Introduction

Health care professionals worldwide are confronted with unprecedented challenges due to the emergence of the novel coronavirus disease-2019 (COVID-19) caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). The virus’s high infectivity, ability to transmit during the asymptomatic phase and relatively low virulence has resulted in rapid transmission beyond geographic regions, leading to a pandemic. Cardiovascular Disease (CVD) and cardiovascular risk factors enhance vulnerability to COVID-19. Further, COVID-19 can worsen underlying CVD and even precipitate de novo cardiac complications [1]. One area of cardiovascular medicine vulnerable during the pandemic is that of Heart Transplantation (HT). The donors, recipients, and those awaiting HT are at increased risk of infection. The eminent risk for the recipients is more evident given their immunocompromised state. We present the case of a 47-year-old woman who presented with COVID-19 on immunosuppression therapy due to recent heart transplantation four months before admission.

Case Report

A 47-year-old Saudi female patient was referred from a peripheral hospital to our center with a COVID-19 respiratory infection. Her history was significant for long-term diabetes, diabetic nephropathy, and hypertension. Due to cardiomyopathy and excessive heart failure with an Ejection Fraction (EF) of 15%, she underwent HT at a specialized center in Riyadh four months before her admission with COVID-19. She was on full immunosuppression medication with mycophenolate 1000 mg twice daily, prednisolone 5 mg twice daily, and sirolimus 2 mg daily. On admission, she reported dry cough concerns but did not have a fever, chest pain, or shortness of breath. She had no diarrhoea, vomiting, or abdominal pain on clinical examination. The patient was conscious, alert, and oriented, with oxygen saturation at 96% on room air (RA). Her chest x-ray showed peripheral bilateral infiltrates (Figure 1). Echocardiography on admission showed left ventricular dysfunction with hypokinesia of the anterior wall and estimated EF of 40% to 45%, dilated left atrium due to the recent transplant, and moderate tricuspid regurgitation. The electrocardiography directly following her HT showed an EF of 55% with no hypokinesia. We initiated broad-spectrum antibiotics (ceftriaxone 1 g; doxycycline 100 mg every 12 hours) for prophylaxis of hospitalacquired pneumonia and antiviral agents against COVID-19. The transplant team modified her immunosuppressive medications to stop mycophenolate, continue sirolimus and changed prednisolone to dexamethasone 6 mg intravenous (IV) daily.

On day three, the patient required oxygen because her saturation was 88% to 90% on RA. She was connected to a nasal cannula of 4 L/min flow, and her oxygen saturation increased to 96%. A second chest x-ray showed increased bilateral infiltrations, but the patient was still afebrile with no shortness of breath and was not in respiratory distress. Her antibiotic treatment was upgraded to IV piperacillin/tazobactam. Her transplant center in Riyadh was contacted, and they advised initiating tocilizumab 4 mg/kg, but this medication was not available to our hospital at that time. A second echocardiography study showed only mild improvement of her EF. Given her severe leukopenia, the patient was also evaluated by a haematologist who suggested her condition was due to immunosuppressive medications augmented with the viral infection, so filgrastim 300 µg daily (subcutaneous) was administered for three days, and her laboratory values were assessed (Table 1). On day five, she developed shortness of breath, and her oxygen saturation dropped to 85% on RA and 97% with the use of 7 L/ min flow via a simple face mask. After two hours, she developed a fever and increased dyspnoea. She also developed gastrointestinal symptoms (vomiting and diarrhoea).