Interventional Cardiology. Группа авторов

cap disruption whereby the overlying thrombus is in continuity with the underlying necrotic core is the most frequent finding in autopsy studies of patients with sudden cardiac death [115, 120]. Plaque rupture is thought to be consequence of thin‐cap atheroma disruption and inflammation is the key regulator of the structural integrity of the plaque. Recently, circumferential biomechanical forces have been focused and recognized as one of the risk factor leading to plaque development and plaque rupture [121]. OCT is currently the most ideal modality to identify and evaluate plaque rupture. Interestingly, in the preliminary study, the area of ruptured cavity was significantly larger in STEMI compared with non‐ST‐segment elevated ACS (NSTE‐ACS), suggesting that the morphological feature of plaque rupture could relate to the clinical presentation in patients with ACS [122] Additionally, another study conducted 3‐vessel OCT imaging in 38 patients with ACS demonstrated that ruptured culprit plaques had non‐culprit plaques with thinner prevalence of TCFA, wider maximum lipid arc, greater lipid length and thinner fibrous caps compared with non‐ruptured culprit plaques, indicating that the patients with ruptured culprit plaques have increased pan‐coronary vulnerability in non‐culprit plaques which may cause future adverse events [123].

      Plaque erosion

      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.

      Calcified nodule

      Calcified nodule, pathologically defined as, the presence of fracture of a calcified plate protruding into the lumen through a disrupted fibrous cap with an overlying thrombus (Figure 1.4), is the least frequent pathological finding associated with coronary thrombosis [115]. Consistent with the histological findings, clinical OCT evaluation in a study of 126 patients with ACS found a prevalence of 7.9%, with being more common in older patients [132]. Thus, given that the prevalence of plaque rupture and erosion are higher enough to get details compared with calcified nodule, it remains a poorly understood entity. In pathology series, calcified nodules are more commonly found in older individuals in the mid‐right coronary artery or left anterior descending artery where torsion is greatest [115]. Coronary calcification correlates highly with plaque burden and is an independent marker of cardiovascular risk [135]. Furthermore, coronary calcification within a thin fibrous cap can increase the circumferential stress leading to plaque rupture and thrombotic events [136]. OCT is the only tool to depict the thickness of superficial calcium deposits accurately, superior to IVUS [137]. Additionally, a great ability to detect calcified nodules have been reported with a sensitivity of 96% and specificity of 97% [138]. Recently, striking images showing a close correlation between pathological and OCT findings in a human coronary artery were reported [139]. However, more recent studies have raised an important issue with regard to the visualization of intense dorsal shadowing generated by protruding red thrombus and protruding bony calcified spicules [140,141]. Further investigation is required to clarify whether protruding luminal red thrombus emerged directly, or small bony calcified nodules generated intense dorsal shadowing.

      OCT‐derived Vulnerable Plaques

      OCT‐ derived TCFA

With the high resolution of OCT, this modality might be the best for its reliability as a tool to measure the fibrous cap thickness in vivo. A histology study examined 38 human cadavers and showed a good correlation of the fibrous cap thickness between OCT and histology (r=0.90; p<0.001) [142]. In the clinical setting, OCT‐TCFA was reported to be more frequently observed in the culprit lesion in patients with STEMI compared with those with stable coronary artery disease [143], and NSTEMI [122]. In addition, its distribution in the coronary tree was similar to that in the previous pathological observation demonstrating that TCFAs were more commonly found in the proximal distribution of the coronary artery [88, 144]. Subsequently, serial OCT imaging has been employed to assess the natural history and the impact of lipid modification on atherosclerotic coronary plaques. OCT‐TCFA has been shown to be a predictor of subsequent plaque progression and acute coronary events [145]. An early clinical study reported that in patients with AMI, the use of statins for nine months significantly increased fibrous cap thickness compared with placebo control,146 indicating that