Background Hemodynamic depression (HD) is the most common adverse event following carotid artery stenting (CAS). Hypotension and bradycardia are the most frequent manifestations of HD. HD occurs as a result of stretching of the carotid sinus baroreceptors by the balloon and the stent. Therefore, HD occurs mostly at the time of balloon inflation post-stent deployment, and rare before balloon inflation. I report a case symptomatic HD occurring before balloon inflation during carotid angioplasty/stenting.

Methods Case report and review of the literature.

Case report A 64-year-old man was admitted to the Department of Neurology because of transient right hemiparesis. He had hypertension. MRI showed left middle cerebral artery territorial infarction. Diagnostic angiography revealed an 81% stenosis at the left internal carotid artery origin. Percutaneous left carotid angioplasty and stent was planned to prevent recurrent ischemic stroke. Two days later, when the patient arrived at the angiography suite to perform left carotid angioplasty and stent, he had a blood pressure of 134/70 mm Hg and a resting heart rate of 60 beats per minute. He underwent a left common carotid artery angiogram. Immediately after the procedure, his blood pressure was 80/40 mmHg and pulse rate 40/min. He developed global aphasia and right hemiplegia. An atropine 0.5 mg was injected intravenously. And then his blood pressure was 139/67 and pulse rate 62/min. However his neurologic deteriorations persisted. His deteriorations were thought due to hemodynamic depression rather than microembolism from stenotic area. Therefore, left carotid angioplasty and stenting was performed immediately. After completion of the procedure, his symptoms were improved completely.

Conclusion During CAS, hemodynamic depression is caused by the stretch-induced stimulation of the carotid sinus baroreceptors located in the adventitial walls of the carotid bulb. This baroreceptor activation caused by balloon dilatation and stent deployment causes increased afferent signals to the caudal medulla by way of the carotid sinus and glossopharyngeal nerves. The medulla subsequently responds by increasing parasympathetic impulses and decreasing sympathetic vascular tone, which results in bradycardia and hypotension. Reported incidences of HD as well as individual hemodynamic parameters following CAS procedures vary widely in the literature, ranging from 5% to 76% for bradycardia, and 14% to 28% for hypotension. Our case highlights a rare case of symptomatic HD occurring just before carotid balloon inflation during carotid angioplasty/stent.

Disclosures J. Lee: None.