TY - JOUR
T1 - The association between the extent of lipidic burden and delta-fractional flow reserve
T2 - analysis from coronary physiological and near-infrared spectroscopic measures
AU - Murai, Kota
AU - Kataoka, Yu
AU - Nakaoku, Yuriko
AU - Nishimura, Kunihiro
AU - Kitahara, Satoshi
AU - Iwai, Takamasa
AU - Nakamura, Hayato
AU - Hosoda, Hayato
AU - Hirayama, Atsushi
AU - Matama, Hideo
AU - Doi, Takahito
AU - Nakashima, Takahiro
AU - Honda, Satoshi
AU - Fujino, Masashi
AU - Nakao, Kazuhiro
AU - Yoneda, Shuichi
AU - Nishihira, Kensaku
AU - Kanaya, Tomoaki
AU - Otsuka, Fumiyuki
AU - Asaumi, Yasuhide
AU - Tsujita, Kenichi
AU - Noguchi, Teruo
AU - Yasuda, Satoshi
N1 - Publisher Copyright:
© Cardiovascular Diagnosis and Therapy. All rights reserved.
PY - 2021/4
Y1 - 2021/4
N2 - Background: Vulnerable plaque features including lipidic plaque have been shown to affect fractional flow reserve (FFR). Given that formation and propagation of lipid plaque is accompanied by endothelial dysfunction which impairs vascular tone, the degree of lipidic burden may affect vasoreactivity during hyperemia, potentially leading to reduced FFR. Our aim is to elucidate the relationship of the extent of lipidic plaque burden with coronary physiological vasoreactivity measure. Methods: We analyzed 89 subjects requeuing PCI due to angiographically intermediate coronary stenosis with FFR ≤0.80. Near-infrared spectroscopy (NIRS) and intravascular ultrasound were used to evaluate lipid-core burden index (LCBI) and atheroma volume at both target lesion (maxLCBI4mm; maximum value of LCBI within any 4 mm segments) and entire target vessel (LCBIvessel: LCBI within entire vessel). In addition to FFR, delta-FFR was measured by difference of distal coronary artery pressure/aortic pressure (Pd/Pa) between baseline and hyperemic state. Results: The averaged FFR and delta-FFR was 0.74 (0.69–0.77), and 0.17±0.05, respectively. On target lesion-based analysis, maxLCBI4mm was negatively correlated to FFR (ρ=−0.213, P=0.040), and it was positively correlated to delta-FFR (ρ=0.313, P=0.002). Furthermore, target vessel-based analysis demonstrated similar relationship of LCBIvessel with FFR (ρ=−0.302, P=0.003) and delta-FFR (ρ=0.369, P<0.001). Even after adjusting clinical characteristics and lesion/vessel features, delta-FFR (by 0.10 increase) was independently associated with maxLCBI4mm (β=57.2, P=0.027) and LCBIvessel (β=24.8, P=0.007) by mixed linear model analyses. Conclusions: A greater amount of lipidic plaque burden at not only “target lesion” alone but “entire target vessel” was associated with a greater delta-FFR. The accumulation of lipidic plaque materials at both local site and entire vessel may impair hyperemia-induced vasoreactivity, which causes a reduced FFR.
AB - Background: Vulnerable plaque features including lipidic plaque have been shown to affect fractional flow reserve (FFR). Given that formation and propagation of lipid plaque is accompanied by endothelial dysfunction which impairs vascular tone, the degree of lipidic burden may affect vasoreactivity during hyperemia, potentially leading to reduced FFR. Our aim is to elucidate the relationship of the extent of lipidic plaque burden with coronary physiological vasoreactivity measure. Methods: We analyzed 89 subjects requeuing PCI due to angiographically intermediate coronary stenosis with FFR ≤0.80. Near-infrared spectroscopy (NIRS) and intravascular ultrasound were used to evaluate lipid-core burden index (LCBI) and atheroma volume at both target lesion (maxLCBI4mm; maximum value of LCBI within any 4 mm segments) and entire target vessel (LCBIvessel: LCBI within entire vessel). In addition to FFR, delta-FFR was measured by difference of distal coronary artery pressure/aortic pressure (Pd/Pa) between baseline and hyperemic state. Results: The averaged FFR and delta-FFR was 0.74 (0.69–0.77), and 0.17±0.05, respectively. On target lesion-based analysis, maxLCBI4mm was negatively correlated to FFR (ρ=−0.213, P=0.040), and it was positively correlated to delta-FFR (ρ=0.313, P=0.002). Furthermore, target vessel-based analysis demonstrated similar relationship of LCBIvessel with FFR (ρ=−0.302, P=0.003) and delta-FFR (ρ=0.369, P<0.001). Even after adjusting clinical characteristics and lesion/vessel features, delta-FFR (by 0.10 increase) was independently associated with maxLCBI4mm (β=57.2, P=0.027) and LCBIvessel (β=24.8, P=0.007) by mixed linear model analyses. Conclusions: A greater amount of lipidic plaque burden at not only “target lesion” alone but “entire target vessel” was associated with a greater delta-FFR. The accumulation of lipidic plaque materials at both local site and entire vessel may impair hyperemia-induced vasoreactivity, which causes a reduced FFR.
KW - Coronary artery disease
KW - Fractional flow reserve (FFR)
KW - Intravascular ultrasound
KW - Near-infrared spectroscopy (NIRS)
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U2 - 10.21037/cdt-20-1024
DO - 10.21037/cdt-20-1024
M3 - Article
AN - SCOPUS:85105052146
SN - 2223-3652
VL - 11
SP - 362
EP - 372
JO - Cardiovascular Diagnosis and Therapy
JF - Cardiovascular Diagnosis and Therapy
IS - 2
ER -