[OP.1D.05] TYPE 2 DIABETES IS ASSOCIATED WITH GREATER CAROTID STIFFNESS AND GREATER PRESSURE-DEPENDENCY OF CAROTID STIFFNESS -THE MAASTRICHT STUDY

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Abstract

Objective:

Type 2 diabetes (T2D) is associated with increased arterial stiffness. Underlying mechanisms are thought to involve disruption of both the elastin and collagen network within the arterial wall. The pressure-dependency of stiffness is linked to structural alterations of the arterial wall and can be quantified as the systolic-diastolic difference in pulse wave velocity (δPWV). The relationship between δPWV with deteriorating glucose metabolism status (GMS) has not been investigated. In The Maastricht Study, we investigated the association between deteriorating GMS and carotid arterial stiffness (cPWV) and δPWV. Additionally, we investigated the mutual dependency of cPWV and δPWV.

Design and method:

The study population consisted of 746 individuals (415 normal glucose metabolism [NGM], 126 impaired glucose metabolism [IGM] and 205 T2D). cPWV and δPWV were determined by ultrasonography and tonometry. Linear regression analyses were used to investigate the associations of GMS (NGM as reference) with cPWV and δPWV. Models were adjusted for age, sex, mean arterial pressure (MAP), prior cardiovascular disease (CVD), eGFR and smoking, and δPWV or cPWV and anti-hypertensive medication (renin-angiotensin-system(RAS)-inhibitor) as appropriate.

Results:

After adjustment for age, sex, MAP, prior CVD, eGFR and smoking, T2D was associated with greater cPWV (β (95% CI; 0.376 (0.119; 0.632) and δPWV (0.301 (0.013; 0.589)). Additional adjustment for use of RAS-inhibitor did not change these associations. After additional adjustment for δPWV or cPWV the associations of T2D with cPWV and δPWV were attenuated (0.294 (0.048; 0.539) and 0.173 (−0.103; 0.449), respectively). IGM was not associated with either cPWV or δPWV.

Conclusions:

In T2D, but not in IGM, both cPWV and δPWV are increased and only partly dependent on each other. Thereby, δPWV provides additional insight into arterial wall structure behavior with deteriorating GMS. Our future research goal is to further explore the roles of elastin degradation and collagen-crosslinking herein.

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