Abstract
Background and Aims: Lipoprotein(a) [Lp(a)] is a causal genetic risk factor for atherothrombotic events. The homology between plasminogen and apolipoprotein(a) (apo(a)) suggests that Lp(a) might promote thrombosis through inhibition of fibrinolysis. This hypothesis is supported by in vitro studies but has not been tested in humans due to lack of specific Lp(a) lowering agents.
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