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.