Lipid Interventions in Aortic Valvular Disease.
Aortic valve stenosis is the most common valvular disease in the elderly population. Presently, there is increasing evidence that aortic stenosis (AS) is an active process of lipid deposition, inflammation, fibrosis and calcium deposition. The pathogenesis of AS shares many similarities to that of atherosclerosis; therefore, it was hypothesized that certain lipid interventions could prevent or slow the progression of aortic valve stenosis. Despite the early enthusiasm that statins may slow the progression of AS, recent large clinical trials did not consistently demonstrate a decrease in the progression of AS. However, some researchers believe that statins may have a benefit early on in the disease process, where inflammation (and not calcification) is the predominant process, in contrast to severe or advanced AS, where calcification (and not inflammation) predominates. Positron emission tomography using 18F-fluorodeoxyglucose and 18F-sodium fluoride can demonstrate the relative contributions of valvular calcification and inflammation in AS, and thus this method might potentially be useful in providing the answer as to whether lipid interventions at the earlier stages of AS would be more effective in slowing the progression of the disease. Currently, there is a strong interest in recombinant apolipoprotein A-1 Milano and in the development of new pharmacological agents, targeting reduction of lipoprotein (a) levels and possibly reduction of the expression of lipoprotein-associated phospholipase A2, as potential means to slow the progression of aortic valvular stenosis.
Department of Medicine (KJC), University of Chicago Medical Center, Chicago, Illinois; Department of Medicine (CT), General Hospital of Piraeus "Hippocrates," Piraeus, Greece; Department of Medicine (SL), Emory University School of Medicine, Atlanta, Georgia; St. Francis Hospital, The Heart Center (RM, TJV), Division of Cardiology, Center for Advanced Cardiac Therapeutics, Roslyn, New York; and Zena and Michael A. Wiener Cardiovascular Institute (CEK), Icahn School of Medicine at Mount Sinai, New York, New York.
Kwang Jin
KJ
Choi
Christiana
C
Tsomidou
Stamatios
S
Lerakis
Raef
R
Madanieh
Timothy J
TJ
Vittorio
Constantine E
CE
Kosmas
D001011:Aorta / Q000473:pathology*; D001021:Aortic Valve; D016632:Apolipoprotein A-I / Q000378:metabolism; D000082882:Bicuspid Aortic Valve Disease; D002309:Cardiology / Q000379:methods; D002986:Clinical Trials as Topic; D003251:Constriction, Pathologic / Q000628:therapy*; D005462:Fluorine Radioisotopes; D019788:Fluorodeoxyglucose F18; D005786:Gene Expression Regulation; D006330:Heart Defects, Congenital / Q000628:therapy*; D006349:Heart Valve Diseases / Q000628:therapy*; D006350:Heart Valve Prosthesis; D006801:Humans; D008055:Lipids / Q000737:chemistry*; D017270:Lipoprotein(a) / Q000378:metabolism; D049268:Positron-Emission Tomography; D011446:Prospective Studies; D012189:Retrospective Studies; D012969:Sodium Fluoride
D016632:Apolipoprotein A-I; D005462:Fluorine Radioisotopes; D008055:Lipids; D017270:Lipoprotein(a); D019788:Fluorodeoxyglucose F18; D012969:Sodium Fluoride