inhibitors in systolic-dysfunction heart failure.

Aldosterone blockade:

• Use in post–myocardial infarction patients, without significant renal dysfunction or hyperkalemia, who are already receiving therapeutic doses of an ACE inhibitor and ß-blocker, have a left ventricular ejection fraction 40%, and have either diabetes or heart failure.

ß-BLOCKERS:

• Start and continue indefinitely in all patients who have had myocardial infarction, acute coronary syndrome, or left ventricular dysfunction with or without heart failure symptoms, unless contraindicated.

Consider chronic therapy for all other patients with coronary or other vascular disease or diabetes unless contraindicated.

INFLUENZA VACCINATION:

Patients with cardiovascular disease should have an influenza vaccination.

> Patients covered by these guidelines include those with established coronary and other atherosclerotic vascular disease, including peripheral arterial disease, atherosclerotic aortic disease, and carotid artery disease. Treatment of patients whose only manifestation of cardiovascular risk is diabetes will be the topic of a separate AHA scientific statement. ACE indicates angiotensin-converting enzyme.

> Pregnant and lactating women should limit their intake of fish to minimize exposure to methylmercury.

> When LDL-lowering medications are used, obtain at least a 30% to 40% reduction in LDL-C levels. If LDL-C <70>50% in LDL-C levels by either statins or LDL-C–lowering drug combinations.

> The combination of high-dose statin+fibrate can increase risk for severe myopathy. Statin doses should be kept relatively low with this combination. Dietary supplement niacin must not be used as a substitute for prescription niacin.

> Patients with very high triglycerides should not consume alcohol. The use of bile acid sequestrant is relatively contraindicated when triglycerides are >200 mg/dL.

Nutrients, Herbs, etc for Atherosclerosis

2009-04-08T19:40:00.000-07:00

The following are the nutrients, herbs, and other recommendations beneficial to thwart atherosclerosis:

NUTRIENTS

Supplement	Suggested dosage	Comments
*Calcium & Magnesium plus* *Vitamin D3*	1500 mg daily, taken at bedtime 750 mg daily, taken at bedtime 400 mg daily	Needed to maintain proper muscle tone in the blood vessels. Use chelate forms. Aids calcium uptake; enhances immune system
*Coenzyme Q₁₀*	100 mg daily	Improves tissue oxygenation
*Essential fatty acids (flaxseed oil, MaxEPA, or omemga-3 oil complex)*	As directed on label	Reduces blood pressure, lowers cholesterol levels, and helps to maintain proper elasticity of blood vessels. Be sure to use a product that contains Vitamin E to keep essential fatty acids from being rancid.
*Garlic (Kyolic from Wakunaga)*	As directed on label	Has a lipid (fat) regulating effect
*Multivitamin and mineral complex*	As directed on label	All nutrients are needed for protection
*Vitamin C (Ester-C with flavonoids*	2000 mg daily	Antioxidant that acts as a free radical scavenger

Source: Nutritional Healing by Phyllis Balch

Herbs

The following herbs are useful if you suffer from atherosclerosis: cayenne (capsicum), chickweed, and hawthorn berries

Citrin (an extract of the Garcinia cambogia plant) is an herbal produc that inhibits synthesis of potentially dangerous fats in the body.

Ginkgo biloba has been called “nature’s circulation wonder”. It can improve circulation, increasing oxygen and blood flow in the arms, brain, and heart.

Green tea lowers cholesterol and lipid levels, thus decreasing chances of atherosclerosis. Drink green tea ( we suggest one to four cups a day) or take it in extract form. A recent Japanese study recommends not only green tea but also black tea to lower your rate of lipoprotein oxidation, a chemical reaction that makes fat in the blood more likely deposited in the arteries.

Recommendations:

Eat high fiber foods that are low in fat and cholesterol. Fruits, vegetables, and grains should be your primary foods.

Eat plenty of foods rich in Vitamin E to improve circulation. Good choices include dark, green leafy vegetables, legumes, nuts, seeds, soybeans, wheat germ, and whole grains.

Use only pure cold-pressed olive oil or unrefined canola oil (in moderate amounts) as fats in the diet. These may aid in lowering cholesterol. Do not heat these oils.

Drink steam-distilled water only.

Do not eat any candies, chips, fried foods, gravies, high-cholesterol foods, junk foods, pies, processed foods, red meat, or saturated fats.

Avoid egg yolks, ice cream,, salt, and all foods containing white flour and/or sugar. Do not use stimulants such as coffee, colas, and tobacco. Also eliminate alcohol and high-spiced foods.

Maintain a healthy weight for your height. Obesity causes unfavorable changes in serum lipoprotein levels.

Reduce stress and learn techniques to help you handle stress that can not be avoided.

Get regular moderate exercise. A daily walk is good.

Periodically monitor your blood pressure and take steps to lower it as necessary.

DO NOT smoke. Avoid exposure to second hand smoke. Cigarette smoke contains large quantities of free radicals, many of which are known to oxidize low density lipoproteins (LDL, the so-called bad cholesterol), making them more likely to be deposited on the walls of blood vessels. In addition, smoking increases levels of LDL, lowers levels of high density lipoproteins (HDL or good cholesterol), and increases the blood’s tendency to form clots.

On Friday, April 10, see the overview of current clinical practice guidelines for atherosclerosis.

On Atherosclerosis

2009-04-05T08:09:00.000-07:00

Arteriosclerosis and atherosclerosis involve the buildup of deposits on the insides of the artery walls, which causes thickening and hardening of the arteries. In arteriosclerosis, the deposits are composed largely of calcium; in atherosclerosis, the deposits consist of fatty substances, and artery walls lose elasticity and harden. Both conditions have about the same effect on circulation, causing high blood pressure and ultimately leading to angina (chest pain brought on by exertion), heart attack, stroke, and/or sudden cardiac death.

Although arteriosclerosis causes high blood pressure, this can occur the other way around. Calcium based and fatty deposits typically form in areas of the arteries weakened by high blood pressure or strain. The consequent narrowing of the arteries makes blood pressure even higher. As the arteries become less pliable and less permeable, cells may experience ischemia (oxygen starvation) due to insufficient circulation. The fatty plaques can be either stable or unstable. Unstable plaque allows particles to break away and cause further blockage downstream, in the smaller vessels, so it is of more immediate clinical importance.

If one of the coronary arteries get obstructed by accumulated deposits or by a blood clot that has either formed or snagged on the deposit, the heart muscle starves for oxygen and the individual may suffer from a heart attack (myocardial infarction) or angina. When the arteriosclerosis occludes the blood supply to the brain, a cerebrovascular accident or stroke occurs.

Peripheral atherosclerosis, also called arteriosclerosis obliterans, is a type of peripheral vascular disease in which the lower limbs are affected. In the early stages, the major arteries carrying blood to the legs and the feet become narrowed by fatty deposits. Atherosclerosis of the leg and foot not only can limit a person’s mobility, but can also lead to loss of a limb. People who have diseased arteries in the leg or foot are likely to have them elsewhere, mainly in the heart or brain. Early signs of peripheral atherosclerosis are aching muscles, fatigue, and cramping pains in the ankles and legs.

Depending on which arteries are blocked, there may also be pain in the hips and thighs.

Pain in the legs ( most often in the calf, but sometimes in the foot, thigh, hip, or buttocks) brought on by walking and quickly relieved by rest is called intermittent claudication. This is typically the first symptom of peripheral atherosclerosis. Additional symptoms include, numbness, weakness, and a heavy feeling in the legs. These symptoms occur because of the amount of oxygenated blood passing through the plaque-covered arteries is insufficient to meet the needs of the exercising leg muscles. The closer the problem lies in the abdominal aorta – the central artery that branches into the legs- the more tissue affected and the more dangerous the condition.

On Wednesday April 8, we'll deal with herbs and nutrients found to be beneficial against the disorder.

Medical Treatment of abscesses

2009-04-03T08:43:00.000-07:00

A. Specific Measures

Incision and drainage is recommended for all locilated suppurations and is the mainstay of therapy.

Systemic antibiotics are indicated (chosen on the basis of cultures and sensitivity tests, if possible). Sodium dicloxacillin or cephalexin 1.5 gm daily in divided doses by mouth for 10 days, is usually effective. Erythromycin in similar doses may be used in penicillin allergic individuals in communities with low populations of erythromycin-resistant staphylococci or if the particular isolate is sensitive. Ciprofloxacin 500 mg twice daily, is effective against strains of staphylococci resistant to other antibiotics.

Recurrent furunculosis may be effectively treated with a combination of dicloxacillin, 250-500 mg four times daily for 2-4 weeks and rifampicin 300 mg twice daily for 5 days during the period. Clindamycin 150-300 mg daily for 1-2 months, may also cure recurrent furunculosis.

Family members and intimate contacts may need evaluation for staphylococcal carrier state and perhaps concomitant treatment. Applications of topical 2% mupirocin to the nares, axillae, and anogenital area twice daily for 5 days eliminates the staphylococcal carrier state.

B. Local Measures

Immobilize the part and avoid over manipulation of inflamed areas. Use moist heat to help “larger” lesions localize. Use surgical incision and debridement AFTER the lesions are “ripe”. It is not necessary to incise and drain an acute staphylococcal paronychia. Inserting a flat metal spatula and sharpened hardwood stick into the nail fold where it adjoins the nail will release pus from a mature lesion.

Inflamed epidermal cysts may be treated in the initial stages with intralesional injections of triamcinolone acetonide into the borders of the lesions, attempting not to puncture the cyst itself. Drainage of fluctuant lesions results in rapid resolution and reduction of pain.

The traditional approach to abscess

2009-04-01T14:30:00.000-07:00

The following herbs are beneficial for healing abscesses and cleansing the blood:

Burdock root, cayenne (capsicum), red clover, dandelion root, and yellow dock root

Chamomile tea is good for treating dental abscesses. Drink a cup three or four times a day. If your face is swollen from the infection, chamomile can be prepared as a poultice and applied to the outside of the cheek once or twice a day for five to ten minutes until the infection is gone.

Consuming distilled water with fresh lemon juice, plus 3 cups of Echinacea, goldenseal, and astragalus or suma tea every day is helpful. Golden seal can also be made into a poultice and applied directly to the abscess. Or apply, alcohol-free doldenseal extract to sterile gauze and place the gauze over the abscess.

Cautions: Do not use astragalus in the presence of fever. Do not take Echinacea if you have an autoimmune disorder. Do not take golden seal on a daily basis for more than one week at a time, and do not use it for pregnancy. If you have a history of cardiovascular disease, diabetes, or glaucoma, use it only under a doctor’s supervision.

Echinacea tea or extract in water can be used as a mouthwash for dental abscesses. Be sure to prepare it warm and rinse your mouth with it every two hours.

Caution: Do not take Echinacea if you have an autoimmune disorder.

A poultice that combines lobelia and slippery elm bark is soothing and fights infection.

Milk thistle, taken in capsule form, is good for the liver and aids in cleansing the bloodstream.

Tea tree oil, applied externally, is a potent natural antiseptic that kills infectious organisms without harming healthy cells. Mix 1 part tea tree oil with 4 parts water and apply the mixture with a cotton ball three times a day. This will destroy the bacteria, hasten healing, and prevent infection from spreading.

Basic recommendations would be the following:

Eat fresh pineapple daily. Pineapple contains bromelain, an enzyme that fights inflammation and aids healing.
Include garlic and onions in your diet. They are high in sulfur and can help both cure and prevent abscesses.
Perform a liquid fast using fresh juices for twenty four to seventy two hours.
Add kelp to the diet for beneficial minerals.
For an external abscess, apply honey to the affected area. Honey destroys bacteria and viruses, apparently by drawing moisture out of them.
To cleanse the affected area, apply chlorophyll liquid mixed with water several times a day.
If you must take antibiotics, supplement your diet with the B vitamins and products containing the “friendly” bacteria such as acidophilus and yogurt plus vitamin B.
If pain, redness, bleeding, or discharge increases, then consult your doctor.

Source: "Prescription for Nutritional Healing", Mr Phyllis Balch

On Friday April 3, learn how licensed medical practitioners approach and treat this problem.

Week 1: Abscesses

2009-03-29T00:14:00.000-07:00

An abscess is formed when pus accumulates in a tissue, organ, confined space in the body due to an infection. An abscess can form in the brain, lungs, teeth, gums, under arms, GI tract, abdominal wall, ears, tonsils, sinuses, bones, breasts, kidneys, prostate gland, rectum, scrotum, and to almost any part of the body. They may indeed be located externally or internally and may result from injury or a lowered resistance to infection.

The affected area may be swollen, inflamed, hot, red, and tender. The individual may also experience fatigue, weight; loss, anorexia, and alternating bouts of fever and chills. Rupture of the abscess and in severe cases, bacteremia (blood infection) can occur. The material inside an abscess consists of living and dead white blood cells, bacteria, dead tissue, and toxins – all of which can be discarded from the body.

An abscess is said to be acute if it appears suddenly ( in a matter of a few hours or overnight) and is termed chronic is it has been present for a period of days or weeks. Acute abscesses generally respond better to treatment in a matter of days.

Basically, an abscess is a sign that the body is trying to rid itself of impurities. The impurities may be half-starved cells, deficient in nutrients such as sulfur, or toxins that accumulate because of a failure of the normal eliminative processes. Such a situation stems from poor diet and exposure to environmental pollutants, chemicals, or harmful substances. Eating junk food not only clutters the system with food lacking in nutrients, but also prevents the cellular wastes from being eliminated efficiently by causing problems such as constipation and a sluggish liver, spleen, and kidney function.

On the next post this Wednesday April 1, learn some traditional and nutritional modalities used to control and heal abscesses.

Welcome to "The Doctor is In"

2009-02-23T07:48:00.000-08:00

Hello! In this website, I would share to you my ideas as a licensed health professional (medical internist) on various health issues, diseases, and topics. I would also tackle (with reference to other health books) the viewpoint of non Western medicine on such topics. Yep, you are free to comment, share your thoughts, and even consult for advice. Don;t expect me to prescribe you a drug here with exact dosage; if you want to, visit my clinic. :)