Characteristics and clinical significance of myocardial injury in patients with severe coronavirus disease 2019

Abstract

Aims: To investigate the characteristics and clinical significance of myocardial injury in patients with severe coronavirus disease 2019 (COVID-19).

Methods and results: We enrolled 671 eligible hospitalized patients with severe COVID-19 from 1 January to 23 February 2020, with a median age of 63 years. Clinical, laboratory, and treatment data were collected and compared between patients who died and survivors. Risk factors of death and myocardial injury were analysed using multivariable regression models. A total of 62 patients (9.2%) died, who more often had myocardial injury (75.8% vs. 9.7%; P < 0.001) than survivors. The area under the receiver operating characteristic curve of initial cardiac troponin I (cTnI) for predicting in-hospital mortality was 0.92 [95% confidence interval (CI), 0.87-0.96; sensitivity, 0.86; specificity, 0.86; P < 0.001]. The single cut-off point and high level of cTnI predicted risk of in-hospital death, hazard ratio (HR) was 4.56 (95% CI, 1.28-16.28; P = 0.019) and 1.25 (95% CI, 1.07-1.46; P = 0.004), respectively. In multivariable logistic regression, senior age, comorbidities (e.g. hypertension, coronary heart disease, chronic renal failure, and chronic obstructive pulmonary disease), and high level of C-reactive protein were predictors of myocardial injury.

Conclusion: The risk of in-hospital death among patients with severe COVID-19 can be predicted by markers of myocardial injury, and was significantly associated with senior age, inflammatory response, and cardiovascular comorbidities.

Keywords: Coronavirus disease 2019; Mortality; Myocardial injury; Risk.

Figure 1

Flowchart of participant selection.

Figure 2

Receiver operating characteristic analysis of the clinical prediction model. Prediction of in-hospital mortality by levels of CK-MB, MYO, and cTnI; the area under the curve was 0.87, 0.88, and 0.92, respectively. All P < 0.001. AUC, area under the receiver operating characteristic curve; CI, confidence interval; CK-MB, creatinine kinase-myocardial band; MYO, myoglobin; cTnI, cardiac troponin I.

Figure 3

Kaplan–Meier plots and contour plot of survival probability in hospitalized patients with severe COVID-19. (A) Mortality was significantly higher in patients with CK-MB > 2.2 ng/mL, MYO > 73 μg/L, and cTnI > 0.026 ng/mL, all P <0.001 by log-rank test. (B) Higher initial levels of CK-MB, MYO, and cTnI were consistently associated with higher mortality, which was pronounced in patients with senior age. CK-MB, creatinine kinase-myocardial band; MYO, myoglobin; cTnI, cardiac troponin I.

Figure 4

Multivariable Cox regression analysis of clinical indicators of in-hospital mortality in patients with severe COVID-19. (A) In multivariable model 1, CK-MB > 2.2 ng/mL, cTnI > 0.026 ng/mL, and NT-proBNP > 900 pg/mL were risk factors; these cardiac indicators were transformed into categorical variables according to the cut-off points, and procalcitonin, C-reactive protein, and NT-proBNP were transformed into categorical variables according to the 99th percentile upper reference limit. (B) In multivariable model 2, senior age, C-reactive protein, MYO, cTnI, and NT-proBNP were risk factors; these biomarkers were performed as continuous variables. HR, hazard ratio; CI, confidence interval; CK-MB, creatinine kinase-myocardial band; MYO, myoglobin; cTnI, cardiac troponin I; NT-proBNP, N-terminal pro-B-type natriuretic peptide.

Figure 5

Distribution and dynamic profiles of myocardial indicators. (A) Contour plot showing the levels of CK-MB, MYO, and cTnI displayed a rising trend with age, and were significantly higher in the death group than those in the survivors group. (B) Line chart showing a dynamic growth of myocardial indicators in the death group (n = 31), these values were log-transformed for analysis. CK-MB, creatinine kinase-myocardial band; MYO, myoglobin; cTnI, cardiac troponin I.