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Immunology of cardiac tumors.

  • Maisch, B
Published Article
The Thoracic and cardiovascular surgeon
Publication Date
Aug 01, 1990
38 Suppl 2
PMID: 2237895


Whereas abundant literature is available on mechanisms imposed by neoplastic diseases on the immune system, only few details are known about immunological parameters of autoreactive mechanisms directed against the heart. This report will focus on cardiac autoreactivity in patients with endomyocardial types of cardiac tumors (e.g. atrial myxomas), Hodgkin's disease, and with neoplastic pericardial effusion. In patients with atrial myxomas antimyolemmal antibodies were significantly increased when compared to non-cardiac controls. Antisarcolemmal antibodies were positive in 100% of trivalent immunoglobulin binding. Antiendothelial antibodies of the IgG type could be found in 86% of patients with atrial myxoma. Circulating immune complexes were present in 6 out of 7 patients. In 107 patients with Hodgkin's disease without pericarditis the presence of antimyolemmal antibodies was lower than in healthy controls. The incidence of antimyolemmal antibodies in 10 patients with pericarditis lymphogranulomatosa was 10%, whereas in postradiation pericarditis 8 of 15 patients demonstrated antimyolemmal antibodies. Antiendothelial antibodies were positive in 7 out of 15 patients. The number of patient lymphocytes available for functional assays is yet too small to permit further conclusions on cellular autoreactive mechanisms in Hodgkin's disease. Antimyocardial antibodies were found both in the serum and in the effusions at least in lower titers in all patients. With regard to in-vitro analysis it can not be excluded that a balance between protective and cytolytic antibodies keeps a normal mean of antibody-mediated cytolysis. Analysing the first line of defense, the natural killer cell activity was found significantly increased in neoplastic pericardial effusions, whereas peripheral blood and pericardial effusion showed no lymphocytotoxicity with isolated myocardial cells.

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