Читать книгу Interventional Cardiology - Группа авторов - Страница 35

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 its effects of stabilization on vulnerable atherosclerotic coronary plaques. Subsequently, the effect of atorvastatin therapy on fibrous cap thickness in coronary atherosclerotic plaque assessed by optical coherence tomography (EASY‐FIT) trial compared the efficacy of 20 mg and 5 mg atorvastatin on plaque microstructures acquired from OCT in 70 patients with unstable angina pectoris. The increase in fibrous cap thickness was significantly greater with the higher dose of atorvastatin (69% vs 17%, p<0.001), along with more favourable changes in lipid arc (–27% vs –8%, p<0.001) and macrophage grade (–38% vs –24%, p<0.001) [147].