Abstract Introduction Neurologic manifestations presenting symptoms of aortic dissections are noted in a minority of cases, and usually result from direct extension into cerebral vessels. We report an uncommon presentation of a Stanford Type A aortic dissection manifesting as repeated transient ischemic attacks (TIAs) caused by intermittent hypoperfusion of the left common carotid artery due to dissection flap extension into the vessel. Case Presentation A 46 year old male with a history of obstructive sleep apnea, otherwise healthy, developed sudden nonsensical speech while eating dinner in the evening prior to admission. On arrival at the emergency department, he exhibited expressive aphasia (NIHSS 6) without motor deficits. CT angiography of the head and neck demonstrated left internal carotid artery occlusion with distal reconstitution; CT perfusion was negative for infarction. He received aspirin and ticagrelor loading with complete resolution of symptoms after one hour (NIHSS 0), but had recurrent aphasia several hours later (NIHSS 6). Further work-up at that time included an MRI brain which showed no acute infarct. Initial troponins were elevated (126,166,141 ng/L) despite EKG showing no ischemic changes.Subsequently he developed chest discomfort and new-onset atrial fibrillation with rapid ventricular response. Stat transthoracic echocardiography revealed a 6.7 cm ascending aortic aneurysm with an intimal flap and moderate to severe aortic regurgitation. CT angiography of the chest confirmed a Type A dissection originating proximal to the great vessels and extending into the innominate and left common carotid arteries, with a short segment of decreased contrast opacification suggesting reduced carotid flow. These findings correlated with his transient neurologic deficits, consistent with intermittent left carotid hypoperfusion. He was stabilized with intravenous esmolol and nitroprusside infusions, intubated for respiratory support, and urgently transferred to a tertiary center for root and ascending aortic replacement. Discussion This case highlights a nuanced etiology and critical diagnostic pitfall in evaluating for stroke like symptoms. Transient or fluctuating neurologic deficits without a clear radiographic cause, accompanied by chest pain or hemodynamic instability should prompt consideration of acute aortic syndrome, especially prior to initiating antiplatelet or anticoagulant therapy. Furthermore in patients with carotid dissection on imaging, CTA of the chest should be considered to exclude concurrent Type A dissection, as this may potentially represent distal propagation. Early recognition through comprehensive vascular imaging can prevent catastrophic outcomes by expediting surgical intervention. This abstract is funded by: None
Ghumman et al. (Fri,) studied this question.