Electrical and histological remodeling of the pulmonary vein in 2K1C hypertensive rats: Indication of initiation and maintenance of atrial fibrillation.

OBJECTIVE: Hypertension 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. METHODS: Fifty 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-ß1 (TGF-ß1), 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. RESULTS: At 4 months, the 2K1C hypertensive rats developed LA dilation. Col deposition in LSPV and left atrium and expression of TGF-ß1, 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. CONCLUSION: Hypertension 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.

Myocardial injury resulting from radiofrequency catheter ablation: comparison of circumferential pulmonary vein isolation and complex fractionated atrial electrograms ablation.

BACKGROUND: Radiofrequency catheter ablation (RFCA) necessarily produces an area of myocardial necrosis. However, the difference of the extent of myocardial injury between circumferential pulmonary vein isolation (CPVI) and complex fractionated atrial electrograms (CFAE) ablation in patients with atrial fibrillation (AF) has not been investigated before. METHODS: Twenty-nine consecutive male patients (n = 29) with either paroxysmal or persistent AF were selected for CPVI or CFAE ablation. The CPVI or CFAE ablation was performed with a three-dimensional electroanatomical mapping system (CARTO). Serum cardiac biomarkers, for example, cardiac troponin T (cTnT), aspartate transaminase (AST), lactate dehydrogenase (LDH), creatine kinase (CK), and creatine kinase myocardial bound (CKMB) were determined by the Elecsys STATE immunoassay. Cardiac structure and function were measured with echocardiography. RESULTS: Echocardiography showed that there was no significant difference of atrioventricular structure or function parameters between the CPVI group and the CFAE ablation group. Serum cTnT showed a significant increase in the CFAE ablation group over the CPVI group at 12 and 24 hours after the procedure (P < 0.05, respectively), and then it was reduced to a normal level after 48 hours. Serum AST showed a significant increase in the CFAE ablation group over the CPVI group at post-procedure, 4 and 12 hours after the procedure (P < 0.05, respectively), and then it reached to a normal level after 24 hours. There was no significant difference in LDH, CK, or CKMB levels between the CFAE ablation group and the CPVI group at any time point (P > 0.05). CONCLUSIONS: cTnT and AST other than LDH, total CK or CKMB activity significantly increased more in the CFAE ablation group than the CPVI group. However, the difference of the serum levels of cTnT, AST between two groups was temporary.