Abstract
Atrial fibrillation (AF) is a highly prevalent cardiac arrhythmia characterized by atrial remodeling. Complement C1q tumor necrosis factor-related protein 3 (CTRP3) is one of the adipokines associated with obesity, diabetes, and coronary heart disease. The association between plasma CTRP3 levels and AF is uncertain. The aim of this study was to investigate whether plasma CTRP3 concentrations were correlated with AF. Our study included 75 AF patients who underwent catheter ablation at our hospital and 47 sinus rhythm patients to determine the difference in plasma CTRP3 concentrations. Blood samples before the ablation were collected, and ELISA was used to measure the concentrations of CTRP3. Plasma CTRP3 concentrations were significantly lower in AF patients compared with control group (366.9 ± 105.2 ng/ml vs. 429.1 ± 100.1 ng/ml, p = 0.002). In subgroup studies, patients with persistent AF had lower plasma CTRP3 concentrations than those with paroxysmal AF (328.3 ± 83.3 ng/ml vs. 380.0 ± 109.2 ng/ml, p = 0.037). The concentrations of plasma CTRP3 in the recurrence group after radiofrequency catheter ablation of AF were lower than those in the nonrecurrence group (337.9 ± 77.3 ng/ml vs. 386.6 ± 108.1 ng/ml, p = 0.045). Multivariate regression analysis revealed the independent correlation between plasma CTRP3 level and AF. Plasma CTRP3 concentrations were correlated with the presence of AF and AF recurrence.
Highlights
Atrial fibrillation (AF) is one of the most common arrhythmia in clinical practice
Current studies suggest that atrial remodeling [2], inflammatory factors [3], oxidative stress [4], and the effects of the autonomic nervous system [5] are mechanisms related to AF development
The correlation between adiponectin and CITP in patients with persistent AF suggested that adiponectin was involved in atrial remodeling, which was related to the occurrence and maintenance of atrial fibrillation
Summary
Atrial fibrillation (AF) is one of the most common arrhythmia in clinical practice. Research has identified a multitude of pathophysiological processes contributing to the initiation, maintenance, and progression of AF. Many aspects of AF pathophysiology have not yet been fully elucidated. Current studies suggest that atrial remodeling [2], inflammatory factors [3], oxidative stress [4], and the effects of the autonomic nervous system [5] are mechanisms related to AF development. The treatment of atrial fibrillation is essential. Catheter-based ablation technologies which have made the procedure safer, more comfortable to perform, and more effective after a single attempt have greatly improved the outcomes, but AF recurrence is still common [1, 6]
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