Myocardial Damage and Cardiac Arrhythmias After Intracranial Hemorrhage. A Critical Review

Abstract

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.

Histomorphogenesis of Soman-Induced Encephalocardiomyopathy in Sprague-Dawley Rats

“…Also, in vitro studies demonstrated that anoxic neuronal changes differ considerably from those caused by direct exposure to soman (42 (14,15,44,49 Although the possibility that soman may exert (co-participant) a direct toxic effect on the myocardium has not been entirely excluded (57,80) (1,10,13,23,26,32,34,48,51,54,60) and to the lesions induced in this study by soman. A common factor in the pathogenesis of heart damage is thought to be the exposure of the myocardium to a massive or sustained delivery of unphysiologic amounts of catecholamines (79). The cardiac damage seen in this study is thought to represent a secondary response to the protracted excitation of the CNS caused by the soman-induced acetylcholinesterase inhibition.…”

Subarachnoid hemorrhage in middle-Finland: incidence, early prognosis and indications for neurosurgical treatment.

“…The results, however, have been contradictory, 1 "- 18 and the most recent reports on both epsilon-aminocaproic acid" and tranexamic acid 11 give little support for therapeutic benefits of these drugs. The electrocardiographic abnormalities after SAH, 22 their prognostic significance, 23 and probable association with autonomic nervous system overactivity 24 ' 28 have suggested the use of adrenergic blocking drugs. The clinical results have, however, been meager.…”

Cardiac arrhythmias in acute stroke.

“…Cardiac arrhythmias produced by experimental cerebral ischemia can be prevented by autonomic blockade. 19 The well documented cases of cardiac arrhythmias and ECG changes secondary to intracranial hemorrhage 20 may be explained by the finding of significantly elevated levels of plasma catecholamines. 21 In a serial analysis of serum creatine phosphokinase (CPK) in 224 patients with acute cerebrovascular lesions 22 elevated levels were found in 5% of cases.…”