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. METHODS AND RESULTS: Observational cohort study that included 342 patients with ischemic cardiomyopathy, an ICD implanted for primary or secondary prevention, and a coronary angiography performed shortly before ICD implantation. The ICD was implanted for primary prevention in 163 patients (48%). IRA-CTO was found in 161 patients (47%). During a median follow-up of 33 months, 41% of patients experienced at least one appropriate ICD therapy. Patients with IRA-CTO had higher proportions of appropriate ICD therapies (57% vs. 26%, P < 0.001) and appropriate ICD shocks (40% vs. 17%, P < 0.001). At multivariate Cox regression, IRA-CTO was the only variable that consistently resulted as independent predictor of appropriate ICD therapies and shocks both in the global population of the study (HR 2.3, P < 0.001 and HR 3, P < 0.001, respectively) and when analyzing separately patients with primary or secondary prevention ICD. CONCLUSIONS: IRA-CTO is an independent predictor of appropriate ICD therapies, including appropriate ICD shocks. This association is consistent across all the subgroups analyzed. Patients with IRA-CTO have a very high risk of appropriate ICD therapies. These findings may help improving risk stratification as well as the management of ventricular arrhythmias in patients with ischemic cardiomyopathy.

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.

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. Recent studies and continued development of evidence to support catheter ablation for AF has brought into question the traditional belief in equivalence between rate and rhythm control. Indeed, recent trials, in particular the CASTLE-AF (Catheter Ablation versus Standard Conventional Therapy in Patients with Left Ventricular Dysfunction and Atrial Fibrillation) study, suggest that catheter ablation for AF improves survival and rates of hospitalisation in patients with concomitant HF and AF, threatening a paradigm shift in the management of this patient cohort. The evident mortality benefit from clinical trials suggests that catheter ablation for AF should be considered as a therapeutic intervention in all suitable patients with the AF-HF syndrome as these patients may derive the greatest benefit from restoration of sinus rhythm. Further research is needed to refine the evidence base, especially to determine which subgroup of HF patients benefit most from catheter ablation and what is the optimal timing.

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. In this report, we review evidence for the occurrence of endothelial cell senescence in vivo. We will also examine the causes, mechanisms and regulation of this process as they emerge from our studies in cell culture, focusing in particular on the roles of oxidative stress, telomerase, growth factors and nitric oxide.