Hypertension and Coronary Heart Disease

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Hypertension and Coronary Heart Disease






Persistent high blood pressure, or hypertension, became recognized as a diagnosable medical condition in the 1930s, with rudimentary treatments emerging in the late 1940s. A decade or more before this, colonial physicians in Africa had already developed an interest in the apparent paucity of hypertension among indigenous black populations, which they attributed, in part, to the absence of modern stresses and cultural dissonances. This explanation persisted for decades, especially in apartheidera South Africa, where it conformed to the ideology of black homelands as salubrious respites from a more complex urban life for which native people were thought to be inherently unsuited (Donnison 1929; Packard 1989).

Hypertension is an important precursor of coronary heart disease (CHD), which involves a narrowing of the coronary arteries that supply oxygenated blood to the heart muscle. The blood-carrying capacity of the coronary arteries becomes restricted by fat and cholesterol deposits on the artery walls until the affected person experiences a chest pain called angina, or until a sufficient obstruction of the coronary artery occurs to precipitate a heart attack. Often, a heart attack results from a sudden closure of the artery due to a blood clot forming at a point where the artery is already narrowed.


Observations of heightened levels of hypertension and average blood pressure in African Americans arose in the early 1900s, with primitive population-based survey results dating to at least as early as 1932. These findings were in direct contrast to the apparent absence of hyper-tension in rural African populations, and also with a relatively low risk for CHD among African Americans. By the 1960s there was extensive evidence from community-based surveys, such as the Evans County (Georgia) Study, to indicate that black Americans experienced nearly twice the clinically defined hypertension than that experienced by white Americans. At the same time, however, these epidemiologic surveys confirmed that CHD risk was lower for blacks than for whites in the United States. Rather than precipitating heart disease, untreated hypertension in African Americans was more likely to manifest in cerebrovascular disease and stroke mortality.

The observation of differential risk for hypertension and CHD between racial groups led many physical anthropologists and medical researchers in the first half of the twentieth century to focus on identifying inherent anatomic and physiological differences between groups that might explain this disparity. A large number of research reports resulted, with putative racial variation identified in nearly every component of the cardiovascular apparatus. For example, one study involved postmortem examinations of the hearts of seventeen whites, fifteen Africans, and two African Americans in the early 19#s. This study concluded that the Africans had an extra large branch of the left coronary artery, to which protection from coronary heart disease was attributed (Phillips and Burch 1960).

There was a similar preoccupation with the comparative sizes and weights of organs, such as the observation that blacks had smaller or lighter kidneys than whites. Similarly, it was widely held that blacks had a natural resistance to a number of common diseases, including hookworm, gall stones, tuberculosis, syphilis, pneumonia, and whooping cough, and thus it was thought that they might also possess a lower risk for coronary heart disease as an intrinsic racial trait (Lewis 1942; Phillips and Burch 1960).

A consequence of the persistent observation of racial/ethnic disparity in hypertension and CHD risk has been the ongoing use of language that casts blacks and whites as fundamentally distinct in terms of innate biology or physiology. For example, scientific articles often carry titles such as “Hypertension in Blacks: Is it a Different Disease?” (Megs 1985).

This predominant ideology of essential biologic difference has precipitated numerous unsubstantiated assertions in the peer-reviewed medical literature. For example, hypertension is often described as intrinsically more virulent among blacks. But assertions that blacks “tend to experience greater cardiovascular and renal damage at any level of [blood] pressure” (Kaplan 1994, p. 4#) have no clear empirical basis.

Likewise, despite voluminous research on environmental and behavioral factors that contribute to hypertension and CHD risk, the long-standing paradigm of viewing racial/ethnic groups as representing human subspecies has led many discussions of the cardiovascular disease disparity in the biomedical literature to be couched reflexively in terms of hypothesized genetic factors. For example, in an exhaustive review of more than 400 articles on racial differences in cardiovascular disease in 1960, John H. Phillips and George E. Burch sought to caution against a completely essentialist interpretation by concluding, judiciously, that “it appears that many racial differences reflect not only genetic and racial factors but [also] variations in the medical care available and extended to the Negro, and the Negro’s cooperation and participation in this medical care” (p. 274). In the subsequent four decades, however, the general emphasis on intrinsic as opposed to social factors remained largely intact. For example, writing in the British Medical Journal in 1997, Sarah Wild and Paul McKeigue concluded that “excess mortality from cerebrovascular and hypertensive diseases in migrants from both West Africa and the Caribbean suggests that genetic factors underlie the susceptibility to hypertension in people of black African descent” (p. 705).


An abiding faith in innate biologic predisposition as the explanation for observed racial patterning in disease has led to a surfeit of ad hoc hypotheses, such as relating blood pressure disregulation directly to skin pigmentation, or to excess testosterone levels in black men. The most widely disseminated of these “just so” stories is the slavery hypertension hypothesis, an evolutionary theory that relates excess hypertension risk in New World blacks to selection during the “Middle Passage” for phenotypes that were sodium retentive. The theory was posited at least as early as 1983, and it was adopted in the late 1980s by the hypertension researcher Clarence Grim, who has since championed the idea energetically. Grim speculated that sodium loss from sweating, diarrheal stools, and vomit during the transatlantic voyage led to high levels of mortality from dehydration, and therefore to selection pressure against genes coding for greater sodium excretion. Though the slavery hypertension hypothesis lacks any empirical support and has been widely criticized from the historical as well as the biomedical arenas, it continues to capture the popular and scientific imagination as a tidy explanation for elevated levels of hypertension in African Americans, and it is routinely cited in medical textbooks, scientific journal articles, and the popular press. For example, in a feature article about the young Harvard economist Roland Fryer Jr., published in the New York Times Magazine in March 2005, the hypothesis is depicted as a new and exciting idea from the rising academic superstar. (Grim, Henry, and Myers 1995; Kaufman and Hall 2003).

The unexpectedly low prevalence of coronary heart disease observed in African Americans in the first half of the century led to similar speculation regarding some categorical racial protection, either cultural or genetic. But these theories of innate resistance to atherosclerotic progression quickly evaporated as the racial disparity flipped in the 1960s and 1970s. Indeed, by the 1980s and 1990s it was black Americans who had a higher CHD risk than whites (driven largely by a wider disparity for women). This reversal in the racial disparity was largely explained by changes in risk-factor distributions in the two populations, such as more diabetes, more atherogenic lipid profiles, less physically active occupations, and greater levels of obesity among blacks. Nonetheless, the scientific discourse soon shifted to speculation about an innate characteristic that predisposed blacks to develop CHD, rather than to avoid it.


By the last quarter of the twentieth century, the CHD death rate was falling for all groups, although more slowly for blacks, which further exacerbated the disparity. At younger ages (less than sixty-five years), the relative black excess became particularly pronounced. The mortality risk at these young ages is low in absolute terms, but the racial disparity is as much as two-fold. This produces a relatively small difference in the number of attributable cases of CHD death, but a larger number of excess years of life lost, due to the young ages of the cases.

Another important cause of cardiovascular mortality is congestive heart failure, which may result from CHD, hypertension, or any of several other cardiovascular pathologies. There are roughly five million Americans with congestive heart failure, and another half a million are diagnosed with the condition every year, making it the one major category of cardiovascular disease that has continued to increase in the United States over the last several decades. Like hypertension and CHD, a racial predisposition to heart failure incidence or mortality has been proposed numerous times in the medical literature, especially to account for a more extreme excess of black risk at younger ages.

Heart failure is unique in being the target of a race-specific pharmacotherapy. The new drug, marketed under the commercial name BiDil, is simply a combination of two previously existing generic vasodilators, isosorbide dinitrate and hydralazine. In June 2005, based on the successful results of a clinical trial called A-HeFT, which enrolled only self-defined African-American heart failure patients, this drug combination was approved by the U.S. Food and Drug Administration (FDA) for sale in the United States as the first “ethnic drug” (Taylor et al. 2004).

To justify a trial restricted to one racial group, the AHeFT investigators proposed that African Americans have lower average rennin-angiotensin system activity, which leads to reduced tissue availability of nitric oxide, a molecule that facilitates the vasodilation necessary for healthy blood pressure regulation. The A-HeFT investigators then asserted that retrospective analyses of data from previous heart-failure trials strongly suggested that black patients had an especially pronounced response to the BiDil combination. However, in the only study that was cited to support this assertion, a statistical test for racial heterogeneity found no significant difference in response between blacks and whites (Carson et al. 1999). It has therefore been suggested that the decision to test and market the drug only for blacks appears to be motivated by concerns that are commercial, rather than scientific, in nature (Kahn 2004).

The whole notion of creating ethnic-specific drugs for cardiovascular conditions remains controversial. Racial groups are not discrete genetic categories, and they overlap considerably with respect to the relevant etiologic and physiologic factors that influence pharmacological effects. Therefore, all available data suggest that any drug determined to work on most blacks will also work on most members of any other group, and vice versa. This phenomenon was demonstrated quantitatively by a recent meta-analytic review by Ashwini Sehgal (2004). Despite numerous claims that antihypertensive therapies have differential efficacy across racial groups, Sehgal showed that the distributions of blood pressure reductions for various common classes of antihypertensive medications overlapped by 83 to 93 percent. This suggests that basing clinical decisions on race may disadvantage the majority of patients of any group, who would respond equivalently to a drug that is presumed to have an effect specific to some other group.


In contrast to the very ambiguous basis for race-specific therapies, the evidence for differential treatment of cardiovascular conditions is now extensive, including differential access to screening and to diagnostic and therapeutic interventions. These differences persist even when controlling for insurance status and socioeconomic level. For example, in an experimental design in which physicians were shown videotapes of actors reading identical scripts of a case presentation of chest pain, the odds that a black woman actor would be referred for right-heart catheterization were only 40 percent of the odds for a white man, even though the vignettes contained identical medical and social histories and identical symptoms (Schulman et al. 1999).

A large number of factors may contribute to differences in access to care and to differential treatment within the medical system, including patient knowledge, patient trust in the physician (and in the healthcare system as a whole), patient-physician communication, patient noncompliance, physician stereotyping, and overt discrimination. For example, when a physician gains less information from a patient of a different race because of cultural or educational barriers in the communication process, the natural response is to stereotype the patient (i.e., to treat the patient based on assumptions about the average member of the group, instead of according to the patient’s individual values). This stereotyping, even if entirely well-intentioned and factually unbiased, will tend to exacerbate disparities between groups by adding more random error to the transfer of information necessary for appropriate treatment. If the stereotype is factually incorrect, then the disparity may be exacerbated even further (Balsa and McGuire 2003). There is also extensive evidence to suggest that physicians have many irrational stereotypes about racial-minority patients. For example, in experimental studies, medical students rated black women as having a lower quality of life than white men (Rathore et al. 2000), while psychiatrists asked to make diagnoses from standardized patient vignettes rated black men as being more hostile and dangerous than males from other groups (Loring and Powell 1988).

Cardiovascular disorders have complex etiologies involving diet, physical activity, and genetic factors, as well as a person’s psychosocial and physical environment. Moreover, they are ascertained and treated differentially with respect to social position and cultural identity. As such, these conditions are very sensitive to social contexts, and they tend to show wide disparities when the relevant factors vary across population groups. These disparities have long fueled hypotheses of innate group predispositions, but rapid shifts in patterns over space and time belie such facile speculation. For example, the West African diaspora, stretching from the population groups of origin through the Caribbean, Brazil, the United Kingdom, and the United States, represents a group of genetically related peoples who were dispersed widely over dramatically different social environments. Yet despite a common geographic origin, these groups now evidence some of the widest variations in cardiovascular risk factors and disease prevalences in the world (Cooper et al. 1997). Nonetheless, the emergence of race-based therapeutics as the latest approach to cardiovascular disease disparities demonstrates that many of the most important lessons of the last several decades of epidemiologic research have not yet been fully assimilated.

SEE ALSO Diseases, Racial.


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Jay S. Kaufman