Characterization of perioperative contralateral stroke after carotid endarterectomy

Abstract

Objective: Contralateral stroke is an infrequent cause of perioperative stroke after carotid endarterectomy (CEA). Whereas the risks of ipsilateral stroke complicating CEA have been discriminated, factors that lead to contralateral stroke are poorly defined. The purpose of this study was to identify the risk of perioperative (30-day) contralateral stroke after CEA as well as predisposing preoperative and operative factors. Its specific effect on long-term survival was interrogated.

Methods: The Vascular Study Group of New England (VSGNE) was queried from April 1, 2003, to February 29, 2016, for all CEAs. Duplicated patients and those without complete data were excluded. Patients sustaining contralateral stroke after CEA in the 30-day postoperative period were identified. Demographic, preoperative, and operative factors were analyzed to identify discriminators between those with and those without contralateral stroke. Logistic regression modeling was performed to identify factors independently associated with contralateral stroke. The effect of contralateral stroke on 5-year survival was compared with patients with ipsilateral stroke and no stroke using the Kaplan-Meier method. Log-rank testing compared survival curves.

Results: There were 10,837 CEAs performed during the study. Average age was 70.4 ± 9.3 years; 6605 (61%) patients were male, and 40% (n = 4324) were performed for symptoms. Most were current or former smokers (n = 8619 [80%]). Coronary artery disease and congestive heart failure were identified in 31% and 8.6%, respectively. Overall, there were 190 strokes within 30 days of CEA (1.8%); 131 were ipsilateral (1.3%), and 59 (0.5%) patients were identified as having contralateral perioperative stroke. Thirteen patients sustained bilateral stroke (0.1%). Significant univariate associations included urgency (P = .0001), ipsilateral stenosis severity (P = .004), length of operation (P = .0001), CEA with coronary artery bypass graft (P = .0001), CEA with other arterial surgery (P = .01), and CEA with proximal endovascular procedure (P = .03). Contralateral occlusion (P = .06) and degree of contralateral carotid stenosis (P = .14) did not correlate. After logistic regression analysis of significant univariate anatomic and operative factors, length of procedure (odds ratio [OR], 1.08/15 minutes; 95% confidence interval [CI], 1.01-1.15; P = .02), urgency of operation (OR, 2.5; 95% CI, 1.3-4.6; P = .006), and concomitant proximal endovascular intervention (OR, 8.7; 95% CI, 4.5-31.2; P = .001) remained predictors of contralateral stroke after CEA. Occurrence of both ipsilateral (P < .001) and contralateral (P = .023) stroke significantly reduced 5-year survival compared with those without stroke. There was no difference in the negative survival effect based on laterality of stroke (P = .24).

Conclusions: Contralateral stroke after CEA is rare, affecting 0.5% of patients. Traditional risk reduction medical therapy does not affect occurrence. Degree of contralateral stenosis, including contralateral occlusion, does not predict perioperative contralateral stroke. Urgency of operation, length of operation, and performance of concomitant, ipsilateral endovascular intervention predict contralateral stroke risk with CEA. Contralateral stroke affects long-term survival similar to ipsilateral stroke after CEA.