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MYOCARDIAL DAMAGE:Myocytolysis-CAUSED BY SUBARACHNOID HEMORRHAGE Makoto Sugiura 1,6 , Yoshinobu Yozawa 2 , Osami Kubo 3 , Koichi Kitamura 3 , Shinichi Kimata 4 , Haruo Hagiwara 5 , Hisashi Joshita 5 1Division of Neurosurgery, Isesaki Sogo Center of Health 2Division of Internal Medicine, Isesahi Sogo Center of Health 3Department of Neurosurgery, Neurological Institute, Tokyo Women's Medical College 4Department of Cardiology,the Heart Institute of Japan,Tokyo Women's Medical College,Tokyo 5Division of Pathology,Central Laboratory, Schoo of Medicine, Gumma University 6Present Address:Department of Neurosurgery Neurological Intitute, Tokyo Women's Medical College pp.1155-1161
Published Date 1985/12/1
DOI https://doi.org/10.11477/mf.1406205623
  • Abstract
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A case of subarachnoid hemorrhage complicated by neurogenic pulmonary edema and neurogenic myocardial damage is reported.

A 50-year-old woman was admitted following the sudden onset of headache and disturbance of consciousness due to a ruptured internal carotid posterior comminucating artery aneurysm on the right side. She showed respiratory failure dueto pulmonary edema, which subsequently improved with the mechanical ventilation. After that, she manifested chest distress and hypotensive episode then occurred. An ECG showed QS wave and ST elevation which suggested the presence of infero-lateral myocardial damage. Subsequent rises in serum GOT, GPT, LDH and CPK were noticed. CPK-MB and LDH I and V isozyme levels rose. An echo cardiogram showed hypokinesis of the apical half of the left ventricular septum. The patient died on 5 th hospital day due to rerupture of the cerebral aneurysm. Autopsy revealed diffuse myocytolysis with coagulation necrosis of the heart muscle without occlusion of coronary arteries. A small hemorrhagic lesion was found in the hypo-thalamus. We suggested that a hypothalamic lesion due to subarachnoid hemorrhage stimulated the sympathetic nervous system which in turn dis-charged endogenic catecholamine. This was pro-bably accompanied by vasospasm of the coronary arteries and systemic peripheral arterioles. Fur-thermore, myocardial oxygen consumption could have been increased by the increase in catecho-lamine. Finally, it gave rise to neurogenic pul-monary edema and extensive diffuse myocytolysis of the heart occurred.


Copyright © 1985, Igaku-Shoin Ltd. All rights reserved.

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電子版ISSN 2185-405X 印刷版ISSN 0006-8969 医学書院

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