Arteriosclerosis is importantly influenced by blood cholesterol level, blood pressure, and cigarette smoking. Each of these major risk factors is influenced by behavioral choices made by individuals and supported by societies. Behavioral medicine has a rich tradition of dealing with individuals and small groups. The public health perspective of disease challenges behavioral medicine to develop new strategies and tactics for behavioral modification for health promotion on a population-wide basis. Additional research is needed to test effective methods for influencing population behavior, population risk factors, and ultimately population morbid and mortal event rates. Several major community projects are now investigating the health promotion process targeting individuals, small groups, organizations, and the entire community. School, worksites, and churches are particularly conducive to health promotion programming. Each has unique advantages and disadvantages; each deserves careful experimentation to determine its efficacy for population-wide health promotion efforts. A public health dimension to behavioral change promises widespread impact, generalization to other health promotive behaviors, maintenance of new cultural behavioral norms, and significant reductions in the incidence of many chronic diseases.

This article reviews the epidemiologic evidence linking psychological factors and various indexes of coronary heart disease (CHD) that has been gathered since the Amelia Island Conference in 1978. In general, studies of populations not selected according to CHD risk support the conclusion that the global type A construct is predictive of increased risk of coronary events. In high-risk groups, including patients undergoing coronary angiography, the evidence with respect to global type A is much less clear. This stems from the fact that most of these studies, although generally failing to find statistically significant relationships between coronary events and type A behavior, are flawed in a number of ways, including inadequate statistical power of results, use of less than adequate instruments, and failure to take an apparent interaction between type A behavior and age into account. Nevertheless, taken together, these findings suggest that it may be possible to identify measures of coronary-prone behavior that are more powerful than the global type A measure. Extensive evidence suggests that such measures may be found in the domain of hostility and anger. Measures of hostility and anger coping styles have been found to be associated with coronary atherosclerosis in populations in which global type A was not related to disease, and measures of hostility have predicted increased coronary events and total mortality in prospective population samples followed for from 20 to 25 years. Preliminary evidence suggests that hostility/anger characteristics may account for the increased coronary risk associated with global type A behavior.(ABSTRACT TRUNCATED AT 250 WORDS)

A sociocultural perspective on biobehavioral factors is important both for studies of the cause of coronary heart disease and for efforts to prevent the disease. One-to-one programs are limited because coronary heart disease is so prevalent and because people have great difficulty in changing their behavior to lower their risk. Data are now available regarding several psychosocial risk factors that shed light on possible environmental influences. These factors include social mobility, stressful life events, type A behavior, and social support. These factors are now being studied in bus drivers to illustrate the ways in which sociocultural interventions can be developed to prevent disease.

A variety of "emotional" response patterns can be elicited at the limbic-hypothalamic level by challenging environmental stimuli, and such mechanisms may contribute to the multifactorial etiology of primary hypertension. The "defense reaction" is of particular interest because of its widespread neurohormonal excitatory influences and frequent, although mild, engagement in daily life events. Evidence is presented showing how common genetic variants of primary hypertension, both in man and spontaneously hypertensive rats, are characterized by a genetically linked central hyperreactivity to psychosocial stimuli. As a result, the previously mentioned central response pattern--with its differentiated excitatory and tropic effects that also involve salt-volume regulation--is more commonly elicited by even trivial environmental stimuli, therefore constituting an important triggering influence in these variants of primary hypertension. Also discussed is the potential genetic nature of this central hyperreactivity and, further, how it interacts with other genetic-environmental influences and with the early induction of structural cardiovascular adaptation, by which the entire system is gradually reset to operate at a raised pressure equilibrium.

Increasing evidence indicates that sudden death resulting from ventricular fibrillation may be triggered in some patients by behavioral and neural factors. In animal preparations, diverse psychologic stressors and augmented sympathetic neural traffic to the heart lower the vulnerable period threshold for ventricular fibrillation. Epidemiologic studies have demonstrated increased cardiac fatality after bereavement and unemployment, as it relates to social class and cultural dislocation, and as a function of level of education, psychologic stress, and social isolation. Ventricular premature beats (VPBs), which may be risk indicators of susceptibility to sudden death, are not affected by perturbations of the peripheral autonomic nervous system. However, differing psychologic stressors increase, whereas their abatement diminishes, VPB frequency and grade. The most potent stressors relate to the recall of emotionally charged experiences. Such stressors are uniquely individual and cannot be readily replicated. Among the most significant factors to reduce VPBs are non-rapid eye movement sleep and increases in vagal neural activity. Psychological precipitants are demonstrable in about 20% of patients experiencing malignant ventricular arrhythmias. A promising new avenue for investigation relates to the role of various central neurotransmitters and their dietary precursors in cardiac neural traffic. Augmenting central serotonin by administering its tryptophan precursor reduces sympathetic neural activity and protects the heart against ventricular fibrillation.

Potential causes for the development of acute myocardial ischemia include extracardiac factors, rapid progression of atherosclerosis, dynamic coronary artery thrombosis, platelet activation in diseased vessels, abnormal constriction of a coronary artery, and abnormal arachidonic acid metabolism. It is entirely possible that all or many of these potential causes may be occurring in the individual patient.

Ambulatory electrocardiographic (ECG) monitoring of ischemia in patients with coronary artery disease (CAD) provides a new technique for the assessment of ischemic activity and the evaluation of therapies outside of the hospital. Numerous studies have demonstrated that the majority of patients with CAD have episodes of symptomatic and asymptomatic ST segment depression during routine daily activities. Rubidium-82 positron-emission tomographic studies have provided evidence for decreased myocardial perfusion during these episodes of ST segment depression. The prognostic importance of asymptomatic ischemia has been shown in patients with unstable angina to be a marker for early unfavorable cardiac events. Preliminary results suggest a poorer outcome for those patients with chronic stable angina who show episodes of ischemia as well. Ambulatory monitoring studies suggest that total ischemic activity may be underestimated by conventional testing. Whether all ischemic activity detected by ambulatory monitoring requires treatment awaits further study.

Because vasodilator therapy has become an established approach to the treatment of patients with severe chronic heart failure, there has been increasing interest in the use of the calcium channel-blocking drugs in the management of this disorder. This approach has particular appeal because approximately 60% of patients with heart failure have severe left ventricular dysfunction associated with coronary artery disease, and left ventricular systolic and diastolic performance in these patients may improve after interventions directed at improving myocardial blood flow. Unfortunately, all available calcium channel-blocking drugs possess potent negative inotropic effects; these are normally offset in patients without heart failure by activation of the sympathetic nervous system. Patients with severe left ventricular dysfunction, however, are exquisitely dependent on the transmembrane transport of calcium for maintenance of contractile function and show marked attenuation of adrenergic reflexes, which can no longer serve a homeostatic support function; hence, such patients are likely to experience notable cardiodepressant effects after calcium-channel blockade. In clinical trials, although some patients with severe chronic heart failure have been reported to benefit from short-term calcium-channel blockade, the hemodynamic benefits seen are modest compared with those from conventional vasodilator drugs, and little long-term improvement has been observed in randomized, double-blind trials. In addition, 10% to 40% of patients who receive short- and long-term therapy with verapamil, nifedipine, and diltiazem show evidence of serious hemodynamic or clinical deterioration.(ABSTRACT TRUNCATED AT 250 WORDS)

The hemodynamic properties of the calcium entry-blocking agents result principally from the inhibition of transcellular calcium flux in the myocardium and in vascular smooth muscle. The composite effect(s) of these compounds on cardiovascular function derive from a complex interplay between their direct (myocardial depression) and indirect (afterload reduction by peripheral arterial vasodilation, reflex sympathetic stimulation) actions. While qualitatively similar, the currently available agents (diltiazem, nifedipine, verapamil) differ considerably in relative negative inotropic, vasodilator, and reflex properties. The hemodynamic actions of a particular calcium blocker also critically depend on the baseline cardiocirculatory status. Current information regarding these issues from basic and clinical investigations is reviewed.

The interpretation of a change in coronary flow that accompanies administration of a calcium-entry blocker or other pharmacologic agent remains complicated by the variety of factors potentially altered by the agent that can themselves affect flow. These factors are reviewed in the context of steady-state coronary pressure-flow relationships, emphasizing the complexities induced by coronary artery disease. Limitations of currently available approaches for the measurement of coronary reserve, examination of flow heterogeneity, and the calculation of coronary vascular resistance are also addressed. Calcium entry-blocking agents have a number of hemodynamic effects that are likely to augment coronary flow favorably. However, parodoxical and potentially deleterious effects on local flow also seem possible in selected situations.

This review focuses on the potential use of the calcium antagonists diltiazem, nifedipine, and verapamil in the treatment of hypertensive emergencies. Prompt reduction of blood pressure can be achieved after either intravenous administration of diltiazem or verapamil or sublingual/oral administration of nifedipine. Effects on cardiac hemodynamics with these drugs are variable. Effects on the kidney are predictable; administration is associated with prompt diuresis and natriuresis. Effects on the cerebral circulation are more complex; although cerebral vasodilation may occur, the potential exists for uneven cerebral perfusion and an increase in intracranial pressure. Precipitous decreases in mean arterial pressure may decrease cerebral blood flow below the lower limit of autoregulation, inducing cerebral ischemia. Because of the complex interaction of these drugs on the heart, kidney, and brain, short-term therapy should be instituted only in the hospital setting, with appropriate supervision and hemodynamic monitoring.

This review compares the calcium antagonists with diuretics in the management of mild-to-moderate essential hypertension. The antihypertensive efficacy of calcium antagonists appears comparable to that of oral diuretics such as hydrochlorothiazide when used as monotherapy. Peripheral vascular dilation appears to be the principal mechanism of the long-term blood pressure-lowering effects of both calcium antagonists and diuretics. Peripheral vasoconstrictor responses to cardioreflex-mediated sympathetic nervous system activation is attenuated by calcium antagonists but not by diuretics. Long-term calcium antagonist therapy is generally not associated with reflex activation of the sympathetic nervous system or of the renin-angiotensin-aldosterone axis, whereas diuretic therapy results in considerable activation of the renin-angiotensin-aldosterone system. Calcium antagonists appear to have a greater beneficial effect than diuretics with respect to maintenance of renal blood flow and glomerular filtration rate. Calcium antagonists, because of their effects on coronary blood flow and heart rate-blood pressure product, offer advantages over diuretics in the treatment of hypertensive patients with concomitant ischemic heart disease. Metabolic abnormalities associated with diuretic antihypertensive therapy, such as hypokalemia, hypercalcemia, hyperuricemia, lipid changes, and hyperglycemia, are generally not observed with calcium antagonists. Many of these deleterious metabolic changes observed with diuretic therapy may be minimized by the use of smaller doses of these agents than have generally been employed in the past. Diuretics are less expensive and require less frequent dosing than calcium antagonists. Thus, they continue to be preferable first-line antihypertensive agents in many patients with mild-to-moderate hypertension.

The rationale for evaluating the efficacy and safety of calcium entry-blocking drugs to prevent secondary complications in patients after myocardial infarction is presented. The data currently available from postinfarction trials involving verapamil, nifedipine, and diltiazem are critically reviewed, and a comparison of the findings from three major trials of calcium entry-blocking drugs is provided.

Sustained-release diltiazem (D-SR) and sustained-release verapamil (V-SR) when given twice a day have been successfully used to treat both essential hypertension and angina pectoris. Review of available studies indicates that 120 to 180 mg D-SR twice a day and 240 mg V-SR once or twice a day can lower diastolic pressure in 40% to 80% of patients with essential hypertension and that the drugs may be especially useful in patients with low-renin hypertension such as elderly and black populations. D-SR and V-SR prolong treadmill capacity and reduce frequency of angina in patients with stable effort angina. Improvement is mediated primarily by a reduction in resting and submaximal exercise heart rate. Biopharmaceutics of D-SR and V-SR feature a prolonged apparent plasma half-life and reduced peak-to-trough plasma concentration ratios during steady-state dosing.

Cardiovascular disease is the major cause of death in American adults. The chief form of cardiovascular disease is coronary heart disease (CHD). Prevention of CHD depends on the identification of risk factors in asymptomatic individuals. The American Heart Association recommends that all adults be examined periodically for the presence of silent cardiovascular disease and coronary risk factors. The major risk factors for CHD are smoking, high blood pressure, and high blood cholesterol. Additional factors associated with CHD are high blood triglycerides, reduced levels of high-density lipoproteins, diabetes mellitus, obesity, sedentary lifestyle, and certain behavioral characteristics. Available data suggest that the predominance of CHD among Americans can be attributed to these risk factors, and increasing evidence indicates that appropriate modification of these factors will markedly reduce coronary risk. The purpose of this report is to identify the risk factors, indicate their relation to coronary disease, and recommend an approach to their detection in adults during periodic health examinations.