cme.staging.medscape.com This article is a CME certified activity. To earn credit for this activity visit: http://cme.staging.medscape.

com/viewarticle/708548

From MedscapeCME Cardiology

Rethinking Hypertension in the 21st Century: An Overview of the Expanded Definition and Classification of Hypertension CME
Thomas D. Giles, MD CME Released: 09/14/2009; Valid for credit through 09/14/2010

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]

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]

The Interrelationship of High Blood Pressure and Other Cardiovascular Risk Factors
Another 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, risk stratification based on BP levels alone often underestimates CV risk. This is because above-optimal BP levels rarely occur in isolation, and patients seen in clinical practice frequently have multiple CVD markers or risk factors (eg, overweight, insulin resistance, dyslipidemia) that point to greater overall risk.[1,9-13] What is particularly significant, from the perspective of defining hypertension beyond BP thresholds, is that many of these disease processes are intimately interrelated and interact via common pathobiologic processes involving oxidative stress and endothelial dysfunction (Figure).[14] Moreover, the presence of risk factors and disease markers defines the earliest stage in this CVD continuum, well before overt CVD and target-organ damage can be measured in the clinic.[14] From this perspective, above-optimal BP (a risk factor) is not necessarily synonymous with hypertension (a disease representative of progressive CVD and tissue injury).[6]

Figure. Cardiovascular and renal pathophysiologic continuum. CV = cardiovascular; MI = myocardial infarction; CHF = congestive heart failure; ESRD = end-stage renal disease. Adapted from Dzau VJ, et al.[14] Another 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, based on thresholds for each

individual risk factor alone. This is highlighted by the particularly deleterious condition known as the cardiometabolic syndrome, in which individual risk factors combine to increase CV risk synergistically, rather than additively. [12,15] Ultimately, a more clinically meaningful assessment of CV risk can be obtained by global assessment of a patient's risk, rather than focusing solely on whether a patient has crossed a particular BP threshold. Taken together, this evidence suggests that it may be more useful to view BP as 1, but not the only, biomarker for the disease hypertension, and to view above-optimal levels of BP in an individual patient as those that, when sustained, cause damage to the vasculature. [6] This forms the basis of the revised definition of hypertension, as shown in Table 1. Table 1. Revised Definition of Hypertension From Hypertension Writing Group 2009 Hypertension is a progressive CV syndrome arising from complex and interrelated etiologies Early markers of the syndrome are often present before BP elevation is sustained; therefore, hypertension cannot be classified solely by discreet BP thresholds Progression is strongly associated with functional and structural cardiac and vascular abnormalities that damage the heart, kidneys, brain, vasculature, and other organs, and lead to premature morbidity and death Reduction of elevated BP generally confers a reduction in the risk for CV events. Note that HWG separates elevated BP (one manifestation of the disease) from hypertension (the disease) BP = blood From Giles T, et al.[6] pressure; CV = cardiovascular

Because hypertension is defined by as "a progressive cardiovascular syndrome," it is clinically helpful to categorize, or stage, patients (Table 2), 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.[6] Table 2. Revised Definition and Classification of Hypertension From Hypertension Writing Group 2009 Classification Descriptive category Normal Stage Hypertension 1 Stage 2 Stage Hypertension Hypertension or Sustained BP elevations OR BP Marked sustained elevations 3 and BP

Normal BP or Occasional rare BP intermittent elevations elevations

AND OR no identifiable early CVD CVD Cardiovascular risk factors (see Table 3) None or few

progressive CVD

OR advanced CVD

Several risk Many risk Many risk factors factors present factors present present Usually present Overtly present Overtly present with progression Early present signs Overtly present with or without CVD events disease

Early disease None markers (see Table 4) Target-organ disease (see Table 5) None

None

BP = blood From Giles T, et al.[6]

pressure;

CVD

cardiovascular

In the broadest sense, individuals are classified as either normal or hypertensive based on their CV status (ie, the absence or presence of identifiable CVD), regardless of their BP pattern. The stages within the hypertension category are further refined, based on BP patterns or the extent of CVD (early, advanced, or progressive). Each hypertension stage is further characterized by the cumulative presence or absence of risk factors for CVD (Table 3);markers of hypertensive CVD, such as microalbuminuria or mild left ventricular hypertrophy (Table 4); and evidence of target-organ damage, such as frank albuminuria or moderate-to-severe left ventricular hypertrophy (Table 5).[6] The occurrence of a major cardiac event clearly places the progression of hypertensive CVD at a more advanced stage.[6] Table 3. Cardiovascular Risk Factors Increasing age Elevated BPa High heart rate Overweight/obesity Increased BMI Central obesity Increased abdominal circumference Increased abdominal adiposity (waist-to-hip ratio)a Dyslipidemia

 Elevated LDL or non-HDLb cholesterol Low HDL cholesterola Elevated triglyceridesa Elevated blood glucose, insulin resistance, or diabetes mellitusa Chronic kidney disease Smoking Family history of premature CVD (age < 50 yr in men, < 60 yr in women) Sedentary lifestyle Psychosocial stressors Elevated hs-CRP BMI = body mass index; BP = blood pressure; CVD = cardiovascular disease; HDL = high-density lipoprotein; hs-CRP = high-sensitivity C-reactive protein; LDL = lowdensity lipoprotein a Components of the metabolic syndrome b Non-HDL cholesterol = total cholesterol minus HDL cholesterol Table 4. Early Markers of Hypertensive Cardiovascular Disease System Blood pressure Loss of nocturnal BP dipping Exaggerated BP responses to exercise or mental stress Salt sensitivity Widened pulse pressure Cardiac Left ventricular hypertrophy (mild) Increased atrial filling pressure Decreased diastolic relaxation Increased natriuretic peptide Renal Microalbuminuria (urinary albumin excretion of 30-300 mg/day)a Reduced estimated GFR (60-90 mL/min) Physiologic Alteration

Cerebrovascular Stroke Transient ischemic attack Decreased cognitive function Dementia Loss of vision BP = blood pressure; GFR a Also a marker of microcirculatory disease = glomerular filtration rate

Table 5. Hypertensive Target-Organ Damage and Overt Cardiovascular Disease System Cardiac Left ventricular hypertrophy (moderate to severe) Systolic or diastolic cardiac dysfunction Symptomatic heart failure Myocardial infarction Angina pectoris Ischemic heart disease or prior revascularization Vascular Peripheral arterial disease Carotid arterial disease Aortic aneurysm Renal Albuminuria (urinary albumin excretion > 300 mg/day) Chronic kidney disease (estimated GFR < 60 mL/min) or ESRD Cerebrovascular Stroke Transient ischemic attack Evidence of Target-organ Damage and Cardiovascular Disease

Decreased cognitive function Dementia Loss of vision ESRD = end-stage renal disease; GFR = glomerular filtration rate

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 Clinical Category Characterization Optimal BP levels Normal BP Pattern Practical Implications

Resting BP levels Includes some patients usually < 120/80 mm identified as having Hg prehypertension (based on JNC 7 criteria)

No identifiable early Occasional BP markers of CVD elevations, even to 140/90 mm Hg, may occur Early CVD markers BP levels > 115/75 mm Earliest identifiable stage present Hg of hypertensive disease Frequently 1 or more BP may be frankly CVD risk factors elevated, particularly present with environmental stress No evidence of target-organ damage Diffuse disease markers present OR evidence (limited) of early target-organ damage Stage 2 Sustained resting BP Equivalent to JNC 7 stage frequently 140/90 1 hypertension mm Hg, with much higher elevations induced by physiologic or psychologic Includes individuals with prehypertension (based on JNC 7 criteria) who also have CVD risk factors or early disease markers

Stage 1

stressors Indicates disease progressive

Risk factors, if not attenuated, continue to contribute to progressive target-organ disease Overt CVD present Sustained resting BP Equivalent to JNC 7 stage levels 140/90 mm Hg 2 hypertension usual (untreated or inadequately treated) 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

Stage 3

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]

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.

Post-Assessment: Measuring Educational Impact

Thank you for participating in the CME activity. Please take a few moments to read the following cases and complete the questions that follow to help us assess the effectiveness of this medical education activity. Questions answered incorrectly will be highlighted. In your experience, which of the following is the most significant barrier to the optimal management of patients with hypertension? Concerns about drug-drug interactions Lack of uniform clinical practice guidelines Lack of adequate pharmacologic treatments Potential side effects of pharmacologic treatments In your experience, which of the following is the most significant patient-related barrier to optimal management of patients with hypertension? Lack of patient adherence to nonpharmacologic therapies Inconvenience of taking multiple pills per day Delayed presentation to clinicians due to lack of symptoms in early stages of hypertension Delayed presentation to clinicians due to lack of insurance Case #1: Martin, a 47-year-old man, presents to your office for an initial visit. He has no specific complaints but wants to discuss his blood pressure (BP). "My wife has high blood pressure and has this home blood pressure monitor she uses," Martin says. "I've been checking my own numbers over the past couple of months." He presents you with a

logbook containing 6 BP readings: 119/78, 118/72, 130/92, 148/80, 122/72, and 120/70. Martin has no other medical problems, takes no medications, and has a family history notable for diabetes in his mother, diagnosed at age 65 years. He does not smoke cigarettes but does drink 1-2 alcoholic beverages daily and admits to eating fast food frequently. Martin jogs 4 days per week. In the office, his BP is 144/92 and his pulse is 68 beats/min. His body mass index (BMI) is 23 kg/m 2 and his waist circumference is 34 in. Fasting lipid panel reveals: total cholesterol 141 mg/dL, high-density lipoprotein cholesterol (HDL-C) 48 mg/dL, triglycerides (TG) 145 mg/dL, and low-density lipoprotein cholesterol (LDL-C) 68 mg/dL. Fasting blood glucose is 78 mg/dL and creatinine is 1.0 mg/dL. Which of the following additional tests would you consider in assessing cardiovascular disease (CVD) risk and hypertension category in this patient? Erythrocyte sedimentation rate (ESR) Urinary albumin Exercise treadmill test Stress echocardiogram Case #1, continued: Completed test results revealed no abnormality. Which of the following best classifies this patient's hypertension category, based on the classification scheme of the Hypertension Writing Group (HWG)? Normal Stage 1 hypertension Stage 2 hypertension Stage 3 hypertension Which of the following would you consider a more accurate marker of CVD risk in your patients? The presence of elevated BP to > 140/90 The presence of narrowed pulse pressure Office diastolic BP reading Systolic BP pattern Which of the following management steps would you take? Initiate antihypertensive monotherapy in addition to dietary changes Initiate antihypertensive combination therapy in addition to dietary changes Recommend dietary changes Advise against continued ambulatory BP monitoring Case #2: Cecilia, a 57-year-old woman with osteoarthritis, presents to your office for follow-up. Medications include acetaminophen and naproxen, and her family history is notable for stroke in her mother at age 53 years. Cecilia smokes half a pack of cigarettes per day, drinks no alcohol, and exercises infrequently. Her BMI is 27.2 kg/m 2 and her waist circumference is 39 in. Her BP is 120/82 and her pulse is 92 beats/min. BP

recordings that Cecilia has made at her local pharmacy over the preceding 3 months range from 110 to 128 systolic and 68 to 85 diastolic. Fasting lipid panel reveals: total cholesterol 198 mg/dL, HDL-C 32 mg/dL, TG 175 mg/dL, and LDL-C 131 mg/dL. Fasting blood glucose is 84 mg/dL and creatinine is 0.9 mg/dL. Which of the following best classifies this patient's hypertension category (based on the classification scheme of the HWG)? Normal Stage 1 hypertension Stage 2 hypertension Stage 3 hypertension Which of the following is characteristic of this patient's condition? Loss of nocturnal dips in BP may provide clearer evidence of early hypertensive disease than absolute BP Narrowing of pulse pressure may provide clearer evidence of early hypertensive disease than absolute BP According to the JNC 7 classification, this patient has stage 1 hypertension According to the JNC 7 classification, this patient has stage 2 hypertension Which of the following additional tests would you consider in assessing CVD risk in this patient? ESR High-sensitivity C-reactive protein (hs-CRP) Hemoglobin A1c Plasma aldosterone-to-renin ratio Which of the following management steps would you take? Initiate antihypertensive monotherapy in addition to dietary changes Initiate antihypertensive combination therapy in addition to dietary changes Recommend dietary changes Initiate an antiplatelet agent Approximately how many patients do you see each week? Approximately what percentage of your patients has CVD risk?

Save and Proceed

This activity is supported by an independent educational grant from Pfizer.

This article is a CME certified activity. To earn credit for this activity visit: http://cme.staging.medscape.com/viewarticle/708548 [ CLOSE WINDOW ] References 1. Weir MR. Risk-based classification of hypertension and the role of combination therapy. J Clin Hypertens (Greenwich). 2008;10:4-12. 2. Giles TD. Assessment of global risk: a foundation for a new, better definition of hypertension. J Clin Hypertens (Greenwich). 2006;8:5-14. 3. Khosia N, Black HR. Expanding the definition of hypertension to incorporate global cardiovascular risk. Curr Hypertens Rep. 2006;8:384-390. 4. Giles TD, Berk BC, Black HR, et al. Expanding the definition and classification of hypertension. J Clin Hypertens (Greenwich). 2005;7:505-512. 5. Chobanian AV, Bakris GL, Black HR, et al; National Heart, Lung, and Blood Institute Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure; National High Blood Pressure Education Program Coordinating Committee. The Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure: the JNC 7 report. JAMA. 2003;289:2560-2572. 6. Giles TD, on behalf of the Hypertension Writing Group. Definition and classification of hypertension: an update. J Clin Hypertens (Greenwich). In press. 7. Sierra C, de la Sierra A. Early detection and management of the high-risk patient with elevated blood pressure. Vasc Health Risk Manag. 2008:4;289-296. 8. Franklin SS, Khan SA, Wong ND, et al. Is pulse pressure useful in predicting risk for coronary heart disease? The Framingham Heart Study. Circulation. 1999;100:354-360. 9. Basile J. Management of global risk across the continuum of hypertensive heart disease. J Clin Hypertens (Greenwich). 2006;8:21-30. 10. Khot UN, Khot MB, Bajzer CT. Prevalence of conventional risk factors in patients with coronary heart disease. JAMA. 2003;290:898-904. 11. Neaton JD, Wentworth D; the Multiple Risk Factor Intervention Trial Research Group. Serum cholesterol, blood pressure, cigarette smoking, and death from coronary heart disease: overall findings and differences by age for 316,099 white men. Arch Intern Med. 1992;152:56-64. 12. Meigs JB, D'Agostino RB Sr, Wilson PW, et al. Risk variable clustering in the insulin resistance syndrome: the Framingham Offspring Study. Diabetes. 1997;46:1594-1600. 13. Gregg EW, Cheng YJ, Cadwell BL, et al. Secular trends in cardiovascular disease risk factors according to body mass index in US adults. JAMA. 2005;293:18681874. 14. Dzau VJ, Antman EM, Black HR, et al. The cardiovascular disease continuum validated: clinical evidence of improved patient outcomes: Part I: pathophysiology and clinical trial evidence (risk factors through stable coronary artery disease). Circulation. 2006;114:2850-2870.

15. Hoerger TJ, Ahmann AJ. The impact of diabetes and associated cardiometabolic risk factors on members: strategies for optimizing outcomes. J Manag Care Pharm. 2008;14:S2-S14. 16. Pickering TG, White WB; American Society of Hypertension Writing Group. ASH position paper: home and ambulatory blood pressure monitoring. When and how to use self (home) and ambulatory blood pressure monitoring. J Clin Hypertens (Greenwich). 2008;10:850-855. 17. Julius S, Nesbitt SD, Egan BM, et al; Trial of Preventing Hypertension (TROPHY) Study Investigators. Feasibility of treating prehypertension with an angiotensin-receptor blocker. N Engl J Med. 2006;354:1685-1697. 18. The Trials of Hypertension Prevention Collaborative Research Group. Effects of weight loss and sodium reduction intervention on blood pressure and hypertension incidence in overweight people with high-normal blood pressure: the Trials of Hypertension Prevention, phase II. Arch Intern Med. 1997;157:657-667. 19. PROGRESS Collaborative Group. Randomised trial of a perindopril-based bloodpressure-lowering regimen among 6,105 individuals with previous stroke or transient ischaemic attack. Lancet. 2001;358:1033-1041. [CLOSE WINDOW]

Authors and Disclosures

As an organization accredited by the ACCME, MedscapeCME requires everyone who is in a position to control the content of an education activity to disclose all relevant financial relationships with any commercial interest. The ACCME defines "relevant financial relationships" as financial relationships in any amount, occurring within the past 12 months, including financial relationships of a spouse or life partner, that could create a conflict of interest. MedscapeCME encourages Authors to identify investigational products or off-label uses of products regulated by the US Food and Drug Administration, at first mention and where appropriate in the content.

Author(s)
Thomas D. Giles, MD

Professor of Medicine, Tulane University School of Medicine, New Orleans, Louisiana Disclosure: Thomas D. Giles, MD, has disclosed the following relevant financial relationships: Received grants from: AstraZeneca Pharmaceuticals LP; Novartis Pharmaceuticals

Corporation Served as an advisor or consultant for: Boehringer Ingelheim Pharmaceuticals, Inc.; Bristol-Myers Squibb Company; Daiichi Sankyo, Inc.; Forest Laboratories, Inc.; Merck & Co., Inc.; NicOx; Novartis Pharmaceuticals Corporation; Pfizer Inc.; sanofi-aventis

Editor(s)
Ariana Del Negro Scientific Director, MedscapeCME

Ariana Del Negro has disclosed no relevant financial relationships. Disclaimer The material presented here does not necessarily reflect the views of MedscapeCME or companies that support educational programming on www.medscapecme.com. These materials may discuss therapeutic products that have not been approved by the US Food and Drug Administration and off-label uses of approved products. A qualified healthcare professional should be consulted before using any therapeutic product discussed. Readers should verify all information and data before treating patients or employing any therapies described in this educational activity. MedscapeCME Cardiology 2009 MedscapeCME This article is a CME certified activity. To earn credit for this activity visit: http://cme.staging.medscape.com/viewarticle/708548 [ CLOSE WINDOW ]

CME Information
CME Released: 09/14/2009; Valid for credit through 09/14/2010

Target Audience
This activity is intended for physicians specializing in cardiology, family medicine/primary care, nephrology, diabetes/endocrinology, as well as physician assistants, nurses, and other healthcare professionals who manage patients with or at risk for hypertension and related diseases.

Goal

The goal of this activity is to describe the complex relationship between hypertension and other related diseases and how this relationship influenced the updated definition and classification of hypertension proposed by the Hypertension Writing Group.

Learning Objectives
Upon completion of this activity, participants will be able to: 1. Describe the interrelationship between high blood pressure and other cardiovascular (CV) risk factors 2. Delineate the definition and classification of hypertension according to the Hypertension Writing Group consensus statement 3. Discuss strategies for and the clinical implications of treating patients along a continuum of global CV risk

Credits Available
Physicians - maximum of 1.00 AMA PRA Category 1 Credit(s) All other healthcare professionals completing continuing education credit for this activity will be issued a certificate of participation. Physicians should only claim credit commensurate with the extent of their participation in the activity.

Accreditation Statements
For Physicians

The American Society of Hypertension is accredited by the Accreditation Council for Continuing Medical Education to provide continuing medical education for physicians. The American Society of Hypertension, Inc. (ASH) designates this educational activity for a maximum of 1.0 AMA PRA Category 1 Credit(s) . Physicians should only claim credit commensurate with the extent of their participation in the activity. Contact This Provider For questions regarding the content of this activity, contact the accredited provider for this CME/CE activity noted above. For technical assistance, contact CME@medscape.net

Instructions for Participation and Credit

There are no fees for participating in or receiving credit for this online educational activity. For information on applicability and acceptance of continuing education credit for this activity, please consult your professional licensing board. This activity is designed to be completed within the time designated on the title page; physicians should claim only those credits that reflect the time actually spent in the activity. To successfully earn credit, participants must complete the activity online during the valid credit period that is noted on the title page. Follow these steps to earn CME/CE credit*: 1. Read the target audience, learning objectives, and author disclosures. 2. Study the educational content online or printed out. 3. Online, choose the best answer to each test question. To receive a certificate, you must receive a passing score as designated at the top of the test. MedscapeCME encourages you to complete the Activity Evaluation to provide feedback for future programming. You may now view or print the certificate from your CME/CE Tracker. You may print the certificate but you cannot alter it. Credits will be tallied in your CME/CE Tracker and archived for 6 years; at any point within this time period you can print out the tally as well as the certificates by accessing "Edit Your Profile" at the top of your Medscape homepage. *The credit that you receive is based on your user profile.

Hardware/Software Requirements
MedscapeCME is accessible using the following browsers: Internet Explorer 6.x or higher, Firefox 2.x or higher, Safari 2.x or higher. Certain educational activities may require additional software to view multimedia, presentation or printable versions of their content. These activities will be marked as such and will provide links to the required software. That software may be: Macromedia Flash, Adobe Acrobat, or Microsoft PowerPoint.