CASE REPORT
Informed consent was obtained from the patient for publication of this case report and any accompanying images and was approved by the New York Presbyterian-Queens Institutional Review Board.
A 60 year-old male with hypertension, hyperlipidemia, non-insulin dependent diabetes, initially with unstable angina and associated dyspnea. Catheterization revealed severe triple vessel coronary artery disease. The following day he underwent an urgent three-vessel CABG (left internal mammary to left anterior descending, and separate saphenous vein grafts to posterior descending and first circumflex marginal). The postoperative echocardiogram showed normal ventricular function. His postoperative course was uncomplicated and he was discharged on postoperative day 4. Thirteen days following discharge he presented the emergency department with 4 days of progressive shortness of breath associated with a productive cough and intermittent blood tinged sputum. He denied any chest pain on presentation. His vital signs were significant for mild tachycardia and hypoxia requiring a 100% nonrebreather mask to obtain a saturation of 97%. Admission electrocardiogram (EKG) showed anterior and inferior ischemia with ST elevations (Figure 1). Pertinent laboratory blood work showed initial troponin-t of 0.537 ng/ml with a peak of 4.1 ng/ml, a D-Dimer of 11, 344 ng/ml, and a C-reactive protein 5.55 mg/dl. A chest radiograph revealed bilateral pulmonary infiltrates typically seen with COVID-19 (Figure 2). His presentation to the ED occurred at the very beginning of the COVID-19 surge. Given his community risk of exposure to COVID-19 in Queens, NY, a SARS-CoV-2 RT PCR was performed and detected the presence of the virus. A transthoracic echocardiogram demonstrated new severe left ventricular global hypokinesis with akinesis in the basal inferior and inferolateral segments. The estimated ejection fraction was 20%.
He was started on intravenous heparin and dual antiplatelet therapy (with aspirin and clopidogrel) for the STEMI for high suspicion of a COVID-19 associated hypercoagulable state. Given the patient’s hemodynamic stability, absence of chest pain, and scarcity of resources during the initial COVID-19 surge, a cardiac catheterization was deferred. During the early period of the initial COVID-19 surge, his treatment included a five-day course of hydroxychloroquine and azithromycin with close monitoring for hypoxia with supplemental oxygen as needed.
The patient’s subsequent hospital course over the next week was complicated by ventricular tachycardia requiring electrical cardioversion and subsequent paroxysmal atrial fibrillation. The patient continued treatment with heparin anticoagulation and dual antiplatelet therapy. Despite therapeutic anticoagulation his hospital course was further complicated by emboli to his toes and a left hemiparesis. Computerized axial tomography and magnetic resonance imaging of the brain were consistent with acute embolic infarcts involving both cerebellar hemispheres, right thalamus, left temporal lobe and both occipital/frontal and parietal lobes. A repeat echocardiogram was performed which ruled out both apical and left atrial thrombus.
Repeat imaging showed no hemorrhagic conversion of the stroke allowing for transition to oral anticoagulation for his atrial fibrillation. The patient continued to require supplemental oxygenation and hospital admission. He remained asymptomatic from his STEMI, with residual left sided motor weakness. He continued to work with physical and speech therapy and was discharged to a skilled nursing facility on hospital day 45. Two months following discharge he was noted to have made a near full recovery. He is ambulatory without assistance. Transthoracic echocardiogram demonstrated an ejection fraction of 40% with inferior hypokinesis.