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患者は78歳,女性.2002年3月,肥大型心筋症疑いの診断,2004年3月,大動脈弁閉鎖不全,高血圧性心疾患によるうっ血性心不全にて入院,加療を行った.2004年5月,心不全の急性増悪にて再び入院となった.ベンチレーター使用にて治療中,胸痛症状,心電図上肢誘導,胸部誘導の広範囲にてST上昇を認め,トロポニンT定性試験陽性であった.心臓カテーテル検査を施行し,冠動脈に有意狭窄なく,左室造影所見からたこつぼ心筋症と診断された.その後心不全の治療継続中,循環・呼吸状態の急激な悪化を認め永眠された.剖検にて,心基部に比して心尖部の心筋変性,心外膜病変が著明であり,組織学的にも心筋の変性(膨化,空胞,融解),線維化が混在した所見を呈していた.その成因について文献的考察を含めカテコラミンの関与を疑った.
A 78-year-old woman was admitted to our hospital with heart failure. She had a history of “suspicion of hypertrophic cardiomyopathy” in March, 2002 and “congestive heart failure due to aortic regurgitation and hypertension” in March, 2004. During the management of circulation and respiration, she complained of chest pain. An electrocardiogram showed ST elevation in I, II, III, aVF, aVL and V2~V6. Troponin T test showed positive. Though emergent coronary angiography showed no arterial stenosis, ventriculography confirmed the presence of apical ballooning with basal hypercontraction (ejection fraction 52%). We diagnosed this patient as having ampulla cardiomyopathy. However, several days after the chest pain, the condition of her circulation and respiration worsend and she died.
We performed an autopsy and confirmed that she suffered degeneration of heart muscle (hydropic swelling vacuolation, lysis), fibrosis and epicardial hemorrhage. The damage in the heart muscle was more distinct in the apical region than at the base of the heart. It might be thought that the pathogenesis of the case was related to the release of catecholamine during heart failure.
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