Safety and efficacy of early radiofrequency catheter ablation in patients with paroxysmal atrial fibrillation complicated with amiodarone-induced thyrotoxicosis

Background: Amiodarone is an antiarrhythmic drug that is frequently used to control atrial fibrillation (AF). Many patients with AF are afraid of the risk of ablation and take amiodar­one, some patients develop amiodarone-induced thyrotoxicosis (AIT). The purpose of the study was to investigate the safety and efficacy of early radiofrequency catheter ablation in patients with paroxysmal AF complicated with AIT. Methods: From the 146 consecutive patients with paroxysmal AF who had been treated with amiodarone and underwent 3-dimensional mapping system guided circumferential pulmonary vein isolation (PVI) at our center from January 2013 to June 2014, 20 had developed AIT. Thirty controls with normal thyroid function and matched for baseline characteristics were selected. Results: Pulmonary vein isolation was completed in all patients without serious complications and with similar procedural (170.60 ± 14.80 vs. 158.18 ± 9.06 min; p = 0.062) and X-ray exposure (16.48 ± 2.15 vs. 15.36 ± 1.57 min; p = 0.058) time in AIT vs. control groups; however, upon coronary sinus catheter pacing (from 300 ms to 200 ms) after intrave­nous isoproterenol administration 30 min post PVI, rates of induction of AF (35% vs. 3.33%; p = 0.005) and of non-pulmonary vein-related atrial tachyarrhythmias (50% vs. 6.67%; p = 0.01) were higher, while those for atrial flutter (15% vs. 3.33%; p = 0.17) and atrial tachycardia (15% vs. 6.67%; p = 0.31) were similar, as was the recovery of conduction of pulmonary vein potential (15% vs. 30%; p = 0.191). In AIT vs. control group, atrial tachyarrhythmia recurrence rate was higher at 3 months (45% vs. 16.67%, p = 0.032) but not between 3 and 12 months (30% vs. 23.33%; p = 0.418) follow-up. Conclusions: Early catheter ablation for paroxysmal AF in patients with AIT appeared safe and effective albeit with higher atrial tachyarrhythmia recurrence rate up to 3 months but not beyond 12 months after PVI relative to controls.

The Changing Landscape for Stroke\ua0Prevention in AF: Findings From the GLORIA-AF Registry Phase 2

Background GLORIA-AF (Global Registry on Long-Term Oral Antithrombotic Treatment in Patients with Atrial Fibrillation) is a prospective, global registry program describing antithrombotic treatment patterns in patients with newly diagnosed nonvalvular atrial fibrillation at risk of stroke. Phase 2 began when dabigatran, the first non\u2013vitamin K antagonist oral anticoagulant (NOAC), became available. Objectives This study sought to describe phase 2 baseline data and compare these with the pre-NOAC era collected during phase 1. Methods During phase 2, 15,641 consenting patients were enrolled (November 2011 to December 2014); 15,092 were eligible. This pre-specified cross-sectional analysis describes eligible patients\u2019 baseline characteristics. Atrial fibrillation disease characteristics, medical outcomes, and concomitant diseases and medications were collected. Data were analyzed using descriptive statistics. Results Of the total patients, 45.5% were female; median age was 71 (interquartile range: 64, 78) years. Patients were from Europe (47.1%), North America (22.5%), Asia (20.3%), Latin America (6.0%), and the Middle East/Africa (4.0%). Most had high stroke risk (CHA2DS2-VASc [Congestive heart failure, Hypertension, Age  6575 years, Diabetes mellitus, previous Stroke, Vascular disease, Age 65 to 74 years, Sex category] score  652; 86.1%); 13.9% had moderate risk (CHA2DS2-VASc = 1). Overall, 79.9% received oral anticoagulants, of whom 47.6% received NOAC and 32.3% vitamin K antagonists (VKA); 12.1% received antiplatelet agents; 7.8% received no antithrombotic treatment. For comparison, the proportion of phase 1 patients (of N = 1,063 all eligible) prescribed VKA was 32.8%, acetylsalicylic acid 41.7%, and no therapy 20.2%. In Europe in phase 2, treatment with NOAC was more common than VKA (52.3% and 37.8%, respectively); 6.0% of patients received antiplatelet treatment; and 3.8% received no antithrombotic treatment. In North America, 52.1%, 26.2%, and 14.0% of patients received NOAC, VKA, and antiplatelet drugs, respectively; 7.5% received no antithrombotic treatment. NOAC use was less common in Asia (27.7%), where 27.5% of patients received VKA, 25.0% antiplatelet drugs, and 19.8% no antithrombotic treatment. Conclusions The baseline data from GLORIA-AF phase 2 demonstrate that in newly diagnosed nonvalvular atrial fibrillation patients, NOAC have been highly adopted into practice, becoming more frequently prescribed than VKA in Europe and North America. Worldwide, however, a large proportion of patients remain undertreated, particularly in Asia and North America. (Global Registry on Long-Term Oral Antithrombotic Treatment in Patients With Atrial Fibrillation [GLORIA-AF]; NCT01468701

Efficacy and effects on cardiac function of radiofrequency catheter ablation vs. direct current cardioversion of persistent atrial fibrillation with left ventricular systolic dysfunction.

OBJECTIVE:To evaluate the effect of catheter ablation vs. direct current synchronized cardioversion (DCC) in patients with persistent atrial fibrillation (AF) and left ventricular systolic dysfunction, and to define baseline features of patients that will get more benefit from ablation. METHODS:From July 2013 to October 2014, 97 consecutive single-center patients with persistent AF and symptomatic heart failure (left ventricular ejection fraction (LVEF) 20% or to over 55%) in 31 (54.39%) patients with worse baseline cardiac function and ventricular rate control. CONCLUSIONS:Catheter ablation relative to cardioversion of persistent AF with symptomatic heart failure yielded better 12-month SR maintenance and cardiac function. Compared with non-responders, patients with improved LVEF post-ablation had poorer ventricular rate control and cardiac function at baseline, suggesting a significant component of tachycardia-induced cardiomyopathy in this group

Emodin protects H9c2 cells from hypoxia-induced injury by up-regulating miR-138 expression

Myocardial infarction (MI) is a common presentation for ischemic heart disease, which is a leading cause of death. Emodin is a Chinese herbal anthraquinone used in several diseases. However, the effect of emodin in hypoxia-induced injury in cardiomyocytes has not been clearly elucidated. Our study aimed to clarify the functions of emodin in hypoxia-induced injury in rat cardiomyocytes H9c2 and explore the underlying mechanism. The effects of emodin on cell viability and apoptosis were analyzed by the Cell counting kit-8 assay and flow cytometry assay, respectively. The cell proliferation- and cell apoptosis-related proteins were detected by western blot. qRT-PCR was used to determine the relative expression of miR-138. Cell transfection was performed to alter miR-138 and MLK3 expression. miR-138 target was performed by dual luciferase activity assay. Sirt1/AKT and Wnt/β-catenin pathways-related factors phosphorylation were analyzed by western blot. Emodin inhibited hypoxia-induced injury in H9c2 cells by promoting cell viability and reducing cell apoptosis. miR-138 was down-regulated by hypoxia treatment but up-regulated by emodin. Up-regulation of miR-138 alleviated hypoxia-induced cell injury. Down-regulation of miR-138 attenuated the growth-promoting effect of emodin on hypoxia-induced injury, whereas up-regulation of miR-138 enhanced the growth-promoting effects of emodin. The underlying mechanism might be by inactivating Sirt1/AKT and Wnt/β-catenin pathways. MLK3 was negatively regulated by miR-138 expression and inactivated Sirt1/AKT and Wnt/β-catenin pathways. Emodin alleviated hypoxia-induced injury in H9c2 cells via up-regulation of miR-138 modulated by MLK3, as well as by activating Sirt1/AKT and Wnt/β-catenin pathways

Changes in LA, LVEDD and heart function in patients maintaining or not SR post ablation.

<p>Changes in LA, LVEDD and heart function in patients maintaining or not SR post ablation.</p

Variables affecting Marked improvement in LVEF post ablation.

<p>Variables affecting Marked improvement in LVEF post ablation.</p

Comparison of baseline clinical characteristics between the two study groups.

<p>Comparison of baseline clinical characteristics between the two study groups.</p

Rho GTPase‑activating protein 1 promotes apoptosis of myocardial cells in an ischemic cardiomyopathy model

Background: Ischemic cardiomyopathy (ICM) leads to heart failure by causing apoptosis of cardiac myocytes. It is generally believed that a therapy targeting apoptosis of cardiac myocytes would improve the prognosis of patients with ischemic heart disease. Aims: We aimed to investigate the role of Rho GTPase‑activating protein 1 (ARHGAP1) in ICM. Methods: The cellular model of myocardial ischemia (H9c2 cell model) and a rat model of ICM were established to explore the expression of ARHGAP1. The overexpression of ARHGAP1 was induced in H9c2 myocardial cells to assess protein function. Results: The expression of ARHGAP1 as a result of hypoxic conditions in the cellular and rat models was observed. Its overexpression induced apoptosis of cultured H9c2 cells under normal atmospheric conditions. ARHGAP1 was also shown to initiate the apoptosis pathway by regulating the cell death modulators B‑cell lymphoma 2 (Bcl‑2) and Bcl‑2‑associated X protein. Conclusions: Our results show that the ARHGAP1 expression is closely associated with apoptosis of myocardial cells, which in turn leads to ICM. Thus, ARHGAP1 may become a novel molecular marker of the hypoxia‑induced apoptosis pathway and serve as a potential therapeutic target in patients with ICM