Key result
Lipid-rich plaques linked to ~3.1-fold higher odds of post-PCI coronary microvascular dysfunction.
Why the study?
Coronary lipid-rich plaque (LRP) is likely to cause distal embolization and microvascular injury during PCI, and this study evaluated the impact of NIRS-IVUS-identified LRP on coronary microvascular function using the novel index of microvascular resistance reserve (MRR).
Does the presence of NIRS-IVUS-identified lipid-rich plaque (maxLCBI4mm ≥500) impair microvascular resistance reserve (MRR) after percutaneous coronary intervention?
Observational (n=100)
Does the presence of NIRS-IVUS-identified lipid-rich plaque (maxLCBI4mm ≥500) impair microvascular resistance reserve (MRR) after percutaneous coronary intervention?
In coronary lesions with lipid-rich plaque identified by NIRS-IVUS, microvascular resistance reserve significantly decreases during PCI despite improvements in epicardial physiology, establishing maxLCBI4mm ≥500 as an independent predictor of post-PCI microvascular dysfunction.
Answers are grounded in this paper and cite their sources.
Lipid-rich plaques may increase post-PCI microvascular dysfunction risk; hypothesis-generating for NIRS-IVUS-guided strategies.
Background/Purpose Coronary lipid-rich plaque (LRP) is likely to cause distal embolization during PCI, which is associated with microvascular injury. Microvascular resistance reserve (MRR) is a novel index of coronary microvascular function regardless of epicardial stenosis. This study assessed the impact of LRP identified by NIRS-IVUS on coronary microvascular function including MRR during PCI. Methods We retrospectively analyzed 100 patients who underwent NIRS-IVUS–guided PCI. Coronary physiological assessment using a pressure–temperature sensor guidewire was performed pre- and post PCI. Lesions were stratified into two groups with or without LRP (maxLCBI4mm ≥500) and physiological measurements were compared. Results In total, lesions with LRP were identified in 39 patients (39%). Baseline clinical characteristics were similar between two groups. Fractional flow reserve (FFR) and resting full-cycle ratio (RFR) improved in both groups, whereas MRR decreased significantly in LRP lesions (ΔMRR −1.49±0.46 vs −0.32±0.37, p=0.04). On multivariable logistic regression, maxLCBI4mm ≥500 emerged as an independent predictor of post-PCI coronary microvascular dysfunction defined by MRR (odds ratio 3.06, 95% confidence interval 1.01–9.29). Conclusion In lipid-rich lesions, MRR decreased during PCI despite of improvement in epicardial physiological indices, suggesting that MRR may be superior index to predict coronary microvascular dysfunction.
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Kusumoto et al. (2026) conducted an observational in Coronary artery disease undergoing NIRS-IVUS-guided PCI (n=100). Lipid-rich plaque (maxLCBI4mm ≥500) vs. Lesions without lipid-rich plaque (maxLCBI4mm <500) was evaluated on Change in microvascular resistance reserve (ΔMRR) and post-PCI coronary microvascular dysfunction defined by MRR (OR 3.06, 95% CI 1.01-9.29, p=0.04). Lipid-rich plaques (maxLCBI4mm ≥500) decreased microvascular resistance reserve during PCI and predicted microvascular dysfunction.
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