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Atrial fibrillation (AF) is the most common cardiac arrhythmia. Currently more than six million people in Europe are affected by AF and this number is expected to increase twofold during the next 30–50 years, partly due to the ageing population.1 AF is not a benign disease as it is responsible for an increased risk of death, stroke, and heart failure, reduced exercise capacity and left ventricular dysfunction, and an impaired quality of life. It is therefore important to develop safe treatment strategies for AF in order to improve outcome and to promote healthy ageing. Treatment of AF, however, is not straightforward due to the progressive nature of the arrhythmia, the wide range of associated diseases, and differences in presentation between patients. The complexity of the ‘syndrome’ requires that AF treatment should be tailored to the individual patient. The purpose of this article is to review new treatment options for AF to optimise patient tailored therapy, in the context of the natural time course and complexity of AF, and with the main focus on rhythm control.
Natural time course of AF
AF has a multifactorial aetiology, the pathophysiology of AF being complex and incompletely understood. Over the past years the role of structural remodelling in the initiation and perpetuation of AF has increasingly become apparent. Structural remodelling can be caused by: well known risk factors of AF development such as age, hypertension, heart failure, valve disease, and diabetes; less well known risk factors such as endurance training, obesity, sleep apnoea syndrome, and chronic obstructive pulmonary disease; and other factors such as altered metabolism, autonomic changes, and genetic and environmental influences.1 2 These factors induce atrial structural changes through various pathways including the renin–angiotensin–aldosterone system (RAAS) and inflammation, leading to enlarged atria, …
Competing interests In compliance with EBAC/EACCME guidelines, all authors participating in Education in Heart have disclosed potential conflicts of interest that might cause a bias in the article. Isabelle van Gelder has received consulting fees/honoraria from Medtronic, MSD, Sanofi-Aventis, Boehringer Ingelheim, and Aga medical, and research grants from the Netherlands Heart Foundation, the Interuniversity Cardiology Institute the Netherlands, and from Astra Zeneca, Biotronik, Medtronic, Sanofi-Aventis, Boehringer Ingelheim, St Jude Medical, and Boston Scientific.
Provenance and peer review Commissioned; internally peer reviewed
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