Diagnostic relevance of humoral and cell-mediated immune reactions in patients with acute viral myocarditis.

TLDR

The study examined sera from 177 acute myocarditis patients, testing for heart and skeletal muscle autoantibodies via indirect immunofluorescence and assessing antibody‑dependent cytolysis, lymphocytotoxicity, and cellular cytotoxicity using viral rat cardiocytes as targets. Anti‑sarcolemmal antibodies were found in most coxsackie B, influenza, mumps, and 65 of 144 undefined myocarditis cases, correlated with cardiocyte cytolysis, and could be absorbed by viral antigens, indicating diagnostic and etiological relevance, whereas cytomegalovirus cases lacked these antibodies and lymphocyte cytotoxicity was generally absent except in a few unknown‑origin patients.

Abstract

Sera of 177 patients with acute myocarditis (10 coxsackie B 3/4, four influenza, four mumps, 15 cytomegalovirus, 144 undefined) were tested by indirect immunofluorescence for autoantibodies against heart and skeletal muscle and vital or air-dried adult cardiocytes. Antibody-dependent cytolysis, lymphocytotoxicity and antibody-dependent cellular lymphocytotoxicity were assessed using viral adult rat cardiocytes as target cells. Muscle-specific anti-sarcolemmal antibodies of the anti-myolemmal type--often associated with non-organ-specific anti-endothelial antibodies--were demonstrated in nine out of 10 patients with coxsackie B, in all patients with influenza and mumps and in 65 out of 144 patients with undefined myocarditis. In contrast, 13 out of 15 patients with cytomegalovirus myocarditis lacked anti-sarcolemmal antibodies but had low titre anti-inter fibrillary antibodies instead. In the presence of complement, anti-myolemmal antibodies induced cytolysis of vital cardiocytes, whereas hepatocytes remained unaffected. Titres of anti-myolemmal antibodies correlated with the degree of cardiocytolysis. The anti-myolemmal immunofluorescent pattern and the cytolytic serum activity could be absorbed with the respective viral antigens suggesting that these antibodies cross-react with moieties of the virus itself and may be both diagnostic and aetiological markers in acute viral myocarditis. Lymphocyte-mediated cytotoxicity against heterologous cardiac target cells could not be observed in our patients with myocarditis of proven viral aetiology. However, lymphocyte-mediated cytotoxicity was demonstrated in 10 ASA-positive and one ASA-negative patient with myocarditis of unknown origin. ASA-positive sera blocked lymphocytotoxicity in three of these patients.