Novel Therapeutic Targets in the Management of Atrial Fibrillation
Novel Therapeutic Targets in the Management of Atrial Fibrillation
Atrial fibrillation (AF) is the most common cardiac arrhythmia, contributing to increased morbidity and reduced survival through its associations with stroke and heart failure. AF contributes to a four- to fivefold increase in the risk of stroke in the general population and is responsible for 10–15 % of all ischemic strokes. Diagnosis and treatment of AF require considerable health care resources. Current therapies to restore sinus rhythm in AF are suboptimal and are limited either by their proarrhythmic effects or by their procedure-related complications. These limitations have necessitated identification of newer therapeutic targets to expand the treatment options. There has been a considerable amount of research interest in investigating the mechanisms of initiation and propagation of AF. Despite extensive research focused on the pathogenesis of AF, a thorough understanding of various pathways mediating initiation and propagation of AF still remains limited. Research efforts focused on the identification of these pathways and molecular mediators have generated a great degree of interest for developing more targeted therapies. This review discusses the potential therapeutic targets and the results from experimental and clinical research investigating these targets.
Atrial fibrillation (AF) is the most common cardiac arrhythmia encountered in clinical practice, contributing to increased morbidity and reduced survival through its associations with stroke, thromboembolism and heart failure. Current antiarrhythmic drugs remain limited in their efficacy and carry the risk of adverse effects, including proarrhythmia. The landmark discovery by Haïssaguerre et al. that arrhythmogenic triggers in the pulmonary veins contributed to some cases of AF led to the development of pulmonary vein isolation as an effective interventional therapy for symptomatic drug-refractory AF. Catheter ablation, although efficacious, remains limited because of its invasive nature and possible procedural complications. The current medical and invasive AF rhythm control strategies necessitate research focused on the identification of newer therapeutic targets to expand available treatment options. Despite the fact that the pathophysiology of AF has been extensively investigated for almost a century, the precise mechanisms leading to and maintaining AF still remains elusive. This review focuses on the ° mechanisms of AF that might represent targets for future novel AF therapies.
Abstract and Introduction
Abstract
Atrial fibrillation (AF) is the most common cardiac arrhythmia, contributing to increased morbidity and reduced survival through its associations with stroke and heart failure. AF contributes to a four- to fivefold increase in the risk of stroke in the general population and is responsible for 10–15 % of all ischemic strokes. Diagnosis and treatment of AF require considerable health care resources. Current therapies to restore sinus rhythm in AF are suboptimal and are limited either by their proarrhythmic effects or by their procedure-related complications. These limitations have necessitated identification of newer therapeutic targets to expand the treatment options. There has been a considerable amount of research interest in investigating the mechanisms of initiation and propagation of AF. Despite extensive research focused on the pathogenesis of AF, a thorough understanding of various pathways mediating initiation and propagation of AF still remains limited. Research efforts focused on the identification of these pathways and molecular mediators have generated a great degree of interest for developing more targeted therapies. This review discusses the potential therapeutic targets and the results from experimental and clinical research investigating these targets.
Introduction
Atrial fibrillation (AF) is the most common cardiac arrhythmia encountered in clinical practice, contributing to increased morbidity and reduced survival through its associations with stroke, thromboembolism and heart failure. Current antiarrhythmic drugs remain limited in their efficacy and carry the risk of adverse effects, including proarrhythmia. The landmark discovery by Haïssaguerre et al. that arrhythmogenic triggers in the pulmonary veins contributed to some cases of AF led to the development of pulmonary vein isolation as an effective interventional therapy for symptomatic drug-refractory AF. Catheter ablation, although efficacious, remains limited because of its invasive nature and possible procedural complications. The current medical and invasive AF rhythm control strategies necessitate research focused on the identification of newer therapeutic targets to expand available treatment options. Despite the fact that the pathophysiology of AF has been extensively investigated for almost a century, the precise mechanisms leading to and maintaining AF still remains elusive. This review focuses on the ° mechanisms of AF that might represent targets for future novel AF therapies.
Source...