Kato Takao, Ban Yoko, Kuruma Saori, Ishida Seiko, Doi Chikako, Iura Tamae, Terawaki Hiromi, Inoko Moriaki, Nohara Ryuji
Cardiovascular Center, Kitano Hospital, Tazuke Kofukai Medical Research Institute, Osaka, Japan.
Echocardiography. 2013 Apr;30(4):E92-4. doi: 10.1111/echo.12139. Epub 2013 Feb 14.
We report 2 cases of reversible ventricular hypertrophy in patients with takotsubo cardiomyopathy (stress-induced cardiomyopathy) during recovery of cardiac function. The first case involved a 72-year-old woman who presented with cerebral infarction. On admission, an elevated troponin I and decreased apical wall motion were observed with normal myocardial perfusion imaging. The second case involved a 79-year-old woman who presented with angina, anxiety resulting from emotional stress, slightly decreased apical wall motion, and normal epicardial arteries. In both cases, apical hypertrophy of the left ventricle was observed at approximately 3 weeks after onset, when the wall motion had improved. The ventricular wall gradually became thinner over time. To our knowledge, this is the first report of reversible ventricular hypertrophy in patients with takotsubo cardiomyopathy. We hypothesize the hypertrophic signaling in the myocardium was stimulated by catecholamines, which are the suggested etiology of takotsubo cardiomyopathy, and the hypertrophied myocardium gradually returned to normal as the syndrome receded.
我们报告了2例应激性心肌病（takotsubo心肌病）患者在心脏功能恢复过程中出现可逆性心室肥厚的病例。第一例为一名72岁女性，因脑梗死入院。入院时，肌钙蛋白I升高，心尖壁运动减弱，心肌灌注成像正常。第二例为一名79岁女性，因情绪应激导致心绞痛、焦虑，心尖壁运动略有减弱，心外膜动脉正常。在这两例中，发病后约3周，当壁运动改善时，均观察到左心室心尖肥厚。随着时间的推移，心室壁逐渐变薄。据我们所知，这是应激性心肌病患者可逆性心室肥厚的首次报告。我们推测，心肌中的肥厚信号是由儿茶酚胺刺激的，儿茶酚胺是应激性心肌病的推测病因，随着综合征的消退，肥厚的心肌逐渐恢复正常。
