Vascular Damage and Glycometabolic Control in Older Patients with Type 2 Diabetes

Diabetes is one of the main risk factors for vascular damage, including endothelial dysfunction and arterial stiffness. The aim of this study was to compare selected parameters of vascular damage in patients with type 2 diabetes (T2D) in different age categories and to determine their relationship to indicators of glycometabolic control. A total of 160 patients with T2D were included in this cross-sectional study. They were divided into four age quartiles (with mean ages of 42.1 +/- 4.5, 51.6 +/- 1.4, 59.2 +/- 3.0, and 69.8 +/- 3.8, respectively). All subjects were evaluated for indicators of glycometabolic control and for arterial stiffness parameters along with markers of endothelial damage-tissue plasminogen activator (tPA), plasminogen activator inhibitor-1 (PAI-1) and von Willebrand factor (vWF). The oldest compared to the youngest participants showed significantly increased parameters of arterial stiffness (augmentation pressure 13.4 +/- 8.6 vs. 6.7 +/- 4.4 mm Hg, augmentation index 26.2 +/- 11.3 vs. 19.6 +/- 9.2 mm Hg, aortic pulse pressure 47.7 +/- 17.1 vs. 33.7 +/- 10.4 mm Hg, and pulse wave velocity 11.9 (10.1-14.3) vs. 8.2 (7.7-9.8) m/s) despite having similar glycometabolic control. Arterial stiffness parameters were mainly associated with age and blood pressure. Age and systolic blood pressure were major determinants of arterial stiffness regardless of glycometabolic control. The oldest patients also had the highest levels of vWF (153.7 +/- 51.9 vs. 121.7 +/- 42.5 %) but the lowest levels of PAI-1 (81.8 +/- 47.5 vs. 90.0 +/- 44.9 ng/mL). Markers of endothelial dysfunction correlated with metabolic parameters, but did not correlate with arterial stiffness. Age and systolic blood pressure are major determinants of arterial stiffness in patients with T2D regardless of glycometabolic control, whereas an unfavorable metabolic profile is mainly related to endothelial dysfunction. These results suggest a differential contribution of cardiometabolic risk factors to vascular damage in T2D patients over their lifetime.