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IAC 2018



Nalini M. Rajamannan, M.D., Mayo Clinic, Rochester, MN, and Most Sacred Heart of Jesus Cardiology and Valvular Institute, Sheboygan WI, Corvita, Chicago IL, USA


In 2009, NHLBI coordinated a working group on Calcific aortic valve disease. For decades, the disease was thought to be due to a degenerative process. In 2018, the disease mechanisms are still under intense investigation which has resulted in two RFA call for applications by the NIH to further explore the disease process and potential targeted therapies which will result in bench to bedside future clinical trials in the field.
Over the past nine years, the field has recognized that the strong evidence that lipoprotein(a) [Lp(a)] plays a critical role in the development of CAVD. However, the biology of Lipoprotein(a) remains elusive and the role in the development of calcific aortic valve disease is under intense investigation.
This abstract will review the 2018 state of the art position perspectives on CAVD, Lp(a) in the pathology, epidemiology and genetic studies which provide the strong evidence that Lipoprotein(a) is a causal mediator of calcific aortic valve disease and the current NHLBI combined working group recommendations in the field of CAVD and Lp(a) as it affects research from bench to bedside.



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