Background: LDL plays a key role in development and progression of atherosclerosis. Elevated LDL amplifies the atherosclerotic process but the significance of modified LDL in pathogenesis of vascular complications is unclear. We aimed to assess plasma modified LDL levels and their relationship with vascular function in African American diabetic patients.

Methods: 125 patients with type-2 diabetes were enrolled. Levels of glycated LDL (g-LDL), carbamylated LDL (c-LDL), nitrated LDL (n-LDL) and oxidized LDL (ox-LDL) were quantified by ELISA. Microvascular function was assessed by vascular reactivity index (VRI), which assesses changes in digital temperature before and after release of arterial cuff occlusion. Carotid-femoral pulse wave velocity (PWV) assessed arterial stiffness using applanation tonometry. B-mode ultrasound image analysis assessed Carotid intima-media thickness (CIMT). Patient population was divided into well-controlled: HbA1c ≤7.0%, N=54; poorly-controlled: HbA1c >7.0%, N=71.

Results: Age 60±8 years; 64% Female, 80% Hypertension, 90% Dyslipidemia and 15% CKD. HbA1c level 8.1±2.2%, diabetes duration 10.29±3.79 years. Mean plasma g-LDL, c-LDL, n-LDL and ox-LDL were 1.56±0.64 mg/dL, 0.85±0.11 mg/dL, 2.33±0.39 ng/mL, and 61.93±9.25 ng/mL. Ox-LDL was positively correlated with CIMT in well-controlled patients (r= 0.45, p=0.001), but not in poorly-controlled (r= 0.12, p=0.30). Multi-regression analysis revealed ox-LDL was independently associated with CIMT, but neither with PWV nor VRI after adjustment for variables such as age, gender, weight, smoking, total cholesterol, HDLc, triglycerides, and LDLc (β= 0.003, p= 0.012; r2= 0.38).

Conclusion: Ox-LDL offered better predictive value for CIMT in well-controlled patients than other forms of modified LDL. These data favor ox-LDL as potential marker to identify diabetic patients at risk of developing atherosclerotic 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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