Mechanisms of behaviorally induced arrhythmias.

Significant progress has been made in the past few years in defining the role of behavioral stress in the precipitation of cardiac arrhythmias. This is largely attributable to the development of relevant biobehavioral models and the advent of quantitative methods for assessing myocardial electrical stability in conscious animals. Classic and instrumental aversive conditioning has been shown to decrease electrical stability even in the normal heart. During evolving myocardial ischemia or infarction, the stress states can precipitate major arrhythmias, including ventricular fibrillation. Natural emotions have also been shown to be capable of altering the propensity to fibrillation. Notably, provocation of an angerlike state has been shown to decrease the vulnerable period threshold by 40% to 50%. The poststress phase can be particularly hazardous, as suggested by the profound myocardial perfusion abnormalities that have been observed within 1 to 3 min after cessation of anger. Cryogenic blockade of the thalamic gating system or its output from the frontal cortex to the brainstem blunts significantly the profibrillatory influence of stress. This indicates that discrete pathways within the central nervous system mediate the deleterious influence of aversive states on heart rhythm. Adrenergic factors appear to constitute the major effector component. This is supported by the observation that pharmacologic or surgical sympathectomy is capable of annulling the arrhythmogenic influence of diverse types of stress. The generally deleterious influence of the adrenergic system appears to be counteracted by vagal activity. The underlying mechanism is a muscarinically mediated inhibition of norepinephrine release from sympathetic nerve endings and a blunting of the actions of the adrenergic transmitters at the receptor level.(ABSTRACT TRUNCATED AT 250 WORDS)