Cardiovascular clinics最新文献

Development of strategies to prevent CHD in blacks is impeded by the virtual absence of clinical trials demonstrating the feasibility and effectiveness of interventions in blacks. The wholesale generalization that interventions effective (or ineffective) in whites are similarly effective in blacks may risk the employment of worthless or even dangerous interventions in blacks. Using available epidemiologic data, a number of risk factors may be more important in blacks than whites by virtue of higher prevalence, increased relative risk, or both. These may include hypertension, lipoprotein (a), smoking, diabetes, and obesity. Thus, health agencies might emphasize these risk factors when developing preventive programs targeted at black populations. Prevention programs may best seek to prevent the onset of risk factors found highly prevalent in black communities, rather than the costly and side-effect-prone interventions to treat risk factors once established. Thus, there is a role for community-based as well as a high-risk approaches. The community-based approaches should seek to work with organizations such as churches, which traditionally play strong roles in the black community. Physicians treating black patients should be aware of the potentially different roles played by risk factors, and treat aggressively those individuals identified to be at high risk. Risk factor management should be emphasized, rather than reduced, in patients with already established CHD. CHD has been clearly shown to be preventable; both blacks and whites should benefit from specific interventions aimed toward this worthy goal.

Contrary to early impressions of blacks' relative immunity to CHD, it is now clear that African Americans experience greater mortality from CHD than whites. The natural history of CHD differs between blacks and whites in three important respects: First, greater prevalence of established risk factors among blacks suggests that they may be at greater risk for heart disease than their white counterparts. Second, health care seeking differences are evident between blacks and whites, leading to lower rates of identification of early disease and slower seeking of services for acute events. However, risk factor differences and health care seeking behaviors do not appear to account for all of the differences in the natural history of heart disease between the ethnic groups, such as survival rate differences during treatment. Economic factors appear to account for only a portion of these differences in risk factors and health care seeking. Beyond differences in risk factors and health care seeking, other, as yet undetermined, factors seem to be involved. These unknown influences could include physiologic, behavioral, and/or psychologic differences.

Although blacks may differ from whites in the response of hypertension to therapy, present data do not suggest that potential racial differences in cardiac structural adaptation to hypertension by themselves mandate a difference in therapeutic strategy. The results of large racially mixed trials of therapy that monitor LV mass regression, such as the VA Cooperative Monotherapy Trial, will be of interest in this regard.

Despite an overall limited range of social and economic opportunities in the recent past, blacks of lower socioeconomic status have experienced marked excesses in hypertension-related burdens compared with their more advantaged peers: the incidence, prevalence, and severity of hypertension and its end-organ sequelae increased with decreasing educational achievement and the 5-year mortality was two times higher for black hypertensives of lower than higher educational achievement under conditions of usual care in U.S. communities in the 1970s. The Stepped Care program of antihypertensive pharmacologic therapy of the HDFP reduced all-cause mortality by 19% for black hypertensive men and 28% for black women. The HDFP also eliminated the association of mortality with educational achievement; the favorable impact of the program was greatest in the group at highest risk, blacks of lowest socioeconomic status.

The primary focus of both nonpharmacologic and pharmacologic therapy should be to control systemic blood pressure in a simple, affordable, and nontoxic fashion that provides an adequate quality of life. Although newer agents provide hope for greater capability of preventing renal dysfunction, their cost may prevent their broad availability in the black hypertensive population (see Chapter 5). Judicious use of traditional therapies, combined with newer approaches when possible, may offer prescribing physicians the best opportunity to control blood pressure in ways to avoid renal dysfunction. The lessons of the past 20 years have taught us that lowering blood pressure by any means helps in reducing target organ damage. More recent observations in hypertensive blacks illustrate the need for improved therapies to prevent renal dysfunction. A more physiologic approach to blood pressure control in the black patient that conserves perfusion to the kidney may delay the development of nephrosclerosis. Increased awareness, educational support, and encouragement will be necessary to insure compliance with therapy for a disease that is largely asymptomatic.

In summary, for reasons that are not clear, some persons seem to be extremely good at retaining sodium on a high-sodium diet or poor at excreting sodium on a high-sodium intake. This is more frequent in Western hemisphere blacks than in whites in the West or in blacks in Africa. These geographic/ethnic differences in sodium handling ability may be related to environmental factors or, more likely, to inherited differences in the ability to conserve sodium based on the evolutionary principle of survival fo the fittest for the ability to conserve sodium. The frequency of this salt-conserving (thrifty) genotype in Western hemisphere blacks may have been further increased as a consequence of severe selection pressures for survival based on the ability to conserve sodium during the slavery period of history in the West. One characteristic of the blood pressure control systems of Western hemisphere blacks is suppression of plasma renin activity without suppression of aldosterone production. In addition there is greater nephrosclerosis in blacks than whites and a more rapid decline in creatinine clearance with age. When more sodium is ingested than the kidneys are able to handle (excrete), there is a (transient) slight positive sodium balance; as a result sodium, chloride, and water are retained, resulting in an expansion of plasma volume (Fig. 7-3). The initial physiologic responses include (increased) secretion of atrial natriuretic peptides and the digitalis-like substance (natriuretic hormone), and inhibition of vasopressin and aldosterone secretion. The net effect is directly enhanced natriuresis and diuresis, and a reduction in plasma volume, with no significant effect on blood pressure. However, if there is a continuing tendency to sodium retention and volume expansion, the capacity of the aforementioned mechanisms to control plasma volume will be exceeded; then, the chronically elevated level of the digitalis-like substance will inhibit the sodium pumps in the arterial and venous smooth muscle cells and in the sympathetic neurons. The increased venous tone will help to reduce plasma volume directly by reducing central venous volume. Arterial tone will be increased by direct action of the digitalis-like substance on the arterial smooth muscle and, indirectly, via the hormone's action on the sympathetic neurons. Initially, of course, blood pressure will be maintained in the normal range (but will be labile) because of the compensating cardiovascular reflexes. Once the capacity of these reflexes to control blood pressure is exceeded, however, the blood pressure will begin to rise; this will induce a pressure natriuresis to help restore plasma volume to normal.(ABSTRACT TRUNCATED AT 400 WORDS)