Key result
Empagliflozin reduces monocyte CTF-1 expression ~13-fold vs. placebo in post-PCI STEMI with diabetes.
Why the study?
The effect of Empagliflozin on Cardiotrophin-1 and GDF-15 gene expression in type 2 diabetic patients after myocardial infarction undergoing PCI was not previously investigated.
Does empagliflozin 10 mg daily reduce the mRNA expression of atherosclerosis-associated biomarkers CTF-1 and GDF-15 in patients with type 2 diabetes and recent STEMI undergoing primary PCI?
RCT (n=33)
Double-blind
Coded assignment without replacement
No
Does empagliflozin 10 mg daily reduce the mRNA expression of atherosclerosis-associated biomarkers CTF-1 and GDF-15 in patients with type 2 diabetes and recent STEMI undergoing primary PCI?
Effect estimate: 13-fold reduction
Absolute Event Rate: 0.3% vs 5.66%
p-value: p=0.003
Empagliflozin significantly reduces the expression of inflammatory and atherosclerosis-related biomarkers CTF-1 and GDF-15 in post-STEMI patients with type 2 diabetes, suggesting a potential pleiotropic cardioprotective mechanism.
May support empagliflozin post-STEMI in T2D; extends RCT evidence for SGLT2i effects on CTF-1 and GDF-15.
Introduction: Given the proven cardiovascular benefits of Empagliflozin (EM), we aimed to investigate the effect of Empagliflozin on Cardiotrophin-1 (CTF-1) and growth differentiation factor-15 (GDF-15) expressions in circulating monocytes in type 2 diabetic patients after MI. Methods: This randomized, double-blind, placebo-controlled study included 33 patients referred to Ayatollah Mousavi Hospital in Zanjan between 5 of September to 25 of December, 2024. Eligible patients with type 2 diabetes and MI who underwent primary percutaneous coronary intervention (PCI) were randomly assigned (17:16) to receive either 10 mg of EMPA daily or placebo for 12 weeks. Target genes expression levels were quantified by real time PCR, and data were analyzed by SPSS version 26. Results: Thirty-three patients were included in this study (mean age: 61.27±9.07, 66% male), mean diabetes duration was longer in intervention group (7.82±5.13) compared to placebo group (3.75±2.74), hypertension was the most common comorbidity (57%). CTF-1 expression in the intervention group was 0.3±0.28 and in placebo group was 5.66±6.52. GDF-15 expression in the intervention group was 0.198±0.22 and in placebo group was 1.66±1.04. EMPA significantly reduced expression of CTF-1 (13-fold) (P=0.003) and GDF-15 (7-fold) (P ˂ 0.0001). The CTF-1 and GDF-15 expression reduction were not associated with any other clinical variables. Significant reduction observed in LDL (P=0.045) and triglycerides (P=0.013) after intervention. Conclusion: EMPA significantly reduced the expression of CTF-1 and GDF-15 in type 2 diabetic, post MI patients, which are associated with atherosclerosis, and suggest that potential anti-atherosclerotic effect of EMPA mediated through modulation of GDF-15 and CTF-1 gene expression.
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Rastgoo et al. (2026) conducted an RCT in Type 2 diabetes and ST-Segment Elevation Myocardial Infarction (n=33). Empagliflozin vs. Placebo was evaluated on Cardiotrophin-1 (CTF-1) mRNA expression in circulating monocytes (13-fold reduction, p=0.003). Empagliflozin reduced the mRNA expression of CTF-1 by 13-fold (p=0.003) and GDF-15 by 7-fold (p<0.0001) compared to placebo in patients with type 2 diabetes and STEMI undergoing primary PCI.
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