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RESEARCH PRODUCT

Endothelial dysfunction and carotid lesions are strong predictors of clinical events in patients with early stages of atherosclerosis: a 24-month follow-up study

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Background The purpose of this study was to investigate whether the vasodilator response to brachial artery and the presence of carotid lesions may have a prognostic significance in patients with early stages of atherosclerosis. Methods and results Vascular echography was performed to analyze flow-mediated vasodilatation (FMD) at the brachial artery and intima–media thickness (IMT) of carotid arteries in 84 asymptomatic patients. At baseline, we evaluated all the established traditional cardiovascular risk factors. Transient ischemic attack, stroke, effort or unstable angina, acute myocardial infarction, peripheral arterial disease and cerebrovascular and cardiovascular death served as outcome variables over a follow-up period of 24 months. Brachial FMD was correlated inversely with carotid IMT (P=0.003), systolic blood pressure (P=0.0001) and age (P=0.0001). IMT was positively correlated with systolic blood pressure (P=0.0001), waist circumference (P=0.004) and age (P=0.01). At the end of the follow-up cardiovascular and cerebrovascular events were registered in 29% of the patients and in a multivariate analysis, including all the variables evaluated at baseline, male sex [odds ratio (OR) 1.6, P=0.005], the presence of baseline carotid lesions (OR 3.5, P=0.02) and FMD below the median (OR 3.2, P=0.03) were the only variables predictive of clinical events. Conclusion In this study, endothelial dysfunction and carotid lesions significantly increased the risk of vascular events in asymptomatic patients with early stages of atherosclerosis. Assessment of systemic vasoreactivity and carotid IMT evaluation may provide, in this category of patients, important prognostic information in addition to that derived from traditional established cardiovascular risk factors. Coron Artery Dis 19:139–144 c 2008 Wolters Kluwer Health | Lippincott Williams & Wilkins. Coronary Artery Disease 2008, 19:139–144