'Stronger' Evidence of Myocardial Injury in COVID-19

Megan Brooks

April 16, 2020

Editor's note: Find the latest COVID-19 news and guidance in Medscape's Coronavirus Resource Center.

The clinical features of four end-stage heart failure patients with COVID-19 provide strong supportive evidence that the virus can cause cardiac injury, researchers from China conclude in a small study.

Emerging evidence suggests that COVID-19 preferentially afflicts the elderly, particularly those with chronic comorbid conditions, yet the clinical picture of COVID-19 in refractory heart failure patients is unknown, Nianguo Dong, MD, PhD, and colleagues from Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China, write in their report, published online April 7 in JACC: Heart Failure.

To investigate, they did a retrospective study of four patients (all male) with severe heart failure who were hospitalized with confirmed COVID-19 infection. It's believed that three patients became infected while in the hospital because they had been in the same ward before isolation. At the time of diagnosis, they had just mild cough or fatigue; none developed fever during the illness.

20-Fold Increase in Troponin I

All four patients had significantly enlarged left ventricles and reduced left ventricular ejection fractions and New York Heart Function grade IV. Only two patients had typical ground-glass imaging changes in lung CT.

The two patients who required ICU died 10 days after the first positive nucleic acid test. Three patients had elevated troponin I (TNI) in the later period, especially the two who died, with TNI increasing significantly a few days before death.

The "most novel" observation was a greater than 20-fold increase in TNI level of the two critically ill patients, indicating myocardial injury, Dong and colleagues report.

They note that previous reports of myocardial damage in COVID-19 patients have mostly been based on nonspecific indicators, such as creatine kinase-MB (CK-MB) and lactate dehydrogenase (LDH), "which could be confounded by many other factors in clinic."

In fact, CK-MB and LDH were not significantly increased in those reports. "Our findings provided definitely stronger evidence of myocardial injury by COVID-19," they write.

The team also observed significantly higher levels of C-reactive protein (CRP) and brain natriuretic peptide in the two patients who died. In line with evidence in other populations, critically ill COVID-19 patients with heart failure also had typical lymphopenia, they note.

On the basis of these cases, the clinicians say it appears that patients with end-stage heart failure seem to have a "high mortality rate after infection." Older age, more comorbidities, poor general condition, and severe myocardial injury may be risk factors.

The exact mechanism of myocardial injury caused by the novel coronavirus is not completely clear, they say, but through previous reports and this case series, it is clear that the infection can cause myocardial injury and is closely related to disease progression.

Dong and colleagues say that long-term studies in a larger cohort of heart failure patients are needed to understand the prognosis of the disease.

The study had no specific funding. The authors have no relevant disclosures.

JACC Heart Fail. Published online April 7, 2020. Full text

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