Despite considerable progress in linking behavioral stress to the genesis of cardiac arrhythmias, little has been learned about the effects of sleep on electrical stability of the heart. Historically sleep has been regarded to be the antithesis of stress, being little more than a state of profound relaxation. We now realize of course that this is a gross oversimplification and that sleep is a non-homogeneous state which exerts complex influences on all physiologic systems. This precisely integrated state of changing autonomic nervous system activity provides a valuable opportunity to gain new insights into the dynamic mechanisms regulating myocardial perfusion and ventricular electrical stability. The proposed experimental work will be guided by the following objectives:
Specific Aims 1. To define the influences of sleep on coronary hemodynamic function and vulnerability to ventricular fibrillation (VF) in the normal heart. 2. To examine the effects of myocardial ischemia and infarction on sleep-induced changes in coronary hemodynamic function and vulnerability to VF. 3. To examine the contribution of peripheral adrenergic activity in mediating sleep-induced changes in myocardial perfusion and vulnerability to VF. 4. To define the role of sympathetic-parasympathetic interactions in modulating the coronary hemodynamic and cardiac electrophysiologic effects of the sleep-wake cycle. The methods to be employed will include electroencephalographic recording, behavioral monitoring of the sleep-wake cycle using video display, coronary hemodynamic monitoring, left ventricular metabolic measurements, plasma catecholamine determinations and cardiac electrical testing. These investigations will serve to define underlying mechanisms mediating the effects of sleep on coronary hemodynamic function and cardiac rhythm. Important clinical benefits may also emerge from a better understanding of the neurophysiologic factors controlling heart rhythm. Indeed, if certain sleep stages are found to exert antiarrhythmic effects, therapeutic insights may be provided for the management of malignant arrhythmias.

Agency
National Institute of Health (NIH)
Institute
National Heart, Lung, and Blood Institute (NHLBI)
Type
Research Project (R01)
Project #
1R01HL032905-01A1
Application #
3344446
Study Section
Cardiovascular and Pulmonary Research B Study Section (CVB)
Project Start
1985-09-30
Project End
1988-09-29
Budget Start
1985-09-30
Budget End
1986-09-29
Support Year
1
Fiscal Year
1985
Total Cost
Indirect Cost
Name
Harvard University
Department
Type
Schools of Public Health
DUNS #
082359691
City
Boston
State
MA
Country
United States
Zip Code
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