Basilar Artery Occlusion Secondary to Cocaine-Associated Cardiomyopathy: A Case of Cardioembolic Stroke With Poor Outcome Despite Successful Reperfusion

Basilar artery occlusion (BAO) is a neurologic emergency associated with high morbidity and mortality, in which successful reperfusion does not consistently translate into favorable functional outcomes. While futile recanalization has been well described, the underlying mechanisms contributing to poor outcomes remain incompletely understood. We present the case of a 54-year-old male with polysubstance use who presented with altered mental status and focal neurologic deficit, and was found to have BAO. He underwent emergent endovascular thrombectomy with complete reperfusion (thrombolysis in cerebral infarction (TICI) grade 3). Despite this, post-procedural imaging demonstrated extensive multifocal infarctions involving the posterior circulation and supratentorial territories. Further evaluation revealed newly diagnosed severe systolic dysfunction with an ejection fraction of 20%, raising concern for a cardioembolic source. In the context of confirmed cocaine use, this finding suggests cocaine-associated cardiomyopathy as a potential underlying mechanism contributing to thrombus formation and embolization. The pattern of widespread infarction across multiple vascular territories supports a systemic embolic process rather than isolated large vessel occlusion. Despite hemodynamic stability and appropriate medical management, the patient remained significantly functionally impaired. This case highlights cocaine-associated cardiomyopathy as a likely underrecognized and clinically important cardioembolic mechanism in posterior circulation stroke. It underscores the importance of early cardiac evaluation in patients with multifocal infarction patterns and substance use, and demonstrates how severe systolic dysfunction may contribute to poor neurologic outcomes despite technically successful reperfusion.