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We analyzed (a) insulin sensitivity (IS), (b) plasma insulin (PI), and (c) plasminogen activator inhibitor-1 (PAI-1) in type 2 diabetes (T2D) patients with (group A) and without (group B) atherothrombotic ischemic stroke (ATIS), nondiabetics with ATIS (group C), and healthy controls (group D). IS was determined by minimal model (Si). Si was lower in A versus B ( 1.18 ± 0.67 versus 2.82 ± 0.61 min−1/mU/L × 104; P < 0.001 ) and in C versus D ( 3.18 ± 0.93 versus 6.13 ± 1.69 min−1/mU/L × 104; P < 0.001 ). PI and PAI-1 were higher in A versus B (PI: 19.61 ± 4.08 versus 14.91 ± 1.66 mU/L; P < 0.001 , PAI-1: 7.75 ± 1.04 versus 4.57 ± 0.72 mU/L; P < 0.001 ) and in C versus D (PI: 15.14 ± 2.20 versus 7.58 ± 2.05 mU/L; P < 0.001 , PAI-1: 4.78 ± 0.98 versus 3.49 ± 1.04 mU/L; P < 0.001 ). Si correlated with PAI-1 in T2D patients and nondiabetics, albeit stronger in T2D. Binary logistic regression identified insulin, PAI-1, and Si as independent predictors for ATIS in T2D patients and nondiabetics. The results imply that insulin resistance and fasting hyperinsulinemia might exert their atherogenic impact through the impaired fibrinolysis.

Decreased Insulin Sensitivity and Impaired Fibrinolytic Activity in Type 2 Diabetes Patients and Nondiabetics with Ischemic Stroke