Comparative outcomes of heart failure among existent classes of anti-diabetic agents: a network meta-analysis of 171,253 participants from 91 randomized controlled trials.

Background: The cardiovascular (CV) safety in terms of heart failure among different classes of treatment remains largely unknown. We sought to assess the comparative effect of these agents on heart failure outcomes.

Methods: This study was registered in the International Prospective Register of Systematic Reviews (CRD 42016042063).

Comparative cardiovascular outcomes in the era of novel anti-diabetic agents: a comprehensive network meta-analysis of 166,371 participants from 170 randomized controlled trials.

Background: Cardiovascular (CV) safety of one anti-diabetic medication over another remains partially delineated. We sought to assess the comparative effect on CV outcomes among novel anti-diabetic agents.

Methods: This study was registered with the International Prospective Register of Systematic Reviews (CRD 42016042063).

Association between paced QRS duration and atrial fibrillation after permanent pacemaker implantation: A retrospective observational cohort study.

Right ventricular pacing often results in prolonged QRS duration (QRSd) as the result of right ventricular stimulation, and atrial fibrillation (AF) may result. The association of pacing-induced prolonged QRSd and AF in patients with permanent pacemakers is unknown.We selected 180 consecutive patients who underwent pacemaker implantation for complete/advanced atrioventricular block.

More favorable response to cardiac resynchronization therapy in women than in men.

Background: Data on sex difference in response to cardiac resynchronization therapy (CRT) remain controversial. We conducted a meta-analysis to summarize all published studies to determine whether sex-based differences in response to CRT exist.

Methods And Results: We performed a literature search using MEDLINE (source PubMed; January 1966 to March 2014) and EMBASE (January 1980 to March 2014) with no restrictions.

AVE0991, a Nonpeptide Compound, Attenuates Angiotensin II-Induced Vascular Smooth Muscle Cell Proliferation via Induction of Heme Oxygenase-1 and Downregulation of p-38 MAPK Phosphorylation.

The nonpeptide AVE0991 is an agonist of the angiotensin-(1-7) (Ang-(1-7)) Mas receptor and is expected to be a putative new drug for treatment of cardiovascular disease. However, the mechanisms involved in the antiproliferative effects of AVE0991 are not fully understood. We saw that the compound attenuated proliferation in an angiotensin II-induced rat vascular smooth muscle cells (VSMC) proliferation model.

Acute myocardial ischemia directly modulates the expression of brain natriuretic peptide at the transcriptional and translational levels via inflammatory cytokines.

Cardiomyocyte stretching has been reported to be a major trigger for brain natriuretic peptide (BNP) release; however, an increase in circulating BNP is observed in patients with acute myocardial ischemia in the absence of increased left ventricular wall stress or cardiomyocyte stretching. In the present study, to investigate the direct and independent effects of acute myocardial ischemia on BNP expression and its mechanism, we established an in vitro glucose-free ischemia and hypoxia injured model of cultured rat cardiomyotes and proved hypoxia upregulated expressions of interleukin-6(il-6) and BNP. Further treatment with il-6 elicited dose- and time-dependent increases in BNP mRNA and protein expression as well as an upregulation in transforming growth factor-β1 (TGF-β1)/Smad2 expression, which was partially suppressed by a neutralizing antibody.

Illness perception among Chinese patients with acute myocardial infarction.

Objective: To explore illness perception (IP) and its predictors among Chinese patients with myocardial infarction (MI).

Methods: The revised Illness Perception Questionnaire (IPQ-R) was used in the present study. A cross-sectional, descriptive design was employed.

[Angiotensin-(1-7) reduced postangioplasty vascular fibrosis in abdominal aorta of rabbits].

Objective: To explore the effects of Angiotensin (ANG)-(1-7) on postangioplasty fibrotic remodeling and the involvement of TGF-beta/Smad signaling pathway in this process.

Methods: Thirty two healthy New Zealand white rabbits were randomly divided into 4 groups: sham group, control group, ANG-(1-7) group and ANG-(1-7) + A-779 group. Rabbits underwent angioplasty in the abdominal aorta or sham surgery.

The nonpeptide AVE0991 attenuates myocardial hypertrophy as induced by angiotensin II through downregulation of transforming growth factor-beta1/Smad2 expression.

The nonpeptide AVE0991 is expected to be a putative new drug for cardiovascular diseases. However, the mechanisms for the cardioprotective actions of AVE0991 are still not fully understood. We planned to determine whether AVE0991 attenuates the angiotensin II (AngII)-induced myocardial hypertrophy and whether these AVE0991 effects involved transforming growth factor beta1 (TGF-beta1) and Smad2.

B-type natriuretic peptide attenuates cardiac hypertrophy via the transforming growth factor-ß1/smad7 pathway in vivo and in vitro.

1. Previously, we showed that long-term treatment of rats after myocardial infarction (MI) with B-type natriuretic peptide (BNP) prevented ventricular remodelling. However, it is unclear whether long-term BNP treatment affects cardiac hypertrophy and, if so, its mechanism of action.

Chronic angiotensin-(1-7) administration improves vascular remodeling after angioplasty through the regulation of the TGF-beta/Smad signaling pathway in rabbits.

Objective: Angiotensin-(1-7) [ANG-(1-7)] has been reported to attenuate neointimal formation after vascular injury and stent implantation in rats, but the mechanism remains mostly unresolved. Interestingly, the levels of circulating transforming growth factor-beta1 (TGF-beta1) after myocardial infarction were suppressed by ANG-(1-7), which suggests a possible downstream target for the anti-remodeling action of ANG-(1-7). Our study focused on the effects of ANG-(1-7) on vascular remodeling, including neointimal formation and collagen synthesis, and determining whether or not these effects were dependent upon the TGF-beta signaling pathway.

[Side effects of non-steroidal anti-inflammatory drugs on gastric mucosa and preventive effects of teprenone].

Objective: To evaluate the side effects of non-steroidal anti-inflammatory drugs (NSAID) on gastric mucosa, and to study the preventive effects of teprenone in patients.

Methods: 108 patients taking NSAID for more than 3 months with no infection of helicobacter pylori (Hp) were collected. All patients were screened by endoscopy and their upper gastrointestinal symptoms were evaluated.

Epigallocatechin-3-gallate attenuates cardiac hypertrophy in hypertensive rats in part by modulation of mitogen-activated protein kinase signals.

1. It has been demonstrated that epigallocatechin-3-gallate (EGCG) inhibits cardiac hypertrophy through its antihypertensive and anti-oxidant effects. However, the underlying molecular mechanism is not clear.

[Effects of rhBNP on left ventricular remodeling in rats with acute myocardial infarction].

Objective: To assess the effects of rhBNP on left ventricular (LV) remodeling in rats with acute myocardial infarction (AMI).

Methods: AMI was induced by ligating coronary artery in male Sprague Dawley rats. Two days after surgery, AMI rats received intravenous infusion of rhBNP (15 microg/kg or 5 microg/kg once daily, n = 15 each) or saline (placebo control, n = 15) through Jugular Vein.

[Effect of chronic enhanced external counterpulastion on gene expression profiles of arterial endothelial cells of pigs fed with high-cholesterol diet].

Objective: To investigate the effect of chronic enhanced external counterpulastion (EECP) on gene expression profiles of arterial endothelial cells (ECs) of pigs fed with high-cholesterol diet.

Methods: Eight male pigs were fed with high-cholesterol diet for 12 weeks to induce arteriosclerosis and subjected to EECP for accumulative 36 h (2 h every other day for 18 sessions). Another 8 pigs on cholesterol-enriched diet and 6 normally fed pigs served as the arteriosclerosis model group and normal control group, respectively, and the high-cholesterol diet was maintained until the end of EECP treatment.

[An experimental study of expression of angiotension converting enzyme 2 in myocardium and effect of telmisartan treatment in pressure-overloaded rats].

Objective: To study the effect of hypertension and telmisartan treatment on the protein and gene expression of cardiac angiotensin-converting enzyme 2 (ACE2) in pressure-overloaded rats.

Methods: Coarctation of suprarenal abdominal aorta was reproduced in 8 week-old male Sprague-Dawley (SD) rats and then randomized into 4 groups, including a sham group (n=15), a suprarenal aortic coarctation group (model group, n=12), a suprarenal aortic coarctation with low-dose Telmisartan treatment group (low-dose group, 2 mgxkg(-1)xd(-1), n=11) and a suprarenal aortic coarctation with high-dose Telmisartan treatment group(high-dose group, 10 mgxkg(-1)xd(-1), n=13). Telmisartan or equivalent amount of normal saline was gavaged 24 hours before the operation and once every day afterwards for 3 weeks.

[Ischemic postconditioning attenuates ischemia/reperfusion injury in isolated hypertrophied rat heart].

Objective: To explore the effects of ischemic postconditioning on ischemia/reperfusion injury in isolated hypertrophied rat heart and investigate the signal transduction pathway changes induced by ischemia postconditioning.

Methods: Cardiac hypertrophy was induced in rats by abdominal aortic banding, and isolated hypertrophied rat heart ischemia/reperfusion model was made by Langendorff technique to evaluate the effects of ischemia postconditioning on left ventricular systole pressure, coronary artery flow, creatine phosphokinase (CPK) and lactate dehydrogenase (LDH) release, myocardial infarction size, and the level of myocardial phospho-protein kinase B/Akt (Ser473), phospho-glycogen synthase kinase-3beta (Ser9). Following groups were studied (n = 12 each group): IR, 30 min ischemia (I)/60 min Reperfusion (R); Post: 30 min ischemia, 6 circles of 10 s I/10 s R followed by 60 min R; Post Wort: 30 min ischemia, 6 circles of 10 s I/10 s R, wortmannin (10(-7) mol/L) followed by 60 min R; Wort: 30 min ischemia, wortmannin (10(-7) mol/L) followed by 60 min R.

[Study on up-regulation of the expression of angiotensin-converting enzyme-2 in human umbilical vein endothelial cells by telmisartan].

Objective: To investigate the effect of telmisartan on the protein and gene expression of angiotensin-converting enzyme-2 (ACE2) in human umbilical vein endothelial cells (HUVECs).

Methods: HUVECs were treated with various concentrations of telmisartan (10(-7), 10(-6) and 10(-5) mol/L) for 24 hours. In a time-control experiment, HUVECs were treated with telmisartan at the final concentration of 10(-6) mol/L for 6, 12 and 24 hours, respectively.

[Effects of enhanced external counterpulsation in atherosclerosis and NF-kappaB expression: a pig model with hypercholesterolemia].

Objective: To study the effects of enhanced external counterpulsation (EECP) on the vascular morphology, and endothelial function using experimentally induced hypercholesterolemic pigs.

Methods: Thirty five male pigs were randomly divided into three groups: 7 normal control animals, 11 hypercholesterolemic animals, and 17 hypercholesterolemic animals receiving EECP. Serum cholesterol was measured.

[Effects of ACE inhibitor on the calcium transient and calcium handling proteins in ventricular myocytes from rats with heart failure].

Objective: To investigate the influence of ACE inhibitor (perindopril) on the contractility and calcium transient and calcium handling proteins in ventricular myocytes from rats with experimental heart failure.

Methods: Male Wistar rats were randomized to heart failure group treated with perindopril (CHF-T, 3 mg.kg(-1).

[Angiotensin-(1-7) modulates fibrinolytic imbalance induced by oxidized low-density lipoprotein in cultured human umbilical vein endothelial cells].

Objective: To study the effect of angiotensin-(1-7)[Ang-(1-7)]on fibrinolytic imbalance induced by oxidized low- density lipoprotein (ox-LDL) in cultured human umbilical vein endothelial cells (HUVECs).

Method: Cultured HUVECs were incubated for 24 h in the presence of Ang-(1-7), ox-LDL and A-779 at different concentrations either separately or in combination. The final concentrations of Ang-(1-7) were 10, 100 and 1,000 nmol/L, and those of ox-LDL were 25, 50 and 100 mg protein/L.

Effect of angiotensin converting enzyme inhibitor on the calcium transients and calcium handling proteins in ventricular myocytes from rats with heart failure.

Background: Chronic heart failure (CHF) is associated with calcium transients and calcium handling proteins. Angiotensin converting enzyme (ACE) inhibitor has been demonstrated to have beneficial effect on CHF. Yet studies addressed to the relationship between ACE inhibitor and calcium transients in CHF are rare.

Chronic administration of angiotensin-(1-7) attenuates pressure-overload left ventricular hypertrophy and fibrosis in rats.

Objective: To test the hypothesis that chronic administration of angiotensin-(1-7) [Ang-(1-7)] attenuates cardiac hypertrophy in rats in vivo.

Methods: Coarctation of the suprarenal abdominal aorta was performed in 41 8-week-old male Sprague Dawley rats. Twenty-four hours after the operation, osmotic minipumps were surgically implanted subcutaneously in the rats, which were randomly divided into 3 groups, including a sham-operation group (n=15) receiving infusion with normal saline, a suprarenal aortic coarctation group (n=12), and a suprarenal aortic coarctation group (n=14) with Ang-(1-7) treatment at the dose of 25 mug x kg(-1) x h(-1).

[Effects of angiotensin-(1-7) on remodeling of myocardial collagen network in pressure-overloaded rats].

Objective: To investigate the effects of angiotensin-(1-7) on remodeling of myocardial collagen network in pressure-overloaded rats.

Methods: A rat model of pressure-overloaded heart was induced by constriction of abdominal aorta. Seventy-five male Sprague Dawley rats were randomized to sham-operated group, model control group and angiotensin-(1-7) group.