Saint Joseph's Translational Research Institute/Saint Joseph's Hospital of Atlanta, Atlanta, Georgia 30342, USA.
JACC Cardiovasc Interv. 2009 Mar;2(3):253-62. doi: 10.1016/j.jcin.2008.11.009.
We sought to evaluate coronary epicardial and intramyocardial resistance, arterial vasomotor function, local inflammatory reaction, and superoxide anion (O(2)(.-)) production after overlapping paclitaxel-eluting stent (PES) implantation in a porcine model.
PES implantation has been shown to elicit coronary vasomotor dysfunction. However, underlying mechanisms remain largely unknown.
Nine pigs received overlapping PES and bare-metal stents (BMS) in the coronary arteries, and 3 sham animals were naïve. At 1 month, inflammatory response at the overlapped region was assessed by histopathology and scanning electron microscopy. Endothelial vasomotor function and O(2)(*-) at nonstented coronary reference segments were measured by angiography and organ chamber tensiometry, and lucigenin luminometry; vasomotor function of distal resistance arteries was measured by myography.
Paclitaxel-eluting stents showed reduced late lumen loss, but inflammation and luminal inflammatory cell adherence were higher than for BMS (p < 0.001) at overlapped segments. Endothelium-dependent relaxation to substance P was significantly impaired in PES at nonstented coronary reference segments (>or=15 mm proximally and distally) and perfusion bed resistance arteries (p < 0.05). In contrast, endothelium-independent relaxation to nitroglycerin and sodium-nitroprusside was similar between groups. Local O(2)(-) production at both proximal and distal nonstented coronary reference segments was elevated for PES when compared with O(2)(-) production in BMS and naïve arteries (p < 0.001).
Abnormal endothelium-dependent relaxation at both coronary conduit and resistance arteries was demonstrated after overlapping PES implantation. Profound localized inflammatory reaction, as well as enhanced local oxidative stress, may contribute to vasomotor dysfunction.
我们旨在评估重叠紫杉醇洗脱支架（PES）植入后猪模型的冠状心外膜和心肌内阻力、动脉血管舒缩功能、局部炎症反应和超氧阴离子（O(2)(.-)）产生情况。
PES 植入已被证明会引起冠状血管舒缩功能障碍。然而，其潜在机制在很大程度上仍不清楚。
9 只猪的冠状动脉中接受重叠 PES 和裸金属支架（BMS）植入，3 只假手术动物作为对照。1 个月后，通过组织病理学和扫描电子显微镜评估重叠区域的炎症反应。通过血管造影和器官室张力计及黄嘌呤氧化酶发光法测量非支架冠状参考段的内皮血管舒缩功能和 O(2)(*-)；通过肌动描记术测量远端阻力血管的血管舒缩功能。
PES 显示晚期管腔丢失减少，但重叠段的炎症和管腔炎症细胞黏附高于 BMS（p < 0.001）。非支架冠状参考段（近端和远端 >15 毫米）和灌注床阻力血管的 PES 对物质 P 的内皮依赖性松弛显著受损（p < 0.05）。相比之下，两组间内皮非依赖性松弛对硝酸甘油和硝普钠相似。与 BMS 和未处理动脉相比，PES 在近端和远端非支架冠状参考段的局部 O(2)(*-)产生均升高（p < 0.001）。
重叠 PES 植入后，在冠状导管和阻力血管中均显示出异常的内皮依赖性松弛。明显的局部炎症反应以及增强的局部氧化应激可能导致血管舒缩功能障碍。
