Case Presentation: A 51-year-old morbidly obese male without any significant past medical history presented to the hospital for evaluation of one month history of worsening dyspnea on exertion associated with orthopnea and PND. He was hemodynamically stable and physical examination revealed 2+ bilateral lower extremity pitting edema. Initial laboratory workup was significant for high-sensitivity troponin elevation to 66 ng/L[Normal less than 45 ng/L] and brain-natriuretic peptide elevation to 554 pg/ml [Normal less than 100 pg/ml]. Chest x-ray was unremarkable, and electrocardiogram was significant for sinus tachycardia. Notably, he was admitted to the hospital three months ago for COVID-19 infection. Further workup with transthoracic echocardiography revealed a severely reduced left ventricular systolic ejection fraction of 15 to 20% without wall motion abnormalities. A follow-up left heart catheterization to evaluate the etiology of new-onset heart failure did not reveal any significant coronary artery disease. The patient was diagnosed with non-ischemic cardiomyopathy secondary to COVID-19 infection, and he was initiated on guideline-directed medical therapy with metoprolol, sacubitril-valsartan, and empagliflozin. Patient’s symptoms improved drastically as euvolemia was achieved with diuretics and he was discharged home. On follow-up visit three months later, he appeared symptom-free with a recovered ejection fraction of 40-45% on repeat cardiac echocardiographic imaging.
Discussion: Myocarditis refers to inflammation of cardiac muscles, with COVID-19 being identified as one of the causes [1]. It can present with a myriad of symptoms ranging from asymptomatic presentation to severe cardiomyopathy and fatal arrhythmias [2]. We present a clinical case of late-onset COVID-19-induced myocarditis in an otherwise healthy adult. COVID-19 infection induces a systemic inflammatory response that can affect cardiac muscles for up to several weeks after the initial infection. Most cases of COVID-19-induced myocarditis have been reported within the first seven days of infection, with one case highlighting the late symptom onset, one month post-infection [1]. Our case signifies the possibility of late-onset myocarditis with our patient displaying a unique presentation two months after the initial infection.
Conclusions: Clinicians should be aware of the delayed presentation of COVID-19-induced myocarditis, which can guide towards early diagnosis and management. This would also entail prolonged surveillance after resolution of the initial infection.