Friday, October 30, 2009

New Joint Statement Streamlines Definition of Metabolic Syndrome

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.

Wednesday, October 28, 2009

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

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.

Sunday, October 25, 2009

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

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)
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

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

Thursday, October 22, 2009

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

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+++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Monday, October 19, 2009

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

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]

Friday, October 16, 2009

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

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]

Tuesday, October 13, 2009

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

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."

Friday, October 9, 2009

Music Therapy Lowers Blood Pressure and Reduces Reinfarction Rates in ACS

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.