Characterization of plaque hemorrhage with optical coherence tomography imaging in statin-treated patients with coronary artery disease: comparison with noncontrast T1-weighted MRI

Abstract Background Plaque hemorrhage is a phenotypic feature of coronary lesions associated with future coronary events. Noncontrast T1-weighted MRI has a potential to non-invasively identify plaque hemorrhage. Plaque to myocardium ratio (PMR) evaluated by noncontrast T1-weighted MRI has been shown to pathohistologically correspond to plaque hemorrhage. In several case reports comparing OCT images with coronary specimens, low intensity area without its attenuation was observed at lesions presenting plaque hemorrhage. However, whether the association of this OCT-derived feature with PMR remains to be elucidated yet. Purpose To characterize plaque hemorrhage in vivo by comparing with OCT and noncontrast T1-weighted MRI. Methods The current study prospectively enrolled 80 statin-treated patients with coronary artery disease requiring elective PCI. A total of 103 target lesions were imaged by both noncontrast T1-weighted MRI and OCT prior to PCI. Plaque hemorrhage on noncontrast T1-weighted MRI was defined as PMR>1.0. On OCT imaging analysis, low intensity area without attenuation (LIA) was defined according to the following criteria; (1) area presenting homogeneous low intensity signals, (2) clear border and (3) no signal attenuation behind its area. The maximum arc of LIA was manually measured. OCT-derived plaque features were compared in lesions with and without PMR>1.0. Results PMR>1.0 was observed at 49.5% of analyzed lesions. Patients with PMR>1.0 were more likely older (72 vs. 66 years, p=0.02), whereas there was no significant difference in on-treatment LDL-C levels (median: 80 vs. 77 mg/dL, p=0.62) (Table). On lesion-based analysis, while fibrous cap thickness was similar between the two groups (80 vs. 100um, p=0.10), a larger lipid arc (270 vs. 230º, p=0.02) and a greater frequency of macrophage (90.2 vs. 53.9%, p<0.01), layered plaque (62.8 vs. 32.7%, p=0.003) and cholesterol crystal (70.6 vs. 30.8%, p<0.001) were observed at lesions with PMR>1.0. Furthermore, lesions with PMR>1.0 more frequently exhibited LIA (66.7 vs. 19.2%, p<0.001) and its greater maximum arc (33 vs. 0º, p<0.001) (Figure). Of note, PMR was significantly correlated to the maximum arc of LIA (r=0.51, p<0.001) (Figure). Multivariate analysis demonstrated LIA and cholesterol crystal as independent OCT-derived features associated with PMR>1.0 (Table). Conclusion In statin-treated patients, 49.5% of analyzed lesions presented PMR>1.0. Coronary lesions with PMR>1.0 more frequently harbored LIA and cholesterol crystals, in addition to other vulnerable OCT features. Our findings suggest OCT-derived LIA as a potential signature of plaque hemorrhage. Given that cholesterol crystal was another feature of PMR>1.0, plaque inflammation driven by cholesterol crystallization may exist at plaque hemorrhage despite statin use. Whether anti-inflammation agent could modulate plaque hemorrhage requires future investigation.