Case Presentation: A 63 year old African American female with history of hypertension was admitted to the hospital for COVID-19 and hypoxia. She was treated with Remdesivir, dexamethasone and convalescent plasma in January 2021. Symptoms improved and she was discharged on steroids and anticoagulation. Six weeks later she started complaining of shortness of breath. CTA chest ruled out pulmonary embolism. She continued to test positive for COVID-19 for two months after her initial diagnosis. After 4 months her shortness of breath persisted and she developed palpitations and fatigue so presented to the emergency room. Examination revealed tachypnea, tachycardia and bilateral pitting pedal edema. EKG showed left ventricular hypertrophy. Her troponin was noted to be mildly elevated and BNP- 745 pg/ml. Chest X-ray revealed bilateral infiltrates and pulmonary edema. COVID-19 test was negative this time. A repeat CTA chest was negative for pulmonary embolism but continued to reveal bilateral ground glass opacities and revealed cardiomegaly which was a new finding. Echocardiogram revealed left ventricular ejection fraction 20-24%, grade I diastolic dysfunction, normal right ventricular size and function. Subsequently she underwent left heart catheterization with no evidence of coronary artery disease. Repeat Echocardiogram three months later continued to show ejection fraction of 20%.
Discussion: Viral myocarditis during acute infection is a known complication of respiratory viral infections including Severe Acute Respiratory Syndrome Coronavirus-2 (SARS COV-2) infection. There are reports of developing Takotsubo cardiomyopathy and myocarditis during active COVID-19 infection (1). However developing cardiomyopathy several weeks post COVID-19 infection is uncommon. So far only one case report has been published with non-ischemic cardiomyopathy (2). This is a second case report to our knowledge of non-ischemic cardiomyopathy in a patient who developed cardiomyopathy long after her initial COVID-19 episode. Patient continued to test positive for COVID-19 for 2 months after her initial diagnosis. During the initial hospitalization with COVID-19, troponin levels were normal suggesting against acute myocarditis. EKG and chest X-ray were negative for cardiomegaly during the initial admission for COVID-19. During her subsequent admission to the hospital, patient revealed signs and symptoms of congestive heart failure. She was known to have normal cardiac function a year prior to COVID-19. Following discharge from the hospital her echocardiogram three months later continued to reveal low ejection fraction. Mechanism of delayed development of cardiomyopathy is unknown. Pathophysiology of development of cardiomyopathy during active COVID-19 infection is broadly considered due to myocardial injury caused by myocarditis, myocardial infarction or related to stress (3). During active infection it is hypothesized that SARS COV-2 viruses can cause direct injury to the heart due to the effect of SARS COV-2 on cells which express ACE2 receptors and also indirectly by mediating an immune response that in turn causes an inflammatory response to the heart (4). Non-ischemic cardiomyopathy should be considered in post COVID-19 patients as part of the differential diagnosis to avoid delays in management.
Conclusions: This case report emphasizes considering non- ischemic cardiomyopathy as part of the differential diagnosis in post COVID-19 infection patients presenting with shortness of breath.