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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).

      Acute coronary syndromes: identification of the culprit plaque and distinction rupture/erosion

Schematic illustration of plaque classification algorithm by optical coherence tomography (OCT).

      Source: Jia et al. 2013 [47]. Copyright (2013), with permission from Elsevier.

      Although plaque rupture is the most common cause of ACS, pathology has shown that more than 20–30% of events are caused by plaque erosion, or more rarely by thrombosis triggered by the presence of superficial protruding calcific nodules shown on OCT (Figure 9.3). The subtle changes induced by erosion can be detected and confirmed in vivo only by OCT. Plaque erosion can be suspected in the presence of different patterns: white thrombus on an intact fibrous cap, lack of thrombus with an irregular lumen surface, overlying thrombus with underlying plaque without superficial lipid or calcification immediately proximal or distal to the site of thrombus [47]. The characteristics of 51 culprit plaques and 216 nonculprit plaques were analyzed in 51 ACS patients (37 men; mean age 58.7 years). Compared with patients with culprit plaque rupture, ACS patients with culprit plaque erosion had a smaller number of nonculprit plaques. A prospective series of 822 patients suggests that people with plaque erosion tend to be younger, with a relatively high rate of post‐menopausal women and smokers, without traditional coronary risk factors, with lack of multi‐vessel disease. Low lesion severity, larger vessel size and nearby bifurcation were significantly associated with plaque erosions [48,49]. The importance of OCT in detecting plaque disruption and categorize plaque morphology in vivo [47] could aid in the derivation of treatment strategies [50], with no PCI required in non critical stenoses with plaque erosions.

Schematic illustration of optical coherence tomography in coronary interventions. Schematic illustration of baseline angiogram of the the right coronary system shown on the left with a red arrow at the site of maximal stenosis in the mid-RCA.

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