Introduction: The incidence and clinical outcome of pericardial and pleural effusion after cryoballoon ablation (CBA) or radiofrequency catheter ablation (RFCA) of atrial fibrillation (AF) have not been fully investigated.Methods: A total of 60 patients with paroxysmal AF were treated with either CBA (n = 30) or RFCA (n = 30) groups, with assessment of serum troponin I level, left atrial pulmonary vein computed tomography (CT) angiography and echocardiography within 24 hours before ablation, and serum troponin I level at 12 hours, and chest CT and echocardiography within 24 hours postablation. Repeat chest CT was performed 1 month after the index procedure in patients with pericardial or pleural effusion.Results: With similarly distributed baseline characteristics, the CBA group relative to the RFCA group had postablation: higher serum troponin I level (13.48 vs 1.84 µg/L, P < .001); similarly high pericardial effusion rates on chest CT (80% vs 93.3%, P > .05), with chest CT yielding significantly higher detection rate than echocardiography; similarly high pleural effusion rates on chest CT (73.3% vs 80%, P > .05); and smaller maximum depths on chest CT cross-section of pericardial effusion (5.21 ± 3.37 vs 7.13 ± 2.68 mm, P < .05) and pleural effusion bilaterally (left: 4.16 ± 4.90 vs 6.96 ± 5.42 mm; right: 5.04 ± 4.46 vs 7.55 ± 4.95 mm, both P < .05). The effusions selfresolved within a mean period of 1 month.Conclusions: Both CBA and RFCA were associated with high rates of pericardial and pleural effusion, with RFCA yielding numerically higher incidence and significantly higher effusion extent, and chest CT significantly higher detection rates than echocardiography. K E Y W O R D S atrial fibrillation, catheter ablation, pericardial effusion, pleural effusion

RFW APs resistant to conventional catheter ablation might be due to unique anatomic AP features such as more epicardial course at the annulus level with atrial insertion distant from the tricuspid annulus. Electroanatomic mapping is helpful to accurately localize the atrial insertion sites of these APs and facilitates catheter ablation.

ObjectiveHypertension is a significant risk factor for atrial fibrillation (AF). The role of pulmonary vein (PV) remodeling in the mechanistic association between hypertension and AF is not definitive. In this study, we aimed to identify changes in the electrophysiology and histology in PVs in two-kidney, one-clip (2K1C) hypertensive rats.MethodsFifty male Sprague-Dawley rats were classified into the 2K1C and sham-operated groups. The systolic blood pressure was measured every 2 weeks. The left atrial diameter was measured by transthoracic echocardiography. Left superior PV (LSPV) and left atrial (LA) fibrosis was evaluated by Masson’s trichrome staining. The expression of fibrosis markers [angiotensin II (Ang II), transforming growth factor-β1 (TGF-β1), matrix metalloproteinase-2 (MMP-2), and collagen I (Col I)] and ion channels [Kir2.1, Kir2.3, Cav1.2, and Nav1.5] in LSVP was quantified by western blot. Conventional microelectrodes were used to record the action potential duration at 90% repolarization (APD90) and effective refractory period (ERP) in isolated LA.ResultsAt 4 months, the 2K1C hypertensive rats developed LA dilation. Col deposition in LSPV and left atrium and expression of TGF-β1, MMP-2, and Col I in LSPV were significantly increased in 2K1C hypertensive rats. In addition, hypertension reduced the expression of Nav1.5 and Kir2.1, although there were no significant differences in APD90; ERP; and expression of Ang II, Kir2.3, and Cav1.2 between the two groups.ConclusionHypertension may lead to changes in the electrophysiology and histology of rats PVs, which is characterized by significant reduction in the expression of Nav1.5 and Kir2.1 and increase in interstitial fibrosis. These observations may clarify the role of PVs in the mechanistic association between hypertension and AF.