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LIPOPROTEIN(A) DOES NOT HAVE A CLINICALLY SIGNIFICANT ARTERIAL OR VENOUS PROTHROMBOTIC EFFECT
Abstract
Background and Aims
Lipoprotein(a) is an apoB-containing lipoprotein attached to an apolipoprotein(a) and is causally associated with the risk of cardiovascular disease. Because the apo(a) moiety has sequence homology with plasminogen, Lp(a) may be prothrombotic. We therefore sought to determine whether Lp(a) has a clinically significant venous or arterial prothrombotic effect.
Methods
We used Mendelian randomization to evaluate the causal effect of Lp(a) on the risk of venous thromboembolism (VTE) among participants in the UK-Biobank. We then evaluated the causal effect of Lp(a) on the risk of myocardial infarction (MI) in the entire study sample, and stratified by genetic scores that mimic the effect of antiplatelet and antithrombin therapies.
Results
Among 445,774 participants (mean age 57.3 years, 54% female), a total of 15,973 had a VTE event, and 15,465 had a first MI. Lp(a) was not associated with the risk of VTE (OR: 0.99, 95%CI:0.96-1.02). By contrast, Lp(a) was strongly associated with the risk of MI (HR: 1.35 per 100 nmol/L higher Lp(a), 95%CI:1.32-1.38). Furthermore, the antiplatelet score was associated with a dose-dependent step-wise decrease in the risk of MI, and the antithrombin score was associated with a dose-dependent step-wise decrease in the risk of VTE. However, the effect of Lp(a) on the risk of MI was not diminished by either genetically determined lifelong platelet or thrombin inhibition (Figure).
Conclusions
Lp(a) does not have a clinically significant venous or arterial prothrombotic effect. Therefore, the increased risk of MI caused by elevated Lp(a) is unlikely to be reduced by treatment with either an antiplatelet or antithrombin therapy.