Accelerated coronary atherosclerosis in type 2 diabetes: findings from a large coronary CT angiography cohort

Background

Type 2 diabetes (T2D) is associated with premature cardiovascular disease, yet the extent to which it influences coronary plaque burden and phenotype on computed tomography angiography (CCTA) remains incompletely characterized. We hypothesized that T2D is associated with an accelerated vascular aging phenotype on CCTA and that cumulative and glycemic exposure further influence plaque characteristics.

Methods

In this retrospective single center study patients who were referred for CCTA because of suspected CAD in 2022 and 2023 were included. multivariable regression models were constructed adjusting for age, sex, body mass index, smoking history, family history of coronary artery disease (CAD), hypertension, low-density lipoprotein cholesterol, and lipid-lowering therapy. Analyses were stratified at 65 years, with additional adjustment for continuous age within strata. Outcomes included any CAD (any coronary plaque), obstructive CAD (stenosis degree > 50%) , segment involvement score (SIS), and plaque composition. Vascular age was derived by translating the excess T2D-associated risk into age equivalents. Within the T2D group, associations of diabetes duration (per 5 years) and glycated hemoglobin (HbA1c; per 10 mmol/mol) with plaque phenotypes were assessed.

Results

4,211 patients were included, of which 341 patients with T2D (8.1%). T2D was independently associated with higher odds of any CAD (odds ratio [OR] 1.97 [1.37–2.81], p<0.001) and obstructive CAD (OR 1.68 [1.28–2.21], p<0.001), and with greater plaque burden reflected by higher SIS (β 0.56 [0.29–0.83], p<0.001). These associations corresponded to approximately +7.3 years of vascular aging for any CAD and +6.5 years for obstructive CAD. Predicted probability curves demonstrated a leftward shift in patients with T2D, particularly in those <65 years.

Within patients with T2D, longer diabetes duration was associated with obstructive CAD (OR 1.22 per 5 years [1.00–1.47], p=0.047) and a higher SIS in patients < 65 years (β 0.70 per 5 years [0.10–1.30], p=0.03). Higher HbA1c was associated with increased non-calcified plaque segments (β 0.20 per 10 mmol/mol [0.00–0.30], p=0.047) and, in individuals <65 years, with higher SIS (β 0.20 per 10 mmol/mol [0.00–0.50], p=0.032).

Conclusion

In a large CCTA cohort, T2D was associated with a clinically meaningful acceleration of coronary atherosclerosis equivalent to approximately 7 years of vascular aging, particularly in younger patients. Cumulative and glycemic exposure further influence plaque burden and phenotype. These findings provide imaging-based evidence of accelerated vascular aging in type 2 diabetes and support earlier and more intensive cardiovascular risk management, particularly in younger individuals.Forest plots multivariate regressionsAdjusted predicted probability