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Does not support targeting myocardial autoantibodies therapeutically; leaves open their value as biomarkers of cardiac injury.
Clinicians have long recognized the importance of immune mechanisms in certain cardiovascular syndromes. Myocardial autoantibodies (HAb) occur in a number of cardiac states as a result of myocardial injury due to infection, infarction, surgery, or trauma to the heart or pericardium. Cavelti's demonstration of cross-reactivity of the rat heart andStreptococcusantigen in acute rheumatic fever went unheralded for a decade before HAb were implicated in the pathogenesis of this disease.1Kaplan and Meyeserian's work confirmed that HAb occurred after streptococcal infection in response to a cross-reactive antigen of group AStreptococcusto myofibrils.2The importance of HAb in the progression of rheumatic heart disease was studied by Ehrenfeld et al by using tanned RBC hemagglutinins in a variety of cardiac and noncardiac diseases.3His studies indicated HAb was not a cause but a consequence of tissue destruction. High titers of HAb did not lead to histologic
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James V. Talano (1977) studied this question.
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