COVID-19 Resource Center

COVID-19 Resource Center

Disclosures: The study and editorial authors report no relevant financial disclosures.
March 27, 2020
3 min read
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Myocardial injury may be key in predicting COVID-19 fatalities

Disclosures: The study and editorial authors report no relevant financial disclosures.
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New data from Wuhan, China, indicate that myocardial injury appears to be associated with death in patients with COVID-19. However, the association may not be as strong in patients with COVID-19 and underlying CVD but no evidence of myocardial injury, according to a retrospective single-center case study.

Researchers analyzed 187 patients with COVID-19 (mean age, 59 years), of whom 23% died and 35.3% had underlying CVD, including hypertension, CHD and cardiomyopathy.

Among the cohort, 27.8% had myocardial injury, defined as serum troponin T levels above the 99th percentile upper reference limit, Tao Guo, MD, cardiologist from Zhongnan Hospital of Wuhan University, and colleagues wrote in JAMA Cardiology.

Differences by myocardial injury

The primary outcome of COVID-19-associated death occurred in 69.44% of patients with both underlying CVD and myocardial injury, 37.5% of patients with myocardial injury but no underlying CVD, 13.3% of patients with underlying CVD but no myocardial injury and 7.62% of patients without underlying CVD or myocardial injury, according to the new data.

Myocardial injury was observed in 54.5% of patients with underlying CVD and 13.2% of patients without underlying CVD, Guo and colleagues wrote.

The researchers reported plasma troponin T levels were correlated with C-reactive protein levels (beta = 0.53; P < .001) and N-terminal pro-B-type natriuretic peptide levels (beta = 0.613; P < .001).

Among patients who died, plasma troponin T and NT-proBNP levels increased during hospitalization (P = .001 and P < .001, respectively), but that was not true in patients who survived (P = .96 and P = .16, respectively), Guo and colleagues wrote.

Patients with myocardial injury were more likely than those without myocardial injury to have malignant arrhythmias, need glucocorticoid therapy (71.2% vs. 51.1%) and need mechanical ventilation (59.6% vs. 10.4%), according to the researchers.

The rate of mortality was higher, 36.8%, for patients who were taking ACE inhibitors or angiotensin receptor blockers, compared with 25.6% for those not taking these medications, according to the new data.

“For patients with underlying CVD, including hypertension, coronary heart disease and cardiomyopathy, viral illness can further damage myocardial cells through several mechanisms including direct damage by the virus, systemic inflammatory responses, destabilized coronary plaque and aggravated hypoxia. Therefore, patients with CVD are more likely to experience myocardial injury after COVID-19 infection and higher risk of death,” Guo and colleagues wrote. “However, it is also notable that the 16% of patients with underlying CVD but with normal troponin T levels had a relatively favorable outcome in this study. These data suggest that myocardial biomarkers should be evaluated in patients with CVD who develop COVID-19 for risk stratification and possible early and more aggressive intervention.”

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Wake-up call has been delivered’

Robert O. Bonow

In a related editorial, Robert O. Bonow, MD, MS, vice chair for development and innovation, Max and Lilly Goldberg Distinguished Professor of Cardiology and professor of medicine at Northwestern University Feinberg School of Medicine and past president of the American Heart Association, and colleagues, wrote: “The current observations ... regarding the important association of myocardial injury with adverse outcomes begin to provide insights into other possible mechanisms, including demand ischemia that devolves into myocardial injury or plaque disruption stimulated by intense systemic inflammatory stimuli. As with other coronaviruses, SARS-CoV-2 can elicit the intense release of multiple cytokines and chemokines that can lead not only to vascular inflammation and plaque instability but also to myocardial inflammation. Direct viral infection of the myocardium is another possible causal pathway of myocardial damage and one that requires further investigation.

“The wake-up call has been delivered,” Bonow and colleagues concluded. “We have a similar profile of elderly patients with cardiovascular disease in the U.S. and other Western countries in which the toll of COVID-19 could be daunting. While remarkable efforts to unravel the mechanisms of myocardial injury are ongoing and candidate therapies are already entering clinical trials ... one message resonates with us: prevention.” – by Erik Swain

Disclosures: The study and editorial authors report no relevant financial disclosures.