Preclinical Structural and Functional Vascular Involvement in Young Subjects With Type 1 Diabetes Without Overt Complications.

Background: Increased carotid intima-media thickness (IMT), endothelial dysfunction and arterial stiffness (AS) have been reported in young subjects with type 1 diabetes (DM1). However, the relations between these vascular abnormalities remain unknown. Aim of the Study: To assess by a multiparametric approach the preclinical vascular involvement in young patients with early onset DM1 and adequate glycaemic control. Methods: 31 DM1 patients, free of macro- and microvascular complications (20 males, age 19.3 +/- 3.1, BMI 22.1 +/- 2.7 kg/m2, disease duration: 11 +/- 5 years, average HbA1c: 7.7 +/- 1.0%), and 31 controls (NL: 16 males, age 20.1 +/- 1.6; BMI 21.6 +/- 2.1 kg/m2) were studied. IMT was measured by radiofrequency-based ultrasound (Q-IMT, Esaote MyLab70). AS was estimated by carotid-femoral pulse wave velocity (PWV, Complior), and endothelial function by forearm reactive hyperemia index (RHI, EndoPAT). Carotid augmentation index (AIx) was measured by applanation tonometry (Pulsepen, Diatecne). Results: Compared to controls, DM1 patients, although normotensive, had significantly higher (p 7.5 % than in those with HbA1c < 7,5 % and NL (1.5 +/- 0.35; 2.1 +/- 0.69 and 2.1 +/- 0.53). Lipid profile was comparable in DM1 vs NL. Within vascular parameters, in the entire population, Q-IMT was directly related with AIx (r = 0.53, p < 0.005) and inversely with RHI (r = -0.33, p < 0.05). In multivariate models, DM1 was independent predictor (p < 0.001) of SBP (together with sex and BMI, R2 = 0.62), Q-IMT (together with sex and RHI, R2 = 0.39), PWV (together with age and SBP, R2 = 0.28) and AIx (together with Q-IMT, R2 = 0.45). Conclusions: In young subjects with adequately controlled DM1 free of overt complications, a mildly increased IMT is associated with augmented wave reflection and reduced RHI. Higher HbA1c levels are associated with endothelial dysfunction, suggesting that an aggressive glycaemic control may be a critical factor for preventing preclinical vascular involvement