Copyright © 1991 by the European Society of Cardiology.
© 1991 The European Society of Cardiology
Dilated cardiomyopathy and myocarditis: monoclonal antibodies to diseased heart tissues
British Heart Foundation Cardiovascular Immunology Group, Department of Cellular and Molecular Sciences, St. George's Hospital Medical School London, UK
Address for Correspondence: Prof. Christopher Spry, BHF Cardiovascular Immunology Group, Department of Cellular and Molecular Sciences, St George's Hospital Medical School, Cranmer Terrace, London SW17 ORE, UK
This study looked for the presence of abnormal contractile protein antigens and alterations in contractile protein expression in dilated cardiomyopathy (DCM). Monoclonal antibodies were raised to extracts from hearts removed at cardiac transplantation from two patients with dilated cardiomyopathy (DCM), and one with myocarditis. The specificities of the antibodies were assessed on cryostat sections from eight hearts with DCM. Although an extensive search was made for DCM-specific antibodies among over 1500 clones, none were found. However, a panel of antibodies was prepared and characterized, including antibodies to human adult myosin heavy chain β, actin and troponin-I, which were selected for their value as reagents for immunocytochemical studies on cardiac, skeletal and smooth muscle. No significant alteration in the distribution of the epitopes recognized by these antibodies was found in DCM although more atrial myocytes in patients with DCM contained myosin adult heavy chain-β. As a similar increase was found in atrial from patients with other diseases who had a normal filling pressure, it was concluded that this alteration was unrelated to filling pressure, and was not specific for DCM. Further work with well defined monoclonal antibodies to other cardiac components in DCM could be useful in defining the alterations which lead to the functional defects in DCM and other cardiac diseases of unknown cause.
Key Words: Actin antibodies-monoclonal cardiomyopathy-congestive aetiology-of-disease immunocyto-chemistry myosin troponin-l
* Since the writing of this paper we report, with regret, that Dr Tai has died.