Abstract
BackgroundRaised plasma lipoprotein(a) (Lp(a)) concentration is an independent and causal risk factor for atherosclerotic cardiovascular disease. Several types of pharmacological approaches are under evaluation for their potential to reduce plasma Lp(a) levels. There is suggestive evidence that statins and fibrates, two frequently employed lipid-lowering drugs, can lower plasma Lp(a). The present study aims to compare the efficacy of fibrates and statins in reducing plasma concentrations of Lp(a) using a meta-analysis of randomized head-to-head trials.MethodsMedline and Scopus databases were searched to identify randomized head-to-head comparative trials investigating the efficacy of fibrates versus statins in reducing plasma Lp(a) levels. Meta-analysis was performed using a random-effects model, with inverse variance weighted mean differences (WMDs) and 95% confidence intervals (CIs) as summary statistics. The impact of putative confounders on the estimated effect size was explored using random effects meta-regression.ResultsSixteen head-to-head comparative trials with a total of 1388 subjects met the eligibility criteria and were selected for this meta-analysis. Meta-analysis revealed a significantly greater effect of fibrates versus statins in reducing plasma Lp(a) concentrations (WMD, –2.70 mg/dL; 95% CI, –4.56 to –0.84; P = 0.004). Combination therapy with fibrates and statins had a significantly greater effect compared with statin monotherapy (WMD, –1.60 mg/dL; 95% CI, –2.93 to –0.26; P = 0.019) but not fibrate monotherapy (WMD, –1.76 mg/dL; 95% CI, –5.44 to +1.92; P = 0.349) in reducing plasma Lp(a) concentrations. The impact of fibrates versus statins in reducing plasma Lp(a) concentrations was not found to be significantly associated with treatment duration (P = 0.788).ConclusionsFibrates have a significantly greater effect in reducing plasma Lp(a) concentrations than statins. Addition of fibrates to statins can enhance the Lp(a)-lowering effect of statins.
Highlights
Raised plasma lipoprotein(a) (Lp(a)) concentration is an independent and causal risk factor for atherosclerotic cardiovascular disease
Lp(a) is a low-density lipoprotein-like substance with a core of cholesteryl esters and a surface layer of phospholipids and unesterified cholesterol that contains a single molecule of apolipoprotein B-100 bound to a molecule of apo(a) by a disulfide linkage [6]
It has been reported that plasma Lp(a) levels are decreased by monoclonal antibodies targeting proprotein convertase subtilisin/kexin type 9 (PCSK9) [18,19,20,21]
Summary
Raised plasma lipoprotein(a) (Lp(a)) concentration is an independent and causal risk factor for atherosclerotic cardiovascular disease. Plasma concentrations of Lp(a) are an independent risk factor for early atherosclerotic cardiovascular disease [3,4,5]. Therapeutic strategies to reduce plasma Lp(a) concentrations in patients with hyper-Lp(a) are important to reduce cardiovascular mortality In this regard, various therapeutic interventions for lowering Lp(a) levels have been reported, including apheresis techniques, nicotinic acid, statins, fibrates, and aspirin, among others [14,15,16,17]. Since the availability of LDL-apoB plays a key role in the formation of Lp(a) particles [25], LDL-lowering activity of PCSK9 inhibitors is accompanied by a significant fall in plasma Lp(a) levels, as suggested by pooled analyses and meta-analyses [22,23,24].
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