Hyperinsulinemia and hemostatic abnormalities are associated with silent lacunar cerebral infarcts in elderly hypertensive subjects

OBJECTIVES We sought to study the association of the silent cerebral infarc t (SCI), a predisposing condition of stroke, with hyperinsulinemia and hemo static abnormalities in older hypertensive subjects. BACKGROUND Hypertension is a powerful risk factor for stroke. However, the role of other risk factors for stroke in hypertensive subjects remains inco mpletely understood. METHODS We performed brain magnetic resonance imaging and measured cardiova scular risk factors, by administering the 75-g oral glucose tolerance test and measuring plasma insulin and hemostatic variables, in 123 asymptomatic hypertensive subjects (mean age 69 years). RESULTS At least one SCI was detected in 80 subjects (65%), and multiple SC Is were found in 48 subjects (39%). The presence of SCIs was associated wit h older age, higher levels of 24-h systolic blood pressure, 2-h insulin, th rombin-generation markers (prothrombin fragment 1+2 and thrombin-antithromb in complexes), plasminogen activator inhibitor-1 (PAI-1), D-dimer and von W illebrand factor (vWF), but not with plasmin-alpha(2)-plasmin complex (PIC) levels. The 2-h insulin area under the curve (AUC) was positively correlat ed with PAI-1 and VWF levels (p < 0.01), and the PAI-1 level was negatively correlated with the PIC level (p < 0.02). Multiple logistic regression ana lysis revealed that age and the 2-h insulin AUC were significantly associat ed with SCIs, particularly those located in the subcortical white matter, a nd hemostatic abnormalities were significantly associated with the presence of multiple SCIs, particularly those located in the basal ganglia. CONCLUSIONS In older asymptomatic hypertensive subjects, hyperinsulinemia a ppears to be associated with lacunar-type SCIs, particularly those located in the subcortical white matter, and hemostatic abnormalities show an assoc iation with the presence of multiple SCIs, particularly those located in th e basal ganglia. a Am Coil Cardiol 2001;37:871-7) (C) 2001 by the American College of Cardiology.