Читать книгу Interventional Cardiology - Группа авторов - Страница 33

Plaque erosion, pathologically characterized by luminal thrombus and absence of the endothelium, without evidence of fibrous cap disruption) [115] is frequently followed by plaque rupture in patients with sudden cardiac death, ranging from 30–40% [124–126] especially more frequently in younger female [126] and smokers [127] Given that OCT does not permit the identification of the endothelial lining, the pathological definition of erosion cannot simply be adapted for the OCT definition. Subsequently, OCT‐identified plaque erosion has been defined as the presence of thrombus and an irregular luminal surface in the absence of cap rupture (Figure 1.4) [128]. In contrast to plaque rupture, plaque erosion is distinctly different entity. Firstly, markers of inflammation are significantly lower in plaque erosion with sparse infiltration of macrophages and T lymphocytes within the vessel wall [79, 129]. Consistent with these findings, differential intracoronary cytokine expression between plaque erosion and rupture has been shown by a clinical study that examined 40 STEMI patients who underwent OCT [130]. Secondly, the stenosis of coronary lumen is not always significant in eroded plaques. According to pathological study examined 111 sudden coronary death, the internal elastic area and percent stenosis were significantly smaller in erosions compared with ruptures (p<0.0001 and p=0.02, respectively), where plaque burden was greater (p=0.008) [131]. Thirdly, coronary thrombi exhibit diverse healing phases, depending on the etiology of the underlying culprit plaque. These findings of differences between plaque erosion and plaque rupture attributed to clinical settings in which the frequency of STEMI was significantly higher in the patients with plaque rupture, whereas NSTE‐ACS was predominant in patients with plaque erosion [132]. These findings may require tailored therapy in individual plaque features. Recently, in a small number, non‐randomized study, a potential alternative treatment strategy for patients with ACS who had OCT‐identified plaque erosion without stent implantation has been shown to result in satisfactory clinical outcomes in which none of 12 patients who had plaque erosion treated with thrombectomy and anti‐thrombotic agents without stenting required an additional revascularization after two years [133]. More recently, another prospective study demonstrated that anti‐thrombotic therapy without stent implantation reduced thrombus volume and enlarged the flow area without re‐occlusion of the culprit lesion at one month in ACS patients with OCT derived erosion [134]. These findings may highlight the utility of OCT assessment to optimize a treatment in patients with ACS.

Figure 1.4 OCT appearance of vulnerable plaques (plaque erosion, plaque rupture, calcified nodule). (a) Plaque Erosion: Intact fibrous cap with irregular luminal surface and superficial calcium. (b) Plaque rupture with luminal thrombus. At 11 o’clock a Thin Cap Fibro‐Atheroma (TCFA) is seen (fibrous cap thickness measured 40 microns, marked with small white bar). (c) Calcified nodule: the presence of fracture of a calcified plate protruding into the lumen through a disrupted fibrous cap with an overlying thrombus.

Figure 1.5 OCT appearances of vulnerable plaques (others). (a) Thin‐cap fibroatheroma (7‐9 o’clock of the plaque seen as red arrow): a presence of thin fibrous cap thickness as <65 μm overlying a signal‐poor lesion with diffuse border representing a lipid‐rich plaque. (b) Macrophage infiltration (red arrows): signal‐rich, distinct or confluent punctuate regions with heterogeneous backward shadows. (c) Cholesterol crystals (red arrows): linear, highly backscattering structures within the plaque. (d) Neovascularization (red arrows): black holes with a diameter of 50‐300 µm within plaque that are present on at least 3 consecutive frames.