1 Upjohn Center for Clinical Pharmacology, and the Departments of Internal Medicine and Pharmacology, The University of Michigan Medical Center, Ann Arbor, Michigan 48104
Reprint requests to: Dr. D. J. Weidler, Upjohn Center for Clinical Pharmacology, The University of Michigan Medical Center, Ann Arbor, Michigan 48104
Evidence is presented which supports the theory that intracranial hemorrhage may secondarily cause myocardial damage and cardiac arrhythmias. Fatal intracranial hemorrhage occasionally is accompanied by ECG changes which are consistent with myocardial infarction; histological examination of the heart revealed a variable amount of myocardial damage. After intracranial hemorrhage in animals, myocardial damage was frequent. Similar myocardial damage was produced in animals by intravenous infusion of norepinephrine or acetylcholine and by electrical stimulation of the stellate ganglia, vagus nerve or mesencephalic reticular formation. Atrial and ventricular arrhythmias and various degrees of A-V block were reported in patients suffering from subarachnoid hemorrhage. Similar cardiac arrhythmias were found in animals after intracranial hemorrhage, and with electrical stimulation of the vagus nerve, stellate ganglia or CNS centers. Available data suggest that increased or altered autonomic activity may be the mechanism whereby intracranial hemorrhage produces myocardial damage and cardiac arrhythmias. The efficacy of autonomic blockade in preventing myocardial damage, which was secondary to experimental intracranial hemorrhage in animals, was demonstrated. It is suggested that the initiation of therapy with autonomic blocking drugs, as soon as possible after the onset of intracranial hemorrhage in patients, may be useful in preventing myocardial damage and cardiac arrhythmias.
© 1974 American Heart Association, Inc.
Myocardial Damage and Cardiac Arrhythmias After Intracranial Hemorrhage. A Critical Review
Key Words: intracerebral hemorrhage subarachnoid hemorrhage sympathetic nervous system parasympathetic nervous system autonomic blockade
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