Abstract

It has been proposed that purely unilateral carotid stenosis is due mainly to local hemodynamic factors, whereas more diffuse disease reflects a systemic as well as a local predisposition and should therefore be associated with higher rates of arterial disease in the other territories. However, few studies have tested this hypothesis. We studied angiograms from 2741 patients with a recently symptomatic carotid stenosis from the European Carotid Surgery Trial and categorized them as showing purely unilateral disease (no convincing plaque in the contralateral carotid artery) or bilateral disease. We related the presence and extent of plaque at both bifurcations to the prevalence of past atherothrombotic disease in other arterial territories and the risk of future nonstroke vascular events. The degree of symptomatic carotid stenosis was unrelated to either the prevalence of symptomatic arterial disease in other territories at baseline or to the risk of nonstroke vascular death during follow-up, whereas there were strong associations with the presence of bilateral carotid disease. In multivariate analyses, bilateral carotid disease (n=2076) was associated with previous myocardial infarction (odds ratio [OR]=1.7; 95% CI, 1.2 to 2.4) or peripheral vascular disease (OR=1.5; 95% CI, 1.2 to 2.0) and with subsequent nonstroke vascular death (hazard ratio=2.0; 95% CI, 1.5 to 2.6). The 5-year risk of nonstroke vascular death ranged from 2.7% (95% CI, 1.5% to 4.6%) in patients with no history of coronary or peripheral arterial disease at baseline and purely unilateral carotid disease to 21.4% (95% CI, 17.6% to 26.1%) in those with bilateral carotid disease and a history of either coronary or peripheral arterial disease (P<0.0001). Bilateral carotid disease is associated with higher rates of symptomatic arterial disease in other territories, suggesting a systemic predisposition to atherosclerosis and hence, the need for more aggressive preventive treatment, whereas purely unilateral carotid disease indicates a mainly local hemodynamic etiology.

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