How Does Elevated Lipoprotein(a) Cause Aortic Valve Stenosis?

L ipoprotein(a) [Lp(a)] was discovered in 1963 by Kaare Berg in Norway, and elevated levels were already then considered a cardiovascular risk factor (1). For many years, Lp(a) received only moderate scientific and clinical attention; however, in recent years, important new evidence has emerged, and elevated Lp(a) is now considered a causal risk factor for cardiovascular disease. Genetic variants in the LPA gene, which is responsible for encoding apolipoprotein(a) [apo(a)] and determining elevated Lp(a) levels, are associated with coronary heart disease (2,3). Other exciting new discoveries include evidence that elevated Lp(a) levels likewise are a causal risk factor for aortic valve calcification and stenosis (4,5). In aortic valve stenosis, thickening of the aortic valve cusps limits the outflow of blood from the left ventricle of the heart, a condition that, if untreated, can lead to heart failure and premature death. Aortic valve stenosis affects w2% of individuals $65 years of age, and in those who have symptoms, 5and 10-year mortality approaches 50% and 90%, respectively, without aortic valve replacement (AVR) (6). Randomized trials using statins and other lipid-lowering medications have failed to show an effect on aortic valve stenosis, and to date, the only effective treatment is AVR. Previously, risk factors for aortic valve