Songwen Chen

Procedural Arrhythmia Termination and Long-Term Single-Procedure Clinical Outcome in Patients with Non-paroxysmal Atrial Fibrillation

The influence of procedural arrhythmia termination on long‐term single‐procedure clinical outcome in patients with non‐paroxysmal atrial fibrillation (AF) remains controversial.

Nav1.8 channels in ganglionated plexi modulate atrial fibrillation inducibility

AIMS Emerging evidences indicate that SCN10A/NaV1.8 is associated with cardiac conduction and atrial fibrillation, but the exact role of NaV1.8 in cardiac electrophysiology remains poorly understood. The present study was designed to investigate the effects of blocking NaV1.8 channels in cardiac ganglionated plexi (GP) on modulating cardiac conduction and atrial fibrillation inducibility in the canine model. METHODS AND RESULTS Thirteen mongrel dogs were randomly enrolled. Right cervical vagus nerve stimulation (VNS) was applied to determine its effects on the sinus rate, ventricular rate during atrial fibrillation, PR interval, atrial effective refractory period, and the cumulative window of vulnerability. The NaV1.8 blocker A-803467 (1 μmol/0.5 mL per GP, n = 7) or 5% DMSO/95% polyethylene glycol (0.5 mL per GP, n = 6, control) was injected into the anterior right GP and the inferior right GP. The effects of VNS on the sinus rate, ventricular rate, PR interval, atrial effective refractory period, and the cumulative window of vulnerability were significantly eliminated at 10, 35, and 90 min after A-803467 injection. In separate experiments (n = 8), A-803467 blunted the slowing of sinus rate with increasing stimulation voltage of the anterior right GP at 10 min after local injection. CONCLUSIONS Blockade of NaV1.8 channels suppresses the effects of VNS on cardiac conduction and atrial fibrillation inducibility, most likely by inhibiting the neural activity of the cardiac GP.

Lysophosphatidic Acid Increases the Electrophysiological Instability of Adult Rabbit Ventricular Myocardium by Augmenting L-Type Calcium Current

Lysophosphatidic acid (LPA) has diverse actions on the cardiovascular system and is widely reported to modulate multiple ion currents in some cell types. However, little is known about its electrophysiological effects on cardiac myocytes. This study investigated whether LPA has electrophysiological effects on isolated rabbit myocardial preparations. The results indicate that LPA prolongs action potential duration at 90% repolarization (APD90) in a concentration- and frequency-dependent manner in isolated rabbit ventricular myocytes. The application of extracellular LPA significantly increases the coefficient of APD90 variability. LPA increased L-type calcium current (ICa,L) density without altering its activation or deactivation properties. In contrast, LPA has no effect on two other ventricular repolarizing currents, the transient outward potassium current (Ito) and the delayed rectifier potassium current (IK). In arterially perfused rabbit left ventricular wedge preparations, the monophasic action potential duration, QT interval, and Tpeak-end are prolonged by LPA. LPA treatment also significantly increases the incidence of ventricular tachycardia induced by S1S2 stimulation. Notably, the effects of LPA on action potentials and ICa,L are PTX-sensitive, suggesting LPA action requires a Gi-type G protein. In conclusion, LPA prolongs APD and increases electrophysiological instability in isolated rabbit myocardial preparations by increasing ICa,L in a Gi protein-dependent manner.

A dual-loop bi-atrial macro-reentry flutter during atrial fibrillation ablation.

Dual-loop macro-reentry atrial flutter (AFL) is an atypical AFL, which has two loops of the reentry circuit usually localized within single atrium. In this case report, we present a double-loop bi-atrial flutter during atrial fibrillation ablation, in which the two reentry circuit loops were located around the inferior vena cava (IVC) and the mitral annulus, (MA) respectively.

Renal Denervation Suppresses the Inducibility of Atrial Fibrillation in a Rabbit Model for Atrial Fibrosis.

Renal denervation (RD) was reported to reduce the susceptibility of atrial fibrillation (AF), but the underlying mechanism has not been well understood. This study was performed to investigate the effect of RD on the inducibility of AF in a rabbit model for atrial fibrosis and to explore the potential mechanisms. Thirty-five rabbits were randomly assigned into sham-operated group (n = 12), abdominal aortic constriction (AAC) group (n = 12) and AAC with RD (AAC-RD) group (n = 11). The incidence of AF induced by burst pacing in atriums was determined. Blood was collected to measure the levels of rennin, angiotensin II and aldosterone. Atrial samples were preserved to evaluate protein and gene expression of collagen, connective tissue growth factor (CTGF) and transforming growth factor-β1 (TGF-β1). Our data suggested cardiac structure remodeling and atrial fibrosis were successfully induced by AAC. Compared with the AAC group, the AAC-RD rabbits had smaller ascending aortic diameter and left ventricular end-systolic diameter. For burst pacing at the left atrium (LA), AF was induced in two of the 12 rabbits in the sham-operated group, 10 of the 12 rabbits in the AAC group, and 2 of the 11 rabbits in the AAC-RD group, with great difference among the three groups (P = 0.001). The percentage of LA burst stimulations with induced AF achieved 47.2% in the AAC group, which was higher than those in both the AAC-RD (12.1%) and the Sham-operated (5.6%) groups. Significantly increasing intercellular space in the AAC group (P<0.001) compared with the sham-operated rabbits. RD clearly decreased the volume fraction of collagen in LA and right atrium compared with that of the AAC group (P< 0.01). AAC-induced elevation of collagen I, CTGF and TGF-β1 was suppressed by RD. In conclusion, RD suppressed the inducibility of AF in a rabbit model for pressure associated atrial fibrosis, potentially by modulating renin-angiotensin-aldosterone system and decreasing pro-fibrotic factors.

Multiple Manifested Accessory Atrioventricular Pathways in a Patient without Obvious Structural Heart Disease

A 53-year-old man was referred for treatment of preexcitation syndrome, which was first diagnosed after having had cardioversion for presyncope due to atrial fibrillation. He had hypertension controlled with losantan. The ECG indicated multiple accessory pathways (APs), located on the tricuspid annulus (TVA). Echocardiography revealed a dilated left atrium and slight left ventricular hypertrophy (associated with hypertension) without Ebstein anomaly. The procedure was performed with a three-dimensional (3-D) mapping system (CARTO 3). Manifested APs were mapped

Clinical implications of and factors influencing dissociated pulmonary vein potentials

BACKGROUND Factors influencing dissociated pulmonary vein (PV) potentials (DPVPs) in atrial fibrillation (AF) patients undergoing circumferential PV isolation have not been investigated. Furthermore, the clinical implications of such DPVPs remain controversial. METHODS Circumferential PV isolation as a first ablation procedure was performed in 688 consecutive patients with AF (460 men; mean age, 58.9±10.5 years). The clinical implications of and factors influencing DPVPs were evaluated. RESULTS Acute PV isolation was achieved in 679 (98.7%) patients. A total of 578 (42.6%) ipsilateral PVs with DPVPs were documented in 378 (55.7%) patients (DPVPs group). Multivariate analysis revealed that male gender [odds ratio (OR): 1.894; 95% confidence interval (CI): 1.344-2.667; p<0.001] and paroxysmal AF (OR: 1.715; 95% CI: 1.182-2.488; p=0.005) were independent factors for DPVPs. The incidence of acute and intraoperative PV reconnection (PVR) was higher in the DPVPs group than in the non-DPVPs group (33.1% vs. 17.9%; p<0.001 and 44.4% vs. 28.2%; p<0.001). After the first procedure, 244 (65.6%) DPVPs-group patients and 168 (56.4%; p=0.015) non-DPVPs group patients were free from AF recurrence. During repeat procedures, PVR incidence was similar in the DPVPs group (81.8%) and non-DPVPs groups (83.3%; p=0.863). CONCLUSION Male gender and paroxysmal AF were independent risk factors for DPVPs in patients undergoing circumferential PV isolation. DPVPs had a significant impact on acute and intraoperative PVR. The outcomes of the first ablation procedure were better in patients with DPVPs.

Association of SCN10A Polymorphisms with the Recurrence of Atrial Fibrillation after Catheter Ablation in a Chinese Han Population

The nonsynonymous SCN10A single nucleotide polymorphism (SNP) rs6795970 has been reported to associate with PR interval and atrial fibrillation (AF) and in strong linkage disequilibrium (LD) with the AF-associated SNP rs6800541. In this study, we investigated whether rs6795970 polymorphisms are associated with AF recurrence after catheter ablation. A total of 502 consecutive patients with AF who underwent catheter ablation were included. AF recurrence was defined as a documented episode of any atrial arrhythmias lasting ≥30 s after a blanking period of 3 months. AF recurrence was observed between 3 and 12 months after catheter ablation in 24.5% of the patients. There was a significant difference in the allele distribution (p = 7.86 × 10−5) and genotype distribution (p = 1.42 × 10−5) of rs6795970 between the AF recurrence and no recurrence groups. In a multivariate analysis, we identified the following independent predictors of AF recurrence: the rs6795970 genotypes in an additive model (OR 0.36, 95%CI 0.22~0.60, p = 7.04 × 10−5), a history of AF ≥36 months (OR 3.57, 95%CI 2.26~5.63, p = 4.33 × 10−8) and left atrial diameter (LAD) ≥40 mm (OR 1.85, 95%CI 1.08~3.19, p = 0.026). These data suggest that genetic variation in SCN10A may play an important role in predicting AF recurrence after catheter ablation in the Chinese Han population.

Potential role of cyanidin 3-glucoside (C3G) in diabetic cardiomyopathy in diabetic rats: An in vivo approach

The present study aimed to evaluate the importance of cyanidin 3-glucoside (C3G) of diabetic cardiomyopathy in diabetic rats. The rats were induced with diabetic using streptozotocin and total triglyceride (TG) and total cholesterol (TC) were determined. The range of myocardial enzymes such as aspartate aminotransferase (AST), creatine kinase (CK) and lactate dehydrogenase (LD) were also estimated, further, the Immuno histochemical analysis and western blot investigation were determined for the actual activity of C3G. Results indicated that the marker enzymes such as CK, LD and AST were significantly (P < 0.05) increased in STZ administered rats (DM group), while the levels of these elevated marker enzymes of cardiac injury significantly (P < 0.05) declined in the DM + C3G group, as compared to the diabetic group of rats. Additionally, a decrease in the level of TNF-alpha and interleukin-6, was noticed in the C3G treated group as compared to diabetic group. Finally, blotting analysis clearly confirmed that theC3G treatment resulted to higher level response of Bcl-2 and lower level response of caspase-3 and BAX. In conclusion, C3G a natural antioxidant may prevent cardiovascular complications by ameliorating oxidative damage, inflammation, metabolic dysfunctions and apoptosis pathways in type 2 diabetes.

Lysophosphatidic acid as a potential trigger of atrial fibrillation

Atrial fibrillation (AF) is the most common arrhythmia in clinical practice, but its pathogenesis is incompletely understood. Current evidences have highlighted the progression of atrial fibrosis and electrophysiological remodeling in AF development. Lysophosphatidic acid (LPA), the simplest phospholipid, is associated with fibrotic disease and promotes proliferation of a wide variety of fibroblast. It was demonstrated that LPA stimulation in many cell types such as human endothelial cells, human renal fibroblasts, and myoblasts, significantly upregulates connective tissue growth factor (CTGF) expression, which acts as a downstream signaling effector for transforming growth factor-β1 (TGF-β1) to drive fibrosis. We hypothesized that LPA could also evoke growth factor-like responses to atrial fibroblast, and subsequently induce atrial fibrosis to trigger AF. LPA is also verified to involve in numerous electrophysiological activities in non-myocardiocytes. So LPA is a possible cause of AF by initiating fibrosis response and altering electrophysiological properties in atrium. If the hypothesis is confirmed, LPA will act as a new target for AF treatment and administration of LPA receptor blockers may be applied in the prophylaxis of AF.