Determination of sources of error and improvement in accuracy of left ventricular mass measurement by echocardiography.

Abnormal Left ventricular mass (LVM) prognosticates adverse cardiovascular events. Conventionally, LVM measured by echo assumes a prolate ellipsoid (PE) shape; however, it poorly correlates with reference standard of cardiac magnetic resonance imaging (CMR) derived LVM. PE model assumes LVL = 2 × LVID.

Adipogenic Signaling Promotes Arrhythmia Substrates before Structural Abnormalities in TMEM43 ARVC.

Arrhythmogenic right ventricular cardiomyopathy (ARVC) is a genetic disorder of desmosomal and structural proteins that is characterized by fibro-fatty infiltrate in the ventricles and fatal arrhythmia that can occur early before significant structural abnormalities. Most ARVC mutations interfere with β-catenin-dependent transcription that enhances adipogenesis; however, the mechanistic pathway to arrhythmogenesis is not clear. We hypothesized that adipogenic conditions play an important role in the formation of arrhythmia substrates in ARVC.

Low voltage-guided ablation of posterior wall improves 5-year arrhythmia-free survival in persistent atrial fibrillation.

Introduction: The posterior wall (PW) has been proposed as a standard target for ablation beyond pulmonary vein antral isolation (PVI) in patients with persistent atrial fibrillation (AF). However, studies have shown inconsistent outcomes with the addition of PW ablation. The presence or absence of low voltage on the PW may explain these inconsistencies.

Human Cardiac Mesenchymal Stem Cells Remodel in Disease and Can Regulate Arrhythmia Substrates.

Background: The mesenchymal stem cell (MSC), known to remodel in disease and have an extensive secretome, has recently been isolated from the human heart. However, the effects of normal and diseased cardiac MSCs on myocyte electrophysiology remain unclear. We hypothesize that in disease the inflammatory secretome of cardiac human MSCs (hMSCs) remodels and can regulate arrhythmia substrates.

Improvement in renal function following cryoballoon ablation for atrial fibrillation.

Purpose: Patients with chronic kidney disease are predisposed to heart rhythm disorders including atrial fibrillation (AF). Several studies have suggested that radiofrequency catheter ablation of AF improves renal function. However, little data exists for pulmonary vein isolation with cryoballoon ablation (CBA).

Use of the cryoballoon to ablate pulmonary vein-dependent left atrial flutter.

New atrial flutter (AFL) that arises after pulmonary vein isolation (PVI) by catheter or surgical ablation can originate from reconnection of a pulmonary vein (PV). Reisolation of PVs with cryoballoon ablation (CBA) for treatment of peri-PV AFL after Maze or PVI has not previously been reported. The present case series describes use of CBA to treat post-PVI and post-Maze PV-dependent AFL.

A novel risk model for very late return of atrial fibrillation beyond 1 year after cryoballoon ablation: the SCALE-CryoAF score.

Purpose: Cryoballoon ablation (CBA) is an effective technique for pulmonary vein isolation (PVI). To date, there are no risk models to predict very late recurrence of atrial fibrillation (VLRAF) after CBA.

Methods: Retrospective analysis of a single-center database was performed.

Patient characteristics as predictors of recurrence of atrial fibrillation following cryoballoon ablation.

Background: While several studies have evaluated predictors for atrial fibrillation (AF) recurrence following catheter ablation, there are limited data specific to cryoballoon ablation (CBA).

Methods: We analyzed a prospective registry of patients at a single institution who underwent CBA. Recurrence of AF (RAF) was defined as recurrence of AF by 12-month follow-up, excluding the 3-month blanking period.

Outcomes With Novel Oral Anticoagulants in Obese Patients who Underwent Electrical Cardioversion for Atrial Tachyarrhythmias.

The efficacy of novel oral anticoagulants (NOACs) in severely obese patients is uncertain as volume of distribution is related to weight, and few such patients were enrolled in the pivotal trials. As the month after direct-current cardioversion (DCCV) for atrial fibrillation and atrial flutter is a high-risk period for stroke, we sought to evaluate the safety of performing DCCV in obese patients on NOAC. All patients who underwent DCCV after ≥3 weeks of NOAC or therapeutic warfarin treatment without a previous transesophageal echocardiogram over a 3-year period at a single center were included.

Mesenchymal stem cells suppress cardiac alternans by activation of PI3K mediated nitroso-redox pathway.

Background: The paracrine action of non-cardiac progenitor cells is robust, but not well understood. Mesenchymal stem cells (MSC) have been shown to enhance calcium (Ca(++)) cycling in myocytes. Therefore, we hypothesized that MSCs can suppress cardiac alternans, an important arrhythmia substrate, by paracrine action on Ca(++) cycling.

Clinical and economic studies of eptifibatide in coronary stenting.

Platelet adhesion and aggregation at the site of coronary stenting can have catastrophic clinical and economic consequences. Therefore, effective platelet inhibition is vital during and after percutaneous coronary intervention. Eptifibatide is an intravenous antiplatelet agent that blocks the final common pathway of platelet aggregation and thrombus formation by binding to glycoprotein IIb/IIIa receptors on the surface of platelets.

Platelet-activating factor enhancement of calcium influx and interleukin-6 expression, but not production, in human microglia.

Calcium-sensitive fluorescence microscopy and molecular biology analysis have been used to study the effects of platelet-activating factor (PAF) on intracellular calcium [Ca2+]i and IL-6 expression in human microglia. PAF (applied acutely at 100 nM) elicited a biphasic response in [Ca2+]i consisting of an initial rapid increase of [Ca2+]i due to release from internal stores, followed by a sustained influx. The latter phase of the [Ca2+]i increase was blocked by SKF96365, a non-selective store-operated channel (SOC) inhibitor.

Minocycline inhibits neuronal death and glial activation induced by beta-amyloid peptide in rat hippocampus.

Minocycline, a second-generation tetracycline compound, has been examined as a neuroprotectant in beta-amyloid (A beta)-injected rat hippocampus. At 7 days post-injection, A beta(1-42) caused a significant loss of granule cell layer neurons (28% reduction) compared to control uninjected hippocampus. Hippocampal injection of A beta peptide also led to marked gliosis with numbers of microglia (increased by 26-fold) and immunoreactivity of astrocytes (increased by 11-fold) relative to control, as determined from immunohistochemical analysis.