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Etiology of late cerebrovascular events after carotid endarterectomy
Author(s) -
Fluri F.,
Hatz F.,
Voss B.,
Lyrer P. A.,
Engelter S. T.
Publication year - 2011
Publication title -
european journal of neurology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.881
H-Index - 124
eISSN - 1468-1331
pISSN - 1351-5101
DOI - 10.1111/j.1468-1331.2010.03152.x
Subject(s) - medicine , etiology , carotid endarterectomy , stroke (engine) , stenosis , cardiology , endarterectomy , carotid artery disease , surgery , mechanical engineering , engineering
Background: Progressive carotid artery disease has been shown to cause cerebrovascular events years after a patient’s carotid thromboendarterectomy (CEA). Yet, some late cerebrovascular events in CEA patients are attributable to other etiologies. Objective: We sought to determine frequency and characteristics of late cerebrovascular events in post‐CEA patients attributable to etiologies other than progressive carotid disease. Methods: In a post hoc analysis of data from a CEA‐registry with long‐term follow‐up, all patients with transient ischaemic attack (TIA) or stroke occurring >1 month post‐CEA were identified. The etiologies of these events were dichotomized into the groups large‐artery atherosclerosis (LAA) and that non‐large‐artery atherosclerosis (non‐LAA), i.e. all other etiologies (Trial of Org 10172 in Acute Stroke Trial‐criteria). Frequency and characteristics of both groups were compared. Results: Sixty of 361 post‐CEA patients (16.6%; 95%CI 12.9–20.9%) had late cerebrovascular events after 7 years (median). Thirty patients had ischaemic strokes and 30 had TIAs. These events were attributable to LAA in 48% (29/60) and to non‐LAA in 52% (31/60). In the LAA group, contralateral carotid stenosis (62%; 18/29) was more frequent than recurrent ipsilateral stenosis (38%; 11/29). Amongst non‐LAA patients, cardioembolism (29%; 9/31) and small‐artery‐occlusion (23%; 7/31) were the most frequent causes. LAA and non‐LAA patients did not differ in age, time since CEA, risk factor profile, type of event, and baseline medication. Conclusion: In post‐CEA‐patients, half of the late cerebrovascular events were attributable to etiologies other than LAA. Clinical features did not distinguish LAA‐events from non‐LAA events. Thus, stroke prevention in post‐CEA patients should not be confined to screening for progressive carotid disease but includes efforts to optimize the management of risk factor and cardiac diseases.