Figure 1.
Micropathology of Chagas heart disease.
(A) Acute myocarditis with foci of myocytolytic necrosis and degeneration are seen with an intense inflammatory infiltrate around ruptured pseudocysts of parasite (arrows, in the inset). Intact intramyocyte parasite nest without inflammatory response (arrow heads, in the inset). Hematoxylin and eosin staining. Bar = 100 µm; inset bar = 50 µm. (B) Chronic fibrosing myocarditis. Foci of myocytolytic necrosis associated with mononuclear inflammatory infiltrate and incipient interstitial fibrosis appearing in light blue (arrows). Gomori trichrome staining. Bar = 100 µm. (C) Chronic fibrosing myocarditis. Predominantly perimysial interstitial fibrosis extending to the endomysium (arrow heads) appearing in light blue associated with mononuclear inflammatory infiltrate. Gomori trichrome staining. Bar = 500 µm. (D) Chronic fibrosing myocarditis. Interstitial and diffuse fibrosis manifested by increased amount of thick collagen fibers surrounding muscle fiber bundles (perimysial matrix) and around intramural coronary vessels, combined with a less pronounced increase in the endomysial matrix. Picrosirius red staining. Bar = 500 µm.
Figure 2.
Gross pathology of chronic Chagas cardiomyopathy (four-chamber frontal view).
(A) Cardiomegaly with a left apical aneurysm (arrow). Myocardium hypertrophy. Marked thinning can be noted in the obtuse border of the heart at the submitral area (arrow head). At the apex of the right ventricle, distinct replacement of myocardial tissue by adipose tissue can be seen. (B) Cardiomegaly. Thinning and thrombosis at apices of both ventricles (arrow heads). Dilatation of cardiac ventricular chambers, mainly the right one. Fibrofatty substitution at the apex of the left ventricle and major part of the right ventricular free wall. (C) Normal-sized heart showing an enormous aneurysm at the apex of the left ventricle. Hypertrophy of the right ventricle free wall except for a marked thinned apex can be clearly seen. (D) Mildly enlarged heart showing dilatation of the four chambers. Giant left apical aneurysm. Thinning of left border of the heart immediately below the mitral valve. (E) Globally enlarged chronic chagasic heart with dilatation mainly affecting the right-sided chambers. Adipose replacement of the right ventricular myocardium, particularly at the apical region, associated with bulging can be seen (arrow heads). (F) Transillumination of a chagasic heart showing thinning of the muscle wall “cor bifidum” with aneurysm at the left apex (arrow heads), and marked thinning of the anteroapical region of the right ventricle. RV, right ventricle; LF, left ventricle. All bars = 3 cm.
Figure 3.
Study in mice chronically infected with T. cruzi demonstrating involvement of microcirculation.
(A) Enlarged heart of a mouse infected with T. cruzi 100 days post-infection showing marked thinning of the apex of the left ventricle (apical aneurism). Bar = 2 mm. (B) Myocardium of an infected mouse stained by the Carstairs method for demonstration of platelets. An occlusive platelet thrombus is seen in a small epicardial vessel (arrowhead). Bar = 50 µm. Mononuclear cell infiltration, interstitial edema and fibrosis, and foci of myocytolytic necrosis. (C) Schematic representation of coronal sections through mice hearts infected with T. cruzi 100 days post-infection without (upper panel) and with (lower panel) apical aneurism, showing the extent of foci of myocytolytic necrosis. These areas are scattered throughout the ventricular and atrial myocardium, but are more numerous in the subendocardial and subepicardial regions in the apex, papillary muscles, and base of the ventricles. (D) Electron micrograph showing complete dissolution of myofibrils within a myofiber (*) of an infected mouse with characteristic myocytolysis or myocytolytic necrosis. Bar = 10 µm.
Figure 4.
Changes of coronary perfusion in experimental T. cruzi infection and human chronic Chagas cardiomyopathy.
(A) Microfil injection of the coronary vasculature of A/J mice infected with T. cruzi 15–17 days post-infection. Section of the atrium reveals saccular microaneurysms and vasospasm in the subendocardium. (B) Videomicrographs of representative fields of the microvasculature obtained from the cremaster muscle from T. cruzi–infected mice 20–25 days post-infection (a, arterioles; v, venules). Upper left and right panels: Representative fields showing areas of vasospasm (arrows). Left lower panel: In this field there is an area of segmental microvascular dilation (arrow). Right lower panel: Infected mouse treated with verapamil in which there were no areas of vasospasm or dilatation. Bar = 20 µm (from Tanowitz et al. (1996) Journal of Parasitology 82: 124–130, with permission of Allen Press and the Journal). (C) Planar images (anterior, left anterior oblique, and lateral views of myocardial scintigraphy with Tc-labelled microspheres in a chronic chagasic patient whose complaint was chest pain, but who had angiographycally normal coronary arteries. A prominent perfusion defect is seen in the anterolateral and posterolateral regions of the left ventricle. Courtesy of J. Antonio Marin-Neto, MD.