Group A streptococci can trigger autoimmune responses that lead to acute rheumatic fever (ARF) and rheumatic heart disease (RHD). Some autoantibodies generated in ARF/RHD target antigens in the S2 subfragment region of cardiac myosin. However, little is known about the kinetics of these antibodies during the disease process.
View Article and Find Full Text PDFBackground: Anti-myosin antibodies (AMAs) are often formed in response to myocardial infarction (MI) and have been implicated in maladaptive cardiac remodelling. We aimed to: (1) compare AMA formation in patients with Non-ST-Elevation MI (NSTEMI) and ST-Elevation MI (STEMI); (2) evaluate factors predicting autoantibody formation; and, (3) explore their functional significance.
Methods: Immunoglobulin M (IgM) and Immunoglobulin G (IgG) AMA titres were determined in serum samples collected at admission, 3 and 6 months post MI.