Abstract
There is a possible association between lymphocytic myocarditis and COVID-19 in patients genetically susceptible to cardiomyopathy.
A 50-year-old female with history of hypertension and a family history of sudden cardiac death in two siblings and COVID-19 related myocarditis in a brother presented with persistent shortness of breath at rest, orthopnea, exertional stabbing-type chest pain, and fatigue two weeks after diagnosis of COVID-19. Physical exam was notable for tachycardia, with no fever or signs of volume overload. Patient was found to have elevated troponin and erythrocyte sedimentation rate, with normal brain natriuretic peptide and c-reactive protein. Electrocardiogram showed sinus tachycardia. Computer tomography angiography of the chest was negative for pulmonary embolism, pneumonia, or interstitial lung disease. Echocardiogram revealed lateral wall hypokinesis with ejection fraction 50% and normal ventricular cavity size. Coronary angiogram revealed normal coronaries. Cardiac magnetic resonance revealed anterolateral wall hypokinesis and left ventricular ejection fraction 45% with no scar or edema and no evidence of myocardial or pericardial disease.
The patient received treatment with NSAIDs, furosemide, carvedilol, and colchicine. Symptoms persisted over the next several months. Magnetic resonance FDG-PET revealed increased uptake in the lateral wall of the left ventricle. Subsequent biopsy of this region revealed lymphocytic myocarditis. The patient was started on prednisone 60 mg, with partial improvement of symptoms. Symptomatic treatment also required acetaminophen and aspirin, with continued use of colchicine. Genetic studies revealed a likely pathogenic variant in the MYBPC3 gene involving an altered consensus splice site associated with autosomal dominant hypertrophic cardiomyopathy and dilated cardiomyopathy. Symptoms recurred upon tapering of prednisone, requiring a longer course of treatment. The patient also developed symptoms of postural orthostatic tachycardia syndrome. With continued treatment, symptoms significantly improved.
Our case suggests that lymphocytic myocarditis could be a rare manifestation of coronavirus disease whose risk factors may include hereditary cardiomyopathies. It has potential to become a chronic condition with a challenging symptomatic management.