Читать книгу Interventional Cardiology - Группа авторов - Страница 239

The unique ability of OCT to identify small plaque rupture and to distinguish rupture and erosion offers a major added value in the characterization of patients with ACS before treatment (Figure 9.3). Johnson et al. described plaque rupture as the presence of a disrupted discontinuous fibrous cap overlying a lipid core. It is typically associated with a vessel wall cavity, result of the embolization of its necrotic core. Plaque rupture can be observed in a variety of clinical scenarios and often thrombi are found on rupture edges. Plaque rupture, TCFA, and red thrombus are more frequent in patients with ST‐elevation myocardial infarction (STEMI). Additionally, the size of the ruptured cavities was greater and an aperture opposite to the flow direction was more frequent in patients with STEMI [44]. OCT also showed differences in the morphology of ruptured plaques in non‐STEMI and asymptomatic coronary artery disease (CAD) [45]. Pathologic studies suggest that ruptures do not necessarily lead to ACS, and ruptures can heal and cause plaque progression. Using OCT, healed plaques can be identified as multiple layers of different optical densities overlying a large necrotic core [46].

Figure 9.3 Plaque classification algorithm by optical coherence tomography (OCT). Plaque rupture is defined as the presence of fibrous cap discontinuity associated to a cavity inside the plaque. Definite OCT erosion is identified by the presence of attached thrombus overlying an intact and visualized plaque, whereas probable OCT erosion is defined by: (i) luminal surface irregularity at the culprit lesion in the absence of thrombus; or (ii) attenuation of underlying plaque by thrombus without superficial lipid or calcification immediately proximal or distal to the site of thrombus. A calcified nodule protruding into the lumen with partial cap disruption may also lead to thrombus formation and plaque instability.

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.