Abstract

DIAZ RUIZ, María Valentina; SUAREZ, Claudia B; TREJO, Ernesto  and  HAMANA, Leticia. Caracterización de la angiogénesis en la valvulitis reumática crónica como factor de progresión de las lesiones del aparato valvular mitral. Gac Méd Caracas. [online]. 2008, vol.116, n.4, pp.287-298. ISSN 0367-4762.

Characterisation of angiogenesis in chronic rheumatic valvulopathy and his relation with progression of the valvular injuries is novel in our country. The objective of this study is to quantify neovascularizacion and to relate it with progression of the inflammatory process and fibrosis. We analyzed 40 biopsies with chronic valvulitis rheumatic from patients with representative ages of two evolutionary stages. The average of ages in the Group A, was of 31 ± 1.5 years and in Group B, of 49,7 ± 1,4 years. The histology sections were collored with haematoxylineosin and tricromic of Gomori, and immune marked with CD34. Macroscopic valves of both groups was thickened by fibrosis, although in group B, the changes were more severe being focal calcification, its more important note (50.0 %). Histology cally in both groups, they were observed fibrosis, inflammatory infiltrate without presence of Aschoff.’nodules. The greater degrees of inflammation were observed in group A. The group B there were calcifications in 60 % of the cases versus 5 % of group A. In each case the positive immune neovessels were counted. The vascular density was calculated dividing the total number of vessels by the section’s area (vessels/mm2). The density was 5.98 ± 1.08 vessels/mm2, and 3.55 ± 0.76 (P< 0.001) in the groups A, and B, respectively. We conclude that angiogenesis is constant in all phases of the chronic rheumatic valvulitis and comprises all the courtship of the inflammatory and reparative tissue elements, representing a potential factor of progression of collagen remodelation. Considering that angiogenesis displays morphologic variants produced by different modulators factors, it is probable that they may become therapeutics targets to inhibit this process in order to diminish cicatrisation of the mitral valvular apparatus.

Keywords : Angiogenesis; Chronic rheumatic valvulopathy; Remodelation.