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European Heart Journal 1997 18(2):270-275;
Copyright © 1997 by the European Society of Cardiology.
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© 1997 The European Society of Cardiology

Circulating cardiac-specific autoantibodies as markers of autoimmunity in clinical and biopsy-proven myocarditis

A. L. P. Caforio*,{dagger},, J. H. Goldman*, A. J. Haven*, K. M. Baig*, L. Dalla Libera{ddagger}, W. J. McKenna* and Myocarditis Treatment Trial Investigators§

*Department of Cardiological Sciences, St George's Hospital Medical School London, UK
{dagger}Division of Cardiology, Department of Clinical and Experimental Medicine, Padua University Italy
{ddagger}CNR Unit for Muscle Biology and Physiopathology, Department of Experimental and Biomedical Sciences, University of Padua Italy

revised 20 May 1996; accepted 29 May 1996.

Correspondence: Ahda L. P. Caforio, MD, PhD, FESC, Department of Cardiological Sciences, St. George's Hospital Medical School, Cranmer Terrace, London SW17 ORE, U.K.

Abstract

AIM: Myocarditis and dilated cardiomyopathy may be phases of an organ-specific autoimmune disease of the myocardium. To provide evidence for autoimmune involvement in myocarditis, cardiac autoantibodies were detected in patient sera from the Myocarditis Treatment Trial.

METHODS AND RESULTS: Cardiac antibody status was assessed by indirect immunofluorescence and by anti-{alpha}-myosin enzyme-linked inimunosorbent assay in 53 patients from the Myocarditis Treatment Trial (35 males, aged 42±15 years); all had clinical myocarditis, but only 24 were classified as having histological myocarditis (Dallas criteria). By immunofluorescence, cardiac antibodies were more common in myocarditis (13/53) than in ischaemic (11/186, P=0·0001) or in normal controls (24/270, P=0·001). Abnormally raised anti-{alpha}-myosin antibodies were also more frequent in myocarditis (9/53) than in ischaemic (4/92, P0·01) or normal controls (4/203, P=0·0001); 34% of myocarditis patients were positive with one or both tests. Similar proportions of patients with and without histological myocarditis had antibodies by immunofluorescence (8/24 vs 5/29, P=ns) and by enzyme-linked immunosorbent assay (4/24 vs 5/29, P=ns).

CONCLUSION: The detection of disease-specific cardiac autoantibodies supports autoimmune involvement in a subset of patients with clinical myocarditis. The lack of correlation of antibody with biopsy features suggests that diagnosis of myocarditis should not be made on histology alone. Autoimmune markers may provide adjunct diagnostic tools and identify patients in whom immunosuppression is of potential benefit.

Key Words: Myocarditis • autoimmunity • myosin • cardiac autoantibodies


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