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Rheumatic heart disease is the most severe complication of rheumatic fever. Till date, very few successful animal models of rheumatic valvular disease have been reported. This study aimed at developing a suitable animal model of chronic rheumatic valvulitis for further investigation and prevention of rheumatic heart disease. Lewis rats were immunized with one administration of formalin-killed and sonicated group A streptococci together with Complete Freund's Adjuvant every 7 days for three cycles followed by group A streptococci alone till killing. Control rats were administered adjuvants and saline. Rats in group 1 were killed 12 weeks after the initial injection. Rats in group 2 and control group were killed 24 weeks after the initial injection. Results 62.5% (5/8) of rats in group 1 developed myocarditis and 50% (4/8) developed valvulitis. Histological examination of cardiac sections showed only cellular infiltrates. In contrast, 75% (6/8) of rats in group 2 developed rheumatic-like myocarditis and 62.5% (5/8) developed chronic valvulitis. Histological manifestations of the hearts in group 2 animals involved not only acute damage such as cellular infiltrates, Aschoff-like cells, verrucous vegetation, but also chronic lesions such as fibrosis, vascular neogenesis. None of the rats (0/8) in control group presented myocarditis or valvulitis. Lewis rat repeatedly immunized with formalin-killed GAS may be a suitable animal model of chronic rheumatic valvulitis. It may be useful for future investigation of the pathogenesis and possible preventive strategies of human rheumatic heart disease.

Heart transplantation as a treatment for end-stage heart failure has spawned numerous important challenges in patient care. A heart transplant patient with clinically unsuspected acute rheumatic carditis had an ultimately fatal course marked by refractory rejection and early death after transplantation. The patient had several immune abnormalities. Peripheral blood T lymphocytes (CD2+) were significantly elevated (p < 0.05) by flow cytometry in active rheumatic carditis versus 76 healthy individuals. The CD4+:CD8+ T-cell ratio was 5.5:1 in rheumatic disease and only 2.7:1 in healthy individuals. Numbers of peripheral blood B lymphocytes (CD19+), macrophages (CD14+), and interleukin-2 receptor-positive cells (CD25+) were also elevated in rheumatic disease. Natural killer cells (CD16+) were slightly reduced in number and appeared functionally deficient, and antibody-dependent cellular cytotoxicity was also reduced. Immunohistochemically, infiltrating cells in Aschoff lesions of the rheumatic native heart were mainly T cells, with putative TH/I cells predominating. The striking immune accompaniments of acute rheumatic fever may have heralded profound immune-mediated allograft intolerance leading to the patient's demise. Considering the recrudescence of rheumatic heart disease in this country and its remaining worldwide importance, such patients as the one discussed offer daunting clinical challenges when transplantation is an obvious management choice for severe, end-stage dilated cardiomyopathy.

The histologic findings of 325 necropsies of rheumatic patients at the National Institute of Cardiology in Mexico, between 1980-1985 were studied forty five of them had Aschoff nodules plus valvular inflammation-Out of these 45 cases two groups were formed: children-adolescent group (24 cases) and an adult group (21 cases). The clinical, histologic and laboratory findings were compared. Clinical records were reviewed searching for history of rheumatic fever. Active rheumatic fever was suspected in 16 patients in the younger group (67%) and only in 3 adults (14.2%). As far as Jones' criteria is concerned, the most common finding was carditis, principally in the younger group (83%). In the adult group, it appeared in 50% of the patients. All other criteria were only occasionally seen or could not be identified during the patients lifetime. The most common laboratory finding which could suggest active rheumatic fever were: a high levels of anti-streptolysin in younger patients (95%) and elevation of erythro-sedimentation in adults (83%). We conclude that in active rheumatic fever of the adult; Jones criteria are not met, so the illness is difficult to recognize, and there is clinical-histologic discrepancy. In this context the disease has a "silent" evolution.

To define the cellular subpopulations that infiltrate the heart in human myocarditis, formaldehyde-fixed, paraffin-embedded sections from 18 hearts with histologically proved myocarditis were examined immunohistochemically. Disease was classified on routine stains as follows: mixed mononuclear cell (7 cases), granulomatous (3), giant cell (1), rheumatic (2), and fungal (5) myocarditis, respectively. On immunohistochemical examination, T-lymphocyte and macrophage predominance was found in nearly every case, except in fungal myocarditis, in which polymorphonuclear leukocytes and macrophages prevailed. In contrast, B lymphocytes and natural killer cells were conspicuously absent, regardless of histologic classification. Giant cells in giant cell myocarditis and in the Aschoff lesions of rheumatic carditis expressed macrophage, but not myocyte, antigens, suggesting derivation along macrophage lineage. Immunohistochemical data obtainable in paraffin-embedded tissues supplement the study of myocarditis, providing information potentially relevant to immunopathogenesis, natural history, and therapy.