Recent studies have identified Lp(a) as an independent genetic and causal risk factor for CV disease[31]–[38] with several studies showing that higher plasma levels of Lp(a) and genetic variation in the LPA gene that raise Lp(a) levels increase the risk of myocardial infarction (MI) in patients with and without established coronary heart disease [31], [37], [38], [51]. This evidence concerns the gene LPA and coronary artery disorder.