Key result
Pre-reperfusion dapagliflozin fails to reduce infarct size compared with placebo in STEMI patients.
Why the study?
SGLT2i have shown cardioprotective effects in experimental ischemia-reperfusion models, but whether early administration of dapagliflozin before reperfusion limits infarct size in STEMI patients undergoing primary PCI remained uncertain.
Does pre-reperfusion dapagliflozin loading reduce myocardial infarct size in STEMI patients undergoing primary PCI?
RCT (n=60)
Double-blind
1:1
Does pre-reperfusion dapagliflozin loading reduce myocardial infarct size in STEMI patients undergoing primary PCI?
Pre-reperfusion loading with dapagliflozin in STEMI patients undergoing primary PCI failed to significantly reduce enzymatic or CMR-measured infarct size compared to placebo.
Pre-reperfusion dapagliflozin does not reduce infarct size in STEMI; challenges experimental cardioprotection and does not support pre-PCI loading.
Background Sodium-glucose cotransporter-2 inhibitors (SGLT2i) have demonstrated cardioprotective effects in experimental ischemia–reperfusion models, including reduction of myocardial injury. Whether early administration before reperfusion can limit infarct size in ST-elevation myocardial infarction (STEMI) remains uncertain. Purpose We aimed to investigate the effect of pre-reperfusion dapagliflozin loading on myocardial infarct size measured by cardiac biomarkers and cardiac magnetic resonance (CMR) in STEMI patients undergoing primary percutaneous coronary intervention (PCI). Methods In this prospective, double-blind, randomized trial, 60 STEMI patients presenting within 12 hours of symptoms onset and eligible for primary PCI were randomized 1:1 to dapagliflozin (20 mg loading dose before wire crossing followed by 10 mg daily for 3 months) or placebo. The primary endpoint was infarct size quantified as the area under the curve (AUC) of cardiac troponin I (TnI) over 72 hours. The secondary endpoint was the infarct size change assessed by CMR at baseline and 3 months. Results Baseline clinical, angiographic, and procedural characteristics were comparable between groups (mean age 63.9±8.7 years; 66.7% male; baseline left ventricular ejection fraction [LVEF] from echocardiography 50.8±11.2%). Pre-reperfusion dapagliflozin did not significantly reduce enzymatic infarct size. Median AUC TnI (0–72 h) was 2,812,946 in the dapagliflozin group vs 3,046,243 in placebo (p=0.57), with consistent findings in anterior and non-anterior infarctions. At 3 months, LVEF improved significantly in both groups without a between-group difference (dapagliflozin +5.4±10.1%, p<0.001; placebo +3.6±14.2%, p=0.03). Among patients with serial CMR, infarct size reduction at 12 weeks was numerically greater with dapagliflozin, both in absolute infarct area (7.4±15.3 vs 0.7±8.7) and percentage change (24.6±50.3 vs 8.8±35.3), but differences did not reach statistical significance. Left ventricular volumes, mass, and microvascular obstruction were similar between groups. Conclusions Pre-reperfusion dapagliflozin loading in STEMI patients undergoing primary PCI did not significantly reduce infarct size assessed by cardiac biomarkers or CMR, although a consistent numerical trend toward infarct reduction was observed on follow-up imaging.Figure 1.Median AUC TnI (0-72 hrs)
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Suwannasom et al. (2026) conducted an RCT in ST-elevation myocardial infarction (STEMI) (n=60). Dapagliflozin vs. Placebo was evaluated on Infarct size quantified as the area under the curve (AUC) of cardiac troponin I (TnI) over 72 hours (p=0.57). Pre-reperfusion dapagliflozin did not significantly reduce 72-hour troponin I AUC infarct size compared with placebo in STEMI patients (2,812,946 vs 3,046,243; p=0.57).
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