Adjunctive balloon dilatation after stent deployment: beneficial or deleterious?

The practice of adjunctive balloon post-dilatation is not consistent among interventionalists, particularly in the setting of acute myocardial infarction (AMI). There have been some concerns about the risks of adjunctive balloon post-dilatation, particularly in the setting of acute coronary syndrome (ACS). This review will examine the data on the angiographic and clinical effects, and the risks of adjunctive balloon post-dilatation of stents in the treatment of coronary artery disease.     

Inhibitory effects of aspirin and indometacin on the growth of Helicobacter pylori in vitro

OBJECTIVE: The interactions between non‐steroidal anti‐inflammatory drugs and Helicobacter pylori have not been sufficiently documented to date. The aim of this study was to investigate the possible effects of aspirin and indometacin on the growth of H. pylori and to determine the effects of aspirin on the susceptibility of H. pylori to some antimicrobials. METHODS: Kinetic studies were performed by inoculating strains of H. pylori in brucella broth with different concentrations of aspirin and indometacin. Growth of bacteria in the broth was assessed spectrophotometrically and by viable colony counts after incubation for 24 and 48 h. Bacterial morphology was determined by Gram stain under light microscopy. The minimal inhibitory concentration (MIC) of aspirin and indometacin was determined by the standard agar dilution method. The MIC of amoxicillin, clarithromycin and metronidazole was measured in the presence and absence of aspirin by the E‐test method. RESULTS: Kinetic studies revealed that aspirin and indometacin inhibited the growth of H. pylori in a dose‐dependent manner. The bactericidal activity of these agents was expressed by cell lysis. Aspirin at 400 µg/mL produced an almost 2‐log decrease in the number of CFU/mL at 48 h. Similar inhibitory effects were obtained when 100 µg/mL indometacin was tested. The MIC at which 90% of H. pylori was inhibited was 512 µg/mL and 128 µg/mL for aspirin and indometacin, respectively. Increased susceptibility of H. pylori to amoxicillin, clarithromycin and metro­nidazole was found in the presence of aspirin. CONCLUSIONS: Aspirin and indometacin could significantly inhibit the growth of H. pylori when incubated in brucella broth in vitro. A subinhibitory concentration of aspirin enhanced the susceptibility of H. pylori to some antimicrobial agents.     

Pseudo-no-reflow phenomenon in ostial saphenous vein graft intervention using FilterWire EX protection

Distal protection using FilterWire EX has been shown to be effective in reducing the incidence of debris embolization and no-reflow phenomenon in saphenous vein graft (SVG) intervention. We present a case of mechanical obstruction of antegrade flow by atherothrombotic debris collected in the FilterWire EX after stent implantation of the ostial SVG lesion, masqueraded as no-reflow phenomenon. The condition was promptly reverted by thrombosuction using an Export Aspiration Catheter. A heavy debris burden was recovered by the thrombosuction and there was no evidence of myonecrosis after the procedure. We emphasize that different distal protection device can complement each other in special situations. A brief overview of the various approaches in preventing distal embolization in SVG intervention was also given.     

糖尿病大鼠骨代谢变化与立普妥、胰岛素的干预效应

目的:近年细胞培养实验发现他汀类药物可以促进骨形成,采用动物实验观察胰岛素和他汀类药物立普妥对糖尿病大鼠骨代谢的影响,为糖尿病伴骨质疏松的治疗提供实验依据。方法:实验于2005-08/2006-01在大连医科大学病理教研室完成。①实验分组:SD雄性大鼠55只,随机选择10只为空白对照组,余45只经鼠尾静脉注射链尿佐菌素造成糖尿病大鼠模型。其中40只符合造模标准,随机分为糖尿病未治疗组、胰岛素治疗组、立普妥治疗组及胰岛素 立普妥治疗组,每组10只。②实验方法:所有大鼠皆给予相同普通饮食。胰岛素治疗组及胰岛素 立普妥治疗组于实验第4天接受中效胰岛素治疗,6～8U/d分两次颈背部皮下注射。胰岛素剂量按每只鼠每周血糖进行调整。立普妥治疗组及胰岛素 立普妥治疗组于实验第4天给予立普妥1.25mg/kg灌胃。糖尿病未治疗组和空白对照组给予等量生理盐水灌胃。③实验评估:9周末用乙醚麻醉,每组取4只大鼠去眼球取血之后处死。14周末应用同样方法处死剩余大鼠。均取腰椎骨,常规脱钙石蜡包埋,行苏木精-伊红染色。骨组织形态计量学测量平均骨小梁厚度和平均骨小梁间距或弥散度。血中Ⅰ型胶原氨基端肽测定采用竞争性放射免疫检测方法(碘标记)。结果:实验期间大鼠死亡5只,其中糖尿病未治疗组1只于第3周死亡,胰岛素组2只于第6周死亡,胰岛素 立普妥治疗组2只于第7周死亡。①骨组织病理形态学变化:9周末立普妥治疗组、胰岛素 立普妥治疗组及糖尿病未治疗组光镜下见骨质疏松表现。14周末立普妥治疗组及胰岛素治疗组骨组织微观结构恢复至空白对照组水平。②平均骨小梁厚度:9周末:糖尿病未治疗组、胰岛素治疗组、立普妥治疗组及胰岛素 立普妥治疗组均明显低于空白对照组(P<0.01)。14周末:糖尿病未治疗组及胰岛素 立普妥治疗组均明显低于空白对照组(P<0.05)。③平均骨小梁间距或弥散度:9周末:糖尿病未治疗组及胰岛素 立普妥治疗组均明显高于空白对照组(P<0.05)。14周末:糖尿病未治疗组及胰岛素 立普妥治疗组均明显高于空白对照组(P<0.05)。④Ⅰ型胶原氨基端肽水平:9周末:立普妥治疗组和胰岛素 立普妥治疗组均明显高于空白对照组(P<0.01)。14周末:胰岛素治疗组、立普妥治疗组和胰岛素 立普妥治疗组均明显高于空白对照组(P<0.01)。结论:①糖尿病大鼠造模9周出现明显的骨质疏松。②糖尿病大鼠骨质变化表现为骨吸收超过骨形成作用,主要以骨吸收增强为主。③立普妥及胰岛素可以促进糖尿病大鼠骨质的形成,抑制糖尿病大鼠骨质疏松的发生发展。     

Platelet-endothelial cell adhesion molecule-1 gene polymorphism and its soluble level are associated with severe coronary artery stenosis in Chinese Singaporean

OBJECTIVES: Platelet-endothelial cell adhesion molecule-1 (PECAM-1) mediates the transendothelial migration of circulating leukocytes, a characteristic change in vascular inflammation leading to atherosclerotic plaque development. We hypothesized that genetic variation and soluble level of PECAM-1 could be associated with coronary artery disease (CAD). DESIGN AND METHODS: We analyzed two single nucleotide polymorphisms (SNPs) of PECAM-1 gene C+373G (Leu125Val) at exon 3, which encodes the first extracellular (Ig)-like domain that mediates the homophilic binding of PECAM-1, and G+1688A (Ser563Asn) at exon 8 in 144 angiographically documented (> or =70% stenosis) patients with CAD and 150 age- and sex-matched controls in the Chinese population in Singapore, using a polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) strategy. Level of plasma soluble PECAM-1 (sPECAM-1) was measured by ELISA. RESULTS: The Leu125Val polymorphism was associated with CAD (P < 0.01). Also, the level of sPECAM-1 is was found to be elevated in CAD patients (P = 0.005). Moreover, subjects with the homozygous GG genotype of the Leu125Val polymorphism had higher sPECAM-1 levels (P = 0.005). The level of sPECAM-1 was further correlated to soluble platelet selectin (sP-selectin, also measured by ELISA), platelet count, and total white blood cell count (WBC), suggesting that platelets are a major source of sPECAM-1 and platelet activation and inflammation may contribute to PECAM-1 elevations in CAD patients. CONCLUSION: The Leu125Val polymorphism of PECAM-1 and the level of sPECAM-1 are associated with CAD in Chinese in Singapore. The level of sPECAM-1 is also associated with platelet activation and inflammation and correlated to the Leu125Val polymorphism. Our data suggest that PECAM-1 plays an important role in the development of atherosclerosis.