Key result
HCM is linked to higher serum β1-adrenergic and M2-muscarinic receptor autoantibodies versus normal controls.
Why the study?
Concentrations of β1-adrenergic and M2-muscarinic receptor autoantibodies in HCM patients and their relationship with clinical manifestations have rarely been reported.
Are serum concentrations of β1-adrenergic and M2-muscarinic receptor autoantibodies elevated in patients with hypertrophic cardiomyopathy and correlated with clinical manifestations?
Case-Control (n=174)
Are serum concentrations of β1-adrenergic and M2-muscarinic receptor autoantibodies elevated in patients with hypertrophic cardiomyopathy and correlated with clinical manifestations?
Elevated levels of β1-adrenergic and M2-muscarinic receptor autoantibodies in HCM patients correlate with disease severity and may play a role in the pathogenesis and progression of hypertrophic cardiomyopathy.
Elevated autoantibodies associate with HCM; hypothesis-generating for pathogenesis, should not yet change practice.
New Findings What is the central question of this study? The concentrations of β 1 ‐adrenergic receptor and M 2 ‐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 β 1 ‐adrenergic receptor autoantibody (β 1 ‐AAb) and M 2 ‐muscarinic receptor autoantibody (M 2 ‐AAb) in patients with hypertrophic cardiomyopathy (HCM), and the relationship between β 1 ‐AAb, M 2 ‐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 β 1 ‐AAb and M 2 ‐AAb by enzyme‐linked immunosorbent assay. The clinical data of HCM patients were collected. The serum concentrations of β 1 ‐AAb and M 2 ‐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 β 1 ‐AAb. Female patients and patients with a family history of sudden cardiac death or atrial fibrillation had higher concentrations of M 2 ‐AAb. Maximal wall thickness, interventricular septum thickness and resting left ventricular outflow tract gradient were positively correlated with log β 1 ‐AAb or log M 2 ‐AAb in HCM patients. In conclusion, the serum concentrations of β 1 ‐AAb and M 2 ‐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.
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Duan et al. (2019) conducted a case-control in Hypertrophic cardiomyopathy (n=174). β1-adrenergic and M2-muscarinic receptor autoantibodies vs. Normal controls was evaluated on Serum concentrations of β1-AAb and M2-AAb. Serum concentrations of β1-adrenergic and M2-muscarinic receptor autoantibodies were significantly higher in patients with hypertrophic cardiomyopathy compared to normal controls.
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