Ogungbe Oluwabunmi, Kumbe Baridosia, Fadodun Oluwadamilola Agnes, Latha T, Meyer Diane, Asala Adetoun Faith, Davidson Patricia M, Dennison Himmelfarb Cheryl R, Post Wendy S, Commodore-Mensah Yvonne
Johns Hopkins University School of Nursing, Baltimore, MD, USA.
The University of Lethbridge, Lethbridge, Alberta, Canada.
Int J Cardiol Heart Vasc. 2022 Jun;40:100950. doi: 10.1016/j.ijcha.2021.100950. Epub 2022 Jan 4.
Infection with the SARS-CoV-2 virus can lead to myocardial injury, evidenced by increases in specific biomarkers and imaging.
To quantify the association between biomarkers of myocardial injury, coagulation, and severe COVID-19 and death in hospitalized patients.
Studies were identified through a systematic search of indexed articles in PubMed, Embase, CINAHL, Cochrane, Web of Science, and Scopus, published between December 2019 to August 2021. Effect estimates from individual studies for association between markers of myocardial injury (Troponin), myocardial stretch (N-terminal-pro hormone BNP, NT-proBNP), and coagulopathy (D-Dimer) and death or severe/critical COVID-19 were pooled using inverse variance weighted random-effects model. Odds Ratios (OR), Hazard Ratios (HR), and 95% Confidence Intervals (CI) were pooled separately and reported by outcomes of critical/severe COVID-19 and death. A -analysis of proportions was also performed to summarize the pooled prevalence of co-morbidities in patients hospitalized with COVID-19.
We included 62 articles, with a total of 41,013 patients. The pooled proportion of patients with history of hypertension was 39% (95% CI: 34-44%); diabetes, 21% (95% CI: 18%-24%); coronary artery disease, 13% (95% CI: 10-16%); chronic obstructive pulmonary disease, 7% (95% CI: 5-8%); and history of cancer, 5% (95% CI: 4-7%). Elevated troponin was associated with higher pooled odds of critical/severe COVID-19 and death [Odds Ratio (OR: 1.76, 95% CI: 1.42-2.16)]; and also separately for death (OR: 1.72, 95% CI: 1.32-2.25), and critical/severe COVID-1919 (OR: 1.93, 95% CI: 1.45-2.40). Elevations in NT-proBNP were also associated with higher severe COVID-19 and death (OR: 3.00, 95% CI: 1.58-5.70). Increases in D-dimer levels was also significantly associated with critical/severe COVID-19 and death (pooled OR: 1.38, 95% CI: 1.07-1.79).
This meta-analysis synthesizes existing evidence showing that myocardial injury, and coagulopathy are complications of COVID-19. The durability of these complications and their contributions to long-term cardiac implications of the disease is still being investigated. Patients who have recovered from COVID-19 may benefit from minimally invasive assessment for markers of myocardial injury, stretch and coagulopathy for early risk stratification purposes.
感染新型冠状病毒2(SARS-CoV-2)可导致心肌损伤,这可通过特定生物标志物升高及影像学检查证实。
量化住院患者中心肌损伤、凝血生物标志物与重症新型冠状病毒肺炎(COVID-19)及死亡之间的关联。
通过系统检索2019年12月至2021年8月期间发表在PubMed、Embase、CINAHL、Cochrane、Web of Science和Scopus上的索引文章来确定研究。使用逆方差加权随机效应模型汇总个体研究中关于心肌损伤标志物(肌钙蛋白)、心肌拉伸(N末端前体激素脑钠肽,NT-proBNP)和凝血病(D-二聚体)与死亡或重症/危重型COVID-19之间关联的效应估计值。分别汇总比值比(OR)、风险比(HR)和95%置信区间(CI),并按重症/危重型COVID-19和死亡的结果进行报告。还进行了比例分析,以总结COVID-19住院患者合并症的汇总患病率。
我们纳入了62篇文章,共41013例患者。有高血压病史患者的汇总比例为39%(95%CI:34-44%);糖尿病为21%(95%CI:18%-24%);冠状动脉疾病为13%(95%CI:10-16%);慢性阻塞性肺疾病为7%(95%CI:5-8%);癌症病史为5%(95%CI:4-7%)。肌钙蛋白升高与重症/危重型COVID-19和死亡的较高汇总比值相关[比值比(OR:1.76,95%CI:1.42-2.16)];单独与死亡(OR:1.72,95%CI:1.32-2.25)及重症/危重型COVID-19(OR:1.93,95%CI:1.45-2.40)也相关。NT-proBNP升高也与重症COVID-19和死亡相关(OR:3.00,95%CI:1.58-5.70)。D-二聚体水平升高也与重症/危重型COVID-19和死亡显著相关(汇总OR:1.38,95%CI:1.07-1.79)。
这项荟萃分析综合了现有证据,表明心肌损伤和凝血病是COVID-19的并发症。这些并发症的持续性及其对该疾病长期心脏影响的作用仍在研究中。从COVID-19中康复的患者可能受益于对心肌损伤、拉伸和凝血病标志物的微创评估,以进行早期风险分层。