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Calcific Aortic Stenosis – Inflammatory Disease


Authors: Ivo Šteiner
Authors place of work: Fingerlandův ústav patologie LF UK a FN, Hradec Králové
Published in the journal: Čes.-slov. Patol., 60, 2024, No. 2, p. 124-128
Category: Original Article

Summary

In developed countries, calcific aortic stenosis (CAS) has become the most common acquired valvular disease and cause for valve replacement. The prevalence of the disease increases with age, reaching over 5 % in adults over 75 years of age. The cases of CAS are classified as either of a previously normal (tricuspid) aortic valve (senile, syn. age – related, “sclerotic” type), or based on a congenitally malformed, usually bicuspid aortic valve.

This paper is a brief summary of our 5 previous publications from the years 2007 – 2021, devoted to histopathology of CAS, namely to vascularization, inflammatory infiltrate and metaplastic ossification of the valve, and also to topography of these lesions in individual valve cusps.

We conclude that calcification of the aortic valve is not a passive degenerative lesion, but an active multifactorial inflammatory process driven by cells native to the aortic valve. Pathogenesis of CAS is similar to that of atherosclerosis.

Keywords:

Pathogenesis – Aortic valve – inflammation – calcific aortic stenosis


Zdroje
  1. Vojáček J, Kettner J. Klinická kardiologie (5. vyd). Maxdorf Jessenius; 2022: 588-600.
  2. Šteiner I, Krbal L, Dominik J. Blood vessels and lymphatics in calcific aortic stenosis – in support of its inflammatory pathogenesis. Cesk Patol 2010; 46(2): 33-36.
  3. Šteiner I, Krbal L, Rozkoš T., Harrer J, Laco J. Calcific aortic valve stenosis: Immunohistochemical analysis of inflammatory infiltrate. Pathol Res Pract 2012; 208: 231-234.
  4. Šteiner I, Stejskal V, Žáček P. Mast cells in calcific aortic stenosis. Pathol Res Pract 2018; 214: 163-168.
  5. Šteiner I, Kašparová P, Kohout A, Dominik J. Bone formation in cardiac valves: a histopathological study of 128 cases. Virchows Arch 2007; 450: 653-657.
  6. Šteiner I, Timbilla S, Stejskal V. Calcific aortic valve stenosis – comparison of inflammatory lesions in the left, right, and non-coronary cusp. Pathol Res Pract 2021; 227, 153636.
  7. Kahn HJ, Bailey D, Marks A. Monoclonal antibody D2-40, a new marker of lymphatic endothelium, reacts with Kaposi´s sarcoma and subset of angiosarcomas. Med Pathol 2002; 15: 434-440.
  8. Lerman DA, Prasad S, Alotti N. Calcific aortic valve disease: molecular mechanisms and therapeutic approaches. Eur Cardiol 2015; 10: 108-112.
  9. Rutkovskiy A, Malashicheva A, Sullivan G, Bogdanova M et al. Valve interstitial cells: the key to understanding the pathophysiology of heart valve calcification. J Am Heart Assoc 2017; 6, e006339.
  10. Raddatz MA, Madhur MS, Marryman WD. Adaptive immune cells in calcific aortic valve disease. Am J Physiol Heart Circ Physiol 2019; 317: H141-H155.
  11. Yip CYY, Simmons CA. The aortic valve microenvironment and its role in calcific aortic valve disease. Cardiovasc Pathol 2011; 20:177-182.
  12. de Oliveira Sá MPB, Cavalcanti LRP, Perazzo AM, Gomes RAF et al. Calcific aortic valve stenosis and atherosclerotic calcification. Curr Atheroscler Rep 2020; 22:2.
Štítky
Anatomical pathology Forensic medical examiner Toxicology
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