Neo-Microvasculature: An active Factir in the Inmunopathogenesis of Chronic Chagasic Cardiopathy

pp 201-207

Abstract

The reduction of the capillary bed in chagasic cardiopathy was first demonstrated by Jörg. Later, Cabral et al. found the presence of high endothelium venules (HEV) which normally occur only in lymphatic tissues. This work studies new features on neo-microvessels in chagasic heart disease with cardiac death. We studied the heart samples of patients with death ages of 41 years (n=8) and 62 years (n=9). Five micron slices were prepared with monoclonal antibodies for cells and vessels and classic staining. The neo-microvessels were counted at 400x in 50/hpf. We found HEV on all samples. The hearts of those who died earlier had a higher count of HEV and other venules of flat endothelium (4.1±1.3 versus 1.2±0.3 per hpf; p<0.001) than the older hearts. Both kinds of microvessels, with diameter ranging from 25 to 90 microns, showed lymphocytes (CD45 RO+) and macrophages (CD68+) inside and through their walls, migrating to the cardiac interstice. Anti-CD31 or ICAM-1CD54 monoclonal antibodies stained the endothelium and anti CD44 stained immunocytes. T. cruzi  was not seen. These findings demonstrate the modification of microvasculature in the chagasic heart through the development of neo-venules vessels, which allow an intense traffic of lymphocytes and macrophages in cardiac tissue and alter the normal arrangement of cardiomyocytes, suggesting there may be autoimmune activity in the chagasic process. A larger count of neo-microvessels was associated with heavy infiltration by T-lymphocytes and macrophages, more malignant arrhythmias and earlier deaths. We post an open question: What are the stimuli leading to their production?