Background: Glucagon-like peptide-1 and its receptor agonist-exendin-4 (Ex-4) have been shown to provide beneficial effects for cardiovascular diseases. This study investigated the effects of Ex-4 on ischemia-induced ventricular arrhythmias in rats.
Objective :—This study is to explore the effect of valsartan-eluting stents on neointima formation after stenting and to elucidate possible mechanisms how locally used valsartan prevents in-stent restenosis (ISR). METHOD: valsartan- and carriereluting stents were manufactured by using multi-layer-coated technology. Bare stents, carrier-eluting stents and valsartan– eluting stents were implanted into the abdominal aortas of the rabbits respectively. Quantitative angiography (QA) before, immediately after and 3 months after stent implantation were compared between the groups of bare (n=8), carrier-eluting (n=8) and valsartan-eluting stent (n=10), which allows the comparison of vascular diameters of aortas as well as indices of vascular neointimal formation, i.e. luminal area (LA), neointimal area (NIA), inner elastic membrane luminal area (IELA) and the maximal inner-membrane thickness (MIT) in 15 rabbits. α-Actin protein expression were detected by Envision two-step immunohistochemistry. Mean positive indices (MPI) of the above protein were analyzed semi-quantatively by IMS(Information Management System) cell image analysis system. MPI=positive area×OD (optical density). Collagen deposition in neointima was observed through MASSON stain among the three groups.Result:—the mean aortic diameters were similar in the three groups:bare stents group(n=8), carrier-eluting stents group(n=8) and valsartan eluting stents group(n=10) measured by QA at different time. A larger luminal area and a less neointimal hyperplasia in valsartan eluting-stents group was found compared with the other two groups. The mean luminal areas were 4345548±125822um2; 4302061±167952 um2; 5016269±207934um2 respectively. The mean neointimal areas were 1119635±163503um2; 1135636±136555um2; 441577±74099um2 and the mean maximal inner-membrane thickness were 210±30um;192±21um; 116±12um respectively. α-Actin protein expression was significantly lower in neointima of valsartan eluting-stents group than the other two groups. Through MASSON stain we found that Collagen was much richer in neointima of bare stents group and carrier-eluting stents group than valsartan eluting-stents group.Conclusion:—Valsartan eluting-stents inhibited neointimal hyperplasia after stenting by decreasing collagen deposition and smooth muscle cell proliferation. Therefore it would be potentially effective in preventing in-stent restenosis.Abbreviations:—Quantitative angiography (QA), luminal area (LA), neointimal area (NIA), inner elastic membrane luminal area (IELA), the maximal inner-membrane thickness (MIT), Mean positive indices (MPI), optical density (OD), Drugeluting stents (DES), in-stent restenosis(ISR), percutaneous transluminal coronary angioplasty (PTCA), angiotensin α type 2 receptor (AT2).
OBJECTIVE: To investigate the clinical efficacy and safety of low-energy direct current defibrillation combined with intravenous application of β-receptor blocker in the treatment of ventricular tachycardia storm (VTS). METHODS: A total of 59 patients with VTS were randomly divided into two groups. In the control group (n = 31), intravenous administration of Lidocaine or Amiodarone and routine electrical defibrillation were performed. In the esmolol group (n = 28), intravenous administration of esmolol and low-energy electrical defibrillation were performed in addition to the same drug treatment as the control group.RESULTS: The success rate of terminating recurrent ventricular tachycardia or ventricular fibrillation was significantly higher in the esmolol group than in the control group (89.71% vs. 39.89%, P < 0.05). The necessary discharge times and average discharge energy to terminate ventricular tachycardia or ventricular fibrillation were significantly decreased in the esmolol group compared with control (5.69 ± 1.34 times vs. 8.63 ± 3.79 times, 95.32 ± 13.21J vs. 185.39 ± 25.63J, both P < 0.05). There was no significant difference in the incidence of hypotension (45.16% vs. 39.29%), sinus bradycardia (3.23% vs. 3.57%), and junctional/ventricular escape (38.71% vs. 39.29%) between the esmolol and control groups (all P > 0.05). The mortality was significantly lower in the esmolol group than in the control group (21.43%, 6/28 vs. 77.42%, 24/31, P < 0.01).CONCLUSION: Compared with conventional treatment, intravenous administration of a β-receptor blocker combined with low-energy electrical defibrillation could be a safe and effective therapy to treat VTS.
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