Читать книгу Interventional Cardiology - Группа авторов - Страница 250

The necrotic core region has an abundance of lipid deposition and lacks mechanical stability due to the degradation of fibrous tissue and disappearance of cells. The size of the necrotic core has been significantly associated with the likelihood of plaque rupture. In a previous pathologic study of aortic plaques, ulceration, and thrombosis were characteristic of plaques with >40% of their volume occupied by extracellular lipids [124]. As the lipid core increases plaque vulnerability, the NIRS can potentially be used to identify high risk plaques (Figure 9.7). It has been shown that the target lesions responsible for ACS were in most cases lipid‐rich plaques; additionally, patients with ACS commonly harbored remote, nontarget lipid‐rich plaques [125]. In another study in patients with STEMI, maxLCBI_4mm > 400 in NIRS accurately distinguished culprit from non‐culprit segments within the artery and from the lipidrich plaque‐free autopsy histology segments [126]. In a recently published prospective observational study, NIRS imaging was performed in a non‐culprit coronary artery in 203 patients referred for angiography due to stable angina pectoris or ACS. It was shown that the one year cumulative incidence of a cardiovascular event in patients with an LCBI equal to or above the median value (43.0) was significantly higher than those with an LBCI value below the median [127].

Figure 9.7 A 39‐year‐old man was admitted with unstable angina. Angiography showed significant lesions in right and left anterior descending arteries. After post‐dilatation, near‐infrared spectroscopy–intravenous ultrasound (NIRS‐IVUS) imaging was performed, which revealed lipid core plaque in the mid‐ and distal left anterior descending (LAD) (b and c). Proximal segments were relatively disease free (a). Right coronary artery (RCA) also harbored lipid core plaques.

The Lipid Rich Plaque (LRP) study enrolled 1241 patients with stable or unstable angina and myocardial infarction and studied more than 5000 lesions assessed with NIRS‐IVUS. The study demonstrated that the identification of non‐critical, untreated, lipid‐rich plaques by NIRS imaging is associated with adverse events following PCI for de novo culprit lesions. NIRS allows the assessment of atherosclerotic plaques by the analysis of reflected spectrum of near infrared light, providing a reliable chemogram of the wall lipid content. The lipid core burden index (LCBI) is reported along the entire acquisition segment, or within the 4 mm segment of highest accumulation (LCBI4mm). Commercially available systems allow the simultaneous acquisition of IVUS and NIRS signals, providing the assessment of lipid content, lumen stenosis severity and plaque burden. Four non‐randomized studies, the two largest ATHEROREMO‐NIRS and Spectrum NIRS‐IVUS registry enrolling more than 400 patients, demonstrated that an increased LCBI is associated with the development of subsequent MACE. In the LRP study, NIRS‐IVUS imaging was performed in non‐culprit arteries in 1563 patients with coronary artery disease (46.3% stable angina) who underwent PCI for an index event. Patient‐ and plaque‐level events were followed for two years among those with at least one maxLCBI4mm segment ≥ 250 and a randomly selected 50% of patients with all maxLCBI4mm segments < 250. A representative example is presented in Figure 9.8. The adjusted patient‐level analysis showed that for each 100 unit increase of maxLCBI4mm the risk of non‐culprit MACE increased by 18% and patient with maxLCBI4mm greater than 400 is at 87% higher risk of non‐culprit MACE. Also, the plaque‐level analysis demonstrated a 45% higher risk of events within 24 months with each 100‐unit increase in maxLCBI4mm in a coronary segment, with MACE rates of 3.7% versus 0.8% for plaques with maxLCBI4mm ≥ 400 and < 400, respectively. The results of this trial show that NIRS is a safe and feasible technique able to identify vulnerable plaque and vulnerable patients in whom strategies of tailored secondary prevention could be focused [128].

Figure 9.8 Angiography at baseline without significant stenosis (a). Angiography at one year follow‐up with a stenotic lesion at the region of MaxLCBI4mm from baseline assessment (b). Chemogram (c) from baseline near‐infrared spectroscopy (NIRS) with MaxLCBI4mm = 472 at the site of a future event at one year post index procedure.

The recent IBIS‐3 trial demonstrated that high‐intensity rosuvastatin therapy during one year resulted in a neutral effect on NC and LCBI within non‐stenotic, non‐culprit coronary segments with a relatively low atheroma burden (The Netherlands Trial Register n. 2872).