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Published on: June 28, 2019
Intracoronary nicorandil improves coronary microcirculatory function after primary PCI in first-episode STEMI: an
Qing Yu1, Jie Lin1, Jiashi Ding2
1Department of Cardiology, Shaowu Municipal Hospital of Fujian Province, Shaowu, Fujian, China.
Insights
Intracoronary nicorandil improved microvascular function after ST-elevation myocardial infarction (STEMI) during primary percutaneous coronary intervention (PCI). This pilot study showed reduced angiographic microcirculatory resistance (AMR) and better flow without increased adverse events.
Area of Science:
- Cardiology
- Interventional Cardiology
- Myocardial Infarction Research
Background:
- Microvascular dysfunction significantly impacts outcomes post-STEMI, even after successful primary PCI.
- Nicorandil possesses vasodilatory and KATP-channel opening properties that may enhance reperfusion.
- Current understanding of nicorandil's effect on angiography-derived microvascular function is limited.
Purpose of the Study:
- To assess the impact of intracoronary nicorandil on microvascular function post-primary PCI.
- To evaluate nicorandil's effect on angiographic microcirculatory resistance (AMR) and quantitative flow ratio (QFR).
Main Methods:
- A prospective, single-center randomized trial involving 63 STEMI patients undergoing primary PCI.
- Patients were randomized to receive either intracoronary nicorandil or standard PCI.
- Primary endpoint was post-PCI AMR; secondary outcomes included QFR, reperfusion markers, hemodynamics, and clinical events.
Main Results:
- Intracoronary nicorandil significantly reduced final AMR compared to control (1.4 vs. 2.7, P < 0.001).
- Nicorandil group showed higher rates of TIMI grade 3 flow and improved vessel QFR (P < 0.001).
- No significant differences in peak cardiac biomarkers, LVEF, or short-term MACE were observed.
Conclusions:
- Intracoronary nicorandil administration during primary PCI improved angiography-derived microvascular function indices.
- The treatment was associated with enhanced epicardial physiology without increased peri-procedural instability or short-term adverse events.
- Findings are exploratory, necessitating larger trials for confirmation and outcome validation.
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.
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