Читать книгу Interventional Cardiology - Группа авторов - Страница 32

Plaque rupture, defined by an area of fibrous 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].