Search

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.

We have evaluated the nature of Aschoff cells within Aschoff bodies seen in 35 of 100 excised left atrial appendages from cases of rheumatic mitral stenosis who underwent closed mitral valvotomy. These were tested using a panel of monoclonal and polyclonal antisera by the indirect immunoperoxidase staining for leucocyte common antigen, macrophage, desmin, vimentin, alpha-1-antitrypsin, alpha-1-antichymotrypsin, lysozyme, acid phosphatase and nonspecific esterase. The Aschoff cell gave strong reactivity with monoclonal antisera to vimentin, macrophage and variable reaction with polyclonal antisera known to recognise macrophages/histiocytes in tissues, namely alpha-1-antitrypsin, alpha-1-antichymotrypsin and lysozyme. These were also strongly positive for acid phosphatase and nonspecific esterase. The Aschoff cell lacked affinity for desmin and only an occasional cell in 4 out of 20 and 6 out of 35 cases showed a weak reaction with myoglobin and leucocyte common antigen, respectively. Intense consistent reactivity with several histiocytic markers affirms the genesis of these cells from macrophages/histiocytes and not muscle cells; a controversy which must be laid to rest!

Electron microscopic evaluation of subcutaneous nodules excised from two cases of acute rheumatic fever showed an electron dense and smudgy material which had a distinct filamentous appearance in places. The latter was recognized as collagen. This corresponded to the fibrinoid necrosis seen under the light microscope. In addition, several histiomonocytic cells and fibroblasts were seen. A large number of cells were degenerated. A fair degree of resemblance of the nodule both by light and electron microscopy to the rheumatoid nodule was noted.

Presence of Aschoff nodules and other chronic inflammatory cells in the left atrial appendage even in the absence of rheumatic activity has been reported in a high percentage of patients with chronic rheumatic valvular heart disease. This study was conducted on 37 left atrial appendages resected at the time of closed mitral valvotomy. Aschoff nodules were present in 61.2 percent of resected appendages, positivity being 71.4 percent in the age group of 20 years of less and 53.3 percent in patients more than 20 years of age. The histological findings did not change significantly in the presence of activity. The frequency of Aschoff nodules and chronic inflammatory cells and their subtypes also did not show any correlation with age, sex, duration of symptoms or severity of mitral stenosis.

Fifty left atrial appendages collected fresh during closed mitral valvotomy in patients with chronic rheumatic heart disease, were analysed to determine the frequency of Aschoff nodules and characteristics of mononuclear inflammatory infiltration. Fifty-six percent of specimens demonstrated Aschoff nodules with no clinical or laboratory evidence of acute rheumatic activity in the patients undergoing surgery. Endomyocardial infiltration contained predominantly T cells and occasionally B cells. The relative proportions of T helper-inducer, T suppressor-cytotoxic lymphocytes and macrophages were 45.1 +/- 7.6, 23.5 +/- 4.8 and 29.3 +/- 9.6%, respectively. Frequent presence of Aschoff nodules and heavy mononuclear infiltrates in chronic rheumatic heart disease suggests a possibility of subclinical ongoing carditis.