This Article Figures Only Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Chan, K.-L. Search for Related Content PubMed PubMed Citation Articles by Chan, K.-L.

STATE-OF-THE-ART PAPER

Is aortic stenosis a preventable disease?

^* Division of Cardiology, University of Ottawa Heart Institute, Ottawa, Ontario, Canada

Manuscript received May 1, 2003; accepted May 9, 2003.

^* Reprint requests and correspondence: Dr. Kwan-Leung Chan, University of Ottawa Heart Institute, 40 Ruskin Street, Ottawa, Ontario, Canada, K1Y 4W7.
kchan{at}ottawaheart.ca

Aortic stenosis (AS) is the most common valvular disease requiring valve replacement. Its prevalence increases with age. When the severity of AS is only mild to moderate, it is well tolerated. When it becomes severe, AS confers significant morbidity and mortality. Adverse events can be avoided if it is possible to prevent or retard the progression from mild or moderate AS to severe AS. Progression of AS parallels the progression of sclerotic changes involving the aortic valve, which share histological and immunochemical similarities with the process of atherosclerosis. Far from being just a degenerative process, the development of AS is a complex and highly regulated process with a number of modifiable factors. One of the key factors appears to be lipoproteins, which are intimately involved in several pathways crucial to the development of AS. The importance of lipoproteins is further supported by epidemiological and clinical studies showing a strong association between lipoproteins and AS. The time has come to initiate prospective studies to assess the effect of cholesterol lowering on the progression of AS.

Abbreviations and Acronyms   AS = aortic stenosis   BAV = bicuspid aortic valve   LDL = low-density lipoprotein   TAV = tricuspid aortic valve   TGF = transforming growth factor

This article has been cited by other articles:

				A. M. Greve and K. Wachtell Review: Does lowering cholesterol have an impact on the progression of aortic stenosis? Therapeutic Advances in Cardiovascular Disease, August 1, 2008; 2(4): 277 - 286. [Abstract] [PDF]

				H. I. Michelena, V. A. Desjardins, J.-F. Avierinos, A. Russo, V. T. Nkomo, T. M. Sundt, P. A. Pellikka, A. J. Tajik, and M. Enriquez-Sarano Natural History of Asymptomatic Patients With Normally Functioning or Minimally Dysfunctional Bicuspid Aortic Valve in the Community Circulation, May 27, 2008; 117(21): 2776 - 2784. [Abstract] [Full Text] [PDF]

				R. Ramaraj and V. L Sorrell Degenerative aortic stenosis BMJ, March 8, 2008; 336(7643): 550 - 555. [Full Text] [PDF]

				M. A. Bratos-Perez, P. L. Sanchez, S. Garcia de Cruz, E. Villacorta, I. F. Palacios, J. M. Fernandez-Fernandez, S. Di Stefano, A. Orduna-Domingo, Y. Carrascal, P. Mota, et al. Association between self-replicating calcifying nanoparticles and aortic stenosis: a possible link to valve calcification Eur. Heart J., February 1, 2008; 29(3): 371 - 376. [Abstract] [Full Text] [PDF]

				Z. Zeng, Y. Yin, K.-M. Jan, and D. S. Rumschitzki Macromolecular transport in heart valves. II. Theoretical models Am J Physiol Heart Circ Physiol, June 1, 2007; 292(6): H2671 - H2686. [Abstract] [Full Text] [PDF]

				Z. Zeng, P. Nievelstein-Post, Y. Yin, K.-M. Jan, J. S. Frank, and D. S. Rumschitzki Macromolecular transport in heart valves. III. Experiment and theory for the size distribution of extracellular liposomes in hyperlipidemic rabbits Am J Physiol Heart Circ Physiol, June 1, 2007; 292(6): H2687 - H2697. [Abstract] [Full Text] [PDF]

				D. Messika-Zeitoun, L. F. Bielak, P. A. Peyser, P. F. Sheedy, S. T. Turner, V. T. Nkomo, J. F. Breen, J. Maalouf, C. Scott, A. J. Tajik, et al. Aortic Valve Calcification: Determinants and Progression in the Population Arterioscler. Thromb. Vasc. Biol., March 1, 2007; 27(3): 642 - 648. [Abstract] [Full Text] [PDF]

				M. Briand, I. Lemieux, J. G. Dumesnil, P. Mathieu, A. Cartier, J.-P. Despres, M. Arsenault, J. Couet, and P. Pibarot Metabolic Syndrome Negatively Influences Disease Progression and Prognosis in Aortic Stenosis J. Am. Coll. Cardiol., June 6, 2006; 47(11): 2229 - 2236. [Abstract] [Full Text] [PDF]

				D Skowasch, S Schrempf, C J Preusse, J A Likungu, A Welz, B Luderitz, and G Bauriedel Tissue resident C reactive protein in degenerative aortic valves: correlation with serum C reactive protein concentrations and modification by statins Heart, April 1, 2006; 92(4): 495 - 498. [Abstract] [Full Text] [PDF]

				D M Shavelle Are angiotensin converting enzyme inhibitors beneficial in patients with aortic stenosis? Heart, October 1, 2005; 91(10): 1257 - 1259. [Abstract] [Full Text] [PDF]

				K. Tanaka, M. Sata, D. Fukuda, Y. Suematsu, N. Motomura, S. Takamoto, Y. Hirata, and R. Nagai Age-Associated Aortic Stenosis in Apolipoprotein E-Deficient Mice J. Am. Coll. Cardiol., July 5, 2005; 46(1): 134 - 141. [Abstract] [Full Text] [PDF]

				O. Fondard, D. Detaint, B. Iung, C. Choqueux, H. Adle-Biassette, M. Jarraya, U. Hvass, J.-P. Couetil, D. Henin, J.-B. Michel, et al. Extracellular matrix remodelling in human aortic valve disease: the role of matrix metalloproteinases and their tissue inhibitors Eur. Heart J., July 1, 2005; 26(13): 1333 - 1341. [Abstract] [Full Text] [PDF]

				D. W. Quinn Jr. and S. A. Spinler Efficacy of statins in preventing progression of aortic stenosis Am. J. Health Syst. Pharm., May 1, 2005; 62(9): 979 - 981. [Full Text] [PDF]

				D. Garcia, P. J. C. Barenbrug, P. Pibarot, A. L. A. J. Dekker, F. H. van der Veen, J. G. Maessen, J. G. Dumesnil, and L.-G. Durand A ventricular-vascular coupling model in presence of aortic stenosis Am J Physiol Heart Circ Physiol, April 1, 2005; 288(4): H1874 - H1884. [Abstract] [Full Text] [PDF]