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A 23-year-old man presented to an outpatient cardiology clinic reporting pain on the left side of his chest with physical activity that persists for 30-60 minutes. He had no preexisting conditions and had previously had an active lifestyle that included running two miles a day, 6 days a week without any problems. Three months prior to presentation, though, he said, he had "mild" COVID-19 that had been treated conservatively in an outpatient setting.

All other information in his medical, surgical, and social history was unremarkable, except assessment of systems was positive for fatigue. The patient's vital signs were within normal limits, and he had no evidence of cardiopulmonary abnormalities.

Findings of a comprehensive metabolic panel were similarly unremarkable:

• Serum troponin: 12 ng/L (reference range 0-30 ng/L)

• B-type natriuretic peptide: <10 pg/mL (reference range ≤100 pg/mL)

Clinicians ordered an EKG, which revealed sinus bradycardia and an incomplete right bundle branch block. Subsequent transthoracic echocardiogram showed that his left ventricular ejection fraction (LVEF) was 60% with no valvular or wall motion abnormalities.

Based on his existing symptoms and the recent history of COVID-19, clinicians ordered a cardiac MRI (CMR) to assess the possibility of myocarditis.

The medical team performed several imaging sequences using a 1.5T Siemens scanner -- steady-state free precession cine images, along with tissue characterization using T1 map shortened Modified Look-Locker Inversion recovery sequence, T2 map images, and late gadolinium enhancement (LGE) images using phase-sensitive inversion recovery sequence.

The results showed evidence of mild dilation of the right atrium; the size of the remaining cardiac chambers was normal. The patient had a normal left ventricular ejection fraction of 54%, with evidence of trace pericardial effusion. There was no evidence of myocardial edema – i.e., global native T1 and T2 values were normal.

LGE imaging was consistent with myopericarditis, with several areas of sub-epicardial as well as pericardial enhancement; quantitative LGE burden was 18.6% (using the mean+5 SD method). Clinicians started the patient on treatment with ibuprofen at 600 mg three times daily for 14 days, and colchicine at 0.6 mg twice daily for 3 months.

At a follow-up assessment 1 month later, the patient reported that he no longer had chest pain or other symptoms. A treadmill stress test revealed he had a good exercise capacity, with no symptoms or EKG abnormalities at 17 metabolic equivalents.

At a later assessment 7 months after his initial presentation, repeat CMR showed that his sub-epicardial fibrosis persisted, in the same distribution as the initially detected myopericarditis; LGE burden, however, had improved to 5.1% and the pericarditis had resolved.

Discussion

Clinicians presenting this of a healthy young man with persistent myocardial scarring 10 months after COVID-19 infection note that CMR's capacity for advanced tissue characterization has made the modality useful in a wide variety of COVID patients with cardiac concerns, ranging from asymptomatic to severe disease.

Other sequelae of the disease include myocarditis, pericarditis, arrhythmias, postural orthostatic tachycardia syndrome, and unmasking of underlying CAD, but unfortunately, little is known about either treating these patients, or their prognosis.

While CMR is used acutely to diagnose myocarditis based on the Lake Louis or modified Lake Louis criteria, it also has outside of acute settings, when tissue edema or scarring on CMR are considered markers for the presence of myocarditis. The case authors cited suggesting that a non-ischemic pattern of LGE may persist as long as 6 months after COVID-19 infection, although the clinical significance of this myocardial scarring remains unclear.

The potential for "a young, healthy individual with mild clinical symptoms" to develop myopericarditis "is concerning as it may represent a large population with undetected myocardial involvement with potential future consequences," the authors wrote.

In a study of a COVID-19 test center cohort of 100 patients recently recovered from COVID-19, was found in 78 patients (78%) as evidenced by abnormal CMR findings, including at least one of the following: raised myocardial native T1 (n=73), raised myocardial native T2 (n=60), myocardial LGE (n=32), or pericardial enhancement (n = 22).

In addition, 60 of those patients (60%) had ongoing myocardial inflammation 2-3 months after diagnosis, independently of pre-existing conditions, severity/overall course of the acute illness, and the time from the original diagnosis.

Similarly, the case authors referenced a comparison of in COVID versus non-COVID patients, which found that only 11% of non-COVID patients with symptomatic acute myocarditis had complete resolution of myocarditis at 6-month follow-up.

Individuals with LGE but no myocardial edema "were at increased risk for cardiac arrest, implantable cardiac defibrillator shock, and heart transplant, as well as heart failure hospitalizations (P<0.0001)," and patient prognosis worsened concurrently with increasing extent of LGE at follow-up, the authors said.

Accurate prediction of cardiac complications including myopericarditis in COVID-19 patients remains difficult, and while the disease has worse outcomes when there is myocardial involvement, the presence of myocarditis by itself was not found to be a poor prognosticator.

Conclusion

The team concluded that extensive myopericarditis with persistent myocardial scarring can be detected using CMR in healthy individuals with mild COVID-19 symptoms. The exact prevalence and potential clinical implications of this entity remain unclear and warrant further longitudinal research, the case authors stated.

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