Case description
A 62-year-old man diagnosed with COVID-19 pneumonia presented 8 days after his positive COVID test with a chief complaint of worsening dyspnea. He had a prior history of bacterial pneumonia requiring hospitalizations and hypertension. He did not have any cardiac history. On presentation in the ED, the patient was hypoxic with 76% oxygen saturation on room air and required 15 liters of oxygen/min through a non-rebreather mask to maintain his saturation levels above 90%. Computed tomography (CT) of the chest was negative for pulmonary embolism. He was treated with dexamethasone 6 mg daily (10-day course), therapeutic dose anticoagulation (enoxaparin 1 mg/kg), and oxygen. The patient’s daily complaints were dyspnea and cough, and he denied chest pain. On day 3 of his hospitalization, the patient’s oxygen saturations decreased and the respiratory therapist was called to his room to increase his oxygen requirement. Before his oxygen could be maximized, he had cardiac arrest with pulseless electrical activity (PEA). Following resuscitation efforts, the patient was intubated and transferred to the intensive care unit. The patient’s electrocardiogram was consistent with anterior lead ST-segment elevations (Figure 1). His initial troponin I was 0.012 ng/ml. He was started on aspirin, high-intensity statin, ticagrelor, and low intensity heparin infusion. Urgent coronary angiography revealed multifocal stenosis in the left anterior descending coronary artery (LAD), with myocardial infarction flow 3 (Figure 2). He otherwise had angiographically normal coronary vessels without signs of plaque erosion or rupture. The lesions in the LAD were treated with intracoronary nitroglycerin for suspected coronary spasm, revealing complete resolution of the stenotic segment with normal angiographic appearance of the vessel (Figure 3). Intravascular ultrasound was also performed revealing no significant atherosclerotic disease, remodeling, dissection, or thrombus (Figure 4). The patient’s condition did not improve and he was eventually placed on vasopressor support. He soon developed mixed cardiogenic and septic shock with multiorgan system failure. Laboratory examinations revealed D-dimer of 1119 ng/mL. Inflammatory markers including erythrocyte sedimentation rate, ferritin, and C-reactive protein (CRP) were not evaluated. Owing to the patient’s need for ongoing vasopressor support, he was unable to be started on nitrates or calcium channel blockers.