What question did this study set out to answer?

The study aims to evaluate the impact of GLP1 receptor agonists on coronary artery disease regression in diabetic patients after acute coronary syndrome.

February 6, 2026

GLP1 receptor agonists and CAD regression in diabetic patients after ACS

Key Points

The study aims to evaluate the impact of GLP1 receptor agonists on coronary artery disease regression in diabetic patients after acute coronary syndrome.
Conducted a single-center, prospective design with diabetic patients post-acute coronary syndrome undergoing PCI.
Enrolled patients had atherosclerotic plaques in non-culprit lesions with diameter stenosis >20%.
Assessed CAD progression through coronary computed tomography angiography and blood tests at baseline and one year follow-up.
Stratified diabetic patients based on GLP1 receptor agonist use and performed comprehensive lipidomic, metabolomic, and proteomic analyses.
In GLP1 receptor agonist-treated patients, absolute change in plaque burden was significantly greater than in non-GLP1-ra patients (-5.8% vs. -1.1%, p=0.041).
Percent atheroma volume change was also more favorable in the GLP1-ra group (-6.1% vs. -0.7%, p=0.039).
Lipidomic analysis showed decreased monoacylglycerol and triacylglycerol, while metabolomic analysis indicated a shift toward lipid metabolism.
Proteomic changes pointed toward improved immune regulation and endothelial function in the GLP1-ra cohort.

Abstract

Abstract Background Despite advances in PCI, a significant proportion of ACS patients experience early CAD progression, with an increased risk in diabetics. GLP1 receptor agonists (GLP1-ra), among newer antidiabetic agents, have shown cardiovascular benefits in patients with atherosclerotic disease, but the underlying pathophysiologic mechanism remains unclear. Methods The PROGRESSION study was a single-center, prospective study enrolling patients with non-ST elevation ACS undergoing PCI between 2019 and 2022. To be eligible for inclusion, patients were required to have atherosclerotic plaques in non-culprit lesions (NCL) with diameter stenosis 20%. Coronary computed tomography angiography (CCTA) and blood tests were performed at baseline (during the index hospitalization) and at 1 year follow-up to assess and characterize CAD progression. The present analysis included diabetic patients, stratified by GLP1-ra use at discharge. GLP1-ra–treated patients and randomly-selected controls underwent comprehensive plasma metabolomic, lipidomic, and proteomic analysis at baseline and 1 year. The primary endpoint was the absolute change in NCL plaque burden (ΔPB), with the absolute change in patient percent atheroma volume (ΔPAV) as a key secondary endpoint. PB was calculated for each non-stented, non-hypoplastic (2 mm diameter) NCL without total occlusion or imaging artifacts. Patient PAV was the mean PB across lesions per patient. Results Of 28 diabetic patients, 7 (25%) with 22 NCL were treated with GLP1-ra, and 21 (75%) with 65 NCL received other antidiabetics. At baseline, mean NCL PB was 49.0±16.3%, and median patient PAV was 47.7% (IQR: 42.0, 55.4), with no differences between groups. At 1 year, both ΔPB (-5.8±12.8% vs. -1.1±13.6%, p=0.041) and ΔPAV (-6.1% -7.3, -1.8 vs. -0.7% -2.4, 9.8, p=0.039) were significantly lower in GLP1-ra-treated patients (Fig 1). Change in total atheroma volume was also numerically lower (0.7 mm³ -2.5, 8.7 vs. 25.0 mm³ 4.8, 39.7) in the GLP1-ra cohort, driven by a greater reduction in NCL fibrofatty volume percentage (-2.9±10.1% vs. 1.0±6.8%, p=0.042). Lipidomics analysis revealed a decrease in monoacylglycerol and triacylglycerol and an increase in phosphatidylethanolamine and diacylglycerols in GLP1-ra-treated patients (Fig 2A). Consistently, metabolomics showed a shift from carbohydrate metabolism toward lipid metabolism and hormone regulation, including retinol and steroid biosynthesis. Proteomic analysis demonstrated changes in immune regulation, endothelial function, and structural integrity with GLP1-ra treatment. Conclusion GLP1-ra therapy is associated with a significant CAD regression in diabetic patients at 1 year after an ACS. The effect is supported by consistent lipidomic, metabolomic, and proteomic changes, and suggests a potential role for GLP1-ra in modifying atherosclerosis progression beyond glycemic control.Figure 1

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