Carotid angioplasty and stent-induced bradycardia and hypotension: Impact of prophylactic atropine administration and prior carotid endarterectomy.

OBJECTIVE: We compared the physiologic effect of selective atropine administration for bradycardia with routine prophylactic administration, before balloon inflation, during carotid angioplasty and stenting (CAS). We also compared the incidence of procedural bradycardia and hypotension for CAS in patients with primary stenosis vs those with prior ipsilateral carotid endarterectomy (CEA).
METHODS: A total of 86 patients were treated with CAS at 3 institutions. Complete periprocedural information was available for 75 of these patients. The median degree of stenosis was 90% (range, 60%-99%). Indications for CAS were severe comorbidities (n = 49), prior CEA (n = 21), and prior neck radiation (n = 5). Twenty patients with primary lesions were treated selectively with atropine only if symptomatic bradycardia occurred (nonprophylactic group). Thirty-four patients with primary lesions received routine prophylactic atropine administration before balloon inflation or stent deployment (prophylactic group). The 21 patients with prior CEA received selective atropine treatment only if symptomatic bradycardia occurred (prior CEA group) and were analyzed separately. Mean age and cardiac comorbidities did not vary significantly either between the prophylactic and nonprophylactic atropine groups or between the primary and prior CEA patient groups. Outcome measures included bradycardia (decrease in heart rate >50% or absolute heart rate <40 bpm), hypotension (systolic blood pressure <90 mm Hg or mean blood pressure <50 mm Hg), requirement for vasopressors, and cardiac morbidity (myocardial infarction or congestive heart failure).
RESULTS: The overall incidence of hypotension and bradycardia in patients treated with CAS was 25 (33%) of 75. A decreased incidence of intraoperative bradycardia (9% vs 50%; P < .001) and perioperative cardiac morbidity (0% vs 15%; P < .05) was observed in patients with primary stenosis who received prophylactic atropine as compared with patients who did not receive prophylactic atropine. CAS after prior CEA was associated with a significantly lower incidence of perioperative bradycardia (10% vs 33%; P < .05), hypotension (5% vs 32%; P < .05), and vasopressor requirement (5% vs 30%; P < .05), with a trend toward a lower incidence of cardiac morbidity (0% vs 6%; not significant) as compared with patients treated with CAS for primary carotid lesions. There were no significant predictive demographic factors for bradycardia and hypotension after CAS.
CONCLUSIONS: The administration of prophylactic atropine before balloon inflation during CAS decreases the incidence of intraoperative bradycardia and cardiac morbidity in primary CAS patients. Periprocedural bradycardia, hypotension, and the need for vasopressors occur more frequently with primary CAS than with redo CAS procedures. On the basis of our data, we recommend that prophylactic atropine administration be considered in patients with primary carotid lesions undergoing CAS.