Tumor Necrosis Factor-α Gene Polymorphism (G-308A) and Dilated Cardiomyopathy.

The issue that genetic polymorphism of tumor necrosis factor-α (TNF-α) is associated with dilated cardiomyopathy (DCM) is debatable. We sought to investigate the potential role of TNF-α gene polymorphism (G-308A) in the susceptibility to dilated cardiomyopathy.We retrieved PubMed, EMBASE, and CNKI to collect all articles which reported on the association between TNF-α G-308A polymorphism and dilated cardiomyopathy. Two authors used the Newcastle-Ottawa Scale (NOS) checklist to assess the quality of the included studies. The odds ratio (OR) with 95% confidence intervals (CI) were pooled in a specific genetic model to assess the association and Stata version 14.0 software was used.A total of 9 studies with 1338 patients and 1677 controls were included in this study. The results from this meta-analysis indicated that TNF-α G-308A polymorphism significantly increased the risk of dilated cardiomyopathy in heterozygous comparison (GA versus GG: OR = 1.87; 95%CI = 1.03-3.40; P < 0.05). The increased risk of DCM was also found in Asian populations using a dominant model and heterozygous comparison (GA+AA versus GG: OR = 2.00, 95%CI = 1.02-3.92, P < 0.05; GA versus GG: OR = 1.94, 95%CI = 1.23-3.06, P < 0.05).The current meta-analysis revealed that TNF-α gene polymorphism (G-308A) may be associated with the susceptibility to DCM.

Role of Endothelial Nitric Oxide Synthase Polymorphisms in Atrial Fibrillation: A PRISMA-Compliant Meta-Analysis.

BACKGROUND Research interest in endothelial nitric oxide synthase(eNOS) polymorphisms and atrial fibrillation (AF) has grown in last recent years, but the results of individual studies are inconsistent due to their small sample sizes. MATERIAL AND METHODS We searched databases for eligible studies on eNOS and AF, extracted the relevant data, and rigorously screened them according to inclusion and exclusion criteria. Then, we evaluated the study quality according to the Newcastle-Ottawa scale score, and we pooled the odds ratios (ORs) and 95% confidence intervals (CIs) by using a random-effects model or fixed-effects model based on inter-study heterogeneity. In addition, we performed subgroup analysis and sensitivity analysis and assessed publication bias. RESULTS According to the inclusion and exclusion criteria, we finally found 8 studies in this search. The recessive (OR=0.81; 95% CI=0.67 to 0.97; p=0.988; I²=0.0%) model showed that the eNOS 786T/C polymorphism was relevant to AF. We also found that the eNOS 786T/C polymorphism decreases the risk of AF, especially in white people (OR=0.81; 95% CI=0.67 to 0.97; P=0.023 for recessive model) and in the control population (OR=0.79; 95% CI=0.65 to 0.97; P=0.022 for recessive model). We found no obvious publication bias. CONCLUSIONS The eNOS gene loci 786T/C polymorphism is relevant to the risk of AF. Our results suggest that the 786T/C polymorphism significantly decreases AF risks in white people and control populations. Larger studies are required for further evaluation.

Diagnostic value of cadmium-zinc-telluride myocardial perfusion imaging versus coronary angiography in coronary artery disease: A PRISMA-compliant meta-analysis.

BACKGROUND: Rapid progress has been made in research of cadmium-zinc-telluride (CZT) technology in the last few years, which might serve as a new method to diagnose coronary artery disease. However, compared with coronary angiography, the diagnostic value of CZT is still controversial. We aimed to evaluate diagnosis value of coronary angiography versus CZT in coronary artery disease. METHODS: We searched the database for eligible researches associated with CZT- myocardial perfusion imaging (MPI) and invasive coronary angiography, extracted the relevant data, and rigorously screened it according to the inclusion and exclusion criteria. The accuracy indicators included sensitivity, specificity, accuracy, positive and negative likelihood ratios. RESULTS: According to the inclusion and exclusion criteria, we finally found 20 studies containing 2350 patients in this search. Pooled results showed that sensitivity of CZT-MPI was 0.84% and 95% confidence interval (95% CI): 0.78 to 0.89, specificity was 0.72, 95% CI (0.62-0.76), the specificity was lower apparently. The positive likelihood ratio was 3.0, 95% CI (2.4-3.8), the negative likelihood ratio was 0.22, 95% CI (0.16-0.31), diagnostic odds ratio was 14, 95% CI (7.84-17.42). CONCLUSION: This meta-analysis showed that CZT-MPI had satisfactory sensitivity and specificity for diagnosing coronary artery disease. Larger studies are required for further evaluation.

Role of SH2B3 R262W gene polymorphism and risk of coronary heart disease: A PRISMA-compliant meta-analysis.

BACKGROUND: More susceptibility genes have been proved to be associated with coronary heart disease (CHD). The goal of our study is to evaluate the association between the R262W polymorphism of SH2B3 gene and risk of CHD. METHODS: A systematic search was conducted using PubMed, Embase, Web of Science, CNKI, and WanFang databases up to March of 2018. The data of individual study were individually performed by 2 reviewers. The meta-analysis was performed by Stata software and expressed by the pooled odds ratio (OR) and the 95% confidence interval (CI), which were calculated by specific model according to heterogeneity. RESULTS: Our research was based on 12 studies involving 25,845 patients and 68,910 healthy controls. Significant association between the variant R262W and CHD were found in overall populations (OR = 1.12, 95%CI = 1.09-1.15, P = .389, I = 5.4%), but not found in Asian (OR = 1.05, 95%CI = 0.98-1.12, I = 0.0%) in subgroup analysis by ethnicity. In another subgroup analysis, when classified into CHD and myocardial infarction (MI), there was a significance association between R262W and CHD (OR = 1.11,95% CI = 1.07-1.15, I = 13.5%) and MI (OR = 1.13, 95%CI = 1.08-1.18, I = 0.0%). The Begg's funnel plot revealed no significant publication bias. CONCLUSIONS: The R262W polymorphism is associated with risk of CHD or MI in Europeans, but not in Asians.

Retraction Note: Cardiac structural remodeling in hypertensive cardiomyopathy.

The authors are retracting this article [1]. In their recent work the authors have found that the degree of fibrosis in the different walls of the left atrium in pigs with hypertensive cardiomyopathy is the same. Sirius Red staining (another method to test for fibrosis) showed that there was no difference between the different walls. The authors are unable to explain this inconsistency. All authors agree with this retraction.

In vitro and in vivo differentiation of induced pluripotent stem cells generated from urine-derived cells into cardiomyocytes.

Generation of human cardiomyocytes from cells derived from various sources, including skin biopsy, has been made possible by breakthrough advances in stem cell research. However, it is attractive to build up a negligibly invasive way to create induced pluripotent stem (iPS) cells. In this study, we created iPS cells from human urine-derived epithelial cells by gene transduction using lentiviral vectors in a totally noninvasive manner. Then, we induced the differentiation of iPS cells into functional cardiomyocytes both in vitro and in vivo Action potentials were recorded in putative cardiomyocytes and spontaneous beating cells were observed. Our results offered an alternative method to generate cardiomyocytes in a totally noninvasive manner from an easily accessible source. The availability of urine and its potent reprogramming characteristics will provide opportunities for the use of cells with specific genotypes to study the pathogenesis and molecular mechanisms of disease in vitro.

Association between KCNE1 G38S gene polymorphism and risk of atrial fibrillation: A PRISMA-compliant meta-analysis.

BACKGROUND: Previous case-control studies on association between KCNE1 G38S polymorphism and risk of atrial fibrillation (AF) have been published but because of the conflicting results and small sample size of individual studies, the consolidated result is still controversial. OBJECTIVES: The aim of this study was to explore the relationship between KCNE1 G38S polymorphism and risk of AF. METHODS: We performed a comprehensive literature search on PubMed, Embase, OVID, Web of Science, Wan Fang, and CNKI databases up to March 10, 2017 in English and Chinese languages. Two of the authors individually extracted study data and assessed the study quality using Newcastle-Ottawa scale. Odds ratios (ORs) and 95% confidence intervals (CIs) were combined in different genetic models for evaluation using a random-effect model or fixed-effect model according to interstudy heterogeneity. RESULTS: There were totally 14 independent case-control studies of 2810 patients and 3080 healthy controls included. Significant associations were found between KCNE1 G38S polymorphism and AF in overall population under all genetic models: allelic (OR: 1.34, 95% CI: 1.24-1.45, P < .001), homozygous (OR: 1.90, 95% CI: 1.61-2.24, P < .001), heterozygous (OR: 1.43, 95% CI: 1.21-1.68, P < .001), recessive (OR: 1.42, 95% CI: 1.20-1.69, P < .001), dominant genetic model (OR: 1.62, 95% CI: 1.39-1.89, P < .001). Subgroup analyses indicated similar association in Chinese and white. CONCLUSIONS: The G38S polymorphism in the KCNE1 gene can significantly increase the risk of AF in both Chinese and white.

Association between chemokine CXC ligand 12 gene polymorphism (rs1746048) and coronary heart disease: A MOOSE-compliant meta-analysis.

Recently a large number of investigations have implicated the association between the chemokine CXC ligand 12 gene polymorphism (rs1746048) and risk of coronary heart disease (CHD), but the results remain debatable. The aim of our study was to provide more compelling evidence for the relationship between rs1746048 and CHD risk. Studies eligible for this meta-analysis were identified through electronic search of PubMed, EMBASE, and CNKI. Two authors performed independent literature review and study quality assessment by using the Newcastle-Ottawa Scale checklist. The odds ratios (ORs) with 95% confidence intervals (CIs) were pooled in a specific genetic model to assess the association. The meta-analysis of 48,852 patients and 64,386 controls from 12 studies showed that patients with rs1746048 had 1.11 times of high risk in developing CHD (OR = 1.11; 95% CI = 1.09-1.14; P < .005; I = 35.8%). The increased risk of CHD was also found in both Asian (OR = 1.07; 95%CI = 1.02-1.12; P < .005; I = 40.6%) and Caucasian populations (OR = 1.14; 95% CI = 1.10-1.18; P < .005; I = 22.2%). The results of our meta-analysis suggested that chemokine CXC ligand 12 gene polymorphism (rs1746048) may be linked with susceptibility to CHD.

Cardiac structural remodeling in hypertensive cardiomyopathy.

Heart failure with preserved ejection fraction (HFpEF), which is a primary driver of morbidity and mortality, accounts for approximately half of all heart failure cases. Therefore, it is essential to develop preclinical animal models for HFpEF pharmacological treatment strategies. We created a porcine model of severe hypertension and hyperlipidemia by using a combination of deoxycorticosterone acetate (DOCA, 100 mg kg-1), Western diet (WD) and angiotensin II infusion. Systolic blood pressure, echocardiography and invasive pressure-volume loop were assessed at baseline, 12 weeks and 18 weeks. A detailed histological assessment was also performed to determine the cardiac structural remodeling. Compared with controls (n=10), hypertensive animals (n=10) showed markedly higher systolic blood pressure (181 vs. 86 mm Hg) at 18 weeks. Concentric remodeling, characterized by a normal chamber size with a thicker wall, was observed in hypertensive animals. Left ventricle diastolic function showed a tendency toward decline, according to the echocardiographic data. Hemodynamic data showed that the end-diastolic pressure-volume relationship was elevated without changes in the end-systolic pressure-volume relationship. Histological results revealed that the fibrotic area in hypertensive animals (P<0.05 vs. controls) and the fibrotic area in the posterior wall of hypertensive animals' left atria were larger than other sites of the left atria (P<0.05 vs. other sites). This model can mimic clinical HFpEF to some degree. We found that the posterior wall of the left atrium is more susceptible to atrial remodeling associated with hypertension compared with other regions of the left atrium.