Abstract
AimsCVD is the main cause of morbidity and mortality in individuals with diabetes. It is currently unclear whether daily glucose variability contributes to CVD. Therefore, we investigated whether glucose variability is associated with arterial measures that are considered important in CVD pathogenesis.MethodsWe included participants of The Maastricht Study, an observational population-based cohort, who underwent at least 48 h of continuous glucose monitoring (CGM) (n = 853; age: 59.9 ± 8.6 years; 49% women, 23% type 2 diabetes). We studied the cross-sectional associations of two glucose variability indices (CGM-assessed SD [SDCGM] and CGM-assessed CV [CVCGM]) and time in range (TIRCGM) with carotid–femoral pulse wave velocity (cf-PWV), carotid distensibility coefficient, carotid intima–media thickness, ankle–brachial index and circumferential wall stress via multiple linear regression.ResultsHigher SDCGM was associated with higher cf-PWV after adjusting for demographics, cardiovascular risk factors and lifestyle factors (regression coefficient [B] per 1 mmol/l SDCGM [and corresponding 95% CI]: 0.413 m/s [0.147, 0.679], p = 0.002). In the model additionally adjusted for CGM-assessed mean sensor glucose (MSGCGM), SDCGM and MSGCGM contributed similarly to cf-PWV (respective standardised regression coefficients [st.βs] and 95% CIs of 0.065 [−0.018, 0.167], p = 0.160; and 0.059 [−0.043, 0.164], p = 0.272). In the fully adjusted models, both higher CVCGM (B [95% CI] per 10% CVCGM: 0.303 m/s [0.046, 0.559], p = 0.021) and lower TIRCGM (B [95% CI] per 10% TIRCGM: −0.145 m/s [−0.252, −0.038] p = 0.008) were statistically significantly associated with higher cf-PWV. Such consistent associations were not observed for the other arterial measures.ConclusionsOur findings show that greater daily glucose variability and lower TIRCGM are associated with greater aortic stiffness (cf-PWV) but not with other arterial measures. If corroborated in prospective studies, these results support the development of therapeutic agents that target both daily glucose variability and TIRCGM to prevent CVD.Graphical abstract
Highlights
CVD is the main cause of morbidity and mortality in individuals with type 2 diabetes [1]
Because outcome and covariate data could not be obtained in all individuals (ESM Fig. 1, ESM Table 1), the number of participants who were included in the different regression analyses varied (n = 643–816)
31 (17%) of the 185 individuals with type 2 diabetes were not in the highest tertile of SDCGM, participants with prediabetes were evenly distributed between the tertiles, and 58 (13%) of the 454 individuals with normal glucose metabolism (NGM) were not in the lowest or middle tertiles
Summary
CVD is the main cause of morbidity and mortality in individuals with type 2 diabetes [1]. Individuals with prediabetes are already at an elevated risk of CVD [2] Hyperglycaemia contributes to this CVD risk, in part, by its adverse effects on arterial stiffness [3,4,5], atherosclerosis [1, 6], and large-artery endothelial function [5, 7]. Both achieving and maintaining normoglycaemia are important for reducing CVD risk [1]. A better understanding of the involved pathophysiologic processes could yield new therapeutic targets to further reduce CVD risk
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