Previous studies have shown that HDL isolated from human atherosclerotic lesions and the blood of patients with established coronary artery disease contains elevated levels of nitrated apolipoprotein AI (NT-apoAI). The significance of NT-apoAI in the pathogenesis of vascular diabetic complications is not well understood. We aimed to evaluate the relationship between plasma NT-apoAI and vascular function in African-Americans diabetic patients. 125 patients with type 2 diabetes were enrolled over a 6 months period. Levels of plasma NT-apoAI was quantified by enzyme-linked immunosorbent assays (ELISA). Microvascular function was assessed by vascular reactivity index (VRI). Large artery stiffness was assessed by carotid-femoral pulse wave velocity (PWV). Carotid intima-media thickness (CIMT) was assessed by B-mode ultrasound image analysis. Patients population was divided in two groups (well-controlled: HbA1c ≤7.0%, N=54; poorly-controlled: HbA1c >7.0%, N=71). Mean age 60±8 years; 64% female; 80% had hypertension; 90% had dyslipidemia and 15% had CKD. Mean HbA1c levels were 8.1±2.2% and duration of diabetes was 10.29±3.79 years. NT-apoAI was negatively correlated with levels of apoAI and VRI in well-controlled patients but not in poorly-controlled patients (r= -0.298, p=0.025 and r= -0.265, p=0.042; respectively). Multi-regression analysis revealed that NT-apoAI was independently associated with VRI, but neither with PWV nor CIMT, after adjustment for independent variables such as age, gender, weight, hypertension, stroke, smoking, duration of diabetes, dyslipidemia, total cholesterol, HDLc, triglycerides, and LDLc (β= 0.001, p= 0.025; r2= 0.325 for the model). NT-apoAI, independently of other clinical variables, can predict microvascular dysfunction particularly in well-controlled diabetic patients. NT-apoAI could be used as marker to identify diabetic patients at risk of developing early vascular complications.


A.M. Adedayo: None. A. Eluwole: None. F. Tedla: None. A. Kremer: None. N. Mastrogiovanni: None. C. Rosenberg: None. P. Dreizen: None. J. LaRosa: None. L. Salciccioli: None. M. Boutjdir: None. M. Banerji: Speaker's Bureau; Self; Merck & Co., Inc.. C. Brown: None. M. Salifu: None. J. Lazar: None. A. Bakillah: None.

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