Sueta Daisuke, Kojima Sunao, Izumiya Yasuhiro, Yamamuro Megumi, Kaikita Koichi, Hokimoto Seiji, Ogawa Hisao
Department of Cardiovascular Medicine, Graduate School of Medical Sciences, Kumamoto University, Japan.
Intern Med. 2016;55(22):3291-3294. doi: 10.2169/internalmedicine.55.7234. Epub 2016 Nov 15.
A 79-year-old man was diagnosed with sudden deafness. He had previously experienced a suspected episode of angina pectoris. At a local hospital, after 500 mg of hydrocortisone and 80 mg adenosine triphosphate (ATP) were administered, he became aware of chest discomfort. An electrocardiogram revealed serious ST-segment depressions. He was diagnosed with a non-ST elevated myocardial infarction (NSTEMI). Emergency coronary angiography revealed triple vessel disease, and the lesion was successfully stented. The mechanisms whereby the stable effort angina pectoris destabilized in this case were thought to include a reduction of the local blood flow because of an ATP product and probable thrombus formation in response to the administered steroids.
一名79岁男性被诊断为突发性耳聋。他之前曾经历过一次疑似心绞痛发作。在当地医院，给予500毫克氢化可的松和80毫克三磷酸腺苷（ATP）后，他出现了胸部不适。心电图显示严重的ST段压低。他被诊断为非ST段抬高型心肌梗死（NSTEMI）。急诊冠状动脉造影显示三支血管病变，病变成功置入支架。在这种情况下，稳定型劳力性心绞痛病情恶化的机制被认为包括由于ATP产物导致局部血流减少以及可能因使用类固醇而形成血栓。
