Search

Antisarcolemmal (ASAs) and antimyolemmal antibodies (AMLAs) are serological hallmarks of inflammatory heart muscle disease. They occur in a similar incidence in postcardiac injury syndromes, sarcoid heart disease or in dilated and hypertrophic cardiomyopathy. Rarely but still notably they are found with increasing age or in coronary artery disease. We therefore examined whether they are truly pathogenetic or whether they also possess properties of 'natural antibodies'. AMLAs and ASAs, like natural antibodies, have specificity for preserved structures on the membrane; they possess cross-reactivity and increase with age. In contrast to natural antibodies, however, they occur frequently after viral stimulation or other forms of trauma, are more often of the IgG and IgA than of the IgM isotype and fix complement in the acute stage of the disease. They also possess cytolytic and cytotoxic properties when incubated in vitro with isolated heart muscle cells. Antigenic mimicry has been demonstrated to be operative, since they are cross-reactive to viral proteins.

In this study from two specialized centres 85 patients with histologically proven myocarditis (n = 10) and clinically ascertained perimyocarditis (pericardial effusion and cardiomegaly or segmental wall motion abnormality; n = 75) were followed up for 4.5 + 1.9 years. Immunosuppressive treatment was not applied. After a mean follow-up period of 4.5 + 1.9 years 55% of patients had improved clinically and 35% of patients were completely free of symptoms. Relapses had occurred up to three times. Chronic forms were found in 20% of patients, mostly in those with pericarditis and effusions. Eighteen percent of the patients deteriorated gradually. In 20% of the chronic or deteriorating patients congestive heart failure developed (postmyocarditic heart muscle disease). Fifteen percent of the patients died, mainly from bacterial perimyocarditis and to a lesser extent from inflammatory heart disease from enteroviruses. Patients who succumbed after more than 6 months died either suddenly or from progressive heart failure. A favourable outcome was often accompanied by a decrease in titre, but this decrease was less impressive in those who had antimyolemmal and antisarcolemmal antibodies. The persistence of these antibodies in high titres predominated in patients with poor prognosis and postmyocarditic dilated heart muscle disease, as did cytolytic serum activity.

Antisarcolemmal (ASAs) and in particular antimyolemmal antibodies (AMLAs) are a serologic hallmark of inflammatory heart muscle disease and its sequelae. Since they may also occur to a much lesser incidence with increasing age, it was examined whether they also possess properties of "natural antibodies". As natural antibodies, AMLAs and ASAs have specificity for conserved structures on the membrane. They possess cross-reactivity and increase with age. In contrast to natural antibodies, however, they occur most frequently after viral stimulation, and are more often of the IgG- and IgA- than of the IgM-isotype and fix complement in the acute stage of the disease. They also exhibit cytolytic and cytotoxic properties when incubated in vitro with isolated heart muscle cells. In addition, antigenic mimicry has been demonstrated to be operative, since they are cross-reactive to viral proteins.

The vascular endothelium plays a key role in immunologic reactions that also involve the heart: Increased expression of class 1 and 2 antigens of the major histocompatibility complex a common finding in acute rejection after heart transplantation whereas in myocarditis this finding is less pronounced. Another form of involvement of the endothelial cells in the secondary immune response has been reported only infrequently; anti-endothelial antibodies, which may be cytolytic to living cultured human endothelial cells, were demonstrated to be bound to the endomyocardial biopsies of patients with different forms of rejection and with biopsy proven myocarditis and circulating in the peripheral blood of the patients as cytolytic autoantibodies.