New England Society for Vascular Surgery
August 11, 2005

Stroke After Carotid Endarterectomy Surgery: A Re-Appraisal Of Etiology

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Glenn M LaMuraglia, David H Stone, Mark F Conrad, Ferdinando Buonanno, David C Brewster, Michael T Watkins, Christopher J Kwolek, Richard P Cambria
Massachusetts General Hospital, Boston, MA

Introduction and Objectives:
Only with successful outcomes can carotid endarterectomy (CEA) be effective for treating carotid stenosis. Stroke, the major adverse outcome, has been traditionally attributed to surgical technique, presentation with stroke, or certain patient co-morbidities. This study was undertaken to examine correlates of stroke after CEA in contemporary practice.
Methods:
During the interval 2000-2004, 1109 isolated (non-CABG) CEAs, were performed. The primary study endpoint was post-operative stroke and its associated surgical and clinical variables, which were analyzed by univariate and multivariate methods.
Results:
Postoperative stroke occurred in 16 patients (1.4%) including 3 deaths (0.3%). Strokes were classified as intracranial hemorrhage (1), low-flow watershed (3) and thromboembolic (12, 75%). Embolic strokes (12) were identified at anesthesia emergence (2), during the early post-operative period (9, 75%; range 0.3-8 h), or at a delayed interval(1, 14d). In this subpopulation, postoperative hypercoagulation profiles were positive (6/6) for heparin-induced thrombocytopenia (3), elevated anticardiolipin antibody (2) and elevated (>2.5x) homocysteine (1).
By univariate analysis, only hypercoagulative state (p<0.001) and prior stroke (p<0.01) correlated significantly with development of stroke after CEA, while traditional variables as atrial fibrillation, congestive failure, contralateral occlusion, diabetes, hypertension, valvular disease, and pre-operative aspirin were not found to be significant. Multivariate methods verified only hypercoaguable state (p<0.007, Odd R 3.21) as having a statistical difference.
The average drop in postoperative platelet count was greater (16% vs 4%) in patients with stroke (p < 0.005) verifying the hypercoaguable nature of this cohort. Three control patients with previously identified heparin-induced thrombocytopenia underwent uneventful CEA with intravenous argatroban.
Conclusions:
These data are the first to suggest the significant correlation between a patient’s hypercoaguable state and the development of stroke after CEA. While these parameters need prospective validation, these data delineate the importance of screening subpopulations of patients at risk for thrombo-embolic events before CEA.

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