Читать книгу Interventional Cardiology - Группа авторов - Страница 41

The common denominator for plaque rupture causing ACS is lipid accumulation, either as a lipid core or lipid pools [115]. This has been proved in a study that compared ACS culprit sites with lesions responsible for stable CAD using NIRS [164]. Subsequently, it has been shown that NIRS‐IVUS is highly specific for the identification of ST‐elevation myocardial infarction (STEMI) [165] and non‐ST‐elevation myocardial infarction [166]. According to these studies, a maximum LCBI4mm >400 was the optimal threshold for identification of culprit plaque in patients with both STEMI and non‐STEMI. The visualization of lipid rich plaque on NIRS imaging has been also employed to predict PCI procedural risks and optimize coronary stent implantation. A clinical study examined 62 patients with CAD demonstrated that a maximum LCBI4mm >500 as a discriminatory threshold for the occurrence of periprocedural myocardial infarction after PCI [167]. Moreover, the prognostic value of NIRS‐derived LCBI has been investigated in a study examined 203 patients with CAD [168]. Patients with an LCBI equal to or above the median of 43.0 had a fourfold risk of adverse cardiovascular events during one year follow‐up. Thus, these results indicate the potential of intravascular NIRS imaging for risk stratification of cardiovascular events in patients with CAD. Additionally, the relationship of NIRS‐derived LCBI with cardiovascular disease also indicates the potential benefit of pharmacological lipid rich plaque modulation prior to cardiovascular events. The reduction in yellow plaque by aggressive lipid lowering therapy (YELLOW) trial has demonstrated that short‐term intensive statin therapy reduced lipid content using NIRS in severely obstructive coronary lesions compared with standard therapy [169]. However, in the integrated biomarker and imaging study 3 (IBIS‐3) study, the effect of high intensity Rosuvastatin therapy on coronary plaque composition and LCBI was investigated within non‐stenotic, non‐culprit coronary segments with a relatively low atheroma burden and failed to demonstrate a significant reduction of necrotic core volume or LCBI under high intensity rosuvastatin therapy during one year [170]. Further investigations are required to better understand lipidic materials within vessel wall.