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Contralateral Occlusion and Concomitant Procedures Drive Risk of Non-ipsilateral Stroke After Carotid Endarterectomy
W Darrin Clouse1, Laura T Boitano1, Emel A Ergul1
1Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA.
Insights
Non-ipsilateral stroke after carotid endarterectomy (CEA) is uncommon. Key risk factors include operative urgency, symptomatic disease, and contralateral occlusion, but long-term survival is similar to ipsilateral strokes.
Area of Science:
- Vascular Surgery
- Neurology
- Cardiovascular Medicine
Background:
- Stroke following carotid endarterectomy (CEA) is a known complication.
- Factors contributing to non-ipsilateral stroke risk after CEA require further elucidation.
Purpose of the Study:
- To identify predictors of 30-day non-ipsilateral stroke after CEA.
- To evaluate long-term survival based on stroke laterality post-CEA.
Main Methods:
- Analysis of 80,230 CEA procedures from the Vascular Quality Initiative (VQI) database (2003-2017).
- Multivariable logistic regression to identify stroke risk factors.
- Kaplan-Meier analysis for long-term survival assessment.
Main Results:
- Non-ipsilateral stroke occurred in 0.6% of patients.
- Independent predictors included operative urgency, symptomatic disease, contralateral occlusion, shunt use, and combined procedures.
- Protective factors included dextran use and anti-angiotensin therapy.
- 30-day mortality was lower for non-ipsilateral strokes (6.1%) compared to ipsilateral strokes (10.3%).
- Five-year survival rates were similar for non-ipsilateral (73%) and ipsilateral strokes (76%), but worse than no stroke (88%).
Conclusions:
- Non-ipsilateral stroke post-CEA is rare, driven by systemic disease burden and procedural complexity.
- Contralateral carotid occlusion is an independent risk factor for non-ipsilateral stroke.
- Stroke after CEA, regardless of location, similarly impacts long-term survival.
Objectives:
Stroke after carotid endarterectomy (CEA) has been assessed widely. However, factors enhancing non-ipsilateral stroke risk are poorly defined. The aim of this study was to identify drivers of 30 day non-ipsilateral stroke after CEA in the Vascular Quality Initiative (VQI) and assess long-term survival based on laterality of post-operative stroke.
Methods:
The VQI was queried between April 1, 2003, and March 31, 2017, for all CEA. Bilateral carotid procedures within 30 days were excluded. Thirty day non-ipsilateral strokes were identified. Factors were examined to discriminate between patients with and without non-ipsilateral stroke. Univariable analysis followed by multivariable logistic regression was performed. Kaplan-Meier and log rank methods were used to estimate and compare survival.
Results:
During this 14 year period, 80,230 CEA in 74,928 patients met the criteria. The average age was 70.3 ± 9.3 years. Most were male (48,506; 60%), Caucasian (73,967; 92%), smokers (60,543; 76%), and asymptomatic (43,074; 54%). Contralateral stenosis ≥70% was present in 8033 (10%) with 2239 (3%) having contralateral occlusion. In 491 (0.6%) patients, peri-operative non-ipsilateral stroke occurred. After characterising univariable associations, logistic regression identified independent drivers of non-ipsilateral stroke after CEA. Operative urgency (p = .001), symptomatic disease (p < .001) and contralateral occlusion (p = .001) were pre-operative drivers. Operative predictors included shunt use (p = .008), CEA with cardiac surgery (p = .013), and CEA with concomitant proximal ipsilateral endovascular intervention (p = .01). Use of dextran (p = .005) and anti-angiotensin therapy (p = .03) were protective. Reperfusion syndrome (p < .001), re-exploration (p < .001), myocardial infarction (p < .001), and intravenous treatment of hypotension (p < .001) or hypertension (p < .001) were post-operative correlates. Non-ipsilateral stroke 30 day mortality was less than ipsilateral stroke (6.1% vs. 10.3%; p = .007). Five year survival after non-ipsilateral stroke was 73%, and no different from ipsilateral stroke 76% (p = .16). Both were worse than without stroke (88%; p < .001).
Conclusion:
Non-ipsilateral stroke after CEA is rare. Features driving risk surround global disease burden, combined procedures, and haemodynamic fluctuations. Contralateral occlusion independently increases non-ipsilateral stroke risk. Regardless of laterality or location, effects of stroke after CEA on long-term survival are similar.
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