The relationship between β1‐adrenergic and M2‐muscarinic receptor autoantibodies and hypertrophic cardiomyopathy. Issue 3 (29th January 2020)

• Record Type: Journal Article
• Authors: Duan, Xin; Liu, Rong; Luo, Xiao‐Liang; Gao, Xiao‐Jin; Hu, Feng‐Huan; Guo, Chao; Wang, Juan; Hu, Xiao‐Ying; Chun, Yu‐Shi; Yuan, Jian‐Song; Cui, Jin‐Gang; Yang, Wei‐Xian; Qiao, Shu-Bin
• Is Part Of: Experimental physiology. Volume 105:Issue 3(2020:Mar.)
• Page Start: 522
• Page End: 530
• Publication Date: 2020-01-29
• Subjects: autoantibody -- β1‐adrenergic receptor -- hypertrophic cardiomyopathy -- M2‐muscarinic receptor; Physiology, Experimental -- Periodicals; 571.0724
• DOI: 10.1113/EP088263
• Languages: English
• ISSNs: 0958-0670

Abstract

Abstract : New Findings: What is the central question of this study? The concentrations of β1 ‐adrenergic receptor and M2 ‐muscarinic receptor autoantibodies in hypertrophic cardiomyopathy (HCM) patients and the relationship between the cardiac autoantibodies and clinical manifestations of HCM have rarely been reported. What is the main finding and its importance? We found that the concentrations of the two autoantibodies in HCM patients were significantly higher than those in control subjects. Furthermore, we found that the concentrations of the two autoantibodies could reflect myocardial injury and diastolic dysfunction in HCM patients to some extent and might be involved in the occurrence of arrhythmia. These findings might be valuable in exploration of the mechanisms of occurrence and progression of HCM. Abstract: Increasing attention is being given to the role of immunological mechanisms in the development of heart failure. The purpose of this study was to investigate the concentration of serum β1 ‐adrenergic receptor autoantibody (β1 ‐AAb) and M2 ‐muscarinic receptor autoantibody (M2 ‐AAb) in patients with hypertrophic cardiomyopathy (HCM), and the relationship between β1 ‐AAb, M2 ‐AAb and clinical indices. One hundred and thirty‐four patients with HCM were recruited consecutively into the HCM group. Forty healthy subjects were assigned as the normal controls (NCs). Serum samples were collected to measure the concentrations of β1 ‐AAb and M2 ‐AAb by enzyme‐linked immunosorbent assay. The clinical data of HCM patients were collected. The serum concentrations of β1 ‐AAb and M2 ‐AAb of HCM patients were significantly higher than those of NCs. In HCM patients, those with a left atrial diameter ≥50 mm or moderate‐to‐severe mitral regurgitation had significantly higher concentrations of the two autoantibodies. Patients with a history of syncope had higher concentrations of β1 ‐AAb. Female patients and patients with a family history of sudden cardiac death or atrial fibrillation had higher concentrations of M2 ‐AAb. Maximal wall thickness, interventricular septum thickness and resting left ventricular outflow tract gradient were positively correlated with log β1 ‐AAb or log M2 ‐AAb in HCM patients. In conclusion, the serum concentrations of β1 ‐AAb and M2 ‐AAb of HCM patients were significantly higher than those of NCs. Being female, syncope, a family history of sudden death, atrial fibrillation, left atrial diameter ≥50 mm, moderate‐to‐severe mitral regurgitation, maximal wall thickness, interventricular septum thickness and resting left ventricular outflow tract gradient may affect the concentrations of the two autoantibodies. Abstract :