Glycemic control and coronary plaque characteristics in patients with acute myocardial infarction.

Int J Cardiol

Department of Cardiology, The 2nd Affiliated Hospital of Harbin Medical University, Harbin 150086, China; The Key Laboratory of Myocardial Ischemia, Chinese Ministry of Education, Harbin, China, Harbin 150086, China. Electronic address:

Published: January 2025

Background: The impact of glycemic control on the morphological characteristics of non-culprit lesions (NCLs) in patients with acute myocardial infarction (AMI) remains unclear.

Methods And Results: A total of 800 AMI patients who underwent 3-vessel OCT were divided into three groups based on their serum glycated hemoglobin (HbA1c) levels: poorly controlled diabetes mellitus (DM) (HbA1c ≥8.0 %, n = 79), well controlled DM (6.5 % ≤ HbA1c < 8.0 %, n = 105), and non-DM (HbA1c <6.5 %, n = 616). OCT imaging was performed on all NCLs and plaque characteristics were assessed at both the patient and lesion level, including high-risk features. Separate covariate-adjusted multivariate models were performed to determine whether glycemic control was associated with high-risk plaque features in NCLs. Patients with poorly controlled DM had higher NCL vulnerability compared to those with well controlled DM and non-DM, both at the patient level [thin-cap fibroatheroma (TCFA): 63.3 % vs. 32.4 % vs. 27.1 %] and the lesion level [TCFA: 22.1 % vs. 11.6 % vs. 9.5 %; non-culprit plaque rupture (PR): 8.4 % vs. 4.6 % vs. 4.6 %]. Vulnerable plaque features, including TCFA, non-culprit PR, macrophages, microchannels, cholesterol crystals, layered plaque and calcification, were more prevalent with increasing HbA1c levels. Multivariate analysis revealed that at the patient level, poorly controlled DM was an independent predictor of TCFA and microchannels, whereas at the lesion level it independently predicted TCFA and non-culprit PR.

Conclusions: In AMI patients, poor glycemic control is associated with increased vulnerability of NCLs. As HbA1c levels increase, there is a worsening of plaque characteristics, including greater plaque burden and more advanced features of vulnerability.

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http://dx.doi.org/10.1016/j.ijcard.2025.132988DOI Listing

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