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目的:探讨重症新型冠状病毒肺炎（COVID-19）患者的临床特征及转归。方法:回顾性分析2020年1月12日至2月28日武汉肺科医院收治的64例重症COVID-19患者，男36例，女28例，年龄44~85岁，中位年龄为68（62，72）岁；52例（81%）合并基础疾病。按治疗转归分为死亡组40例，男24例，女16例，年龄49~85岁，中位年龄69 (62，72）岁；合并基础疾病31例（78%）。治愈组24例，男12例，女12例，年龄44~82岁，中位年龄66（61，73）岁；合并基础疾病21例（88%）。收集两组患者的临床资料，包括一般情况、实验室检查、影像学检查、治疗方案等，正态分布的计量资料采用独立样本n t检验；非正态分布的计量资料采用Mann-Whitney n U检验；计数资料采用卡方检验或Fisher精确检验。n 结果:入院第一天，死亡组患者肌酸激酶同工酶水平中位数为19.0（17.0，23.0） U/L，高于治愈组的16.5（13.5，19.6） U/L，两组比较差异有统计学意义（n P=0.014）。死亡组肌钙蛋白水平中位数为0.03（0.03，0.07） μg/L，显著高于治愈组的0.03（0.02，0.03） μg/L，两组比较差异有统计学意义（n P=0.007）。死亡组肌红蛋白浓度为79.5（28.7，189.0） μg/L，高于治愈组的33.1（25.7，54.5） μg/L，差异有统计学意义（n P=0.031）。死亡组D-二聚体水平为2.0（0.6，5.2） mg/L，高于治愈组的0.7（0.4，2.0） mg/L，差异有统计学意义（n P=0.020)。死亡组乳酸脱氢酶水平为465.0（337.5，606.5） U/L，高于治愈组的341.0(284.0,430.0) U/L,差异有统计学意义（n P=0.006)。死亡组丙氨酸氨基转移酶浓度为40.0（30.0，48.0） U/L，高于治愈组的32.5（24.0，40.8） U/L，差异有统计学意义（n P=0.047)。47例行心电图检查的患者中，22例（47%）心电图异常，其中死亡组心电图异常16例（62%），治愈组6例（29%)，两组比较差异有统计学意义（n P=0.024）。死亡原因：重症肺炎并急性呼吸窘迫综合征（ARDS）20例，病毒性心肌炎导致的急性心功能不全9例，心房纤颤3例，多器官功能障碍综合征3例，其他5例。n 结论:病毒性心肌炎导致的急性心功能不全是导致重症COVID-19患者死亡的原因。早期预防心肌损伤，积极治疗疾病进展过程中并发的急性病毒性心肌炎，可能降低重症COVID-19患者的病死率。“,”Objective:To investigate the causes of death in patients with severe COVID-19.Methods:A retrospective analysis was performed on 64 patients with severe COVID-19 admitted to Wuhan Pulmonary Hospital from January 12, 2020 to February 28, 2020. There were 36 males and 28 females, aging from 44 to 85 years[median 68 (62, 72)]. Fifty-two patients (81%) had underlying comorbidities. The patients were divided into the death group (n n=40) and the survival group (n n=24) according to the treatment outcomes. In the death group, 24 were male, and 16 were female, aging from 49 to 85 years [median 69 (62, 72)], with 31 cases (78%) complicated with underlying diseases. In the survival group, there were 12 males and 12 females, aging from 44 to 82 years[median 66 (61,73)], with 21 cases (88%) with comorbidities. Clinical data of the two groups were collected and compared, including general information, laboratory examinations, imaging features and treatments. For normally distributed data, independent groupn t test was used; otherwise, Mann Whitney test was used to compare the variables. χ n 2 test and Fisher exact test was used when analyzing categorical variables.n Results:The median of creatine kinase isozyme (CK-MB) in the death group was 19.0 (17.0,23.0) U/L, which was higher than that in the survival group 16.5 (13.5,19.6) U/L. The median level of cTnI in the death group was 0.03 (0.03, 0.07) μg/L, which was significantly higher than that in the survival group (0.02, 0.03) μg/L, with a statistically significant difference between the two groups ( n P=0.007). The concentration of myoglobin in the death group was 79.5 (28.7, 189.0) μg/L, which was higher than 33.1 (25.7, 54.5) μg/L in the survival group. The level of D-dimer in the death group was 2.0 (0.6, 5.2) mg/L, which was higher than 0.7 (0.4, 2.0) mg/L in the survival group. The LDH level of the death group was 465.0 (337.5,606.5) U/L, which was higher than that of the survibal group, 341.0 (284.0,430.0) U/L, the difference being statistically significant ( n P=0.006). The concentration of alanine aminotransferase in the death group was 40.0 (30.0, 48.0) U/L, which was higher than 32.5 (24.0, 40.8) U/L in the survival group, and the difference was statistically significant (n P=0.047).Abnormal ECG was found in 16 cases (62%) in the death group, which was significantly higher than that in the survival group (29%), the difference being statistically significant (n P=0.024) .The main causes of death were severe pneumonia with acute respiratory distress syndrome (ARDS, n n=20), acute heart failure(n n=9), atrial fibrillation(n n=3) and multiple organ dysfunction syndrome (MODS, n n=3).n Conclusions:ARDS caused by severe pneumonia and acute heart failure and atrial fibrillation caused by acute viral myocarditis were the main causes of death in severe COVID-19 patients. Early prevention of myocardial injury and treatment of acute viral myocarditis complicated with disease progression may provide insights into treatment and reduction of mortality in patients with severe COVID-19.