一名年轻患者的 COVID-19 后心肌和冠状动脉受累:鉴别诊断与综合治疗

O. V. Blagova, V. A. Bryukhanov, M. B. Kislova, V. A. Yumasheva, M. S. Gaeva, D. Ainetdinova, N. Gagarina, E. A. Kogan
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摘要

冠状病毒病2019年最新注册送彩金(COVID-19,冠状病毒病2019年最新注册送彩金)后的心脏状况多种多样,在某些情况下需要进行复杂的鉴别诊断。我们描述了一名 35 岁的吸烟男性患者,他在感染 COVID-19 后的第一个月末出现左心室功能障碍,射血分数下降至 25-30%,并伴有持续性左束支传导阻滞(LBBB)。超声心动图还检测到局部收缩功能紊乱。血液中的抗心肌抗体滴度明显升高。心肌活检显示存在活动性淋巴细胞性心肌炎和冠状病毒核糖核酸,冠状动脉造影显示前室间动脉广泛狭窄。在球囊血管成形术和支架植入术后的第一天,LBBB阻滞消失,心前区导联出现深层负T波,这无法排除之前发生过心肌梗死的可能性。经过心衰治疗和类固醇治疗,到治疗的第二年年底,心脏结构和功能参数以及心电图完全恢复正常。只有在高负荷时仍存在短暂的 LBBB。2 年后的心脏计算机断层扫描显示,心肌内无延迟造影剂积聚,冠状动脉狭窄达 30%。本文讨论了 COVID-19 治疗后心肌和冠状动脉损伤的复杂机制(包括冠状动脉炎在动脉粥样硬化进展中的作用)。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Post-COVID-19 myocardium and coronary involvement in a young patient: differential diagnosis and comprehensive treatment
The state of the heart after a coronavirus disease 2019 (COVID-19, coronavirus disease 2019) is very diverse and in some cases requires a complex differential diagnosis. We described a 35-year-old smoking male patient who, by the end of the first month after COVID-19, developed left ventricular dysfunction with decrease in ejection fraction to 25-30% and persistent left bundle branch block (LBBB). Echocardiography also detected local contractility disorders. A significant increase in blood anticardiac antibody titers was noted. Myocardial biopsy revealed active lymphocytic myocarditis, coronavirus ribonucleic acid, while coronary angiography revealed extensive stenosis of the anterior interventricular artery. On the first day after balloon angioplasty and stenting, the disappearance of LBBB block was noted with the appearance of deep negative T waves in the precordial leads, which did not allow ruling out a previous myocardial infarction. As a result of treatment of heart failure and steroid therapy, the structural and functional cardiac parameters and the electrocardiography were completely normalized by the end of the second year of treatment. Only a transient LBBB remained at high loads. Cardiac computed tomography after 2 years showed no delayed contrast agent accumulation in the myocardium, and coronary stenosis up to 30%.The mechanisms of complex myocardial and coronary damage (including the role of coronaritis in the atherosclerosis progression) after COVID-19 are discussed.
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