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Christian G Schrock, Lipoprotein(a): it is not the cholesterol content: it is the apolipoprotein(a)!, European Heart Journal, Volume 40, Issue 43, 14 November 2019, Page 3576, https://doi.org/10.1093/eurheartj/ehz601
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This commentary refers to ‘High lipoprotein(a) and high risk of mortality’, by A. Langsted et al., 2019;40:2760–2770.
‘High lipoprotein(a) and high-risk mortality’ by Langsted et al.1 concludes that the number of KIV-2 repeats in the apolipoprotein(a) [apo(a)] were associated with high risk of mortality not the cholesterol content of lipoprotein(a) [Lp(a)]. This requires a change in the way we conceptualize, study, and treat elevated Lp(a).
Yes, Lp(a) does have an apoB-100 low-density lipoprotein (LDL) component that carries cholesterol, but the apo(a) component is clearly most significant. Lipoprotein(a) should be considered in terms of its apolipoprotein(a) component and called an apo(a) lipoprotein.
Apolipoprotein(a) is the only apolipoprotein with an intrinsic atherogenic nature. Apolipoprotein(a)’s plasminogen homology can promote the thrombosis leading to myocardial infarction. Apolipoprotein(a) carries 85% of all the oxidized phospholipids which can damage the coronary intima of all individuals and facilitate the development and eventual rupture of plaques.2
Lipoprotein(a)-cholesterol [Lp(a)-c] is included with the ‘LDL-C’ in the Friedewald Formula. Lp(a)-C can be calculated by Lp(a) total mass in mg/dL/3 since ∼33% of the Lp(a) is cholesterol. When Lp(a) total mass is high, the Lp(a)-C contribution to the ‘LDL-C’ is significant. Statin therapy increases the relative contribution of the Lp(a)-C because statins lower actual LDL-C but not Lp(a)-C.
