Lipoprotein a (Lp(a)) genetic variant doubles the causal risk of Aortic valvular calcification.

In the last 15 to 20 years our understanding of aortic valve calcification has changed from just simple degenerative disease to disease secondary to an active process involving endothelial dysfunction, lipid accumulation, an inflammatory infiltrate. With this understanding many potential therapeutic approach have been considered. Statins showed promise in prevention of calcification in retrospective trials but prospective trials did not show benfit. Rennin angiotensin inhibitors have given discordant results in retrospective trials and no randomized control trial is there to prove their efficacy.

Aortic valvular calcification.
Now comes new potential therapeutic  target for prevention aortic valve calcification i.e. Lp(a).Article published in NEJM Feb 7 2013 from Johns Hopkins, Harvard University, McGill University, the University of Iceland and the National Institutes of Health says, there is variant of Lp(a) which is associated with aortic valve calcification. In this publication genomewide association was evaluated for 6942 participants of aortic valvular calcification and 3795 participants of mitral valve calcification, detected by CT scanning.

Previous studies showed association of Lp(a) with calcification of aortic valve. Causal or just marker of calcification was not confirmed, present study shows causal relationship of Lp(a) and aortic valve calcification.

From this causal relationship one may think of targeting Lp(a) for preventing aortic valve calcification. Niacin reduces Lp(a) levels. Although  HPS-2 THRIVE trial (with niacin/laropiprant) which was done for coronary artery disease did not show clinical benfit, still one may keep hope for prevention of aortic valve calcification. Time may tell about us this in future.

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