Endocardial Fibroelastosis is Secondary to Hemodynamic Alterations in the Chick Embryonic Model of Hypoplastic Left Heart Syndrome

0490360 - FGÚ 2019 RIV US eng J - Journal Article
Peševski, Živorad - Kvasilová, A. - Stopková, T. - Naňka, O. - Drobná Krejčí, Eliška - Buffinton, Ch. - Kočková, Radka - Eckhardt, Adam - Sedmera, David
Endocardial Fibroelastosis is Secondary to Hemodynamic Alterations in the Chick Embryonic Model of Hypoplastic Left Heart Syndrome.
Developmental Dynamics. Roč. 247, č. 3 (2018), s. 509-520. ISSN 1058-8388. E-ISSN 1097-0177
R&D Projects: GA ČR(CZ) GAP302/11/1308; GA ČR(CZ) GA16-02972S
Institutional support: RVO:67985823
Keywords : hypoxia * HLHS * left atrial ligation * collagen * chick embryo
OECD category: Anatomy and morphology (plant science to be 1.6)
Impact factor: 2.852, year: 2018

Endocardial fibroelastosis (EFE) is a diffuse thickening of the ventricular endocardium, causing myocardial dysfunction and presenting as unexplained heart failure in infants and children. One of the postulated causes is persistent and increased wall tension in the ventricles. Results: To examine whether reduced ventricular pressure in a chick model of hypoplastic left heart syndrome (HLHS) induced by left atrial ligation (LAL) at embryonic day (ED) 4 is associated with EFE at later stages, myocardial fibrosis was evaluated by histology and immunoconfocal microscopy and mass spectrometry (MS) at ED12. Immunohistochemistry with collagen I antibody clearly showed a significant thickening of the layer of subendocardial fibrous tissue in LAL hearts, and MS proved this significant increase of collagen I. To provide further insight into pathogenesis of this increased fibroproduction, hypoxyprobe staining revealed an increased extent of hypoxic regions, normally limited to the interventricular septum, in the ventricular myocardium of LAL hearts at ED8. Conclusions: Abnormal hemodynamic loading during heart development leads to myocardial hypoxia, stimulating collagen production in the subendocardium. Therefore, EFE in this chick embryonic model of HLHS appears to be a secondary effect of abnormal hemodynamics.
Permanent Link: http://hdl.handle.net/11104/0284607