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Glycemic control impacts plaque progression in premature coronary artery disease: A longitudinal CCTA analysis.

Created on 22 Sep 2026

Authors

Qiyu Zhang, Jinying Zhou, Jingpu Wang, Fang Zhang, Rende Xu, Wei Gao, Yan Xia, Weifeng Guo, Yuanji Ma, Juying Qian, Chenguang Li, Junbo Ge

Published in

Journal of cardiovascular computed tomography. Sep 07, 2026. Epub Sep 07, 2026.

Abstract

Premature coronary artery disease (PCAD) is an escalating public health issue. While diabetes mellitus (DM) is a known risk factor, the specific impact of glycemic control (GC) on those younger patients remains poorly defined.
To investigate the impact of GC on plaque progression and major adverse cardiovascular events (MACE) in PCAD using serial coronary computed tomography angiography (CCTA).
This cohort study enrolled PCAD patients with serial CCTA between 2019 and 2024. Poor GC was defined as HbA1c ≥ 7%. Plaque progression was defined as annualized change in total percent atheroma volume (ΔPAV) >0%. MACE included cardiac death, myocardial infarction, and unplanned revascularization. Causal mediation analysis was performed.
We retrospectively enrolled 225 PCAD patients (age 40.5 ± 3.6 years) with serial CCTA (mean interval: 2.0 years). After multivariable adjustment, poor GC independently predicted plaque progression (OR 2.81, 95%CI 1.21-6.55, p = 0.017) and 3-year MACE (HR 3.08, 95%CI 1.11-8.50, p = 0.030). Notably, patients with good GC showed comparable annualized ΔPAV to non-DM patients (p = 0.434), while poor GC was associated with global acceleration across all plaque subtypes. Mediation analysis revealed that plaque progression mediated 19.6% of the effect of poor GC on MACE (p = 0.044).
In PCAD patients, poor GC was linked to accelerated plaque progression and a higher 3-year risk of MACE, with 19.6% of this association mediated by plaque progression. These findings underscore the necessity of strict glycemic management and the value of serial CCTA-based monitoring for personalized risk stratification in this population.

PMID:
42767889
Bibliographic data and abstract were imported from PubMed on 22 Sep 2026.

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