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緒言
心肥大をきたす疾患として冠状動脈硬化症が注目され始めたのは比較的近年のことである。
Yaterら1)は冠状動脈硬化症例の52%に心肥大をみとめ,またFriedberg2)は心筋硬塞症例の2/3に心肥大があったと述べており,1,000gを越える著明な心肥大例も報告されている。しかし本邦ではかかる報告は少なく,橋本ら4)の心肥大の剖検例でも重量800g以上を示した心13例中に冠状動脈硬化症によると思われる症例はみられない。われわれは著明な心肥大と多彩な心電図変化を示し急激な腹痛発作により死亡した症例を経験した。剖検上,左冠状動脈前下行枝のみの高度の狭窄をもつ特異な冠状動脈硬化症によると思われる心肥大(800g)があり,また刺激伝導系の連続切片による検索で心電図所見を説明するに足る房室束の脂肪・線維化をみとめ,さらに直接死因として上腸間膜動脈閉塞症の存在を確認したので報告する。
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.
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