Flowchart of Study Selection.

<p>Flowchart of Study Selection.</p

Does Enhanced External Counterpulsation (EECP) Significantly Affect Myocardial Perfusion?: A Systematic Review & Meta-Analysis

<div><p>Background</p><p>Enhanced external counterpulsation (EECP) is currently applied for treating coronary artery disease (CAD) patients. However, the mechanism(s) by which EECP ameliorates angina pectoris and long-term left ventricular function remain largely unknown. The aim of this study will be to assess whether EECP significantly affects myocardial perfusion in CAD patients through a systematic review and meta-analysis of the available literature.</p><p>Methods</p><p>MEDLINE, EMBASE, and Cochrane CENTRAL databases were searched for prospective studies on CAD patients that underwent EECP and reported myocardial perfusion data pre- and post-EECP. The impact of EECP was assessed based on the weighted mean difference (WMD) in myocardial perfusion from pre-EECP to post-EECP. Statistical heterogeneity was assessed by the I² index. Publication bias was assessed through visual inspection of the funnel plot as well as Begg’s and Egger’s testing.</p><p>Results</p><p>Standard EECP therapy (i.e., 35–36 one-hour sessions within a seven-week period) significantly increased myocardial perfusion in CAD patients (pooled WMD: -0.19, 95% CI: -0.38 to 0.00, <i>p</i> = 0.049). A random effects analysis was applied on account of significant heterogeneity (I² = 89.1%, <i>p</i> = 0.000). There was no evidence of significant publication bias (Begg’s <i>p</i> = 0.091; Egger’s <i>p</i> = 0.282).</p><p>Conclusions</p><p>Standard EECP therapy significantly increases myocardial perfusion in CAD patients. This study’s findings support the continued use of standard EECP therapy in CAD patients and provides one putative physiological mechanism to help explain the improvements in angina pectoris and long-term left ventricular function observed in CAD patients after EECP therapy.</p></div

Forest Plot of Weighted Mean Differences in Myocardial Perfusion Pre- and Post-EECP.

<p>Forest Plot of Weighted Mean Differences in Myocardial Perfusion Pre- and Post-EECP.</p

Putative Physiological Mechanisms underlying EECP’s Effects on Myocardial Perfusion.

<p>EECP produces a diastolic retrograde aortic flow that enhances coronary artery mean pressure and peak diastolic pressure. This retrograde aortic flow acts to improve coronary vasodilation and angiogenesis through three putative mechanisms. First, through its pressure wave, EECP directly vasodilates existent vessels in the myocardium. Second, EECP increases de novo collateral vessel formation through promoting the release of angiogenic and vasoactive factors such as α-actin, von Willebrand factor (vWF), vascular endothelial growth factor (VEGF), basic fibroblast growth factor (BFGF), and hepatocyte growth factor (HGF). Third, EECP increases shear stress in the vasculature, a process which promotes the release of the angiogenic vasodilator nitric oxide (NO).</p

Newcastle-Ottawa Scale Quality Assessment of Included Studies.

<p>Newcastle-Ottawa Scale Quality Assessment of Included Studies.</p

Funnel Plot of Included Studies.

<p>Funnel Plot of Included Studies.</p

Additional file 1: of Effectiveness and safety of glucosamine and chondroitin for the treatment of osteoarthritis: a meta-analysis of randomized controlled trials

Table S1. The results of sensitivity analysis. Figure S1. Summary of study search and selection. RCT randomized controlled trail. Figure S2. Plots of bias risk. Figure S3. Funnel plot of effect size. (DOCX 4698 kb