What Do the Heart Valves Tell Us?

Öz

Background: The aim of our study was to investigate the histopathological changes of excised cardiac valves due to degenerative heart valve diseases.
Methods: We collected and explored the histopathologic changes in 28 aortic valves and 20 mitral valves from 40 patients with Acquired Heart Valve Disease retrospectively. Both aorta and mitral valve were excised from 8 patients. Clinical diagnostic information about the patients was obtained from the hospital information system. Fragments of cardiac valve were processed using standard histopathological methods and embedded in paraffin tissue blocks. From each block, 3–4 μm-thick histological sections were cut and stained with hematoxylin-eosin. Slides stained with hematoxylin-eosin were evaluated under Olympus BX51 microscope for histopathological changes. In each case, the available histopathological slides were independently reviewed to confirm the original diagnosis and provide assessment of the various microscopic changes.
Results: 21 (53%) of the patients were male and 19 (47%) were female. The age range of the patients was 20-88. The average age was calculated to be 59. The average age of women was 60.7 and the average age of men was 57.5. According to the data obtained from the hospital information system, hypertension in 14 (35%), hyperlipidemia in 12 (30%), diabetes in 9 (23%), smoking history in 10 (25%) and coronary artery disease in 6 (15%) were present. There were varying degrees of fibrosis in all of the valves (100%) in which the normal histological structure was also observed in the focal areas. Calcification was present on 32 valves (67%) . Six valves (13%) showed both bone and cartilage formation. The valves which exhibit bone and cartilage formation were 4 valves (8%) aorta and 2 valves (8%) mitral valve. All areas of bone formation were accompanied by calcification. The average age of bone metaplasia was 60.8. Chronic inflammation was observed in 27 valves (56%). Neoangiogenesis in 11 valves (23%) and necrosis and abscess formation due to endocarditis in one valve (2%) were observed. Chronic inflammation consisted of lymphocytes and plasma cells.
Conclusion: Heart valve degenerations are closely associated with cardiovascular risk factors. it is an active process that develops through multi-step molecular pathways. Valve interstitial cells are the lead player in this process.

Kalp Kapakları Bize ne Diyor?

Öz

Amaç: Çalışmamızın amacı dejeneratif kalp kapak hastalıkları nedeniyle eksize kalp kapakçıklarının histopatolojik değişikliklerini araştırmaktır.
Materyal ve metotlar : Dejeneratif kalp kapağı hastalığı olan 40 hastadan eksize edilen 28 tane aort kapağı ile 20 tane mitral kapak retrospektif olarak araştırmaya dahil edildi. 8 hastadan hem aort hem mitral kapak eksize edilmiştir. Hastalara ait klinik diagnostik bilgiler hastane bilgi sisteminden elde edildi. Kalp kapakları standart histopatolojik metotlar kullanılarak parafine gömüldü ve her bloktan 3-4 μm kalınlığında kesitler alındı. Hematoksilen Eozin ile boyalı preparatlar Olympus BX51 mikroskopu ile histopatolojik değişiklikler açısından değerlendirildi. Her vakanın mevcut histopatolojik slaytları orijinal tanıyı doğrulamak ve çeşitli mikroskobik değişikliklerin değerlendirmesini sağlamak için bağımsız olarak gözden geçirildi.
Bulgular: Hastaların 21(% 53)’ i erkek, 19(% 47)’ u kadındı. Hastaların yaş aralığı 20-88 idi. Ortalama yaş 59 olarak hesaplandı. Kadınların yaş ortalaması 60.7, erkeklerin yaş ortalaması 57.5 idi. Hastane bilgi sisteminden edinilen verilere göre hastaların 14 (% 35)’ünde hipertansiyon, 12 (% 30)’sinde hiperlipidemi, 9 (% 23)’unda diyabetes mellitus, 10 (% 25)’unda sigara öyküsü 6 (% 15)’sında koroner arter hastalığı mevcuttu. Fokal alanlarda normal histolojik yapının da seçilebildiği kapakların tamamında (% 100) değişen derecelerde fibrozis mevcuttu . 32 kapakta (% 67) kalsifikasyon mevcuttu . Altı kapakta (% 13) kemik ve kartilaj oluşumu birlikte izlendi . Kemik ve kartilaj oluşumu izlenen kapakların 4 (% 8)’ü aort, 2 (%4)’si mitral kapaktı. Tüm kemik oluşumu alanlarına kalsifikasyon da eşlik etmekteydi. Kemik metaplazisi görülme yaş ortalaması 60.8 idi. 27 kapakta (% 56) kronik inflamasyon, 11 kapakta (% 23) neoanjiogenezis ve bir kapakta (% 2) endokardite bağlı nekroz ve abse formasyonu izlendi Kronik inflamasyonun lenfositler ve plazma hücrelerinden oluştuğu görüldü.
Sonuç: Kalp kapak dejenerasyonları kardiyovasküler risk faktörleri ile yakından ilişkilidir. Çok basamaklı moleküler yolaklar aracılığıyla gelişen aktif bir süreçtir. Kapak interstisyel hücreleri bu süreçteki başrol oyuncusudur.

Anahtar Kelimeler

• KALP KAPAKLARI
• DEJENERASYON
• HİSTOPATOLOJİ

Kaynakça

1. Referans1. Stacey E. Mills. Histology for Pathologists. 4th Edition. Lippincott Williams. Philedelphia. 2013. 563-84 ISBN 978-1-4511-1303-7
2. Referans2. Kumar V, Abbas A, Aster J. Robbins & Cotran Pathologic Basis of Disease, 9th Edition. Elsevier .2014. Canada. ISBN: 978-0-8089-2402-9
3. Referans3.Galli D, Manuguerra R, Monaco R, Manotti L, Goldoni M, Becchi G et al. Understanding the structural features of symptomatic calcific aortic valve stenosis: A broad-spectrum clinico-pathologic study in 236 consecutive surgical cases. Int J Cardiol. 2017 Feb 1;228:364-374.
4. Referans4.Torre M, Hwang DH, Padera RF, Mitchell RN, VanderLaan PA. Osseous and chondromatous metaplasia in calcific aortic valve stenosis. Cardiovasc Pathol. 2016 Jan-Feb;25(1):18-24
5. Referans5. Steiner I, Krbal L, Rozkoš T, Harrer J, Laco J. Calcific aortic valve stenosis: Immunohistochemical analysis of inflammatory infiltrate. Pathol Res Pract. 2012 Apr 15;208(4):231-4.
6. Referans6. Mohler ER, Chawla MK, Chang AW, et al. Gannon FH. Identification and characterization of calcifying valve cells from human and canine aortic valves. J Heart Valve Dis 1999;8:254-260
7. Referans7.Steiner I, Kasparová P, Kohout A, Dominik J. Bone formation in cardiac valves: a histopathological study of 128 cases. Virchows Arch 2007;450:653-657.
8. Referans8. Mirzaie M, Schultz M, Schwartz P, Coulibaly M, Schöndube F. Evidence of woven bone formation in heart valve disease. Ann Thorac Cardiovasc Surg. 2003 Jun;9(3):163-9.

9. Referans9. 9. Groom DA, Starke WR. Cartilaginous metaplasia in calcific aortic valve disease. Am J Clin Pathol. 1990 Jun;93(6):809-12.
10. Referans10. Mohler ER 3rd. Mechanisms of aortic valve calcification. Am J Cardiol. 2004 Dec 1;94(11):1396-402, A6. Review.
11. Referans11. Akahori H, Tsujino T, Masuyama T, Ishihara M. Mechanisms of aortic stenosis. J Cardiol. 2018 Mar;71(3):215-220.
12. Referans12. Watson KE, Boström K, Ravindranath R, Lam T, Norton B, Demer LL. TGF-beta 1 and 25-hydroxycholesterol stimulate osteoblast-like vascular cells to calcify. J Clin Invest. 1994 May;93(5):2106-13.
13. Referans13. Tintut Y, Demer L. Role of osteoprotegerin and its ligands and competing receptors in atherosclerotic calcification. J Investig Med. 2006 Nov;54(7):395-401.
14. Referans14. Pawade TA, Newby DE, Dweck MR. Calcification in Aortic Stenosis: The Skeleton Key. J Am Coll Cardiol. 2015 Aug 4;66(5):561-77.
15. Referans15. Mohler ER 3rd, Gannon F, Reynolds C, Zimmerman R, Keane MG, Kaplan FS. Bone formation and inflammation in cardiac valves. Circulation. 2001 Mar 20;103(11):1522-8.
16. Referans16. Venardos N, Nadlonek NA, Zhan Q, Weyant MJ, Reece TB, Meng X, Fullerton DA. Aortic valve calcification is mediated by a differential response of aortic valve interstitial cells to inflammation. J Surg Res. 2014 Jul;190(1):1-8.
17. Referans17. West XZ, Malinin NL, Merkulova AA, Tischenko M, Kerr BA, Borden EC, et al. Oxidative stress induces angiogenesis by activating TLR2 with novel endogenous ligands. Nature 2010;467:972–6.
18. Referans18 Jones PL, Jones FS. Tenascin-C in development and disease: gene regulation and cell function. Matrix Biol 2000;19:581–96.
19. Referans19. Yoshioka M, Yuasa S, Matsumura K, Kimura K, Shiomi T, Kimura N, et al. Chondromodulin-I maintains cardiac valvular function by preventing angio-genesis. Nat Med 2006;12:1151–9.