{"title":"Glycemic control impacts plaque progression in premature coronary artery disease: A longitudinal CCTA analysis.","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","doi":"10.1016/j.jcct.2026.08.013","DOIUrl":null,"url":null,"abstract":"<p><strong>Background: </strong>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.</p><p><strong>Aims: </strong>To investigate the impact of GC on plaque progression and major adverse cardiovascular events (MACE) in PCAD using serial coronary computed tomography angiography (CCTA).</p><p><strong>Methods: </strong>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.</p><p><strong>Results: </strong>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).</p><p><strong>Conclusions: </strong>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.</p>","PeriodicalId":94071,"journal":{"name":"Journal of cardiovascular computed tomography","volume":" ","pages":""},"PeriodicalIF":0.0000,"publicationDate":"2026-09-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of cardiovascular computed tomography","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1016/j.jcct.2026.08.013","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0
Abstract
Background: 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.
Aims: To investigate the impact of GC on plaque progression and major adverse cardiovascular events (MACE) in PCAD using serial coronary computed tomography angiography (CCTA).
Methods: 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.
Results: 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).
Conclusions: 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.