Left Ventricular Rupture Associated With Takotsubo Cardiomyopathy

Akashi, Yoshihiro J.; Tejima, Tamotsu; Sakurada, Harumizu; Matsuda, Hisao; Suzuki, Kengo; Kawasaki, Kensuke; Tsuchiya, Katsuhiko; Hashimoto, Nobuyuki; Musha, Haruki; Sakakibara, Masayoshi; Nakazawa, Kiyoshi; Miyake, Fumihiko
June 2004
Mayo Clinic Proceedings;Jun2004, Vol. 79 Issue 6, p821
Academic Journal
A 70-year-old woman was admitted to the hospital with chest discomfort after quarreling with her neighbors. Electrocardiography revealed ST-segment elevation in leads I, II, III, aVL, aVF, and V2 through V6. Coronary angiography demonstrated normal arteries, but left ventriculography showed apical akinesis and basal hyperkinesis. Takotsubo cardiomyopathy was diagnosed on the basis of these characteristic findings. The creatine kinase and creatine kinase-MB concentrations were elevated at admission and reached maximum levels 6 hours after admission. The plasma level of brain natriuretic peptide was 10.7 pg/mL (reference range, <18.4 pg/mL) on the first hospital day. ST-segment elevation in leads I, II, III, aVL, aVF, and V2 through V6 persisted at 72 hours after admission. On the third hospital day, sudden rupture of the left ventricle occurred, and despite extensive resuscitation efforts, the patient died. Takotsubo cardiomyopathy presents in a manner similar to that of acute myocardial infarction, but ventricular systolic function usually returns to normal within a few weeks. To our knowledge, this is the first reported case of fatal left ventricular rupture associated with takotsubo cardiomyopathy. We suggest that takotsubo cardiomyopathy may be a newly recognized cause of sudden cardiac death.


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