A Case of In-Stent Neoatherosclerosis 10 Years after Carotid Artery Stent Implantation: Observation with Optical Coherence Tomography and Plaque Histological Findings

We report a patient''s case of slow progressive in-stent restenosis 10 years after bare-metal stent implantation to his carotid artery. We treated the patient with an additional stent placement under a distal filter protection device. Optical coherence tomographic assessment and plaque histology during the carotid artery stenting (CAS) revealed atheromatous change at in-stent neointima, which contained lipid-rich plaque and calcification deposits. These findings suggest that in-stent neoatherosclerosis may play an important role in the pathogenesis of very late stent restenosis after CAS.     

低能量氦氖激光血管内照射对缺血再灌注心肌超微结构的影响

目的:探讨低能量氦氖激光血管内照射(ILIB)对缺血再灌注心肌组织超微结构的影响。方法:通过结扎冠状动脉阻断冠状动脉血流,复制家兔急性心肌缺血-再灌注损伤动物模型。将家兔随机分为4组:假手术组、心肌缺血30min组、缺血30min再灌注30min组、缺血30min再灌注30min+ILIB组。在透射电镜下观察各组心肌超微结构的变化。结果:假手术组心肌纤维呈阶段性收缩、间质水肿、线粒体轻度肿胀、间质可见闭塞的毛细血管;心肌缺血组心肌纤维排列紊乱、肌浆水肿、线粒体水肿、血管扩张、血管结构破坏、血管内可见白细胞镶嵌;缺血再灌注组心肌纤维排列相对整齐、线粒体水肿不明显、肌浆水肿较轻、心肌间质可见轻度毛细血管扩张淤血;缺血再灌注+ILIB组心肌纤维排列整齐、线粒体无肿胀、间质毛细血管内可见红细胞、无毛细血管内白细胞镶嵌现象、毛细血管管腔通畅、血管壁较完整。结论:IL-IB可使缺血再灌注心肌超微结构基本恢复正常,对心肌有保护作用。     

Compensatory enlargement of human coronary arteries during progression of atherosclerosis is unrelated to atheroma burden: serial intravascular ultrasound observations from the REVERSAL trial.

AIMS: On the basis of the evidence from autopsy studies, it is accepted that compensatory enlargement (remodelling) of coronary arteries during progression of atherosclerosis diminishes once atheroma burden (cross-sectional area stenosis) reaches approximately 40%. Our aim was to evaluate whether atheroma burden is a limiting factor for coronary arterial remodelling using in vivo serial intravascular ultrasound (IVUS). METHODS AND RESULTS: From the cohort of the Reversal of Atherosclerosis with Aggressive Lipid Lowering (REVERSAL) trial, we identified 210 focal coronary lesions at baseline IVUS. Of these, 128 lesions that had an increase in atheroma area at the 18-month follow-up IVUS were included in the analysis. Lesions were matched at baseline and follow-up. The increase in external elastic membrane (EEM) area for each mm(2) increase in atheroma area was not significantly different in lesions with <40 and >or=40% atheroma burden at baseline (1.62 vs. 1.28 mm(2), P=0.30). There were no correlations between atheroma burden at baseline and change in EEM (r=0.02, P=0.86) or change in lumen (r=0.04, P=0.64) areas. CONCLUSION: Assessment of coronary arterial remodelling by serial IVUS revealed that compensatory remodelling is not limited by atheroma burden. Atheroma burden is not a determinant of arterial enlargement during the progression of atherosclerosis.