{"title":"[Can we prevent the progression of aortic valve sclerosis and stenosis? The need for a prospective, randomized trial].","authors":"Sabino Scardi, Antonella Cherubini","doi":"","DOIUrl":null,"url":null,"abstract":"<p><p>Cardiologists long assumed that aortic valve sclerosis/stenosis is a wear-and-tear, degenerative process; recent studies suggested that lipoproteins can play a key role in the development of both sclerosis/stenosis in the aortic valve. Thus, sclerosis/stenosis cannot be considered as a simple degenerative process, but on the contrary it is complex and involves multiple pathogenetic mechanisms. Experimental, clinical and epidemiological data support the link between aortic valvulopathy and atherosclerosis: both are caused by inflammation, lipid deposition, and accumulation of extracellular bone matrix protein. In non-randomized clinical studies, hydroxy-methylglutaryl-coenzyme A reductase inhibitors minimized the progression of aortic valvulopathy. The major pharmacological effect, supposed to underlie the inferred (but still unproven) impact of statins on aortic sclerosis/stenosis is plasma cholesterol reduction. Lately, retrospective clinical studies supported this hypothesis and suggested a key role for statins in delaying the progression of aortic valvulopathy. However, the potential favorable effects of statins require confirmation. Prospective trials in Canada and Europe are now ongoing (ASTRONOMER--Aortic Stenosis Progression Observation Measuring Effects of Rosuvastatin; SEAS--Simvastatin and the Ezetimibe in Aortic Stenosis) and will address the use of cholesterol-lowering drugs in reducing the progression of aortic valve stenosis and in improving clinical outcomes.</p>","PeriodicalId":80290,"journal":{"name":"Italian heart journal. Supplement : official journal of the Italian Federation of Cardiology","volume":null,"pages":null},"PeriodicalIF":0.0000,"publicationDate":"2005-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Italian heart journal. Supplement : official journal of the Italian Federation of Cardiology","FirstCategoryId":"1085","ListUrlMain":"","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0
Abstract
Cardiologists long assumed that aortic valve sclerosis/stenosis is a wear-and-tear, degenerative process; recent studies suggested that lipoproteins can play a key role in the development of both sclerosis/stenosis in the aortic valve. Thus, sclerosis/stenosis cannot be considered as a simple degenerative process, but on the contrary it is complex and involves multiple pathogenetic mechanisms. Experimental, clinical and epidemiological data support the link between aortic valvulopathy and atherosclerosis: both are caused by inflammation, lipid deposition, and accumulation of extracellular bone matrix protein. In non-randomized clinical studies, hydroxy-methylglutaryl-coenzyme A reductase inhibitors minimized the progression of aortic valvulopathy. The major pharmacological effect, supposed to underlie the inferred (but still unproven) impact of statins on aortic sclerosis/stenosis is plasma cholesterol reduction. Lately, retrospective clinical studies supported this hypothesis and suggested a key role for statins in delaying the progression of aortic valvulopathy. However, the potential favorable effects of statins require confirmation. Prospective trials in Canada and Europe are now ongoing (ASTRONOMER--Aortic Stenosis Progression Observation Measuring Effects of Rosuvastatin; SEAS--Simvastatin and the Ezetimibe in Aortic Stenosis) and will address the use of cholesterol-lowering drugs in reducing the progression of aortic valve stenosis and in improving clinical outcomes.