Initially detected in Wuhan, China, COVID-19 rapidly spread worldwide. On March 11, 2020, it was declared a pandemic by World Health Organization.1 COVID-19 is caused by acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Since its emergence, COVID-19 has affected health systems worldwide. It can affect multiple systems of the human body. Known cardiovascular manifestations of this disease include myocarditis, pericarditis, arrhythmia, and venous thromboembolism.2 Patients with an existing cardiovascular condition have a higher risk of morbidity and mortality after having contracted COVID-19.3 Herein, we present the case of a patient with no previous cardiovascular disease who presented with COVID-19 infection.
The patient is a 58-year-old male with a history of hypertension, diabetes mellitus, status post left nephrectomy (history of renal carcinoma), and history of end-stage renal disease on hemodialysis. He came to hospital due to shortness of breath, fever, and low oxygen saturation. He was diagnosed with COVID-19 pneumonia. His cardiac troponin rose to 6.65 ng/mL. Initially, we thought that the rise in troponin could be due to his underlying respiratory tract infection and renal insufficiency. Shortness of breath could be due to respiratory infection. The patient had undergone a Cardiolite (Lantheus Medical Imaging) stress test in March 2019 that showed no ischemia (Figure 1). It was decided to treat the patient with conservative medical therapy and consider non-invasive evaluation (Cardiolite stress test) after initial stabilization. The patient was treated with antibiotics, corticosteroids, and anticoagulation therapy. After he became afebrile, requiring less oxygen therapy, a Cardiolite stress test was performed. It showed a large, reversible defect suspicious for triple-vessel disease (Figure 2). Due to this new, abnormal finding, a diagnostic catheter-based coronary angiogram was performed. Angiography showed mild atherosclerotic coronary artery disease (Figure 3). It is possible that COVID-19 associated thromboinflammation4 may have been the cause of the abnormal stress test. However, further studies are required to confirm this assumption.
Disclosure: Dr. Ahmed reports no conflicts of interest regarding the content herein.
Syed M. Ahmed, MD, can be contacted at firstname.lastname@example.org
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