Ortuno Sofia, Jozwiak Mathieu, Mira Jean-Paul, Nguyen Lee S
Assistance Publique - Hôpitaux de Paris, Centre Cochin University Hospital, Intensive Care Medicine Department, Paris, France.
Centre Médico-Chirurgical Ambroise Paré, Research and Innovation, Research and Innovation of CMC Ambroise Paré, Neuilly-sur-Seine, France.
Front Cardiovasc Med. 2021 Feb 22;8:614562. doi: 10.3389/fcvm.2021.614562. eCollection 2021.
Takotsubo cardiomyopathy is triggered by emotional or physical stress. It is defined as a reversible myocardial dysfunction, usually with apical ballooning aspect due to apical akinesia associated with hyperkinetic basal left ventricular contraction. Described in cases of viral infections such as influenza, only few have been reported associated with novel coronavirus disease 2019 (COVID-19) in the recent pandemic. A 79-years-old man, with cardiovascular risk factors (type 2 diabetes and hypertension) and chronic kidney disease, presented to the emergency room for severe dyspnea after 8 days of presenting respiratory symptoms and fever. Baseline electrocardiogram (ECG) was normal, but he presented marked inflammatory syndrome. He was transferred to an intensive care unit to receive mechanical ventilation within 6 h, due to acute respiratory distress syndrome. He presented circulatory failure 2 days after, requiring norepinephrine support (up to up to 1.04 μg/kg/min). Troponin T was elevated (637 ng/l). ECG showed diffuse T wave inversion. Echocardiography showed reduced left ventricular ejection fraction (LVEF 40%), with visual signs of Takotsubo cardiomyopathy. Cardiac failure resolved after 24 h with troponin T decrease (433 ng/l) and restoration of cardiac function (LVEF 60% with regression of Takotsubo features). Patient died after 15 days of ICU admission, due to septic shock from ventilator-acquired pneumonia. Cardiac function was then normal. Mechanisms of Takotsubo cardiomyopathy in viral infections include catecholamine-induced myocardial toxicity and inflammation related to sepsis. Differential diagnoses include myocarditis and myocardial infarction. Evidence of the benefit of immunomodulatory drugs and dexamethasone are growing to support this hypothesis in COVID-19.
应激性心肌病由情绪或身体应激引发。它被定义为一种可逆的心肌功能障碍,通常因心尖运动不能伴左心室基底节段收缩亢进,呈现心尖气球样改变。在流感等病毒感染病例中有相关描述,在近期的大流行中,仅有少数病例报告与2019新型冠状病毒病(COVID-19)相关。一名79岁男性,有心血管危险因素(2型糖尿病和高血压)及慢性肾脏病,在出现呼吸道症状和发热8天后因严重呼吸困难就诊于急诊室。基线心电图(ECG)正常,但他出现明显的炎症综合征。由于急性呼吸窘迫综合征,他在6小时内被转入重症监护病房接受机械通气。2天后他出现循环衰竭,需要去甲肾上腺素支持(剂量高达1.04μg/kg/min)。肌钙蛋白T升高(637ng/l)。ECG显示广泛T波倒置。超声心动图显示左心室射血分数降低(LVEF 40%),有应激性心肌病的可视征象。24小时后心力衰竭缓解,肌钙蛋白T降低(433ng/l),心脏功能恢复(LVEF 60%,应激性心肌病特征消退)。患者在入住重症监护病房15天后因呼吸机相关性肺炎导致的感染性休克死亡。当时心脏功能正常。病毒感染中应激性心肌病的机制包括儿茶酚胺诱导的心肌毒性和与脓毒症相关的炎症。鉴别诊断包括心肌炎和心肌梗死。免疫调节药物和地塞米松有益的证据越来越多,以支持COVID-19中的这一假说。