Pre post correlation comprehensive meta analysis

#Pre post correlation comprehensive meta analysis how to#

Statins may provide an effective response to reverse endothelial dysfunction via reduction of ADMA levels however, the available evidence is not conclusive. The interplay of inflammation, endothelial dysfunction and oxidative stress might play a crucial role in ADMA pathophysiology and reduction of ADMA levels might be a significant target for preventing endothelial dysfunction 13. The Hoorn Study showed that systemic inflammation was associated with decreased arginine and increased ADMA plasma levels resulting in an unfavorable NOS substrate-to-inhibitor ratio 12. However, the application of L-arginine/ADMA ratio is much limitted due to the fact that L-arginine varies much stronger that ADMA levels in the circulation and therefore the ratio need not reflect the intracellular situation 10. Moreover, in the Coronary Artery Risk Determination investigating the Influence of ADMA Concentration (CARDIAC) study, ADMA was shown to be a risk factor for CAD, independently of traditional predictors 10.ДЇormation of NO is regulated by both substrate availability (L-arginine) and the presence of the inhibitor (ADMA), which in turn may be represented by their ratio 11. Since then, it has been shown that higher ADMA levels are related to increased mortality and adverse clinical outcomes in patients with coronary artery disease (CAD), diabetes, renal disease and ischemic stroke 6, 7, 8, 9. The first study that showed that middle-aged smoking men in the highest quartile of ADMA levels were at an almost 4-fold risk for acute coronary events was conducted in 2001 5. ADMA is a pan-inhibitor of all 3 NO synthases (NOS) isoforms (potent noncompetitive inhibitor of neuronal NOS and week inhibitor of inducible and endothelial NOS) 3 and its plasma concentrations in the general population is 0.4вЂ“0.7вЂ‰ОјM 4. Endothelial dysfunction may be associated with increased circulating asymmetric dimethylarginine (ADMA) levels - an L-arginine analogue, which inhibits NO formation 2. In conclusion, this meta-analysis of available RCTs showed a significant reduction in plasma ADMA concentrations following therapy with hydrophilic statins.Д®ndothelial dysfunction is an early event in atherogenesis characterized by decreased availability of nitric oxide (NO), which diffuses towards the vascular smooth muscle tissues (VSMCs), triggers a rise of intracellular cyclic guanosine monophosphate (cGMP), leading to vasorelaxation 1. There was a significant reduction in plasma ADMA concentrations following statin therapy compared with placebo (WMD:вЂ‰в€’вЂ‰0.104вЂ‰ОјM, 95% confidence interval:вЂ‰в€’вЂ‰0.131 toвЂ‰в€’вЂ‰0.077, ZвЂ‰=вЂ‰в€’вЂ‰7.577, pвЂ‰<вЂ‰0.0001). In total, 1134 participants in 9 selected RCTs were randomized 568 were allocated to statin treatment and 566 were controls. A weighted meta-regression (WMD) using unrestricted maximum likelihood model was performed to assess the impact of statin dose, duration of statin therapy and baseline ADMA concentrations as potential variables on the WMD between statin and placebo group. We searched selected databases (up to August 2014) to identify randomized controlled trials (RCTs) that investigate the effect of statins on plasma ADMA concentrations. Therefore the aim of the meta-analysis was to assess the effect of statins on circulating ADMA levels.

#Pre post correlation comprehensive meta analysis how to#

But I'm not sure how to deal with that.The impact of statin therapy on plasma asymmetric dimethylarginine (ADMA) levels has not been conclusively studied. I also read the chapter in Borenstein et al. I read a few papers that adressed this problem but i didnt find a solution. I tried to use an averaged pre post correlation but also then as result some of these studies have a much higher weight than the independent ones. 08 and its weight is more than 20th times the most precise study with independent groups has. One study showed a pre post correlation of. If the pre- / postscore-correlation is relativ high (e.g.06) the weight of this study shoots up extremly.

To compute the weight for each study I used the inverse of that studyвЂ™s variance. (2009).ДЄs prescribed for studies that use pre post scores I used the correlation between pre- and post-scores to compute the standard deviation within groups and the variance of d. For both study types I computed hedges' g according to Borenstein et al. I'm working on a meta-analysis where i combine different designs: independent groups (treatment and control group) on the one hand and only dependent pre post without control group on the other.