Abstract

A number of awake patients undergoing carotid endarterectomy (CEA) present from test clamp neurological deficits (NDs) during the procedure. Current guidelines advocate tighter Doppler ultrasound (DUS) surveillance in these patients because of probable higher likelihood of hemodynamic stroke (class 1 grade C), although evidence is lacking regarding benefit. The aim for the study is the assumption that patients who present ND have a higher risk of developing a complete stroke if the ipsilateral carotid artery becomes occluded, and for this reason, surveillance over restenosis of endarterectomy in this group is justifiable; hence, the authors would like to contribute to this matter presenting their experience on restenosis in this specific group of patients. Data were prospectively collected between 2009 and 2018 for patients of a university tertiary referral center who underwent CEA under regional anesthesia and developed alterations in the neurologic monitoring during internal carotid artery (ICA) test clamping. Control patients were consecutively selected as the next patient submitted to the same procedure but who did not develop neurologic alterations. Patients who did not present to the first postoperative evaluation were excluded (4-6weeks). Primary outcome was any restenosis (>30%; >50%; >70%) detected by DUS evaluations between 16 and 30months of follow-up. Clinical adverse events such as stroke, myocardial infarction, acute heart failure, and all-cause death were assessed 30days after the procedure and in the subsequent long-term surveillance period. A multivariate analysis of factors with significant associations to restenosis identified in a univariate analysis was performed by binary logistic regression. Kaplan-Meier analysis and life tables were used to evaluate time-dependent variables. Ninety patients with ND and 94 controls were included. Those with ND had a higher prevalence of obesity, mean age, and scores of American Society of Anesthesiologist physical status, as well as a lower mean degree of ipsilateral stenosis (82.3% vs. 85.8%, P=0.032) and a higher mean degree of contralateral stenosis (67.8% vs. 61.1%, P=0.030). The incidence of restenosis after 2years did not differ significantly between groups. The univariate analysis yielded two significant associations to restenosis >50%, which remained significant after adjustment: ipsilateral stenosis (1.927 + -0.656, P=0.02) and peripheral arterial disease (3.006 + -1.101, P=0.048). NDs were not found to be associated to restenosis (P=0.856). After a median follow-up period of 52months, patients with NDs did not have a higher incidence of stroke (90.6%, standard deviation [SD]: 3.5%; ND: 91.1%, SD: 3.6%, P=0.869), major adverse cardiovascular events (ND: 69.2%, SD: 5.5%; control, 73.6%, SD: 5.2%, P=0.377), or all-cause death (ND: 90.6%, SD: 3.5%; control: 91.1, SD: 3.6%, P=0.981) than controls. The presence of any restenosis was not associated with later stroke rate (ND: 89.5%, SD: 3.2%; control: 100%, P=0.515). Cost-effective DUS surveillance after CEA requires the definition of evidence-based factors associated with restenosis and late stroke. The present study does not support the assumption that patients who presented NDs during the ICA test clamping present a higher risk of developing late stroke. This group of patients also did not present a higher incidence of restenosis. For these reasons, tighter DUS surveillance in this group seems not justifiable. Results from other groups are required to support this position.

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