Murai Kota, Kataoka Yu, Nakaoku Yuriko, Nishimura Kunihiro, Kitahara Satoshi, Iwai Takamasa, Nakamura Hayato, Hosoda Hayato, Hirayama Atsushi, Matama Hideo, Doi Takahito, Nakashima Takahiro, Honda Satoshi, Fujino Masashi, Nakao Kazuhiro, Yoneda Shuichi, Nishihira Kensaku, Kanaya Tomoaki, Otsuka Fumiyuki, Asaumi Yasuhide, Tsujita Kenichi, Noguchi Teruo, Yasuda Satoshi
Department of Cardiovascular Medicine, National Cerebral & Cardiovascular Center, Osaka, Japan.
Department of Advanced Cardiovascular Medicine, Graduate School of Medical Sciences, Kumamoto University, Kumamoto, Japan.
Cardiovasc Diagn Ther. 2021 Apr;11(2):362-372. doi: 10.21037/cdt-20-1024.
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.
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 (maxLCBI; maximum value of LCBI within any 4 mm segments) and entire target vessel (LCBI: 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.
The averaged FFR and delta-FFR was 0.74 (0.69-0.77), and 0.17±0.05, respectively. On target lesion-based analysis, maxLCBI 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 LCBI 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 maxLCBI (β=57.2, P=0.027) and LCBI (β=24.8, P=0.007) by mixed linear model analyses.
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.
包括脂质斑块在内的易损斑块特征已被证明会影响血流储备分数（FFR）。鉴于脂质斑块的形成和进展伴随着内皮功能障碍，而内皮功能障碍会损害血管张力，脂质负荷程度可能会影响充血期间的血管反应性，从而可能导致FFR降低。我们的目的是阐明脂质斑块负荷程度与冠状动脉生理血管反应性指标之间的关系。
我们分析了89例因冠状动脉造影显示中度狭窄且FFR≤0.80而需要进行经皮冠状动脉介入治疗（PCI）的患者。使用近红外光谱（NIRS）和血管内超声评估靶病变（最大脂质核心负荷指数[maxLCBI]：任何4毫米节段内LCBI的最大值）和整个靶血管（LCBI：整个血管内的LCBI）的脂质核心负荷指数（LCBI）和动脉粥样硬化体积。除了FFR外，通过基线和充血状态之间冠状动脉远端压力/主动脉压力（Pd/Pa）的差值来测量ΔFFR。
平均FFR和ΔFFR分别为0.74（0.69 - 0.77）和0.17±0.05。基于靶病变的分析中，maxLCBI与FFR呈负相关（ρ=-0.213，P = 0.040），与ΔFFR呈正相关（ρ=0.313，P = 0.002）。此外，基于靶血管的分析显示LCBI与FFR（ρ=-0.302，P = 0.003）和ΔFFR（ρ=0.369，P<0.001）具有相似的关系。即使在调整临床特征以及病变/血管特征后，通过混合线性模型分析，ΔFFR（每增加0.10）与maxLCBI（β=57.2，P = 0.027）和LCBI（β=24.8，P = 0.007）独立相关。
不仅“靶病变”而且“整个靶血管”处更大的脂质斑块负荷与更大的ΔFFR相关。局部部位和整个血管处脂质斑块物质的积累可能会损害充血诱导的血管反应性，从而导致FFR降低。
