Hypertension in African-Americans
Hypertension is a persistent and frequently progressive elevation in blood pressure. The level of systolic and/or diastolic blood pressure at which the elevation assumes the diagnosis of hypertension depends on the presence or absence of coexisting comorbidities. The current classification of blood pressure and the level of blood pressure that defines hypertension for the major comorbid conditions as recommended in the seventh report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of high blood pressure are shown in Table 43–1. The prevalence of hypertension varies with age and sex. It is estimated that 23% of adult Americans between the ages of 20 and 74 years have hypertension. About 75% of women aged 75 years and over have hypertension and about 64% of men aged 75 years and over have hypertension. At all ages and in both sexes African-Americans have the highest prevalence of hypertension in the United States. In African-Americans hypertension tends to develop at an earlier age and tends to be more severe than in other races. Some patients with systemic hypertension will have a specific identifiable cause for the elevated systemic blood pressure. The estimated proportion of the cases of secondary hypertension among patients with systemic hypertension ranges from about 5% to 10% and has not been shown to exhibit racial predilection. Patients with secondary hypertension usually exhibit suggestive constellations of signs and/or symptoms on initial evaluation and should undergo further evaluation for specific causes of hypertension regardless of their race and/or ethnicity.
Blood pressure category | Blood pressure reading, mm Hg | |
|---|---|---|
Systolic | Diastolic | |
Normal range | <120 | and <80 |
Prehypertension | 120–139 | or 80–90 |
Hypertension | ||
Stage 1 | 140–159 | or 90–99 |
Stage 2 | ≥160 | or ≥100 |
Hypertension is one of the major risk factors for cardiovascular disease. Uncontrolled hypertension leads to specific target organ damage that contributes to overall cardiovascular morbidity and mortality. African-Americans exhibit a greater increase in target organ damage than other racial and ethnic groups. In fact, the heart disease mortality rate is 50% higher, the stroke mortality rate is 80% higher, and the incidence of hypertension-related end-stage renal disease (ESRD) is 6-fold higher in African-Americans than in whites. It is apparent that hypertension along with its cardiovascular morbidity and mortality is an even greater challenge for the African-American community than it is for the rest of the nation. Many of the factors responsible for the disparities in the incidence, prevalence, detection, treatment, and control of hypertension have been well described and can be useful in the design and development of programs and policies targeted to the diagnosis and control of hypertension within the population.
Blood pressure is a continuous variable determined by multiple factors and demonstrates a fairly normal distribution within the population. Some of the factors that determine blood pressure level are genetic and may account for about 30–50% of the blood pressure variation in the general population. The development of essential or idiopathic hypertension, however, is believed to require a genetic predisposition and an environmental precipitation in most instances. The search for specific genes responsible for hypertension has resulted in the discovery of some rare monogenetic causes of both high and low blood pressure. While several physiologic characteristics such as low renin levels, lower bioavailability of nitric oxide, increased salt sensitivity, and increased aldosterone levels are more prevalent in African-Americans, specific genetic underpinnings have yet to be identified. In spite of popular expectation there is still no identified genetic basis for the excess prevalence of hypertension in the African-American community. However, several lifestyle and environmental risk factors for hypertension have been identified with important differences among racial and ethnic groups.
Excess body fat, particularly in the upper body, is an important risk factor for hypertension. Whether expressed as overweight or obesity, excess body fat is more common among African-Americans, Hispanics, and several other ethnic minorities. Dietary salt intake in the form of sodium chloride has been associated with the level of blood pressure and the rise in blood pressure with age. As a group, African-Americans have higher salt intake and greater sensitivity to changes in blood pressure in response to dietary salt intake. In contrast a low potassium intake has been associated with hypertension and there is evidence that high dietary potassium, particularly in the form of fresh fruits and vegetables, may offer protection from hypertension and perhaps reduce the need for antihypertensive drug therapy. The diets of many African-Americans are generally low in fruits and vegetables and the average dietary potassium intake among African-Americans is less than that of other major racial and ethnic groups in the United States.
Physical inactivity is a risk factor for hypertension and cardiovascular mortality. Optimum physical activity requires 20–60 minutes of rhythmic and aerobic large-muscle activity such as walking, running, and cycling 3–5 days a week for blood pressure control and cardiorespiratory fitness. Physical activity is suboptimal in over 60% of the U.S. adults, about 25% of whome are totally inactive. Physical inactivity is more common among older adults, women, less affluent people, and Hispanic and African-American adults.
The intake of three or more standard drinks of alcohol per day, where a standard drink is defined as 14 g of ethanol and is contained in 1.5 oz of distilled spirit, a 5-oz glass of table wine, or a 12-oz glass of beer, has been associated with serious adverse psychosocial and health consequences including hypertension. It is estimated that about 60% of Americans ages 18 years and over ingest alcohol and about 30% have five or more standard drinks on the same occasion at least once in that year. Many of these Americans are African-Americans.
The low educational status and high unemployment rate prevalent among minority populations in the United States predispose many minority communities, including African-American, to adverse political and socioeconomic conditions that contribute to environmental and psychosocial stress as well as reduced access to quality health care. Acute stress can transiently raise blood pressure, while chronic stress has been associated with sustained hypertension. The job-strain model of psychosocial conflict, designed to assess the impact of occupational stress on the health of the worker, characterizes jobs into high and low strain jobs. Workers with high decision latitudes exhibit little or no distress because they have more flexibility in deciding how best to meet their work-related demands, while those in occupations that combine high demands with low decision latitudes exhibit high stress levels and its attendant cardiovascular morbidity. African-Americans are more likely to be employed in these positions. Indeed, men employed in these typically blue-collar jobs have a 3-fold increase in hypertension and those who remain in these jobs for 3 or more years have a reported blood pressure that is 11/7 mm Hg higher than men in low strain jobs.
While genetic and biological differences may influence the distribution of blood pressure levels within a population, the prevailing body of evidence seems to suggest that lifestyle and socioeconomic disparities have a greater influence on the expression of hypertension and the disproportionate burden of hypertension and cardiovascular disease in African-Americans. This suggests that it is not genetics alone but the gene–environment interaction that is responsible for the higher prevalence of hypertension among African-Americans. Further evidence supporting the unique role of environment is the fact that the excess risk for hypertension in African-Americans is more strongly linked to being born and living in the United States than with African ancestry.
Racial and/or ethnic differences in combined cardiovascular endpoints assume less significance in hypertensive-treated patients after an adjustment for differences in socioeconomic and demographic factors. The treatment and control of hypertension for optimal outcomes require an appropriate sensitivity to and an understanding of the unique sociocultural aspects of race/ethnicity to maximize effective access to care, adherence to treatment, and scheduled follow-ups. Such approaches will ultimately assist in overcoming many of the barriers to the control of hypertension and will lead to improved cardiovascular outcomes for all Americans.
Severe hypertension and suboptimal blood pressure control rates perpetuate the disproportionate burden of cardiovascular disease (CVD) and premature death among African-Americans. Biobehavioral and socioeconomic factors frequently cited as plausible explanations for the lack of awareness and treatment of high blood pressure among African-Americans may not fully explain the failure to achieve recommended blood pressure goals. Several large-scale multicenter studies with substantial enrollment of African-American patients have demonstrated that blood pressure can be treated to goal levels, although more aggressive therapy may be needed. African-Americans seem to have a slightly greater blood pressure response to diuretics and calcium channel blockers than do other ethnic groups and less response to angiotensin-converting enzyme inhibitors (ACEIs) and β-blockers. Nevertheless, these differences do not seem to translate into different clinical outcomes based on class of antihypertensive therapy as long as target blood pressure levels are achieved. Thus, the search for cardiovascular risk factors and target organ damage, both of which are more prevalent among hypertensive African-Americans, and the selection of the appropriate therapeutic agent by compelling indication based on the coexisting comorbidities should supersede the search for specific agents for blood pressure control among African-Americans.
Hypertension is not only a major risk factor for CVD, but often occurs with one or more cardiovascular risk factors such as obesity, diabetes, and/or dyslipidemia in a syndrome known as the metabolic syndrome. A race-specific role for emerging cardiovascular risk factors such as aldosterone and inflammatory mediators has yet to be determined. The clinical and laboratory search for cardiovascular risk factors and target-organ damage is particularly important for African-American hypertensive patients. The awareness and identification of specific end-organ damage and coexisting cardiovascular risk factors should help prioritize nonpharmacologic recommendations, the selection of compelling evidenced-based medical treatment, and the establishment of appropriate target goals.
Left ventricular hypertrophy is a common complication of hypertension and an independent predictor of increased mortality among hypertensive patients. It is more common among female and African-American patients with hypertension and may account for some of the ethnic and gender differences in cardiovascular mortality rates.
The treatment and control of hypertension by β-blockade and renin–angiotensin inhibition have been associated with regression of left ventricular hypertrophy. The blood pressure reduction and left ventricular mass regression associated with both of these treatments in most studies were similar in African-American and other racial and ethnic participants. A diminished response among African-Americans treated with angiotensin receptor blocker (ARB) therapy in one study may have been related to fewer African-Americans achieving target blood pressure goals, but a differential outcome based on race cannot be excluded.
Congestive heart failure (CHF) in blacks is characterized by a higher frequency of hypertension as the etiology, a worse prognosis, and perhaps less of a response to evidenced-based CHF medical therapy in comparison to their white counterparts. There is abundant evidence that β-blockade and renin–angiotensin inhibition are beneficial for improving both mortality and hospitalization outcomes among patients with CHF, and overall these treatment strategies when adjusted for other covariates appear similar for both African-American and other racial/ethnic patients. While there are reports of higher readmission rates for African-American patients receiving these treatments, posthospitalization mortality data suggest that when quality care is provided, the apparent racial disparities in CHF outcomes dissipate. The treatment of CHF patients should therefore encompass class-specific therapy (eg, ACEI, ARB, β-blocker) in combination with diuretics as indicated for the general population regardless of race or ethnicity. The addition of aldosterone blockade has also led to improved CHF outcomes, although there are no data on racial differences. However, isosorbide dinitrate and hydralazine have been shown to reduce CHF mortality by 43% compared to placebo for African-Americans.
African-American patients with hypertension exhibit the highest stroke rates of any racial or ethnic group. The recent decline in stroke mortality observed in other racial and ethnic groups is attenuated for African-American patients with hypertension. Blood pressure control and antiplatelet therapy remain the principal strategies for reducing stroke events among patients with hypertension. The degree of protection conferred by blood pressure control may vary for different classes of antihypertensive medications. A relative-risk reduction in stroke as high as 40% has been reported for African-Americans with diuretic therapy compared to therapy with ACEIs. Diuretics and calcium channel blockers (CCBs) have emerged as the preferred antihypertensive treatment for reducing stroke events for all hypertensive patients, including African-Americans. There are no reported racial and/or ethnic differences in the prevention of recurrent stroke and myocardial infarction with ticlopidine and aspirin. Aspirin is more cost effective and should therefore be the preferred agent for antiplatelet therapy. Ticlopidine should be reserved for patients with aspirin intolerance and allergy.
ESRD secondary to hypertension is six times more common in African-Americans than in the general population. The use of ACEIs in comparison to β-blockers and dihydropyridine CCBs was associated with a reduction in adverse clinical outcomes (doubling of creatinine, ESRD, or death) for African-American patients with hypertensive nephrosclerosis. Thus, the existing body of evidence suggests that optimal clinical outcomes are achieved when inhibition of the renin–angiotensin system is used as initial antihypertensive therapy with diuretics in African-Americans with hypertensive nephrosclerosis. Diabetes is the leading cause of ESRD for all racial and ethnic groups and over 90% of patients with diabetic nephropathy have hypertension. Multiple studies support the use of ACEIs and ARBs as the mainstay of therapy. The inclusion of nearly 15% African-American participants in two of the pivotal prospective randomized trial studies, suggests that the positive outcomes extend to blacks as well as nonblacks. Thus, interruption of the renin–angiotensin system has emerged as the initial recommended therapy in combination with diuretics for treating hypertensive and diabetic nephropathy, and usually represents the minimum treatment regimen needed to achieve the more aggressive recommended treatment goal of 130/80 mm Hg for patients with chronic kidney disease.
Therapeutic lifestyle changes are equally effective across racial and ethnic groups and sometimes even more effective among African-American patients. These changes are particularly important for African-American patients with hypertension because many of the major risk factors for hypertension in these patients are behavioral and modifiable. The identification and communication of risk-attributable behaviors (such as dietary indiscretion, physical inactivity, excessive alcohol intake, and smoking), particularly within the context of the established burden of cardiovascular disease, should engage and encourage the patient to be proactive in the implementation of therapeutic lifestyle changes.
Practical suggestions for the effective implementation of therapeutic lifestyle changes are listed in Table 43–2. Many of the barriers to successful implementation of therapeutic lifestyle changes among African-Americans are listed in Table 43–3. The recommendations for therapeutic lifestyle changes, such as weight control, dietary salt reduction, regular physical activity, and adherence to clinic visits and a medication regimen, should be provided in specific detail with a practical design, making it possible to break through some of these common barriers and achieve successful implementation. This may frequently necessitate the inclusion of additional healthcare professionals (eg, dietitian, pharmacist, social worker) and/or family members in the dialogue.
Medical target | Practical plan to achieve goal |
|---|---|
Weight loss | Lose weight gradually by making permanent changes in daily diet for the entire family Initiate 800–1500 kcal/day diet and set a reasonable weight loss goal (1–2 lb/week for the first 3–6 months) |
Dietary goals | |
Low fat Low sodium High potassium Adequate calcium | Eat more broiled and steamed foods Eat more grains, fresh fruits, and vegetables Eat fewer fats and use healthier fats, such as olive oil Eat fewer processed foods, fast foods, and fried foods Read labels and pay attention to the sodium, potassium, and fat content of foods Do not add salt when cooking; instead use vinegar, lemon juice, or sodium substitutes such as potassium instead of standard table salt for seasoning Do not season foods with smoked meats, such as bacon and ham hocks If lactose intolerant, try lactose-free milk or yogurt, or drink calcium-fortified juices or soy milk |
No more than two beers, one glass of wine, or one shot of hard liquor per day (even less for women) | |
Physical fitness | Increase physical activity as part of the daily routine: eg, if currently sedentary, get off the bus six blocks from home or walk in the evening with your spouse, a friend, or a group Gradually increase the time spent at an enjoyable physical activity to 30–45 minutes 3–5 days/week |
Adapt a low stress lifestyle | Teach coping skills for specific stressors in the work and/or home environment Meditation, relaxation, yoga, biofeedback, others |
Additional considerations | Maintain a smoke-free environment and limit alcohol intake |
Overweight/obese (body mass index >25/30 kg/m2) | Cultural concern that a thin body habitus is associated with poor health |
High dietary intake of sodium and fat | Cultural food preparation and conditioned tasting likely were initiated or exacerbated during slavery when high salt and fat content were needed for preservation and/or palatability of suboptimal food sources (Salt sensitivity is more common in African-Americans than in whites; if BP is not controlled, check 24-hour urinary sodium excretion to assess dietary adherence) |
Low dietary calcium intake | Low milk and dairy intake due to high prevalence of lactose intolerance |
Inactivity for women | Cultural emphasis on hair styling and relatively high cost of hair maintenance contribute to avoidance of routine exercise with increased heart rate and sweating |
Low adherence to prescribed treatment plan | Assess for medication side effects (particularly impotence among males and increased angioedema among African-Americans taking ACEI) High rate of poverty, low rates of insurance (check prescription plan) and/or ability to pay for prescribed medications (adjust therapy as needed) Assess biobehavioral barriers and family support structure Recognize distrust of the medical establishment |
Missed office appointments | Transportation difficulties: Many patients may not have a car and many cities have poor mass transportation systems Competing priorities such as child/grandchild care and elder care (often related to extended family home structure; child care and elder care facilities are often geographically disconnected from health centers) Limited ability to leave work to attend health care appointments in many job settings |
The mainstay of hypertensive therapy for African-Americans remains diuretics and therapeutic lifestyle changes. The selection of supplemental antihypertensive agents should be tailored to the presence of coexisting risk factors, comorbid medical conditions, and/or the presence of hypertension-related target organ damage. Many of these patients will need two to four antihypertensive agents to achieve target blood pressure goals. The preference for agents that block the renin–angiotensin system as supplemental antihypertensive agents among patients with CHF, diabetes, and kidney disease cannot be overemphasized. It is, however, pertinent to note that the use of some of these agents among African-Americans is associated with a slightly higher rate of side effects, such as angioedema with ACEIs. Thus, strategies for the treatment of hypertension should be driven by the prevalence of coexisting cardiovascular risk factors and an understanding of sociocultural influences that impact access to care and adherence to evidenced-based treatment rather than minor differences in blood pressure response by racial and ethnic categories. Such approaches will ultimately reduce the disproportionate impact of hypertension and CVD within the African-American community.
Hypertension in the Elderly
In the past few years there has been a major paradigm shift in thinking about hypertension, with systolic blood pressure (BP) now accepted as the primary clinical concern in adults. Systolic hypertension is generated principally by functional and structural changes in the aorta and large arteries and can be viewed as a condition that differs distinctly from diastolic hypertension. Isolated systolic hypertension is considerably more difficult to treat than diastolic hypertension and expert clinical judgment is often required in establishing acceptable BP targets and in choosing optimal drug therapy.
Age-related BP patterns in industrialized societies are complex (Figure 43–1): Systolic BP increases linearly with age, while diastolic BP increases until about age 50 years and then declines. Mean arterial pressure (MAP) thus increases until about age 50 years and then plateaus, whereas pulse pressure (PP) is constant until age 50 years and then increases. In adults, systolic hypertension is thus the predominant form of the condition. Contrary to popular belief, systolic hypertension is not just “burned out” diastolic hypertension. Rather, it can arise de novo at any age, either preceding or without the presence of diastolic hypertension. Aging is not inexorably associated with systolic hypertension: In primitive or cloistered societies there is no relationship between age and BP.
Figure 43–1.
Age and blood pressure trends. In the third National Health and Nutrition Examination Survey (NHANES III) of the U.S. population, systolic blood pressure (SBP) increased with age, diastolic blood pressure (DBP) increased until about age 50 years and then declined, mean arterial pressure (MAP) reached a plateau at about age 50 years, and pulse pressure (PP) continued to increase with age especially in later years. Data shown are for white males; trends are similar for all races and both genders. (Adapted with permission from Burt VL et al: Prevalence of hypertension in the US population: results from the Third National Health and Nutrition Examination Survey, 1988–1991. Hypertension 1995;25:305.)
Aging and hypertension dramatically increase the risk for cardiovascular disease (CVD). Overall, each 20 mm Hg increase in systolic BP (or 10 mm Hg increase in diastolic BP) at least doubles the risk of cardiovascular disease or stroke over the range of 115/75 to 185/115 mm Hg. The risk associated with systolic BP is robust and log-linear irrespective of age, while the relationship between diastolic BP and risk is weaker and more complex; the risk for CVD is proportional to diastolic BP until about age 50 years, after which decreased diastolic BP and “wide pulse pressure hypertension” are the major markers of increased risk for CVD.
The value of therapy in isolated systolic hypertension has been clearly established for thiazide-based therapy in the Systolic Hypertension in the Elderly Program (SHEP) and for calcium antagonist-based therapy in the Systolic Hypertension in Europe (Syst-EUR) study. In both of these studies, individuals over age 60 years with stage 2 isolated systolic hypertension (pretreatment systolic BP values >160 mm Hg with diastolic BP values <90 mm Hg) experienced a relative reduction in stroke by about one-third when active therapy was compared to placebo. The net differences in systolic BP between the active and control arms in SHEP and Syst-EUR were about 10–12 mm Hg. To date, no study has been completed that demonstrates an outcome benefit of treating stage 1 systolic hypertension (140–159 mm Hg), but it has recently been found that treating prehypertension (systolic BP 120–139 mm Hg) for 2 years with an angiotensin blocker reduces the subsequent incidence of hypertension for at least 2 years after cessation of therapy.
The predominant clinical form of hypertension in middle-aged and elderly individuals is isolated systolic hypertension (ISH); combined systolic–diastolic hypertension (SDH) is much less common and isolated diastolic hypertension (IDH) is increasingly rare (Figure 43–2). These clinical subtypes are related to the underlying hemodynamic abnormalities, which are quite heterogeneous from a pathophysiologic perspective. In the past, the pathogenesis of hypertension was oversimplified as a syndrome of arteriolar vasoconstriction and vascular smooth muscle hypertrophy leading to high systemic vascular resistance (SVR) with normal cardiac output.
Figure 43–2.
Age and prevalence of systolic and diastolic hypertension. Isolated systolic hypertension (ISH) is much more common in older individuals (age 70–79 years) than in younger individuals (age 40–49 years). Combined systolic-diastolic hypertension (SDH) also diminishes with age. Isolated diastolic hypertension (IDH) almost disappears in older individuals. [Adapted with permission from Franklin SS et al: Predominance of isolated systolic hypertension among middle-aged and elderly US hypertensives: analysis based on National Health and Nutrition Examination Survey (NHANES)III. Hypertension 2001;37:869.]
In reality, hypertension is a collection of hemodynamic anomalies that includes various proportions of (1) increased impedance in large arteries (generating systolic or wide pulse pressure hypertension), (2) decreased luminal diameter of distal arterioles (generating diastolic or mean arterial hypertension), (3) inappropriately high cardiac output, and (4) increased blood pressure reactivity to environmental stimuli, most commonly recognized as the “white-coat syndrome.” In contrast to IDH, the characteristic sign of increased SVR, ISH is associated with significant increases in aortic impedance and sometimes with increased stroke volume, with only minimal to moderate increases in SVR (Figure 43–3
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