Amplification of the genes that codify endothelin-1 and its receptors in rheumatic mitral valves.

Autor: Moura EB; Hospital de Base, Instituto do Coração DF, Universidade de Brasília, Brasília, DF, Brasil. ebmoura@terra.com.br, Gomes MR, Corso RB, Faber CN, Carneiro FP, Pacheco YG
Jazyk: angličtina
Zdroj: Arquivos brasileiros de cardiologia [Arq Bras Cardiol] 2010 Jul; Vol. 95 (1), pp. 122-30. Date of Electronic Publication: 2010 Jun 11.
DOI: 10.1590/s0066-782x2010005000059
Abstrakt: Background: Cardiopathies are high prevalence conditions. Among them, rheumatic carditis is of high relevance in developing countries. Left cardiac chamber changes are associated to endothelial dysfunction and ET-1 levels increase. Pulmonary circulation is then affected, and not seldom leading to pulmonary hypertension (PH). However, the presence of ET-1 and its receptors in the mitral valve itself--promoting pulmonary vascular changes, with increased rheumatic valvular deformation--has not been discussed in the literature.
Objective: To determine the expression of endothelin gene and its receptors in rheumatic mitral valves through techniques of molecular genetics.
Methods: Twenty-seven patients submitted to mitral valve replacement had their valvular tissue examined to determine the presence of ET-1 genes and their A and B receptors. Histological and molecular analysis of the valves was performed (divided into M1, M2 and M3 fragments), with patients' clinical and epidemiological data collected. Patients were divided into 3 groups (mitral valvopathy, mitroaortic valvopathy, and reoperation patients).
Results: The study showed endothelin-1 gene expression in 40.7% specimens and A receptor in all samples; receptor gene B had lower expression (22.2%).
Conclusion: All patients showed A receptor gene expression. No statistically significant difference was observed in regard to condition severity, expressed according to functional class, and subgroups (mitral valvopathy, mitroaortic valvopathy, and reoperation patients).
Databáze: MEDLINE