P1.02 INCREASED CAROTID IMT IN PATIENTS WITH TYPE 2 DIABETES FREE OF CARDIOVASCULAR COMPLICATIONS APPEARS TO BE AN ADAPTIVE MECHANISM TO AN INCREASED WALL STRESS MORE THAN ATHEROMASIC DEGENERATION

• Main Authors: M. Kozakova, C. Morizzo, C. Palombo
• Format: Article
• Language: English
• Published: Atlantis Press 2013-11-01
• Series: Artery Research
• Online Access: https://www.atlantis-press.com/article/125938939/view

Type 2 diabetes (DM2) and poor glycemic control adversely affect common carotid intima media thickness (IMT), considered marker of preclinical atherosclerosis. However, studies evaluating the effect of DM2 and glucose levels on IMT did not consider carotid diameter, known to affect IMT. A certain IMT increase could reflect a mutual adjustment between diameter and wall thickness aimed to maintain constant wall tensile stress (WTS). Aim: To compare carotid IMT, luminal diameter, WTS and local wave speed (WS) between patients with uncomplicated DM2 and healthy controls. Methods: Eighty-four patients with well controlled DM2 (HbA1c <7.8%) and 84 controls matched for sex, age and BMI. were studied by radiofrequency-based carotid ultrasound (QIMT® and QAS®, Esaote). Results: DM2 against controls had higher (p<0.0001) IMT (720±131 vs. 620±76 μm), luminal diameter (6.6±0.6 vs. 6.0±0.7 mm), WS (8.3.6±1.7 vs. 6.5±1.2 m/s) and pulse pressure (58±13 vs. 47±8 mmHg), but comparable WTS (49±8 vs. 50±14 kPa; p=0.82). In the entire population, fasting glucose was not independently related to IMT, but was related to carotid diameter (together with male sex and waist), pulse pressure and local WS (together with age and antihypertensive treatment). In DM2, HbA1c was independently related to carotid diameter, pulse pressure and WS. Conclusions: Chronically increased plasma glucose levels may induce intrinsic stiffening of large artery and widening of pulse pressure. Increased pulsatile load in stiff arteries causes luminal dilatation and increases WTS, triggering an increase in arterial wall thickness. Hyperglycaemia affects arterial wall, but through a “sclerotic” more than “atherogenic” mechanism.