Pulse wave arterial stiffness index (ASI) and pulse pressure (PP) were found to be related to type 2 diabetes (T2D) but had differing patterns in their relationship. These findings were published in Diabetes Care.
Data were sourced from the United Kingdom (UK) Biobank study, which was a national population-based prospective cohort study. Individuals with no history of diabetes or cardiovascular disease (n =152,611) were included in the study. Researchers assessed the relationship between genetic risk for and development of T2D with ASI and PP.
The participants did (n=3000) and did not (n=149,611) develop incident T2D over a median follow-up of 9.5 years. These cohorts were aged mean 58.9 (SD, 7.4) and 56.3 (SD, 8.2) years; 53.9% and 43.5% were men; 83.0% and 91.6% were White; and BMI was 31.5 (SD, 5.6) and 27.1 (SD, 4.6), respectively.
ASI was associated with incident T2D in a dose-response relationship. Compared with quintile 1, individuals in quintile 2 had an adjusted hazard ratio (aHR) of 1.23 (95% CI, 1.07-1.41) increasing to 1.58 (95% CI, 1.39-1.80) among those in the highest ASI quintile. This trend indicated that for every 1-SD increase in ASI, the aHD for incident T2D was 1.03 (95% CI, 1.02-1.04; P <.001).
Genetic risk scores (GRS) for T2D had a significant interaction with ASI (P =.008). Stratified by low, intermediate, and high GRS for T2D, all individuals with low risk and those with intermediate risk in the second and third quintiles of ASI were not associated with elevated T2D risk on the basis of ASI. Individuals with intermediate risk in the fourth and fifth quintiles for ASI and all individuals with high GRS risk had a dose-response relationship between ASI and incident T2D. The highest risk for incident T2D was observed among the high GRS, ASI quintile 5 cohort (aHR, 1.66; 95% CI, 1.29-2.15).
PP was also associated with incident T2D but with a J-shaped curve relationship. Compared with quintile 1, there was no increased risk for T2D among individuals in quintiles 2 or 3. There was increased risk observed for quintiles 4 (aHR, 1.15; 95% CI, 1.01-1.30) and 5 (aHR, 1.24; 95% CI, 1.10-1.41). For every 1-SD increase in PP, the aHR for incident T2D was 1.11 (95% CI, 1.07-1.15; P <.001).
This study may have been biased as the participants were only assessed for ASI and PP on 1 occasion.
The study authors concluded that T2D was associated with ASI in a dose-response relationship and was modified by genetic risk. PP was related to T2D in a J-shaped manner, with little evidence for a genetic risk-modifying effect. “Our findings suggest that arterial stiffness might be an important risk factor for T2D, especially among those with high genetic risk of the disease,” the authors wrote. “Additional studies are warranted to confirm our findings for the better prevention of T2D.”
Wang M, Huang J, Wu T, Qi L. Arterial stiffness, genetic risk, and type 2 diabetes: A prospective cohort study Diabetes Care. Published online January 25, 2022;dc211921. doi:10.2337/dc21-1921
This article originally appeared on The Cardiology Advisor