Conclusions Fibrates 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
Background Raised 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 r and omized head-to-head trials .
Lipoprotein(a) Concentrations, Rosuvastatin Therapy, and Residual Vascular Risk: An Analysis From the JUPITER Trial (Justification for the Use of Statins in Prevention An Intervention Trial Evaluating Rosuvastatin)
Background — Lipoprotein(a ) [ Lp(a ) ] is a low-density lipoprotein – like particle largely independent of known risk factors and predictive of cardiovascular disease . Statins may offset the risk associated with elevated Lp(a ) , but it is unknown whether Lp(a ) is a determinant of residual risk in the setting of low low-density lipoprotein cholesterol after potent statin therapy . Methods and Results — Baseline and on-treatment Lp(a ) concentrations were assessed in 9612 multiethnic participants in the JUPITER trial ( Justification for the Use of Statins in Prevention : An Intervention Trial Evaluating Rosuvastatin ) before and after r and om allocation to rosuvastatin 20 mg/d or placebo , with outcomes reported for whites ( n=7746 ) .  Lp(a ) concentrations ( median [ 25th–75th percentile ] , in nmol/L ) were highest in blacks ( 60 [ 34–100 ] ) , then Asians ( 38 [ 18–60 ] ) , Hispanics ( 24 [ 11–46 ] ) , and whites ( 23 [ 10–50 ] ; P<0.001 ) . Although the median change in Lp(a ) with rosuvastatin and placebo was zero , rosuvastatin nonetheless result ed in a small but statistically significant positive shift in the overall Lp(a ) distribution ( P<0.0001 ) . Baseline Lp(a ) concentrations were associated with incident cardiovascular disease ( adjusted hazard ratio per 1-SD increment in Ln[Lp(a ) ] , 1.18 ; 95 % confidence interval , 1.03–1.34 ; P=0.02 ) . Similarly , on-statin Lp(a ) concentrations were associated with residual risk of cardiovascular disease ( adjusted hazard ratio , 1.27 ; 95 % confidence interval , 1.01–1.59 ; P=0.04 ) , which was independent of low-density lipoprotein cholesterol and other factors . Rosuvastatin significantly reduced incident cardiovascular disease among participants with baseline Lp(a ) greater than or equal to the median ( hazard ratio , 0.62 ; 95 % confidence interval , 0.43–0.90 ) and Lp(a ) less than the median ( hazard ratio , 0.46 ; 95 % confidence interval , 0.30–0.72 ) , with no evidence of interaction . Similar results were obtained when analyses included nonwhites . Conclusion — Among white JUPITER participants treated with potent statin therapy , Lp(a ) was a significant determinant of residual risk . The magnitude of relative risk reduction with  rosuvastatin was similar among participants with high or low Lp(a ) . Clinical Trials Registration — URL : http://www . clinical trials.gov . Unique identifier : NCT00239681
Conclusions Fibrates 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
Background Raised 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 r and omized head-to-head trials .