Tom J O'Donohoe1, Ryan G Schrale2, Suchandan Sikder3, Nuzhat Surve4, Donna Rudd3, Natkunam Ketheesan5. 1. Australian Institute of Tropical Health and Medicine, James Cook University, Townsville, Qld, Australia; College of Medicine and Dentistry, James Cook University, Townsville, Qld, Australia; College of Public Health, Medical and Veterinary Sciences, James Cook University, Townsville, Qld, Australia; St. Vincent's Hospital, Melbourne, Vic, Australia. Electronic address: thomas.odonohoe@svha.org.au. 2. College of Medicine and Dentistry, James Cook University, Townsville, Qld, Australia; Cardiac Services, Townsville Hospital, Townsville, Qld, Australia. 3. Australian Institute of Tropical Health and Medicine, James Cook University, Townsville, Qld, Australia; College of Public Health, Medical and Veterinary Sciences, James Cook University, Townsville, Qld, Australia. 4. Australian Institute of Tropical Health and Medicine, James Cook University, Townsville, Qld, Australia; Seth GS Medical College and KEM Hospital, Mumbai, India. 5. Australian Institute of Tropical Health and Medicine, James Cook University, Townsville, Qld, Australia; College of Medicine and Dentistry, James Cook University, Townsville, Qld, Australia; College of Public Health, Medical and Veterinary Sciences, James Cook University, Townsville, Qld, Australia; University of New England, Newcastle, NSW, Australia.
Abstract
BACKGROUND: 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. The relationship between demographic and clinical data, and antibody formation, was investigated to determine factors predicting antibody formation and functional significance. RESULTS: Forty-three (43) patients were consecutively recruited; 74.4% were positive for IgM at admission, compared with 23.3% for IgG. Mean IgG levels increased by 1.24% (±0.28) at 3 months, and 13.55% (±0.13) at 6 months post MI. Mean antibody levels were significantly higher in the NSTEMI cohort at both follow-up time points for IgG (p<0.001, p<0.0001), but not IgM (p=0.910, p=0.066). A moderately positive correlation between infarct size and increase in mean IgM concentration was observed at 3 months (r(98)=0.455; p=0.015). Anti-myosin antibody formation was not associated with an unfavourable outcome at follow-up. CONCLUSIONS: Anti-myosin antibodies are formed in a significant proportion of patients following MI, particularly among those with NSTEMI. While IgM levels fall after infarction, IgG levels increase and persist beyond 6 months of follow-up. This raises the possibility that they may contribute to long-term myocardial damage and dysfunction. Future research should focus on the specific epitopes that are targeted by these antibodies, and their functional significance. This may result in the emergence of novel therapies to attenuate cardiac dysfunction in MI patients.
BACKGROUND: 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. The relationship between demographic and clinical data, and antibody formation, was investigated to determine factors predicting antibody formation and functional significance. RESULTS: Forty-three (43) patients were consecutively recruited; 74.4% were positive for IgM at admission, compared with 23.3% for IgG. Mean IgG levels increased by 1.24% (±0.28) at 3 months, and 13.55% (±0.13) at 6 months post MI. Mean antibody levels were significantly higher in the NSTEMI cohort at both follow-up time points for IgG (p<0.001, p<0.0001), but not IgM (p=0.910, p=0.066). A moderately positive correlation between infarct size and increase in mean IgM concentration was observed at 3 months (r(98)=0.455; p=0.015). Anti-myosin antibody formation was not associated with an unfavourable outcome at follow-up. CONCLUSIONS: Anti-myosin antibodies are formed in a significant proportion of patients following MI, particularly among those with NSTEMI. While IgM levels fall after infarction, IgG levels increase and persist beyond 6 months of follow-up. This raises the possibility that they may contribute to long-term myocardial damage and dysfunction. Future research should focus on the specific epitopes that are targeted by these antibodies, and their functional significance. This may result in the emergence of novel therapies to attenuate cardiac dysfunction in MI patients.
Authors: Matthew DeBerge; Shuangjin Yu; Shirley Dehn; Igal Ifergan; Xin Yi Yeap; Mallory Filipp; Amanda Becker; Xunrong Luo; Stephen Miller; Edward B Thorp Journal: Am J Physiol Heart Circ Physiol Date: 2019-12-06 Impact factor: 4.733