Case Presentation: This is a case of a 67-year-old male with history of strokes in 2012 & 2014 with residual right (R) sided upper and lower extremity weakness, blindness, and hearing loss, Coronary Artery Disease status post (s/p) Myocardial Infarction (MI) and Congestive Heart Failure s/p AICD, atrial fibrillation (AF) on coumadin, hypertension, hyperlipidemia, chronic kidney disease stage 3, presenting from home with acute kidney injury (Cr 2.2) and R ankle pain causing immobility. After appropriate work-up, patient was diagnosed and treated for gout with resolution of symptoms, and started on Levaquin for a right upper lobe pneumonia incidentally identified on imaging. On hospital day 3, patient’s course was complicated by new bilateral (BL) dysmetria, dysdiadochokinesia, and left sided visual deficits. A stroke code was called, with immediate CT Head showing new acute R parieto-occiptial, and BL subacute cerebellar infarcts. Decision was made not to perform CTA Head/Neck given patient’s acute on chronic kidney disease, and high suspicion for cardioembolic etiology of the new infarcts based on his presentation. A transesophageal echocardiogram (TEE) was sought and performed the same day, revealing severe, complex, bulky atherosclerotic plaque with mobile components throughout the descending aorta and aortic arch, as well as a patent foramen ovale. Of note, patient’s INR on HD 3 was supratherapeutic (3.1).

Discussion: Cardioembolic strokes (CES) are rare, accounting for ~ 20% of all strokes. The characteristic clinical features of CES, many of which were noted in this case, include sudden onset with maximal deficits on initial presentation, infarcts within multiple different vascular (most often posterior) territories, and higher hemorrhagic conversion rate (~42% ) due to propensity for spontaneous dissolution, with peak onset 2-4 days post event. Although transthoracic echocardiograms are the customary diagnostic imaging modality for work-up of new strokes, we elected for TEE because of the high pre-test probability for aortic/valvular pathology, and history of AF in our patient, both of which support TEE as the appropriate first choice. It is essential to note that aortic arch atheromas can only be diagnosed on TEE, and had we proceeded with the archetypal approach, our diagnosis would have been delayed.

Conclusions: Once the etiology of our patient’s CES was elucidated, new questions arose; in patients with stroke due to aortic thrombi, does anticoagulation improve clinical outcomes, and when should it be initiated? To date, there is no evidence to support use of aspirin, clopidogrel, and/or coumadin for management of CES due to aortic atheromas. The ARCH Trial (2015) suggested that use of aspirin and clopidogrel reduced the rate of recurrent stroke, MI, peripheral embolism, and vascular death by 24%, but lacked power required for analysis, and could have been the result of chance (adjusted P=0.5).  More research in this field is required.