BACKGROUND:Latest researches suggest that delayed endothelial repair in drug-eluting stents may cause thrombosis and coronary occlusion.Therefore,a novel kind of drug stent,which is characterized by satisfactory anti-proliferative action as well as inhibitive effects on thrombosis,needs to be developed.OBJECTIVE:To summarize the recent research progress and clinical applications of drug-eluting stents (DES) and to seek the direction of new developments.RETRIEVE STRATEGY:The retrieve staffs were the research personnel for this paper.A computer-based online search was conducted in PUBMED for English language publications containing the key words of "drug eluting stents,percutaneous coronary intervention,coronary disease" from January 2002 to April 2007.Relevant data were also searched in international conference reports on the Internet between January 2005 and June 2007.The number of total retrieved Iiteratures was 15.Inclusion criteria:①reports about drug stents;②reports on research progress in the field of drug stents;③reports on the clinical application of drug stents.Exclusion criteria:low relevance and duplicated articles.LITERATURE EVALUATION:There were 264 articles about research and clinical applications of DES.Of those,42 literatures and 5 conference reports with high relevance and timeliness were included in this report.DATA SYNTHESIS:An ideal DES is comprised of a platform,a drug carrier vehicle and a pharmaceutical compound in harmony with each other.Given the ongoing development of DES materials and drugs,more effective DESs are introduced in the clinical practice.Recently,clinical data on DES encourage the interventional cardiologist to use DES in more challenging coronary lesions,such as chronic total occlusions,complex lesions and multivessel lesions.However,concern that DES may be associated with a risk of late thrombotic events arose,suggesting an imbalance between safety and efficacy of DES.Therefore,novel strategies including bioabsorbable stents,and stents coated with pro-healing agents are promising.CONCLUSION:The development of DES is a breakthrough in interventional cardiology that bring great benefit to patients with coronary disease,especially for restenosis and revascularization.Nevertheless,more endeavour will be necessary to create DES with high efficacy as well as low risk.

Soluble ST2 ( sST2 ) is protein of interleukin-1 ( IL-1 ) receptor family present in the blood which have been identified has the ability to capture IL-33, thereby inhibiting IL-33/ST2 signaling, the mechanical properties overload of myocardial cells was significantly increased .Thus, when at the onset of heart failure or chronic heart failure deteriorated , or at scarring resulted by myocardial infarction , soluble ST2 can be detected in the blood .The purpose of this review is to discuss the role of soluble ST 2 ( sST2) as a new cardiovascular marker.

First of all,all tutors as well as postgraduates should have concept of innovation.Secondly,favorable environment should be built up for innovative thoughts.Finally,tutors should try their best to cultivate students'innovative thoughts and direct their creationary practice.

Stem cell therapy for myocardial repair after myocardial infarction is a new and promising treatment modality.But the mechanism is still not very clear.Currently,stem cells are used in clinical study to evaluate its beneficial effect on repairing infarcted/hibernating myocardium after myocardial infarction and heart failure.But there is no final conclusion on the safety of stem cell transplantation.

Aortic Valve Insufficiency ; therapy ; Heart Valve Prosthesis ; Heart Valve Prosthesis Implantation ; Humans ; Transcatheter Aortic Valve Replacement

Objective:To study the effect and clinical significance of tumor necrosis factor-?(TNF-?) in viral myocarditis(VMC).Methods:Animal model was established by serum TNF-? in VMC mice was assayed by the way of ELISA.In addition,VMC mice were treated by TNF-? mAb and rTNF-?,death rate andmyocardial change of intervention group were compared with control group.Results:Serum TNF-? in VMC mice increased apparently.Inflammatory cell infiltration and myocardial necrosis had ralations with TNF-? in VMC.Inflammatory cell infiltration and myocardial necrosis in the mice of exogenous TNF-? intervention group were more serious than simple VMC group apparently,death rate of mice was also higher than simple VMC group.Inflammatory cell infiltration and myocardial necrosis in the mice of TNF-? mAb intervention group were milder than simple VMC group apparently,death rate of mice was also lower.Conclusion:TNF-? take part in the immunoreaction and pathogenesis of VMC,it has important significance to the therapy of VMC.

Objective To study ultrastructure changes of myocardium and morphic change of cardiomyocyte apoptosis in mice with viral myocarditis(VMC).Methods Our experiment established animal model of VMC by the way of coxsackie virus B3(CVB3) inoculation,then we studied the changes and apoptosis of cardiomyocyte by ways of microscope and electron microscope.Results The myocardial changes and inflammatory cell infiltration were found by ways of microscope and electron microscope from 5 days after virus inoculation in experimental mice,the peak changes were at 7-9 days,and were almost recoverd at 35 days.Apoptotic changes and apoptotic bodies were found by eletron microscope at 7-9 days after virus inoculation in mice with VMC.Conclusions VMC can be caused in mice after CVB3 inoculation,abnormal cardiomyocyte apoptosis can be found in VMC.

50 as group B.All patients were examined by CAG.Plaque morphology was assessed by IVUS in 14 of group A and 38 of group B before intervention.Plaque external elastic membrane,minimal lumen area,plaque area,plaque burden,lipid pool area,thickness of fibrous cap and rupture were measured by IVUS.Results Heavy smoking,excess drinking and positive family history were more frequent in group A than those in group B,while hypertension and diabetes mellitus were more common in group B.The percentage multi-vessel lesions and collateral circulation were higher in group B.IVUS results showed that vulnerable and ruptured lesions were found in most of two groups.The severity of plaque burden is milder in group A.However,they had a bigger lipid core and a thinner fibrous cap.Group B showed a more severe stenosis and bigger plaque area.Conclusion Plaque vulnerability and rupture are the most common cause substrate of AMI.There are different risk factors and different coronary artery characteristics in AMI with different ages,which suggests that different emphases should be taken in preventing AMI in patients with different ages.

10 mm) treated by CBA or BA were retrospectively analyzed. CBA was used in 74 patients and BA in 43 patients. Results Initial success (residual restenosis ≤30% with no major complications) was achieved in 99% of cases in CBA group and 100% in cases of BA group. Follow-up angiography was performed in all patients at (5.8?1.6) months. The diameter stenosis percent after CBA was lower and the instant gain after CBA was larger than that after BA (11.81%?9.17% versus 26.33%?10.04% and 1.96?0.51 mm versus 1.51? 0.54 mm, respectively; P

Objective To investigate the effects of emodin on the migration and proliferation of vascular smooth muscle cell (VSMC) and the metabolism of emodin in VSMC. Methods The effects of emodin on the migration or proliferation of vascular smooth muscle cell were measured by “transwell" migration system and MTT assay. Results The migration of VSMC could be significantly inhibited by emodin and the inhibitory ratio was 83.8% in 5 ?g/mL emodin group. The antiproliferative effect of emodin was in a dose- and time- dependent manner. However, the supernatant concentration of emodin insignificantly dereased after culture for 24 h. The cytotoxicity of emodin and cellular ROS was not influenced by CYP inducer or inhibitor. The mRNA expression of emodin's primary metabolic enzyme (cytochrome p450 oxidase, CYP) up-regulated insignificantly after treatment of emodin for 24 h. Conclusion Emodin can inhibit the migration and proliferation of VSMC and can not be metabolized by VSMC. Emodin may be a choice for the medication of drug-eluting stent.