Читать книгу Interventional Cardiology - Группа авторов - Страница 238

Imaging in acute coronary syndromes (ACS) includes ruptured plaques and histomorphologic features that can be detected by OCT (superficial lipids, fibrous cap thickness as well the presence of macrophages and neovascularization).

A semi‐quantitative definition of the presence of superficial lipids in ≥2 quadrants is used to describe lipid‐rich plaques in OCT studies [21]. However, low penetration depth prevents accurate evaluation of the lipid core thickness. Pathologic studies reported that ruptured plaques harbor a thin fibrous cap being <65 μm in 95% of ruptured plaques [22]. Using OCT, the fibrous cap can be detected as a high signal homogeneous band covering the lipid‐rich core. OCT was shown to provide accurate measurement of fibrous cap thickness (FCT) ex vivo [23]; previous studies demonstrated thinner fibrous caps in patients with ACS [21,24]. A study that aimed to evaluate the relationship between FCT and plaque rupture in vivo found that in 95% of ruptured plaques, the thinnest FCT was <80 μm and so the investigators proposed this value as an alternative in vivo threshold [25].

The progression of atherosclerosis and plaque vulnerability is critically affected by macrophages, identified as high signal regions appearing either distinct or confluent punctate visually. With dedicated software, OCT‐derived indices can be used to identify macrophages [26]. Nonetheless, macrophages should only be considered in the presence of a fibroatheroma, because there have not yet been any studies to confirm macrophages on normal vessel walls or intimal hyperplasia. In addition, high speckle from microcalcifications or cholesterol crystals can also appear similar to macrophages [27].

Plaque neovascularization is considered as a feature of vulnerable plaques. These microvessels are inherently fragile and leaky, giving rise to local extravasation of plasma proteins and erythrocytes [28]. OCT reveals these vessels as small black holes in the atherosclerotic plaque [29]. The presence of these microchannels is associated with vulnerable features such as thin fibrous cap and positive remodeling [30]. In a larger study, microchennels characterized culprit lesions of patients with ACS, and were not present in non‐culprit lesions of patients with ACS or in stable patients [31]. Another study found no difference in the prevalence of microchannels in ACS and non‐ACS patients; however, the closest distance from the lumen to the microchannel was shorter in ACS subjects than in non‐ACS [32].

OCT imaging over time can provide insights on the efficacy of the therapeutic strategies for plaque stabilization. In an initial study, patients on preceding statin therapy were found to have a reduced incidence of ruptured plaques and a trend toward thicker fibrous caps [33]. The influence of statins on fibrous caps was further investigated in a study of 40 patients with previous myocardial infarction. FCT was found to increase in both the statin and control group over time, but more so in the statin group [34]; this was confirmed ensewhere [35]. Atorvastatin therapy at 20 mg/day provided a greater increase in FCT than 5 mg at 18‐month follow‐up [36]. Despite comparable reduction in total cholesterol and low density lipoprotein cholesterol levels with statin therapy in ACS patients, non‐culprit lesions without neovascularization showed greater increase in fibrous cap thickness than lesions with neovascularization at a 6–12 month follow‐up [37]. These important insights into the operative mechanism of statins reveal subtle qualitative rather than gross quantitative arterial wall changes, explaining the reduction of clinical endpoints achieved despite the unchanged angiographic lumen dimensions and minimal volumetric plaque changes by IVUS [38–40]. The dramatic decrease of cholesterol levels obtainable with PCSK9 inhibitors [41,42] showed mild IVUS volumentric changes and inconsistent morphologic changes with virtual histology [43] leading to ongoing OCT serial studies (ClinicalTrials.gov Identifier: HUYGENS clinical trial NCT03570697, PACMAN‐AMI clinical trial NCT03067844).