Frontiers in cardiovascular medicine · 2026
Intracoronary nicorandil improves coronary microcirculatory function after primary PCI in first-episode STEMI: an angiography-derived evaluation using AMR and QFR.
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Yu Qing, Lin Jie, Ding Jiashi, Ye Feifei, Li Peng, Chen Shikun, Zhan Yiling, Cai Wenqin, Ou Jiaqi
Аннотация
BACKGROUND: Microvascular dysfunction remains a major driver of adverse outcomes after ST-segment elevation myocardial infarction (STEMI) despite successful restoration of epicardial patency by primary percutaneous coronary intervention (PCI). Nicorandil has nitrate-like vasodilatory properties and ATP-dependent potassium channel (KATP)-opening properties, effects that may improve reperfusion physiology. However, its effects on wire-free, angiography-derived measures of microvascular function are not well defined. We evaluated whether intracoronary nicorandil administered during primary PCI improves angiography-derived microvascular function assessed by angiographic microcirculatory resistance (AMR) and quantitative flow ratio (QFR).
METHODS: In this prospective, single-center randomized trial, 63 patients with first-episode STEMI undergoing primary PCI were allocated 1:1 to intracoronary nicorandil (2 mg after guidewire crossing; n = 32) or control (standard PCI; n = 31). The prespecified primary endpoint was final post-PCI AMR. QFR-derived indices, reperfusion measures [Thrombolysis in Myocardial Infarction (TIMI) flow grade, no-reflow, ST-segment resolution], hemodynamics, biomarkers, and clinical events were analyzed as secondary/exploratory outcomes, with multiplicity controlled using the Benjamini-Hochberg false discovery rate (FDR) where applicable.
RESULTS: Baseline characteristics were balanced between groups. Compared with control, intracoronary nicorandil was associated with a higher rate of post-PCI TIMI grade 3 flow (96.9% vs. 74.2%; overall P = 0.013). Final AMR was significantly lower in the nicorandil group (1.4 ± 0.5 vs. 2.7 ± 0.5; P < 0.001). Vessel QFR and change in QFR (ΔQFR) also favored nicorandil (both P < 0.001), whereas residual QFR showed only a borderline/non-significant difference after FDR correction (raw P = 0.027; q = 0.051). Peak creatine kinase-MB (CK-MB) and cardiac troponin I (cTnI) were numerically lower with nicorandil but not statistically different; left ventricular ejection fraction (LVEF) at 1 week was similar between groups. Rates of intra-procedural hypotension, in-hospital major adverse cardiovascular events (MACE), and MACE at 3-month follow-up did not differ.
CONCLUSIONS: In this pilot randomized study, intracoronary nicorandil administered during primary PCI was associated with improved angiography-derived surrogate indices of microvascular resistance and epicardial physiology without an observed increase in peri-procedural hemodynamic instability or short-term adverse events. These findings should be interpreted as exploratory and warrant confirmation in larger multicenter studies with longer follow-up and outcome-linked validation.
METHODS: In this prospective, single-center randomized trial, 63 patients with first-episode STEMI undergoing primary PCI were allocated 1:1 to intracoronary nicorandil (2 mg after guidewire crossing; n = 32) or control (standard PCI; n = 31). The prespecified primary endpoint was final post-PCI AMR. QFR-derived indices, reperfusion measures [Thrombolysis in Myocardial Infarction (TIMI) flow grade, no-reflow, ST-segment resolution], hemodynamics, biomarkers, and clinical events were analyzed as secondary/exploratory outcomes, with multiplicity controlled using the Benjamini-Hochberg false discovery rate (FDR) where applicable.
RESULTS: Baseline characteristics were balanced between groups. Compared with control, intracoronary nicorandil was associated with a higher rate of post-PCI TIMI grade 3 flow (96.9% vs. 74.2%; overall P = 0.013). Final AMR was significantly lower in the nicorandil group (1.4 ± 0.5 vs. 2.7 ± 0.5; P < 0.001). Vessel QFR and change in QFR (ΔQFR) also favored nicorandil (both P < 0.001), whereas residual QFR showed only a borderline/non-significant difference after FDR correction (raw P = 0.027; q = 0.051). Peak creatine kinase-MB (CK-MB) and cardiac troponin I (cTnI) were numerically lower with nicorandil but not statistically different; left ventricular ejection fraction (LVEF) at 1 week was similar between groups. Rates of intra-procedural hypotension, in-hospital major adverse cardiovascular events (MACE), and MACE at 3-month follow-up did not differ.
CONCLUSIONS: In this pilot randomized study, intracoronary nicorandil administered during primary PCI was associated with improved angiography-derived surrogate indices of microvascular resistance and epicardial physiology without an observed increase in peri-procedural hemodynamic instability or short-term adverse events. These findings should be interpreted as exploratory and warrant confirmation in larger multicenter studies with longer follow-up and outcome-linked validation.