Abstract
Lipoprotein(a) (Lp(a)) is an independent cardiovascular risk factor playing a causal role for atherosclerotic cardiovascular disease (CVD). Lipoprotein apheresis (LA) is a safe well-tolerated outpatient treatment to lower LDL-C and Lp(a) by 60–70%, and is the ultimate escalating therapeutic option in patients with hyperlipoproteinemias (HLP) involving LDL particles. Major therapeutic effect of LA is preventing cardiovascular events. Lp(a)-HLP associated with progressive CVD has been approved as indication for regular LA in Germany since 2008. The Pro(a)LiFe-study investigated with a prospective multicenter design the long-term preventive effect of LA on incidence rates of cardiovascular events prospectively over a period of 5 years in 170 consecutive patients who commenced regular LA. During a median period of 4.7 years of the pre-LA period, Lp(a) associated progressive CVD became apparent. Apolipoprotein(a) (apo(a)) isoforms and polymorphisms at the apo(a) gene (LPA) were analyzed to assess hypothetical clinical correlations. 154 patients (90.6%) completed 5‑years follow-up. Significant decline of the mean annual major adverse cardiac event (MACE) rate was observed from 0.41 ± 0.45 two years prior to regular LA to 0.06 ± 0.11 during 5 years with regular LA (p < 0.0001). 95.3% of patients expressed at least one small apo(a) isoform. Calculation of isoform specific concentrations allowed to confirm the equivalence of 60 mg/dl or 120 nmol/l as Lp(a) thresholds of the German LA guideline. Results of 5 years prospective follow-up confirmed that LA has a lasting effect on prevention of cardiovascular events in patients with Lp(a)-HLP and afore progressive CVD.
Highlights
Lipoprotein(a) (Lp(a)), consisting of an LDL particle and apolipoprotein(a) (apo(a)) was first described in 1963
Calculation of isoform specific concentrations allowed to confirm the equivalence of 60 mg/dl or 120 nmol/l as Lp(a) thresholds of the German Lipoprotein apheresis (LA) guideline
It took almost 50 years to become fully clear that high Lp(a) concentrations represent an independent and causal risk factor for atherosclerotic cardiovascular disease (CVD) [2, 3]
Summary
Lipoprotein(a) (Lp(a)), consisting of an LDL particle and apolipoprotein(a) (apo(a)) was first described in 1963. Candidate patients must have Lp(a) levels >60 mg/dl along with progressive CVD despite effective treatment of all other cardiovascular risk factors in particular LDL-C [4]. German authorities with their decision stipulated that additional prospective data were required to justify maintenance of this reimbursement guideline. 35.2% of the clinically recognized, highly selected Pro(a)LiFe patients with a small apo(a) phenotype were not tagged by either of these SNPs. At the individual level there was a strong effect that the smaller allele was the major isoform in plasma Molecular analysis of Lp(a) in Pro(a)LiFe patients offered the opportunity to validate and confirm the equivalence of 60 mg/dl or 120 nmol/l by calculation of isoform specific concentrations of Lp(a) ([1]; Fig. 3)
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