Abstract
Introduction: FFR and resting indexes (RI) have been recognized as physiological measures to assess myocardial ischemia. Despite their clinical applicability, discrepancy between two measures infrequently occurs. Mechanistically, inducement of hyperemia is a determinant of FFR but not RI. Since lipidic plaque material could be accumulated through endothelial dysfunction, this plaque phenotype may affect vessel response, contributing to physiological mismatch. Near-infrared spectroscopy (NIRS) enables us to evaluate lipidic burden in vivo. Methods: We analyzed 122 target lesions with FFR≤0.80 in 116 stable CAD subjects receiving PCI. Physiological mismatch was defined as FFR≤0.75 and RI>0.89. Physiological indices [RI, FFR and delta-FFR (=resting Pd/Pa-FFR)] and NIRS/IVUS-derived plaque measures were compared in target lesions stratified according to FFR (≤ or >0.75) and RI (≤ or >0.89) values. Results: The averaged FFR, RI and delta-FFR values were 0.73±0.06, 0.86±0.08 and 0.17±0.05, respectively. Physiological mismatch was observed in 10.7% of analyzed lesions. While there was no significant difference in % diameter stenosis across 4 groups (p=0.36), physiological mismatch was associated with a larger % plaque area (max%PA) (p=0.02). Furthermore, greater maximum 4-mm lipid core burden index (maxLCBI 4mm ) was observed in those exhibiting physiological mismatch (Figure). On multivariate analysis, maxLCBI 4mm but not max%PA predicted physiological mismatch (Table). Further analysis demonstrated that lesions causing physiological mismatch more likely exhibited a larger delta-FFR (p<0.01). Of note, delta-FFR was correlated with maxLCBI 4mm (p=0.03, R=0.20) but not max%PA (p=0.09, R=0.15). Conclusions: Lipidic plaque material was a potential contributor to physiological mismatch, driven by its enhanced hyperemic response. Our findings suggest the potential association of lipidic materials with vasomotion and physiological mismatch.
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