Background: Lymphocytic myocarditis is a rare form of myocarditis, associated with a high mortality rate due a high risk of sudden cardiac death. Lymphocytic myocarditis might present as a relevant late extra pulmonary manifestation after COVID-19 infection.

Case summary: We report a 26-year-old, previously healthy male admitted to our emergency unit with a 1-month history of increasing fatigue, palpitations and shortness of breath. Two month ago he was tested positive for SARS-CoV-2. He had received a 2-dose schedule of the coronavirus disease 2019 (COVID-19) mRNA vaccine Comirnaty® (BioNTech/Pfizer) latest 6 months before. Physical examination revealed besides an increased respiratory rate of 17/minute and heart rate of 123 bpm no pathologies. Blood analysis was noticeable for elevated cardiac markers with a Troponin I of 103ng/l (ref: <34ng/l), D-Dimer of 1,3mg/l (ref: <0,5mg/l) and an N-terminal prohormone of brain natriuretic peptide of 2421ng/l (ref: <125ng/l). A first nasopharyngeal swab for SARS-CoV-2 RNA was negative. The electrocardiogram showed an atrial tachycardia and a right bundle branch block. Transthoracic echocardiogram demonstrated a severely impaired biventricular systolic function with an estimated left ventricular (LV) ejection fraction of 18%. Electric cardioversion restored sinus rhythm. As coronary artery disease could be excluded, LV endomyocardial biopsy (EMB) was performed. A guideline-directed heart failure therapy was initiated. Further diagnostic work-up by Cardiac Magnetic Resonance (CMR) imaging on day 8 after admission confirmed a severely reduced LV systolic function with an ejection fraction of 18% and stroke volume index of 25ml/m². Increased signaling of the interventricular myocardium was noticeable as well as strong midmyocardial late gadolinium enhancement (LGE) basal anteroseptal and inferior as well as medial anterior, anterolateral and inferolateral. LGE was evident also in the right ventricle. Histology of the EMB revealed an acute lymphocytic myocarditis with small myocyte necrosis on day 13. CMR findings were compatible with an underlying myocarditis. Polymerase Chain Reaction (PCR) for common cardiotropic viruses or bacteria and PCR testing for SARS-CoV-2 RNA on the histological specimens of the heart was negative. Thus, with negative infectious findings in the myocardium, and no objections for immunosuppressive therapy, prednisolone was initiated on day 14 (1 mg/kg/day) and continued for two weeks, followed by a dose tapering regimen of 10 mg every four weeks in combination with azathioprine 300mg/day. The patient was equipped with a LifeVest® as wearable cardioverter defibrillator for primary prevention of sudden cardiac death. On day 17, a non-sustained ventricular tachycardia was documented. Conservative heart failure therapy achieved complete remission of symptoms and the patient was discharged on day 18. Follow-up CMR imaging after three months showed an improved LV systolic function with an ejection fraction of 36% and a stroke volume index of 45ml/m². Combined immunosuppressive therapy with prednisolone in a dose tapering regimen in combination with azathioprine 300mg/day was suggested to continue for 6 months.

Conclusion: The case highlights the significance of recognizing lymphocytic myocarditis secondary to COVID-19. It is important to be vigilant of late presentation cardiomyopathy in patients diagnosed with COVID-19 due to high mortality without immediate support.