Lipid-Core Plaque Assessed by Near-Infrared Spectroscopy and Procedure Related Microvascular Injury
- Author:
Hyoung Mo YANG
1
;
Myeong Ho YOON
;
Hong Seok LIM
;
Kyoung Woo SEO
;
Byoung Joo CHOI
;
So Yeon CHOI
;
Gyo Seung HWANG
;
Seung Jea TAHK
Author Information
- Publication Type:Original Article
- Keywords: Percutaneous coronary intervention; Coronary artery disease; Microvessel; Near-infrared spectroscopy
- MeSH: Coronary Artery Disease; Creatine; Humans; Incidence; Microvessels; Myocardial Infarction; Observational Study; Percutaneous Coronary Intervention; Prospective Studies; Retrospective Studies; Spectroscopy, Near-Infrared; Troponin I
- From:Korean Circulation Journal 2019;49(11):1010-1018
- CountryRepublic of Korea
- Language:English
- Abstract: BACKGROUND AND OBJECTIVES: Microvascular damage due to distal embolization during percutaneous coronary intervention (PCI) is an important cause of periprocedural myocardial infarction. We assessed the lipid-core plaque using near-infrared spectroscopy (NIRS) and microvascular dysfunction invasively with the index of microcirculatory resistance (IMR) and evaluated their relationship. METHODS: This study is pilot retrospective observational study. We analyzed 39 patients who performed NIRS before and after PCI, while fractional flow reserve, thermo-dilution coronary flow reserve (CFR) and IMR were measured after PCI. The maximum value of lipid core burden index (LCBI) for any of the 4-mm segments at the culprit lesion (culprit LCBI(4mm)) was calculated at the culprit lesion. We divided the patients into 2 groups using a cutoff of culprit LCBI(4mm) ≥500. RESULTS: Mean pre-PCI LCBI was 333±196 and mean post-PCI IMR was 20±14 U. Post-PCI IMR was higher (15.6±7.3 vs. 42.6±17.6 U, p<0.001) and post-PCI CFR was lower (3.7±2.2 vs. 2.1±1.0, p=0.029) in the high LCBI group. Pre-PCI LCBI was positively correlated with post-PCI IMR (ρ=0.358, p=0.025) and negatively correlated with post-PCI CFR (ρ=−0.494, p=0.001). The incidence of microvascular dysfunction (IMR ≥25 U) was higher in the high LCBI group (9.4% vs. 85.7%, p<0.001). However, there were no significant differences in the incidences of creatine Kinase-MB (9.4% vs. 14.3%, p=0.563) and troponin-I elevation (12.5% vs. 14.3%, p=1.000). CONCLUSIONS: A large lipid-core plaque at the ‘culprit’ lesion is observed higher incidence of post-PCI microvascular dysfunction after PCI. Prospective study with adequate subject numbers will be needed.
