For more than a decade our research has focused on the mechanisms whereby behavioral factors predispose to sudden death, the leading cause of cardiac mortality in the United States. We have developed well-defined behavioral models which simulate stress states and have evolved state-of-the-art methodologies for assessing cardiac electrophysiologic and coronary hemodynamic function in conscious, chronically instrumented animals. The investigations have demonstrated that stress-induced vulnerability results both form direct effects of neurotransmitters on the heart and by indirect influences which result in impaired myocardial perfusion. The latter effect is due to inappropriate coronary vasoconstriction in response to certain stress states. Anger in particular has been shown to increase cardiac vulnerability and predispose to profound coronary vasoconstriction int he period following arousal. This raises the possibility that the physiologic responses associated with the post-stress state may be particularly hazardous. A.
SPECIFIC AIMS; 1. To elucidate further the factors involve in delayed myocardial ischemia. 2. To define the influence of contrasting behavioral states on coronary hemodynamic and cardiac electrophysiologic function. 3. To investigate the mechanisms responsible for cardiac vulnerability during the post-stress state. The techniques will include Doppler flow measurement, radiolabeled microspheres, coronary angiography, biochemical assessment of cardiac metabolism, electrochemical detection of catecholamine levels, and cardiac electrical testing. These studies will serve to define underlying mechanisms mediating the effects of diverse stresses on coronary hemodynamic function and the propensity to life-threatening arrhythmias. Ultimately, the insights derived could lead to improved therapeutic strategies relevant to both behavioral medicine and cardiology.
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