Objectives: Hyperglycemia has been associated with an increased risk of cardiovascular morbidity and mortality. Although numerous studies have demonstrated that hyperglycemia is associated with the atherosis component of atherosclerosis, limited studies have addressed the independent role of hyperglycemia in the pathophysiology of sclerotic vascular disease. We hypothesized that hyperglycemia, as assessed by hemoglobin A1c (HbA1c), would be independently associated two common indices of arterial stiffness (pressure-strain elastic modulus (Ep) and Young's elastic modulus (YEM)). Methods: We examined the cross-sectional association between HbA1c and arterial stiffness using B-mode ultrasound examination of the carotid artery in 9050 participants from the community-based Atherosclerosis Risk in Communities (ARIC) study. We used multivariable linear and logistic regression models to characterize the association between HbA1c and increased Ep and YEM. Results: Higher values of HbA1c were associated in a graded fashion with increased arterial stiffness (. P-trend < 0.001 for both EP and YEM). After adjusting for traditional risk factors, increasing HbA1c deciles were significantly associated with elevated EP (OR for the highest decile of HbA1c compared to the lowest, 2.01, 95% CI: 1.30, 3.11) and YEM (OR = 1.71, 95% CI: 1.15, 2.55). Conclusion: Elevated HbA1c is associated with measures of increased arterial stiffness, even after accounting for arterial wall thickness. This is consistent with the hypothesis that hyperglycemia contributes to arterial stiffness beyond its effects on atherosis and suggests that hyperglycemia is associated with altered material within the arterial wall.
|Original language||English (US)|
|Number of pages||6|
|State||Published - Nov 2012|
Bibliographical noteFunding Information:
The Atherosclerosis Risk in Communities study is carried out as a collaborative study supported by National Heart, Lung, and Blood Institute contracts ( HHSN268201100005C , HHSN268201100006C , HHSN268201100007C , HHSN268201100008C , HHSN2682011000-09C , HHSN268201100010C , HHSN268201100011C , and HHSN2682-01100012C ). J.R. was supported by National Heart, Lung, and Blood Institute grant 5T32HL007024 . E.S. was supported by National Institutes of Health/National Institute of Diabetes and Digestive and Kidney Diseases grant R21 DK080294 and K01 DK076595 . J.C. were supported by National Institutes of Health/National Institute of Diabetes and Digestive and Kidney Diseases grant R01-DK-076770 .