Anti-Myosin Antibodies Following Myocardial Infarction: A Prospective Observational Study

Background: Anti-myosin antibodies (AMAs) are formed in response to leaked myosin following myocardial infarction (MI). These antibodies have been implicated in maladaptive post-MI remodelling. Objectives: (1) Compare AMA formation in patients with STEMI and NSTEMI; (2) evaluate predictors of AMA formation; (3) explore the functional significance of AMA. Methods: This study had a prospective observational design, with follow-up at three- and six-months. Anti-myosin IgM and IgG were determined using an ELISA. Results: A total of 43 patients were recruited. Most (74.4%) were positive for anti-myosin IgM at admission. A smaller proportion (23.3%) were positive for IgG. NSTEMI patients experienced a reduction in IgM throughout follow-up (-0.12 ± 0.14), while IgM levels remained steady in the STEMI group (0.01 ± 0.13; p=0.032). Similarly, although more likely to be positive at baseline (p=0.009), the NSTEMI group had a fall in IgG levels at six-months, compared with an increase in the STEMI cohort (p=0.041). Baseline antibody positivity was a predictor of positivity at both follow-up time-points (p=0.018 and p=<0.0001). We also observed a moderately positive correlation between infarct size and percentage increase in mean IgM concentration at first follow-up (r(98) = 0.455; p = 0.015). Although underpowered for clinical endpoints, AMA formation was not associated with re-infarction, impaired systolic function, poorer patient symptomatology or increased BNP at follow-up. Conclusions: This study provided novel insights into AMA kinetics and clarified the relationship between infarct size and autoantibody formation. Future research should further investigate the functional significance of AMA and identify the relevant immunogenic epitopes.