Myocardial damage from acute cerebral lesions.
Autopsy findings in 58 patients with intracranial lesions were compared with those in 50 control patients for myocardial damage, characterised by a change from a myofibrillar to a granular staining pattern, using a histochemical method for succinic dehydrogenase. Transmurally scattered foci of damaged myocardial fibres were significantly more common (p less than 0.01) in patients with intracranial lesions (62%) compared to controls (26%). No victims of sudden violent deaths showed these cardiac lesions. Focal myocardial damage required at least six hours to develop after onset of the acute neurological event and was not observed after the second week. It was associated with lesions producing a rapid increase in intracranial pressure and was usually absent in patients with slowly enlarging or small cerebral lesions. Similar myocardial changes were seen in patients in the control group dying from prolonged shock or other forms of acute circulatory or metabolic failure. The postulated mechanism of cardiac damage in these patients is increased levels of plasma catecholamines secondary to rapidly increasing intracranial pressure, irrespective of the cerebral pathology.
D000208:Acute Disease; D000328:Adult; D000368:Aged; D001254:Astrocytoma / Q000473:pathology; D001344:Autopsy; D001927:Brain Diseases / Q000473:pathology*; D001932:Brain Neoplasms / Q000473:pathology / Q000556:secondary; D002277:Carcinoma / Q000473:pathology / Q000556:secondary; D002543:Cerebral Hemorrhage / Q000473:pathology; D002544:Cerebral Infarction / Q000473:pathology; D002561:Cerebrovascular Disorders / Q000473:pathology*; D005260:Female; D006651:Histocytochemistry; D006801:Humans; D008297:Male; D008581:Meningitis / Q000473:pathology; D008875:Middle Aged; D009206:Myocardium / Q000201:enzymology / Q000473:pathology*; D013345:Subarachnoid Hemorrhage / Q000473:pathology; D013385:Succinate Dehydrogenase / Q000032:analysis; D013997:Time Factors
D013385:Succinate Dehydrogenase