Role of the sympathetic nervous system in the pathophysiology of cardiovascular disease.

Psychosomatic elements, behavior, and sympathetic overactivity are presumed to underlie many cardiovascular diseases; the most investigated conditions are borderline hypertension and type A/B behavior. Many patients with borderline hypertension show signs of hyperkinetic circulation, that is, elevated heart rate and cardiac index. This elevation is neurogenic, since it can be abolished with a combination of beta-adrenergic and parasympathetic blockade. Response to such stepwise blockade shows a larger beta-adrenergic and a lower parasympathetic change in cardiac tone, characteristic of the functional organization of the medullary integrative centers of cardiovascular control. The most likely cause for this abnormal integration is psychosomatic. These patients may be expected to respond to treatment with behavioral and/or cardioselective beta-adrenergic blocking agents. There is little doubt that type A behavior is a predictor of coronary heart disease. The description of the pathophysiology of these transient but characteristically excessive cardiovascular episodes is difficult, however. Type A individuals do not always hyperreact in the same way; the response can be limited to heart rate, blood pressure, or occasionally exaggerated urinary or plasma catecholamine responses. In our laboratory we concentrated on steady markers of type A behavior. Type A subjects had reproducibly larger pupil size--indicative of increased sympathetic arousal--higher heart rate and diastolic blood pressure, and significantly elevated platelet epinephrine values when challenged by a mental task. Treatment with behavioral methods, beta-blocking agents, or both might be useful for prevention of coronary heart disease in type A individuals.