Читать книгу Interventional Cardiology - Группа авторов - Страница 37

CCs are formed very early in the process of atherogenesis and activate the proinflammatory cytokines interleukin‐1‐beta (IL‐1β) and IL‐18 via activating inflammasomes in neutrophils and monocytes/macrophages [153], which has been postulated to contribute to CC‐mediated plaque destabilization. These findings are supported by the fact that demonstrated CCs are often seen abundantly within atheromatous plaques and at sites of plaque disruption [154]. Cholesterol crystallization in plaque is an important trigger for core expansion, leading to intimal injury [155]. Therefore, CCs have been thought to be one of the factors leading to disruption of the plaque cap and overlying intima. With OCT, cholesterol crystals (CCs) are defined as linear, highly backscattering structures within the plaque (Figure 1.5). Preliminary, Kataoka, et al. demonstrated that plaques containing CCs exhibited distinct OCT‐derived microstructures associated with plaque vulnerability [156]. Recently, in a study that investigated the relationship between CCs and culprit lesion vulnerability in patients with ACS, the frequency of CCs was significantly higher in patients with STEMI compared to NSTEMI (50.8% vs 34.7%, p=0.032). Moreover, culprit lesions with CCs had higher prevalence of macrophage accumulation (77.8% vs 40.0%, p<0.001), microchannels (67.9% vs 24.8%, p<0.001), plaque rupture (58.0% vs 36.0%, p=0.001), thrombosis (66.7% vs 49.6%, p=0.016) and spotty calcification (35.8% vs 10.4%, p<0.001), suggesting that CCs may increase plaque vulnerability and trigger plaque rupture in patients with ACS [157].