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Genome-wide association studies for coronary artery disease/myocardial infarction revealed a 58 kb risk locus on 9p21.3. Refined genetic analyses revealed unique haplotype blocks conferring susceptibility to atherosclerosis per se versus risk for acute complications in the presence of underlying coronary artery disease. The cell proliferation inhibitor locus, CDKN2A, maps just upstream of the myocardial infarction risk block, is at least partly regulated by the noncoding RNA, ANRIL, overlapping the risk block, and has been associated with platelet counts in humans. Thus, we tested the hypothesis that CDKN2A deficiency predisposes to increased platelet production, leading to increased platelet activation in the setting of hypercholesterolemia.

Enhanced Megakaryopoiesis and Platelet Activity in Hypercholesterolemic,B6-Ldlr−/−,Cdkn2a-Deficient Mice

Enhanced Megakaryopoiesis and Platelet Activity in Hypercholesterolemic,B6-Ldlr^−/−,Cdkn2a-Deficient Mice