Veugen Marja G J, Henry Ronald M A, van Sloten Thomas T, Hermeling Evelien, Brunner-La Rocca Hans-Peter, Schram Miranda T, Dagnelie Pieter C, Schalkwijk Casper G, Kroon Abraham A, Stehouwer Coen D A, Reesink Koen D
aDepartment of Internal Medicine, Maastricht University Medical Centre +bCARIM School for Cardiovascular Diseases, Maastricht UniversitycHeart and Vascular CentredDepartment of RadiologyeDepartment of Cardiology, Maastricht University Medical Centre +fCAPHRI School for Public Health and Primary CaregDepartment of Epidemiology, Maastricht UniversityhDepartment of Biomedical Engineering, Maastricht University Medical Centre +, Maastricht, The Netherlands.
J Hypertens. 2017 May;35(5):1052-1060. doi: 10.1097/HJH.0000000000001298.
In type 2 diabetes (T2D), increased arterial stiffening results from accelerated arterial wall matrix remodeling. The associated structural alterations modify the pressure dependency of arterial stiffness, which can be quantified by the systolic-diastolic difference in carotid pulse wave velocity (δPWV). We evaluated the association between T2D and δPWV as marker for matrix remodeling and whether δPWV may contain additional information beyond carotid stiffness (cPWV).
In 746 individuals from The Maastricht Study, 415 with normal glucose metabolism; 126 with prediabetes; and 205 with T2D, carotid pulse wave velocity (cPWV) and δPWV were determined by ultrasonography and tonometry. Multiple linear regression analyses were used to investigate associations of glucose metabolism status (with normal glucose metabolism as reference) with cPWV and δPWV, adjusting for age, sex, mean arterial pressure, prior cardiovascular disease, estimated glomerular filtration rate and smoking, and δPWV or cPWV as appropriate.
After adjustment for age, sex, mean arterial pressure, prior cardiovascular disease, estimated glomerular filtration rate and smoking, T2D was associated with greater cPWV [β (95% confidence interval) 0.376 (0.119; 0.632)] and δPWV [0.301 (0.013; 0.589)]. After additional adjustment for δPWV or cPWV, associations of T2D with cPWV and δPWV were attenuated [0.294 (0.048; 0.539) and 0.173 (-0.103; 0.449), respectively]. Prediabetes was not associated with either cPWV or δPWV.
The systolic-diastolic difference in carotid stiffness is increased in T2D, but not prediabetes. Importantly, the association was not abolished by carotid stiffness, which suggests that systolic-diastolic difference in carotid stiffness carries additional information regarding arterial matrix remodeling.
在2型糖尿病(T2D)中,动脉僵硬度增加是由动脉壁基质重塑加速所致。相关的结构改变会改变动脉僵硬度的压力依赖性,这可以通过颈动脉脉搏波速度的收缩压与舒张压差值(δPWV)来量化。我们评估了T2D与作为基质重塑标志物的δPWV之间的关联,以及δPWV是否可能包含超出颈动脉僵硬度(cPWV)的额外信息。
在马斯特里赫特研究的746名个体中,415人葡萄糖代谢正常;126人患有糖尿病前期;205人患有T2D,通过超声检查和眼压测量法测定颈动脉脉搏波速度(cPWV)和δPWV。采用多元线性回归分析来研究葡萄糖代谢状态(以葡萄糖代谢正常为参照)与cPWV和δPWV之间的关联,并对年龄、性别、平均动脉压、既往心血管疾病、估计肾小球滤过率和吸烟情况进行校正,以及在适当情况下对δPWV或cPWV进行校正。
在对年龄、性别、平均动脉压、既往心血管疾病、估计肾小球滤过率和吸烟情况进行校正后,T2D与更高的cPWV [β(95%置信区间)0.376(0.119;0.632)]和δPWV [0.301(0.013;0.589)]相关。在对δPWV或cPWV进行额外校正后,T2D与cPWV和δPWV的关联减弱[分别为0.294(0.048;0.539)和0.173(-0.103;0.449)]。糖尿病前期与cPWV或δPWV均无关联。
T2D患者颈动脉僵硬度的收缩压与舒张压差值增加,而糖尿病前期患者则不然。重要的是,这种关联并未因颈动脉僵硬度而消除,这表明颈动脉僵硬度的收缩压与舒张压差值携带了有关动脉基质重塑的额外信息。