Experimental studies of psychophysiological factors in sudden cardiac death.
Earlier research in the field of sudden cardiac death is reviewed. Such studies have largely oriented towards the provocation of myocardial injury and asystole in normal animals. However, such investigations constitute an inadequate model to describe the clinical appearance of sudden death, where underlying coronary disease is often present and the precipitating event is usually ventricular fibrillation rather than asystole. This report describes a series of studies designed to investigate the processes underlying cardiac vulnerability and the influence upon it of various psychological stresses. It is concluded that the primary mediator of ventricular vulnerability is the sympathetic nervous system. The efferent vagus appears to exert some protective influence against arrhythmias due to adrenergic stimulation. An appropriate clinical strategy for the treatment of malignant arrhythmias would therefore involve attempts to decrease cardiac sympathetic drive whilst at the same time enhancing vagal tone. Treatments are described which aim to bring this situation about by the use of clonidine, morphine sulphate, l-tryptophan and tyrosine. The use of neurochemical agents in this context appears promising.
D000818:Animals; D001145:Arrhythmias, Cardiac / Q000503:physiopathology; D003327:Coronary Disease / Q000150:complications / Q000523:psychology; D003645:Death, Sudden / Q000209:etiology*; D006801:Humans; D013315:Stress, Psychological / Q000150:complications*; D013564:Sympathetic Nervous System / Q000503:physiopathology; D014630:Vagus Nerve / Q000502:physiology; D014693:Ventricular Fibrillation / Q000150:complications / Q000523:psychology