Case Presentation: A healthy 32-year-old male presented with fever and myalgia followed by multiple episodes of vomiting and diarrhea for the past few days. On admission, patient had a fever of 101F, tachycardia of 118, blood pressure of 118/66 mmHg. His oxygen saturation was 100% on room air. Physical exam was unremarkable. COVID-19 test was positive. Chest X-ray showed no focal consolidation. CT abdomen and pelvis showed mild enteritis. In the emergency department, the patient was given a total of 3.7 liters of isotonic fluids and discharged home. However, he arrived the next day, with continued vomiting, diarrhea and progressive generalized weakness. Physical examination showed tachycardia with heart rate of 129, blood pressure of 96/59 mmHg, increased respiratory rate of 22, oxygen saturation of 100% on room air. Laboratory findings were WBC of 17,460/µl; 26% bands; lactic acid, 6.0 mmol/l; creatinine, 1.59 mg/dl. He received isotonic fluids of 3.7 liters IV as per sepsis protocol again. Within a couple of hours, the patient developed progressive dyspnea and tachycardia of 140. He desaturated to 88% and required BiPAP initiation. Lung auscultation revealed bilateral crackles at lung bases. CT chest showed bilateral pleural effusions, no pulmonary emboli or consolidation. Markers of inflammation and coagulopathy were elevated: CRP, 36.8 mg/dl; fibrinogen, 841 mg/dl; D-dimer greater than 20 µg/ml; ferritin, 4198 ng/ml; LDH, 2092 U/L. Liver function tests showed ALT, 1258 U/l, AST, 1494 U/l. Cardiac workup revealed elevated troponin of 4.76 ng/ml, BNP of 6404 pg/ml. EKG showed sinus tachycardia with a rate of 135. Echocardiography (Echo) showed left ventricular ejection fraction (EF) of 30-35%, with moderate left ventricle global hypokinesia. IV fluids were stopped, and patient was started on IV furosemide, dexamethasone and therapeutic enoxaparin. Over the course of hospitalization, patient’s oxygen requirement drastically reduced. Workup for other causes of cardiomyopathy yielded negative results: parvovirus, EBV, CMV, HSV, HIV, ANA and ANCA serology were negative. SARS CoV-2 IgG antibodies were positive. Patient was hospitalized for a total of 7 days and discharged with a life vest, on lisinopril, metoprolol and furosemide. Follow up Echo in 3 months showed normal EF with no hypokinesis.

Discussion: SARS-CoV-2 (severe acute respiratory syndrome coronavirus 2) can cause myocardial injury due to direct invasion of myocytes and increased production of various cytokines. Here we describe a case of SARS-CoV-2 induced cardiomyopathy in a patient with COVID-19 infection without evidence of pneumonia.

Conclusions: Cardiomyopathy is a known complication of SARS-CoV-2. Recent studies demonstrated increased prevalence of myocardial injury among young adults with multisystem inflammatory syndrome (MIS). A high index of suspicion for SARS-CoV-2 induced cardiomyopathy is critical when evaluating young adults with MIS in the absence of respiratory symptoms. Clinicians should consider a more conservative approach towards IV fluid resuscitation in such cases.