The risk factors for sudden coronary heart disease (CHD) death have been well described. Sudden CHD deaths should be classified as those occurring in individuals with and those in individuals without a prior history of clinical heart disease. The extent of coronary artery disease, left ventricular dysfunction, and cardiac arrhythmias are the primary pathophysiologic determinants of ventricular fibrillation and sudden death. Psychosocial factors influence the threshold of response to the numerous physical and social environmental stimuli that can precipitate sudden death. The degree of pathology is probably inversely related to the intensity of the stimuli necessary to precipitate sudden CHD death. In the presence of extensive disease the precipitants of sudden deaths are probably ubiquitous in the environment and unlikely to be prevented. Thus, prevention of the basic cardiac disease is of higher priority.

Over the past 10 years behavioral approaches to the treatment of coronary heart disease (CHD) have become widely recognized as being a significant complement to traditional medical and surgical therapies. The success of approaches to secondary prevention now relate to quality, as well as quantity, of life. A multifaceted program, including dietary management, smoking cessation, physical exercise, modification of type A behavior, and psychological counseling are components of many cardiac rehabilitation programs. Behavioral interventions are effective in reducing traditional risk factors for CHD events, and for improving the quality of life among victims of a disease with significant psychological, as well as physical, consequences. However, the effectiveness of behavioral interventions for prolonging life is less certain and requires more careful evaluation. The mechanisms by which behavioral treatments may influence clinical CHD end points is also in need of further investigation.

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.