A 54-year-old obese (body mass index 40.8 kg/m²) male with a history of non-ischemic cardiomyopathy complicated by heart failure with a reduced ejection fraction and left ventricular assist device (LVAD) placement was presented as a candidate for orthotopic heart transplant. The patient also had a history of pulmonary sarcoidosis, type 2 diabetes mellitus, and a recent admission for gastrointestinal bleeding due to an arteriovenous malformation that was treated with argon plasma coagulation.

The patient underwent a repeat sternotomy for an orthotopic beating heart transplant. The procedure included removal of the LVAD and implantation of an implantable cardioverter-defibrillator. Due to primary graft dysfunction and an air embolism within the right coronary artery, the patient could not be weaned off the cardiopulmonary bypass and was placed on VA-ECMO via the left femoral vein and right axillary artery. Postoperatively, the patient required high doses of vasopressors (epinephrine, norepinephrine, and vasopressin) to maintain hemodynamic stability, and was managed with continuous renal replacement therapy for acute kidney injury and hyperkalemia. Despite these measures, the patient demonstrated poor cardiac contractility and was subsequently supported with an intra-aortic balloon pump for left ventricular unloading.

Two days after the transplant, while still on ECMO, routine neurological assessment revealed left-sided hemiparesis with brisk responses on the right side. These findings prompted us to suspect that a cerebrovascular event triggered the stroke alert. Further neurological examinations revealed an obtunded state characterized by minimal responsiveness and pinpointed pupils that were sluggishly reactive to light. There were no motor responses to verbal commands on the left side, but brisk responses in the right upper and lower extremities resulted in a National Institute of Health Stroke Scale score of 17. To further evaluate the patient’s neurological status and investigate the cause of hemiparesis, the patient underwent CTP and CTA of the brain.

CTP studies were initially performed using contiguous non-contrast multidetector computed tomography (CT) axial imaging of the brain, followed by helically acquired rapid axial imaging from the aortic arch through the brain with contrast. Multifocal embolic-appearing infarcts were observed throughout the right middle cerebral artery, bilateral posterior cerebral artery territories, and cerebellar hemispheres. The entire brachiocephalic artery, along with the right subclavian and right common carotid arteries, was not visualized. CTA did not reveal any filling of the intracranial vasculature within the right hemisphere, while CTP demonstrated hypoperfusion of the entire right hemisphere (Fig. 1). The left common carotid, left subclavian, and left vertebral arteries were well visualized, with no evidence of occlusion within any of these vessels. Although the patient’s neurological examination was limited by sedation, the findings suggested subcortical dysfunction, which contradicted the CTP results. Four hours later, he was transferred to the angiography suite for digital subtraction angiography (DSA) to better assess the vasculature. There was no occlusion within the brachiocephalic, right subclavian, or right common carotid arteries as the entire right hemisphere was perfused (Fig. 2). The patient’s stroke was confirmed by CT 3 days later, which showed the expected evolution of multifocal subacute infarcts. While magnetic resonance imaging (MRI) would have helped differentiate between true hypoperfusion of the entire right hemisphere and widespread cerebral infarction, it was not feasible initially because of the patient’s condition. However, an MRI scan taken 1 month after this event demonstrated right high frontal and bilateral occipital lobe infarcts, which were now subacute to chronic. Additionally, there were punctate foci of increased fluid-attenuated inversion recovery and diffusion signals within the left frontal lobe without a corresponding apparent diffusion coefficient, suggesting subacute or chronic infarction with residual surrounding edema.

The lack of large vessel occlusion suggested that the patient’s acute ischemic stroke was likely cardioembolic and secondary to his recent cardiac surgery. Given the patient's critical condition and the complexities of managing multiple organ support systems, the primary care team focused on optimizing ECMO flow, managing anticoagulation, and maintaining adequate perfusion pressures. The patient was successfully weaned off vasopressors and ECMO, with plans for rehabilitation to address left-sided hemiparesis.