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.