Objectives: The clinical implications of autoantibodies (Abs) were investigated as upstream indicators of paroxysmal atrial fibrillation in patients with congestive heart failure.
Methods: Circulating Abs against myosin (M-Abs) detected by immunofluorescence, Abs against beta 1-adrenergic receptors (Beta 1-Abs) detected by enzyme-linked immunosorbent assay (ELISA), and Abs against NA-K-ATPase (NKA-Abs) detected by ELISA were screened in 95 congestive heart failure patients with < or = 45% left ventricular ejection fraction (coronary artery disease, n = 48; dilated cardiomyopathy, n = 47) and 48 age-matched control patients with hypertension. No patient received antiarrhythmic therapy. All patients were enrolled with angiotensin converting enzyme inhibitors in the chronic stable state. Relationship of the presence of paroxysmal atrial fibrillation to other clinical variables were assessed by 48-hour Holter monitoring.
Results: No control patient had Abs. However, M-Abs, Beta 1-Abs, and NKA-Abs were detected in 22%, 26% and 16% of patients with congestive heart failure (coronary artery disease; 8%, 10%, and 4%, dilated cardiomyopathy; 36%, 43%, and 28%, respectively). Paroxysmal atrial fibrillation was more frequent in patients with dilated cardiomyopathy than in those with coronary artery disease (47% vs 15%, p < 0.01). Multivariate analysis suggested that NKA-Abs was an independent risk factor for the occurrence of paroxysmal atrial fibrillation (p < 0.01), although there were no differences in other clinical factors: age, sex, New York Heart Association functional class, concomitant medication, left ventricular ejection fraction, left atrial diameter, severity of mitral regurgitation, serum potassium, plasma norepinephrine, and atrial natriuretic peptide concentration.
Conclusions: Autoantibodies against sarcolemmal Na-K-ATPase were closely related to the occurrence of paroxysmal atrial fibrillation in patients with congestive heart failure, so an autoimmune process may be an upstream factor in atrial fibrillation.