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急性期に左室流出路閉塞と僧帽弁収縮期前方運動(SAM)を認めた“たこつぼ”型心筋症の1例を経験した.患者は67歳,女性,胸痛と心電図上のST上昇を認め,急性心筋梗塞を疑われ入院したが,冠動脈造影に異常はなかった.左室造影では心尖部を中心とする広範囲の無収縮と心基部の過収縮を示し,“たこつぼ”型心筋症と診断した.引き抜き圧曲線で左室流出路に25mmHgの収縮期圧較差を認め,心エコー図では非対称性中隔肥厚とSAMを認めた,血清CPK値の上昇は軽度であり,SAMと左室流出路閉塞は第3病日に消失し,左室壁運動は3週間で正常化した.CRP,ウイルス抗体価の上昇はなく,心筋生検にて心筋炎の所見はなかった.慢性期の冠攣縮誘発試験は陰性であった.急性期に認めた一過性の左室流出路閉塞は,肥大した心基部心筋の過収縮によりVenturi効果と乳頭筋位置の偏位が生じ,SAMが引き起こされたことによるものと推察した.
A 67-year-old woman with sustained chest pain wasreferred to the hospital because of suspected acutemyocardial infarction. An electrocardiogram demonstrated ST-segment elevation in leads I, II, aVL, and V2-V6. Emergent coronary arteriography showed normalcoronary arteries. Left ventriculography, however,revealed akinesis of the apex, anterolateral, and diaphragmatic segments with hypercontraction of the basalsegment. The end-systolic shape of the left ventriclecorresponded to “Takotsubo”-like cardiomyopathy. Apressure gradient of 25 mmHg was present at the leftventricular outflow tract. Echocardiography demonstrated asymmetric septal hypertrophy and systolicanterior motion (SAM) of the mitral valve. The peaklevel of serum creatine kinase was 216 IU/l. The SAMand the left ventricular outflow obstruction disappearedby the third day of hospitalization, and the leftventricular wall motion normalized within 3 weeks. C-reactive protein and antiviral antibodies did notincrease, and biopsy specimens showed no evidence ofmyocarditis. Neither intracoronary acetylcholine norergonovine provoked coronary vasospasm at 3 weeksafter the disease onset. Although the patient's leftventricular hypertrophy was considered secondary tohypertension, the SAM provoked by the Venturi effectand the displacement of the papillary muscles, both ofwhich were associated with hypercontraction of thehypertrophied basal wall, were the most likely causes ofthe transient left ventricular out flow obstruction.
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