Abstract 18462: Hickam's Dictum Revisited: A Multifactorial Etiology of Stroke in a Patient With Rheumatic Mitral Stenosis and Atrial Septal Aneurysm

Abstract

A 64-year-old gentleman with rheumatic mitral stenosis (MS), coronary artery disease, and active tobacco abuse was admitted with a left posterior cerebral artery (PCA) territory ischemic cerebrovascular accident (CVA). He presented with confusion, headaches, and alexia with stable vital signs. He denied rest or exertional dyspnea. Physical exam revealed right homonymous hemianopia, mild right upper extremity dysmetria, decreased right facial sensation, and mild prosopagnosia. Initial neuroimaging confirmed an evolving left hemispheric infarct. Laboratory testing showed unremarkable inflammatory markers. Computed tomographic (CTA) and magnetic resonance angiography (MRA) of the head and neck confirmed left PCA territory acute or subacute infarction with occlusion of the left P2 segment. 12-lead electrocardiogram demonstrated normal sinus rhythm. Occult atrial fibrillation was not seen. Transthoracic echocardiogram (TTE) showed no evidence of right-to-left interatrial shunt. Moderate left atrial (LA) dilation, posterior mitral leaflet tip calcification, and a resting mean mitral gradient of 20 millimeters of mercury (mmHg) suggested severe mitral stenosis. Given the discrepancy between the patient’s symptoms and the TTE findings, transesophageal echocardiogram (TEE) was performed (Figure). The patient’s left PCA territory infarct was ascribed to multifactorial cardioembolic etiologies: 1) Atrial septal aneurysm (ASA) 2) Rheumatic MS and 3) Aortic arch atheroma. Anticoagulation was recommended and initiated 14 days after his CVA to minimize risk of hemorrhagic transformation. High-dose atorvastatin and aspirin were instituted. He progressed well through rehabilitation, demonstrating steady neurological improvement. The case underscores the importance of pursuing further investigation when discrepancies exist between clinical and objective data. ASA is an uncommon but under-recognized risk factor for cardioembolic stroke.