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This genetic analysis using data from the UK Biobank population compared the atherogenicity of lipoprotein(a) (Lp[a]) with that of LDL on a per-particle basis and then assessed the risk of coronary heart disease (CHD) in relation to the number of apolipoprotein B–containing particles in Lp(a) and LDL. The authors found that Lp(a) has a significantly higher atherogenic potential than LDL. For each 50 nmol/L increase in apolipoprotein B, the risk of CHD was notably greater for Lp(a) than for LDL, with an approximately sixfold higher atherogenicity observed for Lp(a) on a per-particle basis.
These findings highlight the relevance of monitoring Lp(a) levels as well as the importance of targeting Lp(a) in drug interventions for many individuals at risk for CHD.
Lipoprotein(a) (Lp(a)) is recognized as a causal factor for coronary heart disease (CHD) but its atherogenicity relative to that of low-density lipoprotein (LDL) on a per-particle basis is indeterminate.
The authors addressed this issue in a genetic analysis based on the fact that Lp(a) and LDL both contain 1 apolipoprotein B (apoB) per particle.
Genome-wide association studies using the UK Biobank population identified 2 clusters of single nucleotide polymorphisms: one comprising 107 variants linked to Lp(a) mass concentration, the other with 143 variants linked to LDL concentration. In these Lp(a) and LDL clusters, the relationship of genetically predicted variation in apoB with CHD risk was assessed.
The Mendelian randomization-derived OR for CHD for a 50 nmol/L higher Lp(a)-apoB was 1.28 (95% CI: 1.24-1.33) compared with 1.04 (95% CI: 1.03-1.05) for the same increment in LDL-apoB. Likewise, use of polygenic scores to rank subjects according to difference in Lp(a)-apoB vs difference in LDL-apoB revealed a greater HR for CHD per 50 nmol/L apoB for the Lp(a) cluster (1.47; 95% CI: 1.36-1.58) compared with the LDL cluster (1.04; 95% CI: 1.02-1.05). From these data, we estimate that the atherogenicity of Lp(a) is approximately 6-fold (point estimate of 6.6; 95% CI: 5.1-8.8) greater than that of LDL on a per-particle basis.
We conclude that the atherogenicity of Lp(a) (CHD risk quotient per unit increase in particle number) is substantially greater than that of LDL. Therefore, Lp(a) represents a key target for drug-based intervention in a significant proportion of the at-risk population.