COVID-19 can involve several organs and systems, often with indirect and poorly clarified mechanisms. Different presentations of myocardial injury have been reported, with variable degrees of severity, often impacting on the prognosis of COVID-19 patients. The pathogenic mechanisms underlying cardiac damage in SARS-CoV-2 infection are under active investigation.

We report the clinical and autopsy findings of a fatal case of Takotsubo Syndrome occurring in an 83-year-old patient with COVID-19 pneumonia. The patient was admitted to Emergency Department with dyspnea, fever and diarrhea. A naso-pharyngeal swab test for SARS-CoV-2 was positive. In the following week his conditions worsened, requiring intubation and deep sedation. While in the ICU, the patient suddenly showed ST segment elevation. Left ventricular angiography showed decreased with hypercontractile ventricular bases and mid-apical ballooning, consistent with diagnosis of Takotsubo syndrome. Shortly after the patient was pulseless. After extensive resuscitation maneuvers, the patient was declared dead. Autopsy revealed a subepicardial hematoma, in absence of myocardial rupture. On histology, the myocardium showed diffuse edema, multiple foci of contraction band necrosis in both ventricles and occasional coagulative necrosis of single cardiac myocytes. Abundant macrophages CD68+ were detected in the myocardial interstitium. The finding of diffuse contraction band necrosis supports the pathogenic role of increased catecholamine levels; the presence of a significant interstitial inflammatory infiltrate, made up by macrophages, remains of uncertain significance.

COVID-19可能涉及多个器官和系统，通常具有间接的和不清楚的机制。已经报道了心肌损伤的不同表现，其严重程度各不相同，通常会影响COVID-19患者的预后。正在积极研究SARS-CoV-2感染中心脏损害的潜在致病机制。

我们报道了一名83岁的COVID-19肺炎患者发生的致命性Takotsubo综合征病例的临床和尸检结果。该患者因呼吸困难，发烧和腹泻入急诊科。SARS-CoV-2的鼻咽拭子试验呈阳性。在接下来的一周中，他的病情恶化，需要插管和深度镇静。在ICU期间，患者突然显示出ST段抬高。左心室造影显示，收缩过度的心室基部减少和心尖中部球囊扩张，与Takotsubo综合征的诊断一致。病人很快就无脉。经过广泛的复苏操作后，该患者被宣布死亡。尸检显示心包膜下血肿，无心肌破裂。在组织学上，心肌显示出弥漫性水肿，多个收缩带坏死灶在心室和偶发的单个心肌细胞凝血坏死。在心肌间质中检测到大量巨噬细胞CD68 +。弥散性收缩带坏死的发现支持了儿茶酚胺水平升高的致病作用。由巨噬细胞组成的明显的间质炎性浸润的存在，仍具有不确定的意义。