The Effects of Aerobic Exercise on N-terminal Pro-B-type Natriuretic Peptide and Cardiopulmonary Function in Patients With Heart Failure: A Meta-Analysis of Randomised Clinical Trials.

BACKGROUND: Aerobic exercise (AEx) improves outcomes in heart failure (HF). N-terminal pro B-type natriuretic peptide (NT-pro-BNP) is a prognosticator in HF. There are few data on the association of AEx, NT-pro-BNP, and cardiopulmonary function; hence, robust evidence is needed. The aim of this study was to measure the effects of AEx on NT-pro-BNP levels and cardiopulmonary function in HF. METHOD: Databases (Pubmed, EMBASE, Medline, Cochrane Central Registry, and Scopus) were systematically searched for randomised controlled trials (RCTs) that assessed the association of AEx with NT-pro-BNP and cardiopulmonary function (VE/VCO2 slope, peak VO2, maximal workload, and left ventricular ejection fraction [LVEF]) in HF. RevMan 5.3 (The Nordic Cochrane Centre, The Cochrane Collaboration, Copenhagen, 2014) was used to produce forest plots, and the random-effect model was applied with the effects measure of weighted mean differences (WMD) and 95% confidence interval (CI). RESULTS: Thirteen (13) RCTs recruited 1,503 patients and 1,494 controls. Aerobic exercise was significant in lowering NT-pro-BNP (pg/mL) compared with control group (WMD=-741.69, 95% CI -993.10 to -490.27 [p<0.00001; I2=63%]). VE/VCO2 slope was also significantly reduced (WMD=-3.57, 95% CI -6.48 to -0.67 [p=0.02; I2=97%]). Peak VO2 (mL/kg/min) significantly improved (WMD=3.68, 95% CI 2.39-4.96 [p<0.00001; I2=96%]). Maximal workload (watt) significantly increased following AEx (WMD=22.80, 95% CI 18.44-27.17 [p<0.00001; I2=78%]). Furthermore, there was a significant enhancement of LVEF (%) in the AEx group (WMD=2.42, 95% CI 0.64-4.19 [p=0.008; I2=71%]). CONCLUSIONS: Aerobic exercise improves the NT-pro-BNP, ventilatory efficiency, aerobic capacity, maximal workload, and the left ventricular function in patients with HF.

SCN5A gene mutations and the risk of ventricular fibrillation and syncope in Brugada syndrome patients: A meta-analysis.

Mutations in the gene encoding the main cardiac sodium channel (SCN5A) are the commonest genetic cause of Brugada syndrome (BrS). However, the effect of SCN5A mutations on the outcomes of ventricular fibrillation (VF) and syncope remains uncertain. To clarify this relationship, a meta-analysis was performed. A comprehensive search was conducted to identify all eligible studies from PubMed, MEDLINE, EBSCO, ProQuest, Science Direct, Clinical Key, and Cochrane database for cohort studies of BrS populations that had been systematically tested for SCN5A mutations. We did meta-analysis to see the relationship between SCN5A mutations and the occurrence of VF and/or syncope using RevMan 5.3. Five clinical studies met our criteria and included a total of 665 BrS patients. These studies included 45 patients with VF and 178 patients with syncope. We found that in BrS patients with SCN5A mutations the rate of VF event was 30.7% while in patients without mutations was 28.5% (Risk Ratio [RR] = 1.11, [95% CI: 0.61, 2.00], P = 0.73, I 2 = 0%). The occurrence of syncope events was 35.9% in patients with SCN5A mutations and 34.5% in patients without mutations (RR = 1.12, [95% CI: 0.87, 1.45], P = 0.37, I 2 = 39%). Furthermore, the occurrence of combined VF and syncope events were similar between the 2 groups (RR = 1.12, [95% CI: 0.89, 1.42], P = 0.34, I 2 = 11%). BrS patients with SCN5A mutations exhibit a similar risk of future occurence of VF and/or syncope as compared to those without SCN5A mutations.

Associations between four types of single-nucleotide polymorphisms in PLA2G7 gene and clinical atherosclerosis: a meta-analysis.

BACKGROUND: Previous studies suggested that some types of single nucleotide polymorphisms (SNPs) in PLA2G7 genes, encoding Lp-PLA2 have been reported to yield an antiatherogenic effect, but other studies mentioned otherwise. Thus, a comprehensive study to explore the effect of SNPs in PLA2G7 genes (V279F, A379V, R92H, I198T) toward clinical atherosclerosis is needed. METHODS: We searched eligible studies from PubMed, EBSCO, ProQuest, Science Direct, Springer, and Cochrane databases for case-control studies to assess the between four types of SNPs in PLA2G7 gene with risk of clinical atherosclerosis (CVD = cardiovascular disease, CAD = coronary artery disease, PAD = peripheral artery disease, ischemic stroke). All studies were assessed under Hardy-Weinberg Equilibrium, an additive model. This meta-analysis was performed by RevMan 5.3 to provide pooled estimate for odds ratio (ORs) with 95% confidence intervals (95% CIs). RESULTS: Fourteen clinical studies met our inclusion criteria. Those included 12,432 patients with clinical atherosclerosis and 10,171 were controls. We found that ORs of two variants SNPs (V279F, R92H) were associated with clinical atherosclerosis {V279F, OR = 0.88 (95% CI, 0.81-0.95); p = 0.0007, I2 = 40%}, {R92H, OR = 1.29 (95% CI, 1.09-1.53); p = 0.003, I2 = 73%}. Meanwhile, there was no significant associations between the other two, A379V {OR = 1.08 (95% CI, 0.93-1.26); p = 0.31, I2 = 78%} and I198T {OR = 1.12 (95% CI = 0.79-1.59); p = 0.53, I2 = 81%}. CONCLUSIONS: These results suggested that V279F polymorphism in PLA2G7 gene has a protective effect for clinical atherosclerosis, whereas R92H polymorphism might contribute toward increased risk of clinical atherosclerosis.