Catheter ablation for atrial fibrillation in heart failure: untying the Gordian knot.

Atrial fibrillation (AF) and heart failure (HF) are complex clinical entities that occur concomitantly in a significant population of patients, and their prevalence is rising in epidemic proportions. Traditionally, both rate and rhythm control strategies have been regarded as equivalent in the management of dysrhythmia in this AF-HF cohort with escalation of treatment largely guided by symptoms. Both disorders are involved in an elaborate pathophysiological interplay with shared cardiovascular risk factors that contribute to the development and sustenance of both AF and HF.

Chronic total occlusion in an infarct-related coronary artery and the risk of appropriate ICD therapies.

Introduction: Risk stratification for ventricular arrhythmias in patients with ischemic cardiomyopathy needs to be improved. Coronary chronic total occlusions in an infarct-related artery (IRA-CTOs) have been associated with an increased arrhythmic risk. This study aimed to evaluate the association between IRA-CTOs and appropriate implantable cardioverter-defibrillator (ICD) therapies.

The transfemoral approach for cardiac resynchronization therapy.

Cardiac resynchronization (CRT) is a well-established treatment for heart failure and standard superior implantation has a high success rate with acceptable risk profile. When the superior approach is not feasible, surgical epicardial leads are considered. We present a case of transfemoral CRT as a viable alternative to surgical systems and discuss implant factors including lead choice and deep vein thrombosis.

Mechanisms of endothelial senescence.

When endothelial cells from different vascular beds are grown in culture they show a limited capacity to divide, eventually entering into a permanent and phenotypically distinctive non-dividing state referred to as 'replicative senescence'. Replicative senescence is thought to result from progressive shortening of telomeric DNA and consequent telomere dysfunction. More recently, it has been realised that senescence can also be induced by a variety of insults, including those causing intracellular oxidative stress.