Impact of atrial programmed electrical stimulation techniques on unipolar electrogram morphology.

INTRODUCTION: Intra-atrial conduction abnormalities are associated with the development of atrial fibrillation (AF) and cause morphological changes of the unipolar atrial electrogram (U-AEGM). This study examined the impact of different atrial programmed electrical stimulation (APES) protocols on U-AEGM morphology to identify the most optimal APES protocol provoking conduction abnormalities. METHODS: APES techniques (14 protocols) were applied in 30 patients referred for an electrophysiology study, consisting of fixed rate, extra, and decremental stimuli at different frequencies. U-AEGM morphologies including width, amplitude, and fractionation for patients without (control group) and with a history of AF (AF group) were examined during APES. In addition, sinus rhythm (SR) U-AEGMs preceding different APES protocols were compared to evaluate the morphology stability over time. RESULTS: U-AEGM morphologies during SR before the APES protocols were comparable (all P > .396). Atrial refractoriness was longer in the AF group compared to the control group (298 ± 48 vs 255 ± 33 ms; P ≤ .020), but did not differ between AF patients with and without amiodarone therapy (278 ± 48 vs 311 ± 40 ms; P ≥ .126). Compared to the initial SR morphology, U-AEGM width, amplitude, and fractionation changed significantly during the 14 different APES protocols, particularly in the AF group. In both groups, U-AEGM changes in morphology were most pronounced during fixed-rate stimulation with extra stimuli (8S1-S2 = 400-250 ms). CONCLUSION: APES results in significant changes in U-AEGM morphology, including width, amplitude, and fractionation. The impact of APES differed between APES sequence and between patients with and without AF. These findings suggest that APES could be useful to identify AF-related conduction abnormalities in the individual patient.

Effect of garlic on plasma lipoprotein(a) concentrations: A systematic review and meta-analysis of randomized controlled clinical trials.

OBJECTIVES: Garlic can play an essential role in the prevention of atherosclerosis, but the research addressing the effect of garlic on the concentration of lipoprotein(a) [Lp(a)] has not been fully demonstrated. The aim of this study was to assess the effect of garlic on plasma Lp(a) concentrations through systematic review of literature and meta-analysis of available randomized controlled trials. METHODS: The literature search included SCOPUS, PubMed-Medline, ISI Web of Science, and Google Scholar databases up to March 10, 2015 to identify randomized controlled trials investigating the effect of garlic on plasma Lp(a) concentrations. Two independent reviewers extracted data on study characteristics, methods, and outcomes. Overall, the effect of garlic on plasma Lp(a) levels was reported in six trials. RESULTS: Meta-analysis did not suggest a significant alteration in plasma Lp(a) levels after garlic consumption (weighted mean difference [WMD] = 16.86%; 95% confidence interval, -4.59 to 38.31; P = 0.124). This result was robust in the leave-one-out sensitivity analysis. When the studies were categorized according to the duration of supplementation, there was no effect in the subgroup of trials lasting ≤12 wk (WMD = 2.01%; 95% CI, -14.67 to 18.68; P = 0.813) but a significant elevation of plasma Lp(a) concentrations was found in trials lasting >12 wk (WMD = 54.59%; 95% CI, 30.47-78.71; P < 0.001). Random-effects meta-regression suggested an inverse association between the changes in plasma concentrations of Lp(a) and duration of supplementation (slope 1.71; 95% CI, 0.46-2.97; P = 0.007). CONCLUSIONS: The present meta-analysis did not suggest a significant effect of garlic supplementation on the reduction of Lp(a) levels.

Effects of flaxseed supplements on blood pressure: A systematic review and meta-analysis of controlled clinical trial.

BACKGROUND & AIMS: Many experimental and clinical trials suggested that flaxseed might be a potent antihypertensive, but the evidences concerning the effects of flaxseed supplements on blood pressure (BP) has not been fully conclusive. We aimed to assess the impact of the effects of flaxseed supplements on blood pressure through systematic review of literature and meta-analysis of available randomized controlled trials (RCTs). METHODS: The literature search included PUBMED, Cochrane Library, Scopus, and EMBASE up to February 2015 to identify RCTs investigating the effect of flaxseed supplements on plasma blood pressure. Effect size was expressed as weighed mean difference (WMD) and 95% confidence interval (CI). RESULTS: 15 trials (comprising 19 treatment arms) with 1302 participants were included in this meta-analysis. Random-effects meta-analysis suggested significant reductions in both systolic BP (SBP) (WMD: -2.85 mmHg, 95%CI: -5.37 to -0.33, p = 0.027) and diastolic BP (DBP) (WMD: -2.39 mmHg, 95%CI: -3.78 to -0.99, p = 0.001) following supplementation with flaxseed products. When the studies were stratified according to their duration, there was a greater effect on both SBP and DBP in the subset of trials with ≥12 weeks of duration (WMD: -3.10 mmHg, 95%CI: -6.46 to 0.27, p = 0.072 and -2.62 mmHg, 95%CI: -4.39 to -0.86, p = 0.003, respectively) vs the subset lasting <12 weeks (WMD: -1.60 mmHg, 95%CI: -5.44 to 2.24, p = 0.413, and -1.74 mmHg, 95%CI: -4.41 to 0.93, p = 0.202, respectively). Another subgroup analysis was performed to assess the impact of flaxseed supplement type on BP. Reduction of SBP was significant with flaxseed powder (WMD: -1.81 mmHg, 95% CI: -2.03 to -1.59, p < 0.001) but not oil (WMD: -4.62 mmHg, 95%CI: -11.86 to 2.62, p = 0.211) and lignan extract (WMD: 0.28 mmHg, 95% CI: -3.49 to 4.04, p = 0.885). However, DBP was significantly reduced with powder and oil preparations (WMD: -1.28 mmHg, 95% CI: -2.44 to -0.11, p = 0.031, and -4.10 mmHg, 95%CI: -6.81 to -1.39, p = 0.003, respectively), but not with lignan extract (WMD: -1.78 mmHg, 95% CI: -4.28 to 0.72, p = 0.162). CONCLUSIONS: This meta-analysis of RCTs showed significant reductions in both SBP and DBP following supplementation with various flaxseed products.

Effects of supplementation with green tea catechins on plasma C-reactive protein concentrations: A systematic review and meta-analysis of randomized controlled trials.

BACKGROUND: Promising experimental and clinical trials suggest that green tea decreases the inflammatory process in cardiometabolic diseases, but evidence from epidemiologic studies about the effects on plasma C-reactive protein (CRP) seems inconsistent and ambiguous. Therefore, the aim of this meta-analysis was to evaluate the effects of green tea supplementation on plasma CRP concentrations. METHODS: We searched selected database up to October 26, 2014 to identify randomized controlled trials (RCTs) investigating the effects of green tea supplementation on plasma CRP concentrations. Two independent reviewers extracted data on study characteristics, methods, and outcomes. RESULTS: Meta-analysis of data from 11 RCTs arms did not indicate a significant effect of supplementation with green tea catechins on plasma CRP concentrations (weighted mean difference [WMD], 0.085 mg/L; 95% confidence interval [CI], -0.225 to 0.395; P = 0.592). This effect size was robust in sensitivity analysis and omission of each individual study did not have a significant effect. The nonsignificant effects of green tea catechins on plasma CRP concentrations were also observed in subgroups of studies with green tea supplementation with a duration of <8 wk (WMD, 0.029 mg/L; 95% CI, -0.229 to 0.286; P = 0.828) and ≥8 wk (WMD, 0.099 mg/L; 95% CI, -0.555 to 0.754; P = 0.766). Likewise, there was no significant effect in subgroups of studies with total catechins doses <400 mg/d (WMD, 0.073 mg/L; 95% CI, -0.251 to 0.398; P = 0.658) and ≥400 mg/d (WMD, 0.213 mg/L; 95% CI, -0.148 to 0.574; P = 0.247). The effect sizes were not significant after stratification of studies to those recruiting healthy subjects (WMD, -0.028 mg/L; 95% CI, -0.216 to 0.160; P = 0.769), and those recruiting participants with cardiometabolic diseases (WMD, 0.260 mg/L; 95% CI, -0.815 to 1.334; P = 0.636). CONCLUSIONS: This meta-analysis of data from 11 RCT arms did not indicate a significant effect of supplementation with green tea catechins on plasma CRP concentrations. Furthermore, well-designed trials are necessary to validate these results.

Effect of sour tea (Hibiscus sabdariffa L.) on arterial hypertension: a systematic review and meta-analysis of randomized controlled trials.

BACKGROUND: Hibiscus sabdariffa L. is a tropical wild plant rich in organic acids, polyphenols, anthocyanins, polysaccharides, and volatile constituents that are beneficial for the cardiovascular system. Hibiscus sabdariffa beverages are commonly consumed to treat arterial hypertension, yet the evidence from randomized controlled trials (RCTs) has not been fully conclusive. Therefore, we aimed to assess the potential antihypertensive effects of H. sabdariffa through systematic review of literature and meta-analysis of available RCTs. METHODS: The search included PUBMED, Cochrane Library, Scopus, and EMBASE (up to July 2014) to identify RCTs investigating the efficacy of H. sabdariffa supplementation on SBP and DBP values. Two independent reviewers extracted data on the study characteristics, methods, and outcomes. Quantitative data synthesis and meta-regression were performed using a fixed-effect model, and sensitivity analysis using leave-one-out method. Five RCTs (comprising seven treatment arms) were selected for the meta-analysis. In total, 390 participants were randomized, of whom 225 were allocated to the H. sabdariffa supplementation group and 165 to the control group in the selected studies. RESULTS: Fixed-effect meta-regression indicated a significant effect of H. sabdariffa supplementation in lowering both SBP (weighed mean difference -7.58 mmHg, 95% confidence interval -9.69 to -5.46, P < 0.00001) and DBP (weighed mean difference -3.53 mmHg, 95% confidence interval -5.16 to -1.89, P < 0.0001). These effects were inversely associated with baseline BP values, and were robust in sensitivity analyses. CONCLUSION: This meta-analysis of RCTs showed a significant effect of H. sabdariffa in lowering both SBP and DBP. Further well designed trials are necessary to validate these results.

Effects of coenzyme Q10 on statin-induced myopathy: a meta-analysis of randomized controlled trials.

OBJECTIVE: To evaluate the efficacy of coenzyme Q10 (CoQ10) supplementation on statin-induced myopathy. PARTICIPANTS AND METHODS: We searched the MEDLINE, Cochrane Library, Scopus, and EMBASE databases (November 1, 1987, to May 1, 2014) to identify randomized controlled trials investigating the impact of CoQ10 on muscle pain and plasma creatine kinase (CK) activity as 2 measures of statin-induced myalgia. Two independent reviewers extracted data on study characteristics, methods, and outcomes. RESULTS: We included 6 studies with 302 patients receiving statin therapy: 5 studies with 226 participants evaluated the effect of CoQ10 supplementation on plasma CK activity, and 5 studies (4 used in the CK analysis and 1 other study) with 253 participants were included to assess the effect of CoQ10 supplementation on muscle pain. Compared with the control group, plasma CK activity was increased after CoQ10 supplementation, but this change was not significant (mean difference, 11.69 U/L [to convert to µkat/L, multiply by 0.0167]; 95% CI, -14.25 to 37.63 U/L; P=.38). Likewise, CoQ10 supplementation had no significant effect on muscle pain despite a trend toward a decrease (standardized mean difference, -0.53; 95% CI, -1.33 to 0.28; P=.20). No dose-effect association between changes in plasma CK activity (slope, -0.001; 95% CI, -0.004 to 0.001; P=.33) or in the indices of muscle pain (slope, 0.002; 95% CI, -0.005 to 0.010; P=.67) and administered doses of CoQ10 were observed. CONCLUSION: The results of this meta-analysis of available randomized controlled trials do not suggest any significant benefit of CoQ10 supplementation in improving statin-induced myopathy. Larger, well-designed trials are necessary to confirm the findings from this meta-analysis.