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Lipoprotein(a) Foundation Supports National Heart Valve Disease Month, Highlights Genetic Link between Lp(a) and Aortic Valve Disease
[February 21, 2017]

Lipoprotein(a) Foundation Supports National Heart Valve Disease Month, Highlights Genetic Link between Lp(a) and Aortic Valve Disease


In advance of the first-ever National Heart Valve Disease Awareness Day, the Lipoprotein(a) Foundation is highlighting a number of studies that demonstrate the impact of elevated Lp(a) and its significance as an independent, genetic risk factor for early cardiovascular disease. Recently published research has shown that elevated Lp(a) is the strongest independent genetic risk factor for heart valve disease and individuals with high Lp(a) may also be susceptible to earlier and more aggressive valve disease.

The Lipoprotein(a) Foundation has partnered with the Alliance for Aging Research to promote National Heart Valve Disease Awareness Day on February 22, during National Heart Month. The Lipoprotein(a) Foundation recently issued an Infographic to raise awareness about aortic valve disease, including aortic stenosis, the most common form of valve disease in the Western world. More than 5 million adults in the U.S. are estimated to have some form of aortic valve disease and some 15,000 die every year.1 For more information about patients with high Lp(a) and valve disease, visit www.TESTLpa.org.

George Thanassoulis, MD MSc FRCP(C), Director of Preventive and Genomic Cardiology at the McGill University Health Center and Associate Professor at McGill University, Montreal, and a member of the Lipoprotein(a) Foundation's Scientific Advisory Board, has been involved in three recent studies linking elevated levels of Lp(a) and aortic valve disease.

The study "Estimating the Population Impact of Lp(a) Lowering on the Incidence of Myocardial Infarction and Aortic Stenosis," was recently published in the American Heart Association journal, Arteriosclerosis, Thrombosis, and Vascular Biology. With potent Lp(a)-lowering therapies on the horizon, researchers sought to estimate the potential population impact of Lp(a) lowering that may be achieved by these therapies in primary prevention. Results showed that reducing high Lp(a) could potentially prevent up to 1 in 14 cases of myocardial infarction and 1 in 7 cases of aortic valve stenosis.

"These data demonstrate that among those with high Lp(a), nearly one third of heart attacks and half of all cases of aortic stenosis can be attributed tohigh Lp(a) and may be preventable with Lp(a) lowering therapy. Lowering Lp(a) could significantly reduce the impact of cardiovascular disease," said Dr Thanassoulis.



In "Lipoprotein (a) in calcific aortic valve disease: from genomics to novel drug target for aortic stenosis," published in the Journal of Lipid Research (DOI: 10.1194/jlr.R051870) and "Lipoprotein(a): new insights from modern genomics," published in the January issue of Current Opinion in Lipidology (DOI:10.1097/MOL.0000000000000392), Dr Thanassoulis and colleagues identify Lipoprotein(a) as the strongest independent genetic risk factor for both myocardial infarction and aortic stenosis. According to Dr Thanassoulis, "With mounting epidemiological and genetic findings in support of Lp(a)-mediated valve disease, it is critical to discuss potential mechanisms underlying this observation, and outline the steps to translate this discovery to a much needed novel therapeutic strategy for AV disease. With novel therapies on the horizon, Lp(a) is poised to gain significant clinical relevance and its lowering could have a significant impact on the burden of CVD."

Dr Thanassoulis also announced that he just received a Research Project Grant (RO1) from the National Institutes of Health/ National Heart, Lung, and Blood Institute (NHLBI). The purpose of the grant, titled, "Genetic and molecular epidemiology of Lp(a)-mediated calcific aortic valve disease," is to extend discovery of the role of Lp(a) in aortic stenosis. The objectives are to better understand the molecular determinants of Lp(a) mediated valve calcification and identify causal disease pathways that may be targeted by novel therapeutics.


One in 5 people globally have inherited high Lp(a) - 63 million in the U.S.4 - and Lp(a) is currently the strongest monogenetic risk factor for coronary heart disease and aortic stenosis.2,3 Lp(a) concentrations can be measured by a simple blood test and could be the first step in preventing up to 120,000 cardiovascular events every year;1,5 however, it is not included in most standard lipid panel tests that check cholesterol levels.1

"There is a growing body of research that links high lipoprotein(a) to heart attacks, strokes and now aortic stenosis and heart valve disease. Studies likes the ones conducted by Dr Thanassoulis continue to demonstrate that high Lp(a) is the strongest independent genetic risk factor for many cardiac conditions and therapies under development could have tremendous impact. We are proud to support education and awareness of Heart Valve Disease and will continue to empower patients and prevent cardiovascular events due to high Lipoprotein(a) through proper testing and diagnosis," said Sandra Revill Tremulis, founder of Lipoprotein(a) Foundation.

About The Lipoprotein(a) Foundation

Because approximately 63 million Americans have high Lipoprotein(a) and are at risk of premature cardiovascular disease, the vision for the foundation is: To live in a world where high Lipoprotein(a) is routinely diagnosed, treated and family screened. The mission is to prevent cardiovascular events due to high Lipoprotein(a) by diagnosing this inherited risk for cardiovascular disease; educating and empowering patients and saving lives. Our goal is to save lives by increasing awareness, advocating for routine testing, and supporting research that will lead to a specific treatment for elevated Lipoprotein(a). Based in San Carlos, California, the Lipoprotein(a) Foundation is a patient-founded, 501(c)3 non-profit organization. Learn more about Aortic Valve Disease and high Lp(a) visit: www.TESTLpa.org

Citations available upon request.


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