ABSTRACT
Jõrg demostró reducción del lecho capilar en el corazón chagásico. Después, Cabral y colaboradores hallaron vénulas de endotelio alto (VEA), que normalmente sólo existen en tejidos linfáticos. Aquí estudiamos nuevos aspectos sobre neomicrovasos en la cardiopatía chagásica crónica (CChC) con muerte cardíaca. Estudiamos muestras de corazones de pacientes que murieron a una edad media de 41 años (n = 8) y otros con muerte a una edad media de 62 años (n = 9). Se estudiaron cortes de 5 micrones con coloraciones clásicas y otros con anticuerpos monoclonales e inmunocitoquímica, para células y vasos. Los neovasos-vénulas se contaron a una magnificación Î400, en 50 campos. Resultados: En todos los casos se hallaron VEA. Los corazones con muerte más temprana tuvieron un número mayor de VEA y otras vénulas, de endotelio plano (4,1 ± 1,3 versus 1,2 ± 0,3, por campo) (p< 0,001) con respecto a los corazones con muerte tardía. Ambos tipos de microvasos, cuyo diámetro fue de 25 a 90 micrones, mostraron linfocitos (CD45RO+) y macrófagos (CD68+) en su interior y saliendo hacia el intersticio cardíaco. Mediante anticuerpos anti-CD31 o bien ICAM-1/CD54 se demostró inmunotinción de endotelios y de células con anti-CD44. No se observó T. cruzi. Los datos muestran que en el corazón chagásico se producen modificaciones de la microvasculatura con producción de neomicrovasos venulares que permiten un tránsito linfocitario-macrofágico intenso hacia los tejidos cardíacos y refuerzan los datos que sugieren autoinmunidad en el proceso chagásico. Su mayor cantidad, neomicrovasos e inmunocitos, se asoció con un número más alto de arritmias malignas y muerte temprana. Abrimos la pregunta: ¿qué llevan a su producción?
Subject(s)
Humans , Male , Adult , Female , Middle Aged , Arrhythmias, Cardiac , Chagas Cardiomyopathy/immunology , Chagas Cardiomyopathy/mortality , Autoimmunity , Argentina/epidemiology , Macrophages , T-LymphocytesABSTRACT
UNLABELLED: The purpose of this work was to obtain new data on factors intervening in the production and progression of human chagasic cardiopathy (HChC) with death by cardiac failure. We studied cardiac samples of patients that died at an early mean age versus others that died at older ages. The infiltrating cells were characterized and quantified by means of specific monoclonal antibodies and inmunohistochemical methodology; and by classical histological and histochemical methods. We found intense cardiac infiltration by lymphocytes that reacted with the antibodies anti-CD45RO against activated T-lymphocytes (< 70%). A similar number showed reactivity for CD4. And, in seriate sections, showed PAS+ substances in their cytoplasms. Macrophages were detected in a number of 25%. Few lymphocytes reacted to CD8. There was a low number of B lymphocytes. Other noticeable infiltrated cell were intramiocardial mast cells. Qualitatively, such findings were similar in the two groups of patients. However, the number of T-lymphocytes and of the mast cells was significantly higher in the cases that underwent early cardiac death (p < 0.001). T. cruzi was not found. In cardiomyocytes, damages were found, with T-lymphocytes and macrophages adhered to their sarcolemma, as well as mast cells. CONCLUSIONS: These findings suggest the existence of an active and intense occurrence of immunocellular mechanisms in the production and evolution of severe HChC, in which T-lymphocytes CD4+ intervene, with production and secretion of PAS+ substances; Besides, macrophages, and mast cells, in that order. The quantity of infiltrated cells was positively associated with the occurrence of malignant arrythmyias. We suggest that such facts would be involved in the poor cardiac performance of the chagasic heart disease that leads to cardiac death. Indeed, they seem be worthy of consideration with respect to therapeutic strategies.
Subject(s)
Chagas Cardiomyopathy/pathology , Myocardium/pathology , T-Lymphocytes/cytology , Adult , Antibodies, Monoclonal/analysis , B-Lymphocytes/immunology , Chagas Cardiomyopathy/immunology , Disease Progression , Humans , Immunohistochemistry , Leukocyte Common Antigens/immunology , Mast Cells/pathology , Middle Aged , Myocardium/immunologyABSTRACT
The purpose of this work was to obtain new data on factors intervening in the production and progression of human chagasic cardiopathy (HChC) with death by cardiac failure. We studied cardiac samples of patients that died at an early mean age versus others that died at older ages. The infiltrating cells were characterized and quantified by means of specific monoclonal antibodies and inmunohistochemical methodology; and by classical histological and histochemical methods. We found intense cardiac infiltration by lymphocytes that reacted with the antibodies anti-CD45RO against activated T-lymphocytes (< 70
). A similar number showed reactivity for CD4. And, in seriate sections, showed PAS+ substances in their cytoplasms. Macrophages were detected in a number of 25
. Few lymphocytes reacted to CD8. There was a low number of B lymphocytes. Other noticeable infiltrated cell were intramiocardial mast cells. Qualitatively, such findings were similar in the two groups of patients. However, the number of T-lymphocytes and of the mast cells was significantly higher in the cases that underwent early cardiac death (p < 0.001). T. cruzi was not found. In cardiomyocytes, damages were found, with T-lymphocytes and macrophages adhered to their sarcolemma, as well as mast cells. CONCLUSIONS: These findings suggest the existence of an active and intense occurrence of immunocellular mechanisms in the production and evolution of severe HChC, in which T-lymphocytes CD4+ intervene, with production and secretion of PAS+ substances; Besides, macrophages, and mast cells, in that order. The quantity of infiltrated cells was positively associated with the occurrence of malignant arrythmyias. We suggest that such facts would be involved in the poor cardiac performance of the chagasic heart disease that leads to cardiac death. Indeed, they seem be worthy of consideration with respect to therapeutic strategies.