Abstract
We aimed to assess the impact of L-carnitine on plasma Lp(a) concentrations through systematic review and meta-analysis of available RCTs. The literature search included selected databases up to 31st January 2015. Meta-analysis was performed using fixed-effects or random-effect model according to I2 statistic. Effect sizes were expressed as weighted mean difference (WMD) and 95% confidence interval (CI). The meta-analysis showed a significant reduction of Lp(a) levels following L-carnitine supplementation (WMD: −8.82 mg/dL, 95% CI: −10.09, −7.55, p < 0.001). When the studies were categorized according to the route of administration, a significant reduction in plasma Lp(a) concentration was observed with oral (WMD: −9.00 mg/dL, 95% CI: −10.29, −7.72, p < 0.001) but not intravenous L-carnitine (WMD: −2.91 mg/dL, 95% CI: −10.22, 4.41, p = 0.436). The results of the meta-regression analysis showed that the pooled estimate is independent of L-carnitine dose (slope: −0.30; 95% CI: −4.19, 3.59; p = 0.878) and duration of therapy (slope: 0.18; 95% CI: −0.22, 0.59; p = 0.374). In conclusion, the meta-analysis suggests a significant Lp(a) lowering by oral L-carnitine supplementation. Taking into account the limited number of available Lp(a)-targeted drugs, L-carnitine might be an effective alternative to effectively reduce Lp(a). Prospective outcome trials will be required to fully elucidate the clinical value and safety of oral L-carnitine supplementation.
Highlights
Modulated, and Precocious Coronary Artery Disease (PROCARDIS) study showed that two Lp(a) single nucleotide polymorphisms (SNPs) accounted for 36% of variation in Lp(a) levels[3]
Observational studies suggested that the enhanced CV risk associated with increased Lp(a) levels is no longer observed when low-density lipoprotein (LDL)-C levels are treated to aggressive levels, suggesting intensification of statin therapy and LDL-C lowering as a potential option in subjects with Lp(a) elevation[13,20]
The results suggested that the pooled estimate is independent of L-carnitine dose and duration of treatment (Fig. 6)
Summary
Modulated, and Precocious Coronary Artery Disease (PROCARDIS) study showed that two Lp(a) single nucleotide polymorphisms (SNPs) accounted for 36% of variation in Lp(a) levels[3]. Observational studies suggested that the enhanced CV risk associated with increased Lp(a) levels is no longer observed when LDL-C levels are treated to aggressive levels, suggesting intensification of statin therapy and LDL-C lowering as a potential option in subjects with Lp(a) elevation[13,20]. There are substantial alterations in the metabolism of L-carnitine depending upon whether it is provided as intravenous supplement, such as during hemodialysis, or as oral supplement[34] With the latter route of supplementation, gut microbes have been shown to significantly impact L-carnitine metabolism, and to convert it into alternative metabolites, linked to increased atherosclerosis risk[35,36]. We aimed to assess the impact of L-carnitine supplementation and type of administration on plasma Lp(a) concentrations through systematic review of literature and meta-analysis of available randomized controlled trials (RCTs)
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