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Reversible heart failure was reported in a 2-month-old with COVID-19, which, while rare, may suggest yet another cardiac complication to watch out for.

The boy presented in April with an episode of choking and cyanosis after feeding despite no prior fever, cough, or other signs of infection. By the time paramedics arrived, he wasn't breathing well and required oxygen and bag mask ventilation.

In the pediatric ICU, cardiac injury markers troponin-T and N-terminal pro-B natriuretic peptide were found to be elevated, reported Madhu Sharma, MD, of The Children's Hospital at Montefiore in New York City, and colleagues in

sinus tachycardia, nonspecific ST depression, T wave inversions in the anterolateral and inferior leads, and prominent mid-precordial voltages. The baby's left ventricular ejection fraction (LVEF) was severely depressed (30%), and he also had severe mitral regurgitation. Coronary arteries were unaffected.

"The presentation and clinical course of this patient mirrors four case reports of acute myocardial injury reported in adult patients with COVID-19," the researchers noted. "All four cases presented with severe LV dysfunction, and elevated cardiac biomarkers (TnT, pro-NT BNP), which subsequently normalized."

This is the youngest such known case and expands the range of COVID-related risks for kids, Sharma told 乌鸦传媒.

"Clinicians have to keep in mind that kids present in different ways," Sharma told 乌鸦传媒. "It varies from kids being asymptomatic to cardiac involvement that causes cardiac dysfunction." COVID-related Kawasaki disease and multisystem inflammatory syndrome in children (MIS-C) also frequently have coronary involvement.

While most such cases resolved over time, Sharma noted: "We have to see what the long-term outcome is in those cases, because we are only 6 months into it from when we recognized MIS-C."

The boy got fluids, inotropes, mechanical ventilation for respiratory failure, remdesivir (Veklury, started on day 5 under compassionate use at the time), methylprednisolone (started on day 8), and therapeutic low molecular weight heparin (started on day 10 for increased D-dimer levels).

With the evidence that has accrued, earlier treatment would have been better, Sharma noted. With remdesivir, for example, "if we have a patient like this who presents now, we would have started it earlier on," she said.

The boy's cardiac injury markers started improving on day 8 and LV size and function normalized to an EF of 58% by day 14, although mitral regurgitation took a little longer to improve. He went home without any oral heart failure therapy.

The baby's initial SARS-CoV-2 assay was negative but repeat PCR was positive. He tested negative for any other viral causes of acute myocarditis.

He was infected by a visiting family member the week prior to presentation, though neither of his parents developed COVID-19. He had been born premature at 33 weeks' gestation and spent 3 weeks in the neonatal ICU at that time.

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