CLINICAL STUDIES
Antimyosin autoantibodies are associated with deterioration of systolic and diastolic left ventricular function in patients with chronic myocarditis
Bernward Lauer, MD*,
Mira Schannwell, MD ,
Uwe Kühl, MD ,
Bodo-Eckhard Strauer, MD and
Heinz-Peter Schultheiss, MD
* Klinik für Innere Medizin/Kardiologie, Universität Leipzig-Herzzentrum, Leipzig, Germany
Medizinische Klinik und Poliklinik B, Heinrich-Heine-Universität, Düsseldorf, Germany
Abteilung für Kardiologie, Pneumologie und Angiologie, Universitätsklinikum Benjamin Franklin, Berlin, Germany
Manuscript received January 8, 1999;
revised manuscript received September 3, 1999,
accepted September 13, 1999.
Reprint requests and correspondence: Dr. Bernward Lauer, Klinik für Innere Medizin/Kardiologie, Universität Leipzig—Herzzentrum GmbH, Russenstr. 19, D-04289 Leipzig, Germany
laub{at}server3.medizin.uni-leipzig.de
OBJECTIVES
The study evaluates the clinical course and the development of systolic and diastolic left ventricular function in patients with chronic myocarditis with or without autoantibodies against cardiac myosin.
BACKGROUND
Patients with myocarditis often show autoantibodies against cardiac myosin. The clinical and pathophysiologic significance of these antimyosin autoantibodies (AMAAB) is yet unknown. The results from studies comparing the clinical course and the development of left ventricular function in patients with chronic myocarditis with or without AMAAB are not yet available.
METHODS
Thirty-three patients with biopsy proven chronic myocarditis underwent analysis of AMAAB, right and left heart catheterization and left ventriculography at baseline and after six months. Left ventricular volumes and ejection fraction as well as the time constant of left ventricular relaxation "tau" and the constant of myocardial stiffness "b" were determined at baseline and at follow-up.
RESULTS
In 17 (52%) patients, AMAAB could be detected at baseline. After six months, AMAAB were still found in 13 (76%) initially antibody-positive patients. No initially antibody-negative (n = 16) patient developed AMAAB during follow-up. Clinical symptoms improved slightly in antibody-negative patients and remained stable in antibody-positive patients. Left ventricular ejection fraction developed significantly better in antibody-negative patients (+8.9 ± 10.1%) compared with antibody-positive patients (–0.1 ± 9.4%) (p < 0.012). Stroke volume (SV) and stroke volume index (SVI) also improved in antibody-negative patients (SV: +20 ± 31 ml; SVI: +10 ± 17 ml) compared with antibody-positive patients (SV: –14 ± 43 ml; SVI: –8 ± 22 ml) (SV: p < 0.015; SVI: p < 0.016). Left ventricular end-diastolic and end-systolic volumes and the time constant of left ventricular relaxation "tau" did not change significantly different in antibody-positive and antibody-negative patients. The constant of myocardial stiffness "b" improved significantly in antibody-negative patients (–6.1 ± 10.8) compared with antibody-positive patients (+7.3 ± 22.6) (p < 0.040). Analyzing only the persistently antibody-positive patients yielded essentially the same results.
CONCLUSIONS
Antimyosin autoantibodies are associated with worse development of left ventricular systolic function and diastolic stiffness in patients with chronic myocarditis.
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Abbreviations and Acronyms
| | AMAAB | = antimyosin autoantibodies | | AMAAB(+) | = antimyosin autoantibody-positive | | AMAAB(–) | = antimyosin autoantibody-negative | | EDV | = end-diastolic volume | | EDVI | = end-diastolic volume index | | EF | = ejection fraction | | ELISA | = enzyme-linked immunosorbent assay | | ESV | = end-systolic volume | | ESVI | = end-systolic volume index | | LVEDP | = left ventricular end diastolic pressure | | MHC | = major histocompatibility antigens | | NYHA | = New York Heart Association | | RNA | = ribonucleic acid | | SV | = stroke volume | | SVI | = stroke volume index |
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