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  • Title: Modeling stroke risk after coronary artery bypass and combined coronary artery bypass and carotid endarterectomy.
    Author: Ricotta JJ, Char DJ, Cuadra SA, Bilfinger TV, Wall LP, Giron F, Krukenkamp IB, Seifert FC, McLarty AJ, Saltman AE, Komaroff E.
    Journal: Stroke; 2003 May; 34(5):1212-7. PubMed ID: 12690211.
    Abstract:
    BACKGROUND AND PURPOSE: The goals of this study were to compare the ability of statewide and institutional models of stroke risk after coronary artery bypass (CAB) to predict institution-specific results and to examine the potential additive stroke risk of combined CAB and carotid endarterectomy (CEA) with these predictive models. METHODS: An institution-specific model of stroke risk after CAB was developed from 1975 consecutive patients who underwent nonemergent CAB from 1994 to 1999 in whom severe carotid stenosis was excluded by preoperative duplex screening. Variables recorded in the New York State Cardiac Surgery Program database were analyzed. This model (model I) was compared with a published model (model II) derived from analysis of the same variables using New York statewide data from 1995. Predicted and observed stroke risks were compared. These formulas were applied to 154 consecutive combined CAB/CEA patients operated on between 1994 and 1999 to determine the predicted stroke risk from CAB alone and thereby deduce the maximal added risk imputed to CEA. RESULTS: Risk factors common to both models included age, peripheral vascular disease, cardiopulmonary bypass time, and calcified aorta. Additional risk factors in model I also included left ventricular hypertrophy and hypertension. Risk factors exclusive to model II included diabetes, renal failure, smoking, and prior cerebrovascular disease. Our observed stroke rate for isolated CAB was 1.7% compared with a rate predicted with model II (statewide data) of 1.56%. The observed stroke rate for combined CEA/CAB was 3.9%. When the Stony Brook model (model I) based on patients without carotid stenosis was used, the predicted stroke rate was 2.8%. When the statewide model (model II), which included some patients with extracranial vascular disease, was used, the predicted stroke rate was 3.4%. The differences between observed and predicted stroke rates were not statistically significant. CONCLUSIONS: Estimation of stroke risk after CAB was similar whether statewide data or institution-specific data were used. The statewide model was applicable to institution-specific data collected over several years. Common risk factors included age, aortic calcification, and peripheral vascular disease. The observed differences in the predicted stroke rates between models I and II may be due to the fact that carotid stenosis was specifically excluded by duplex ultrasound from the patient population used to develop model I. Modeling stroke risk after CAB is possible. When these models were applied to patients undergoing combined CAB/CEA, no additional stroke risk could be ascribed to the addition of CEA. Such models may be used to identify groups at increased risk for stroke after both CAB and combined CAB/CEA. The ultimate place for CEA in patients undergoing CAB will be defined by prospective randomized trials.
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