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DOI: 10.1055/s-0042-1758382
Calcific Aortic Valve Stenosis with Aging and Current Development in its Pathophysiology
Autoren
Abstract
Aortic stenosis is the most common valvular heart disease affecting the elderly. While most patients have a prolonged asymptomatic phase, the development of symptoms ushers in a phase clinical deterioration that often leads to sudden death without an intervention. Treatment of aortic stenosis with valve replacement often relieves the symptoms but still leaves behind a remodeled left ventricle which may not recover. Understanding the pathophysiology of aortic stenosis and realizing that the disease process may be a more active biological entity rather than a passive degenerative process will help us prevent it. This review serves to summarize the latest literature on the pathophysiology of aortic stenosis in the elderly.
Keywords
advanced glycosylation end product - aortic valve disease - atherosclerosis - biomarkers - valvular heart disease - cardiovascular risk factorsPublikationsverlauf
Artikel online veröffentlicht:
02. November 2022
© 2022. International College of Angiology. This article is published by Thieme.
Thieme Medical Publishers, Inc.
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References
- 1 Carabello BA. Introduction to aortic stenosis. Circ Res 2013; 113 (02) 179-185
- 2 Eveborn GW, Schirmer H, Heggelund G, Lunde P, Rasmussen K. The evolving epidemiology of valvular aortic stenosis. the Tromsø study. Heart 2013; 99 (06) 396-400
- 3 Martinsson A, Li X, Andersson C, Nilsson J, Smith JG, Sundquist K. Temporal trends in the incidence and prognosis of aortic stenosis: a nationwide study of the Swedish population. Circulation 2015; 131 (11) 988-994
- 4 Mathieu P, Boulanger MC. Basic mechanisms of calcific aortic valve disease. Can J Cardiol 2014; 30 (09) 982-993
- 5 Otto CM, Prendergast B. Aortic-valve stenosis–from patients at risk to severe valve obstruction. N Engl J Med 2014; 371 (08) 744-756
- 6 Miller JD, Weiss RM, Heistad DD. Calcific aortic valve stenosis: methods, models, and mechanisms. Circ Res 2011; 108 (11) 1392-1412
- 7 Katz R, Wong ND, Kronmal R. et al. Features of the metabolic syndrome and diabetes mellitus as predictors of aortic valve calcification in the multi-ethnic study of atherosclerosis. Circulation 2006; 113 (17) 2113-2119
- 8 Novaro GM, Katz R, Aviles RJ. et al. Clinical factors, but not C-reactive protein, predict progression of calcific aortic-valve disease: the Cardiovascular Health Study. J Am Coll Cardiol 2007; 50 (20) 1992-1998
- 9 Zhao Y, Nicoll R, He YH, Henein MY. The effect of statins on valve function and calcification in aortic stenosis: a meta-analysis. Atherosclerosis 2016; 246: 318-324
- 10 Goel SS, Kleiman NS, Zoghbi WA, Reardon MJ, Kapadia SR. Renin-Angiotensin system blockade in aortic stenosis: implications before and after aortic valve replacement. J Am Heart Assoc 2020; 9 (18) e016911
- 11 Ramchand J, Patel SK, Kearney LG. et al. Plasma ACE2 activity predicts mortality in aortic stenosis and is associated with severe myocardial fibrosis. JACC Cardiovasc Imaging 2020; 13 (03) 655-664
- 12 Yan AT, Koh M, Chan KK. et al. Association between cardiovascular risk factors and aortic stenosis: the CANHEART aortic stenosis study. J Am Coll Cardiol 2017; 69 (12) 1523-1532
- 13 Tao G, Kotick JD, Lincoln J. Heart valve development, maintenance, and disease: the role of endothelial cells. Curr Top Dev Biol 2012; 100: 203-232
- 14 Hinton Jr RB, Lincoln J, Deutsch GH. et al. Extracellular matrix remodeling and organization in developing and diseased aortic valves. Circ Res 2006; 98 (11) 1431-1438
- 15 Boström KI, Jumabay M, Matveyenko A, Nicholas SB, Yao Y. Activation of vascular bone morphogenetic protein signaling in diabetes mellitus. Circ Res 2011; 108 (04) 446-457
- 16 Srivatsa SS, Harrity PJ, Maercklein PB. et al. Increased cellular expression of matrix proteins that regulate mineralization is associated with calcification of native human and porcine xenograft bioprosthetic heart valves. J Clin Invest 1997; 99 (05) 996-1009
- 17 Wallby L, Janerot-Sjöberg B, Steffensen T, Broqvist M. T lymphocyte infiltration in non-rheumatic aortic stenosis: a comparative descriptive study between tricuspid and bicuspid aortic valves. Heart 2002; 88 (04) 348-351
- 18 Towler DA. Molecular and cellular aspects of calcific aortic valve disease. Circ Res 2013; 113 (02) 198-208
- 19 Galeone A, Paparella D, Colucci S, Grano M, Brunetti G. The role of TNF-α and TNF superfamily members in the pathogenesis of calcific aortic valvular disease. ScientificWorldJournal 2013; 2013: 875363
- 20 Pawade TA, Newby DE, Dweck MR. Calcification in aortic stenosis: the skeleton key. J Am Coll Cardiol 2015; 66 (05) 561-577
- 21 Miller JD, Chu Y, Brooks RM, Richenbacher WE, Peña-Silva R, Heistad DD. Dysregulation of antioxidant mechanisms contributes to increased oxidative stress in calcific aortic valvular stenosis in humans. J Am Coll Cardiol 2008; 52 (10) 843-850
- 22 Winchester R, Wiesendanger M, O'Brien W. et al. Circulating activated and effector memory T cells are associated with calcification and clonal expansions in bicuspid and tricuspid valves of calcific aortic stenosis. J Immunol 2011; 187 (02) 1006-1014
- 23 Irtyuga O, Malashicheva A, Zhiduleva E. et al. NOTCH1 mutations in aortic stenosis: association with osteoprotegerin/RANK/RANKL. BioMed Res Int 2017; 2017: 6917907
- 24 Foffa I, Ait Alì L, Panesi P. et al. Sequencing of NOTCH1, GATA5, TGFBR1 and TGFBR2 genes in familial cases of bicuspid aortic valve. BMC Med Genet 2013; 14: 44
- 25 Hofmann JJ, Briot A, Enciso J. et al. Endothelial deletion of murine Jag1 leads to valve calcification and congenital heart defects associated with Alagille syndrome. Development 2012; 139 (23) 4449-4460
- 26 Koos R, Brandenburg V, Mahnken AH. et al. Association of fetuin-A levels with the progression of aortic valve calcification in non-dialyzed patients. Eur Heart J 2009; 30 (16) 2054-2061
- 27 Di Minno A, Zanobini M, Myasoedova VA. et al. Could circulating fetuin A be a biomarker of aortic valve stenosis?. Int J Cardiol 2017; 249: 426-430
- 28 Lee SH, Choi JH. Involvement of immune cell network in aortic valve stenosis: communication between valvular interstitial cells and immune cells. Immune Netw 2016; 16 (01) 26-32
- 29 Cagirci G, Cay S, Canga A. et al. Association between plasma asymmetrical dimethylarginine activity and severity of aortic valve stenosis. J Cardiovasc Med (Hagerstown) 2011; 12 (02) 96-101
- 30 Matilla L, Roncal C, Ibarrola J. et al. A role for MMP-10 (matrix metalloproteinase-10) in calcific aortic valve stenosis. Arterioscler Thromb Vasc Biol 2020; 40 (05) 1370-1382
- 31 Lutz M, von Ingersleben N, Lambers M. et al. Osteopontin predicts clinical outcome in patients after treatment of severe aortic stenosis with transcatheter aortic valve implantation (TAVI). Open Heart 2017; 4 (02) e000633