0.05). Minor hematoma occurred in four patients with transradial approach and in 59 with transfemoral approach (1.46% vs 17.78%, P0.05), and two patients required blood transfusion in group F. None of the patients suffered from pseudoaneurysm, arteriovenous fistula, and ischemia of the hand. Conclusion Coronary angioplasty can be performed safely using the transradial approach with relatively few vascular complications and with better patient′s comfort.

Objective To investigate the long-term efficacy of transendocardial injection of vascular endothelial growth factor (VEGF) into ischemic porcine myocardium.Methods Thirty pigs were divided into two groups:control group and treatment group (15 each).A angioplasty balloon was used to occlude the left anterior descending coronary arteries of the animals to reproduce a porcine myocardial ischemic model.Blank plasmid (control group) or constructed pIRES2-EGFP-hVEGF165 eukaryotic expression plasmid (treatment group) was directly injected into the ischemic myocardium through an transendocardial injection catheter of NOGA system,respectively.Before and one year after injection,left ventricular electromechanical mapping (LVEMM) was used to detect local linear shortening (LLS) and unipolar potential (UpV);M-mode local wall motion,cycle variation of integrated backscatter (CVIB) and left ventricular ejection fraction (LVEF) were detected by ultrasonagraphy.One year later,the animals were sacrificed for the observation of the capillary formation in myocardial tissue with immunohistochemical staining.Results One year after injection,as compared with that of control group,local linear shortening (LLS) showed a significant increase (P0.05),and ultrasonagraphy showed better heart function in the treatment group (P

Objective: To explore the effect of autophagy on process of high phosphate salt induced vascular smooth muscle cell (VSMC) calciifcation in experimental rats. Methods: Rats’ model of VSMC calciifcation was induced by phosphate incubation. VSMC were divided into 3 groups:①Control group,②Calciifcation group which included 3 subgroups as 4-day subgroup, the cells were cultured by 3.2 mmol/L phosphate for 4 days, 6-day subgroup and 8-day subgroup,③Calciifcation+ 3-MA (autophagy inhibitor) group, in which the 8-day cells were cultured with 5mmol/L 3-MA. Calcium nodule formation and calcium deposition in VSMC were measured by Alizarin red staining and o-cresolphthaleincomplexone method, protein expressions of Runx2, α-SMA and LC3 II were examined by Western blot analysis, autophagosome formation in VSMC was measured by transmission electron microscope and the localization and expression of Runx2 and LC3 II in VSMC were observed by immunolfuorescent microscope. Results: Compared with Control group, the cells at 8-day subgroup showed more calcium nodules, higher calcium deposition, increased protein expressions of Runx2, LC3 II, more autophagosome and decreased α-SMA expression, allP<0.05. Compared with 8-day subgroup, the cells in Calcification+3-MA group presented increased calcium deposition, decreased lfuorescence distribution of LC3 II and more cells with positive Runx2 protein expression, all P<0.05. Conclusion: Autophagy has the protective effect on process of phosphate induced VSMC calciifcation in experimental rats.

Objective: To explore the effects of Vitamin K2 (VK2) on theaortic artery calciifcation and oxidative stress injury in experimental rats.
Methods: A total of 24 rats were divided into 4 groups:①Control group,②6-week calciifcation group,③12-week calciifcation group and④6-week calciifcation + 6-week VK2 group;n=6 in each group. The arterial calciifcation was induced by warfarin (WFN) treatment. The calcium nodule and deposition in rat’s theaortic artery were detected by Alizarin red staining and o-cresolphthalein complexone method, the reactive oxygen species (ROS) were measured by DHE probe staining and the morphological changes of mitochondria in smooth muscle cells were detected by transmission electron microscopy.
Results: Calciifcation nodule formed in both 6-week and 12-week calciifcation groups, the calciifcation deposition and ROS were higher than Control group,P<0.01. Compared with both calcification groups, the above indexes were decreased in 6-week calciifcation + 6-week VK2 group,P<0.01. Both calciifcation groups showed mitochondria swelling with unclear structure and cytoplasm vacuoles degeneration in vascular smooth muscle cells. The vascular smooth muscle cell volumes were similar between Control group and 6-week calcification + 6-week VK2 group, and no cytoplasm vacuoles degeneration was observed.
Conclusion: Warfarin induced aortic calciifcation is related to oxidative stress injury which may cause the ultra-micro structural damage in smooth muscle cells; VK2 may reduce the oxidative stress injury and improve the condition of vessel calciifcation in experimental rats.

Objective: To explore the effect of oxidative stress injury on the mechanism of vascular smooth muscle cell (VSMC) calciifcation induced by calcium and phosphorus in experimental rats.
Methods: The VSMC calcification was induced by incubating the cells with calcium chloride (CaCl2) andβ-sodium glycerophosphate (β-GP) for 8 days, and the cells were divided into 4 groups: ① Control group, ② Calcification group,③ Calciifcation+H2O2 group, ④ Calciifcation+catalase group. The calcium nodule formation and calcium deposition in VSMC were detected by Alizarin red staining and o-cresolphthalein complexone method, the reactive oxygen species (ROS) was detected by DCFH-DA probe staining and the protein expression of Runx2 was examined by Western blot analysis.
Results: Compared with Control group, Calciifcation group showed the higher ROS production, more calcium nodule and calcium deposition, higher Runx2 protein expression;while compared with Calciifcation group, the above indexes were even higher in Calciifcation+H2O2 group, P<0.05. The ROS production, calcium nodule, calcium deposition and Runx2 protein expression were lower in Calciifcation+catalase group than those in Calciifcation group and Calciifcation+H2O2 group, but still higher than that in Control group. The protein expression of Runx2 was similar between Calciifcation+catalase group and Control group, P>0.05.
Conclusion: CaCl2 andβ-GP treatment may induce VSMC calciifcation via activating ROS-Runx2 signal pathway in experimental rats.