Rapid Identification of Type A Aortic Dissection as a Cause of Acute Ischemic Stroke

Background and Purpose Patients with acute aortic dissection (AAD) sometimes present predominantly with neurological symptoms from cerebral ischemia. Such stroke patients must not receive thrombolysis therapy, which can be fatal. However, patients remain at risk if there is a failure to notice concurrent AAD. We aimed to clarify the characteristics of AAD patients with stroke to identify markers for early AAD detection before thrombolysis. Methods Using the single-center database of Stanford type A-AAD patients between 2007 and 2013, we selected those presenting with acute focal neurological deficits, presumably due to cerebral ischemia. Results of physical, radiological, and blood examinations were assessed in AAD patients with stroke. Results Of 226 AAD patients, 23 (10%) had stroke secondary to AAD. Of the 23 patients, 21 (91%) were primarily examined by stroke physicians and 2 (9%) by cardiologists. Thirteen patients (57%) were potential candidates for intravenous thrombolysis. Only 11 patients (48%) complained of chest/back pain. Positive findings indicating AAD included occlusion or intimal flap of the common carotid artery on carotid ultrasound in 18 (90%) of 20 patients, elevated serum d-dimer values (≥6.9 µg/mL) in 18 (78%) of 23, left hemiparesis as a neurological symptom in 17 (74%) of 23, systolic blood pressure differential above 20 mmHg between the arms in 15 (71%) of 21 patients, and mediastinal widening on chest radiograph in 10 (67%) of 15 patients. All 14 patients who underwent complete evaluation showed 2 or more positive diagnostic findings. Conclusions The combination of physical, radiological, and laboratory findings may be a useful rapid-screening method for AAD as a cause of acute ischemic stroke. Patients with acute aortic dissection (AAD) sometimes present predominantly with neurological symptoms from cerebral ischemia. Such stroke patients must not receive thrombolysis therapy, which can be fatal. However, patients remain at risk if there is a failure to notice concurrent AAD. We aimed to clarify the characteristics of AAD patients with stroke to identify markers for early AAD detection before thrombolysis. Using the single-center database of Stanford type A-AAD patients between 2007 and 2013, we selected those presenting with acute focal neurological deficits, presumably due to cerebral ischemia. Results of physical, radiological, and blood examinations were assessed in AAD patients with stroke. Of 226 AAD patients, 23 (10%) had stroke secondary to AAD. Of the 23 patients, 21 (91%) were primarily examined by stroke physicians and 2 (9%) by cardiologists. Thirteen patients (57%) were potential candidates for intravenous thrombolysis. Only 11 patients (48%) complained of chest/back pain. Positive findings indicating AAD included occlusion or intimal flap of the common carotid artery on carotid ultrasound in 18 (90%) of 20 patients, elevated serum d-dimer values (≥6.9 µg/mL) in 18 (78%) of 23, left hemiparesis as a neurological symptom in 17 (74%) of 23, systolic blood pressure differential above 20 mmHg between the arms in 15 (71%) of 21 patients, and mediastinal widening on chest radiograph in 10 (67%) of 15 patients. All 14 patients who underwent complete evaluation showed 2 or more positive diagnostic findings. The combination of physical, radiological, and laboratory findings may be a useful rapid-screening method for AAD as a cause of acute ischemic stroke.