Acute Myocardial Injury and Rhabdomyolysis in COVID-19 Patients: Incidence and Mortality.
Acute Myocardial Injury and Rhabdomyolysis in COVID-19 Patients: Incidence and Mortality.
复制标题
DOI：
10.7759/cureus.18899
复制
发表时间：
2021-10
期刊：
影响因子：
--
通讯作者：
Iqrar A
中科院分区：
文献类型：
--
作者：
Ali L;Mohammed I;Janjua I;Naeem M;Adeli G;Elalamy O;Alhatou M;Akhtar N;Canibano B;Iqrar A
背景心肌损伤被定义为肌钙蛋白水平升高。住院冠状病毒病2019(新冠肺炎)患者急性心肌损伤的频率从7%到36%不等。患有心血管疾病的新冠肺炎患者的死亡风险是对照组的四倍(优势比为4.33；可信区间为95%，3.16-5.94)。在新冠肺炎住院患者的研究显示，死亡率为18.5%。横纹肌溶解被认为是肌肉坏死，细胞内肌肉元素和酶释放到血液中。在新冠肺炎住院患者的一项回顾性队列研究中，横纹肌溶解的发生率为16.7%。材料与方法对413例新冠肺炎住院患者进行回顾性观察研究。结果新冠肺炎患者急性心肌损伤和横纹肌溶解的发生率分别为23.9%(99例)和15.7%(65例)，其中男大于30 ng/L，女大于20 ng/L。住院新冠肺炎患者并发急性心肌损伤的死亡率(28.3%)显著高于并发横纹肌溶解的患者(13.8%)。探讨SARS-CoV-2病毒与血管紧张素转换酶2的结合是新冠肺炎发病过程中的重要环节。新冠肺炎急性心肌损伤的直接和间接机制可能有多种，包括缺血性损伤、缺氧性损伤(MI 2)、直接病毒性心肌炎、应激性心肌病和全身细胞因子风暴。肌肉骨骼损伤可能直接由病毒性肌炎引起，也可能由宿主免疫高炎性细胞因子风暴反应间接引起，从而导致骨骼肌纤维蛋白分解和纤维化。结论新冠肺炎患者存在急性心肌损伤和横纹肌溶解的漏报。在新冠肺炎住院患者中，急性心肌损伤的发生率和死亡率高于横纹肌溶解。在新冠肺炎合并严重急性心肌损伤的患者中，结果更差。急性心肌损伤和横纹肌溶解症患者可能会从这些康复计划中受益。
Background Myocardial injury has been defined as an elevated troponin level. The frequency of acute myocardial injury of hospitalized coronavirus disease 2019 (COVID-19) patients ranges from 7% to 36%. COVID-19 patients with cardiovascular disease (CVD) have a four-fold higher risk of mortality (odds ratio, 4.33; CI 95%, 3.16-5.94). In COVID-19 hospitalized patients’ study showed mortality rate was 18.5%. Rhabdomyolysis is considered as muscle necrosis and the release of intracellular muscles elements and enzymes into blood. In one of retrospective cohort study of COVID-19 hospitalized patients, incidence of rhabdomyolysis was 16.7%. Materials and methods This retrospective observational study consisted of 413 COVID-19 hospitalized patients. Patients with rhabdomyolysis was defined as creatine kinase level greater than 1,000 U/L and acute myocardial injury was defined as serum high-sensitivity troponin-T for males greater than 30 ng/l and for female greater than 20 ng/l. The primary outcome was in-hospital mortality of COVID-19 patients with acute myocardial injury and rhabdomyolysis. Results The incidence of acute myocardial injury and rhabdomyolysis in hospitalized COVID-19 patients was 23.9% (99) and 15.7% (65), respectively. The mortality rate of in hospitalized COVID-19 patients who developed acute myocardial injury (28.3%) was significantly higher in comparison to patients who developed rhabdomyolysis (13.8%). Discussion The binding of SARS-CoV-2 virus to the angiotensin-converting enzyme 2 (ACE2) is a critical step in the pathophysiology in patients with COVID-19. There may be diverse direct and indirect mechanisms of acute myocardial injury in COVID-19 including ischemic injury, hypoxic injury (MI type 2), direct viral myocarditis, stress cardiomyopathy and systemic cytokine storm. Musculoskeletal injury may be caused by direct viral myositis or indirectly by host immune hyperinflammatory cytokine storm response that leads to skeletal muscle fiber proteolysis and fibrosis. Conclusions Acute myocardial injury and rhabdomyolysis were underreported in COVID-19 patients. The incidence and mortality of acute myocardial injury are higher than that of rhabdomyolysis in COVID-19 hospitalized patients. The outcome was worse in COVID-19 patients with severe acute myocardial injury. Patients with acute myocardial injury and rhabdomyolysis may get benefits from rehabilitation programs.