Background : The role of Helicobacter pylori (H. pylori) in the pathogenesis of coronary artery disease (CAD) is still controversial, and the relation between current H. pylori infection and CAD has not been fully examined. This study evaluated the relation between H. pylori infection as confirmed by gastroduodenoscopic biopsy and CAD.Methods : We determined the presence of H. pylori infections, via gastroduodenoscopy, in 88 patients of the normal coronary angiographic group and also in 175 patients of the CAD group, and the latter patients had more than 50% coronary stenosis angiographically demonstrated. We excluded those patients with a history of previous H. pylori eradication and/or malignancy. A small piece of tissue from the antrum, which was obtained by gastroduodenoscopic biopsy, was stained by Warthin-starry silver stain. We defined a negative staining result that there was no stained tissue in the sample and the stained tissue was also positive for H. pylori infection.Results : There was no significant difference, except for gender, age, smoking and high density lipoprotein cholesterol (HDL-c), of the demographic and laboratory characteristics between the groups. Twenty seven (30.7%) patients of the normal control group and 71 (40.6%) patients of the CAD group were positive of H. pylori infection, yet there was no statistical difference. We angiographically followed up the 80 patients of the CAD group who were treated by percutaneous coronary intervention (PCI) at 6 to 9 months after their primary intervention. Twenty two (37.9%) of the 58 patients of the H. pylori negative group and 10 (45.5%) of the 22 patients of the H. pylori positive group were treated with reintervention, but reintervention was also not significantly different between the group with H. pylori infection and the group without the infection.Conclusions : These data indicated that H. pylori infection had a modest influence on CAD and progressive atheroma, but the showed a tendency to increase. Further studies are needed to evaluate the relationship between H. pylori infection and CAD.

RVA pacing is superior to RVS and RVOT pacing with regard to intraventricular synchrony in normal systolic functioning subjects with normal QRS. Cardiac output at RVA pacing is not inferior to other sites.

The aim of this study was to examine the anti-proliferative and anti-inflammatory effects of ezetimibe/simvastatin (E/S) after drug-eluting stent (DES) implantation in a porcine coronary restenosis model. Pigs were randomized into two groups in which the coronary arteries (23 pigs) had DES. Stents were deployed with oversizing (stent/artery ratio 1.3:1) in porcine coronary arteries. Fifteen pigs were taken 10/20 mg of E/S and eight pigs were not taken E/S. Histopathologic analysis was assessed at 28 days after stenting. In neointima, most inflammatory cells were lymphohistiocytes. Lymphohistiocyte count was not different between two groups (337±227 vs. 443±366 cells, P=0.292), but neointima area was significantly smaller (1.00±0.49 mm2 vs. 1.69±0.98 mm2, P=0.021) and percent area stenosis was significantly lower (23.3±10% vs. 39±19%, P=0.007) in E/S group compared with control group. There were no significant differences in fibrin score (1.99±0.79 vs. 1.81±0.88, P=0.49), endothelial score (1.75±0.66 vs. 1.80±0.59, P=0.79), and the percent of endothelium covered lumen (43±21% vs. 45±21%, P=0.84) between E/S group and control group. Combined therapy with ezetimibe and simvastatin inhibits neointimal hyperplasia, but does not inhibit inflammatory infiltration and arterial healing after DES implantation in a porcine coronary restenosis model.

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Coronary stent fractures have been suggested as a potential new mechanism of restenosis. The mechanical properties of stents were designed not only to prevent vessel recoil, but also to resist the mechanical stress of vessel movement over millions of cardiac cycles. We present a case in which mechanical stress may have contributed to the fracture of a stent implanted in a saphenous vein graft (SVG) to the left coronary artery. The patient was admitted due to chest pain 2 years after receiving a coronary artery bypass graft. A coronary angiography revealed the culprit vessel to be the SVG to the left coronary artery. The graft was stenosed and was stented with a sirolimus-eluting stent. A 6-month follow-up coronary angiography revealed 80% in-stent restenosis with stent fracture. We re-intervened by balloon angioplasty. This is the first report of sirolimus-eluting stent fracture combined with restenosis of SVG in Korea.