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A Case of Coronary Sclerotic Heart Disease with Marked Cardiomegaly and a Peculiar Conduction Disturbance Accompanied by the Superior Mesenteric Artery Occulusion:with a Special Reference to the Pathologic Changes of the Conduction System Hideo Ueda 1 , Yutaka Takabatake 1 , Ryozo Okada 1 , Hitoshi Tagawa 1 1The 2nd Department of Internal Medicine, Faculty of Medicine, University of Tokyo pp.69-74
Published Date 1969/1/15
DOI https://doi.org/10.11477/mf.1404201987
  • Abstract
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A 71-year-old man with marked cardiome-galy and abnormal electrocardiogram is pre-sented. He had been told to have arrhythmia since 10 years ago, without hypertension. He complained of recent onset of exertional palpitation, shortness of breath and occasio-nal edema, and marked cardiomegaly as well as abnormal electrocardiogram (atrial fibril-lation, and idioventricular rhythm with com-plete A-V block) were detected. The patterns of electrocardiograms changed variously in course of time, which suggested migration of the ventricular pace-maker. A year there-after, he died suddenly of an attack of severe acute abdomen.

Autopsy revealed the following: (1) Heart weighed 840 g with marked hypertrophy of left ventricle. Atheromatous stenosis up to 75 % was recognized only at the proximal part of the anterior descending coronary artery. Multiple scattered myocardial fibrosis was seen at the anteroseptal area. Significantstenosis was not detected in the other coro-nary arteries. ( 2 ) A-V conduction system was investigated with serial sections, which demonstrated on interruption by fibrosis and fatty degeneration of the A-V bundle at the terminal portion and the bifurcation with minimal cellular continuity between both branches. The observations were compatible with the electrocardiographic findings. ( 3 ) Intestines showed an extensive necrosis by an occlusion of the main stem of the superior mesenteric artery. ( 4 ) Right kidney had a fresh hemorrhagic infarction.

Though coronary atherosclerosis often ca-uses moderate cardiac enlargement, few casesof marked cardiomegaly such as this case have been reported. Its mechanism has been pos-tulated to be due to persisting heart failure, accompanied hypertension, or bradycardia resulting from conduction disturbance. In this case, however, it might be rather as-sumed that a partial myocardial damage due to localized stenosis of coronary artery caused compensatory hypertrophy of the other part of myocardium irrigated by intact dilated coronary arteries. The complete A-V block may result from ischemic changes due to coronary atherosclerosis and/or from secon-dary damage due to senile sclerotic change of the cardiac skelton.


Copyright © 1969, Igaku-Shoin Ltd. All rights reserved.

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電子版ISSN 1882-1200 印刷版ISSN 0452-3458 医学書院

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