Cipollone F, Fazia M, Iezzi A, Pini B, Costantini F, De Cesare D, Paloscia L, Materazzo G, D'Annunzio E, Bucciarelli T, Vecchiet J, Chiarelli F, Cuccurullo F, Mezzetti A
Department of Medicine and Aging, University of Chieti G D'Annunzio School of Medicine, Chieti, Italy.
Heart. 2003 Jul;89(7):773-9. doi: 10.1136/heart.89.7.773.
To investigate whether enhanced oxidant stress in patients undergoing percutaneous transluminal coronary angioplasty (PTCA) is associated with a higher concentration of non-high density lipoprotein (HDL) cholesterol at baseline, and whether this contributes to the inflammatory reaction and luminal renarrowing after PTCA.
An ex vivo and in vitro study of 46 patients who underwent PTCA and who had repeat angiograms after six months. Blood samples were collected immediately before PTCA, and at 24 hours, 48 hours, and 15 days after.
Tertiary referral centre.
46 patients (30 male, 16 female; mean (SD) age, 62 (5) years) with stable or unstable angina who underwent elective PTCA.
Continuous variable luminal loss as defined by change in minimum lumen diameter during follow up, normalised for vessel size; lag phase of low density lipoprotein to in vitro oxidation; plasma fluorescent products of lipid peroxidation (FPLP); plasma vitamin C and E; interleukin (IL) 1beta secretion from unstimulated monocytes; plasma C reactive protein (CRP).
Restenosis occurred in 12 patients (26%). Oxidant stress after PTCA was greater (p < 0.0001 at 15 days) in the patients with restenosis and showed a significant correlation with the preprocedural concentration of non-HDL cholesterol (p < 0.001). Inflammatory reaction (as reflected by IL-1beta production and CRP) and late lumen loss were linearly correlated (p < 0.001) with lag phase and FPLP throughout the study, and inversely (p < 0.05) with vitamin C and E measured at two and 15 days after PTCA.
This study provides evidence for the critical role of cholesterol dependent oxidant stress in the pathophysiology of restenosis after PTCA. The findings raise the possibility that drugs capable of modulating oxidant status might provide a novel form of adjuvant treatment in patients with hypercholesterolaemia undergoing PTCA.
研究接受经皮冠状动脉腔内血管成形术(PTCA)的患者增强的氧化应激是否与基线时非高密度脂蛋白(HDL)胆固醇浓度较高相关,以及这是否会导致PTCA后的炎症反应和管腔再狭窄。
对46例行PTCA且6个月后进行重复血管造影的患者进行的一项体外和体内研究。在PTCA前、术后24小时、48小时和15天立即采集血样。
三级转诊中心。
46例(30例男性,16例女性;平均(标准差)年龄62(5)岁)患有稳定型或不稳定型心绞痛并接受择期PTCA的患者。
随访期间最小管腔直径变化定义的连续变量管腔丢失,根据血管大小进行标准化;低密度脂蛋白体外氧化的延迟期;脂质过氧化的血浆荧光产物(FPLP);血浆维生素C和E;未刺激单核细胞分泌的白细胞介素(IL)-1β;血浆C反应蛋白(CRP)。
12例患者(26%)发生再狭窄。再狭窄患者PTCA后的氧化应激更大(15天时p<0.0001),且与术前非HDL胆固醇浓度显著相关(p<0.001)。在整个研究中,炎症反应(以IL-1β产生和CRP反映)和晚期管腔丢失与延迟期和FPLP呈线性相关(p<0.001),与PTCA后2天和15天测得的维生素C和E呈负相关(p<0.05)。
本研究为胆固醇依赖性氧化应激在PTCA后再狭窄病理生理学中的关键作用提供了证据。这些发现增加了这样一种可能性,即能够调节氧化状态的药物可能为接受PTCA的高胆固醇血症患者提供一种新的辅助治疗形式。