The role of anti-myosin antibodies in perpetuating cardiac damage following myocardial infarction

- Anti-myosin autoantibodies (AMAs) are formed in some patients following MI.
- AMAs have been causally associated with cardiac dysfunction in animal studies.
- The clinical significance of AMA in human patients remains incompletely understood.
- Immunological therapies have been of some success in attenuating the AMA response.

Recent improvements in the medical and surgical management of myocardial infarction mean that many patients are now surviving with greater impairment of cardiac function. Despite appropriate management, some of these patients subsequently develop pathological ventricular remodelling, which compounds their contractile dysfunction and can lead to congestive cardiac failure (CCF). The pathophysiological mechanism underpinning this process remains incompletely understood. One hypothesis suggests that a post-infarction autoimmune response, directed against constituents of cardiac myocytes, including cardiac myosin, may make an important contribution. Our review summarises the current literature related to the formation and clinical relevance of anti-myosin antibodies (AMAs) in patients with myocardial infarction. This discussion is supplemented with reference to a number of important animal studies, which provide evidence of the potential mechanisms underlying AMA formation and autoantibody mediated cardiac dysfunction.