Mechanisms of lipoprotein(a) pathogenicity: prothrombotic, proatherosclerotic, or both?

High quality, large prospective population-based studies are like well-tended orchards: they take many years to bear fruit, but when they do, they yield a bounty. In this issue of Arteriosclerosis, Thrombosis, and Vascular Biology, fruit is on offer from 2 important Danish population-based studies, the Copenhagen City Heart Study and the Copenhagen General Population Study, which previously provided key evidence that genetically based levels of C-reactive protein were not related to vascular disease, and from 3 case-control studies conducted in Copenhagen. In the present study, Kamstrup et al use a Mendelian randomization study similar to that described in 2009 to probe the relationship between plasmaderived and genetically determined levels of lipoprotein(a) (Lp[a]), and the development of venous thromboembolism (VTE; thrombotic events), vascular stenosis (atherosclerotic events), and myocardial infarction (which they called combined atherosclerotic and thrombotic events).