Atrial fibrillation (AF) is the most common arrhythmia experienced in clinical practice, and is responsible for significant morbidity and mortality.1 It affects more than 6 million people in Europe.1 The lifetime risk of developing AF after the age of 40 is approximately 25 %.1 AF is a major public health burden as it is associated with an increased risk of stroke by fivefold, dementia by twofold, heart failure by threefold and mortality by twofold.1,2
Current therapeutic options include non-invasive treatment using antiarrhythmic agents and invasive methods using catheter ablation.3,4 Although several improvements have been achieved, challenges still remain. Pulmonary vein isolation is now an established treatment, especially for patients with paroxysmal AF, but success rates (freedom from AF) in persistent AF are still insufficient.3,5,6 To further improve AF treatment, mechanisms underlying AF initiation and maintenance have to be further elucidated to better enable identification of the most suitable treatment strategy for each individual patient (in terms of drug toxicity, freedom of AF symptoms and improved quality of life) and recognition of patients at high risk for AF.
In recent years our understanding of AF pathophysiology has markedly improved by the identification of key players in cardiovascular signalling: microRNAs (miRNAs).7 We will provide a comprehensive overview of the role of miRNAs in AF and their potential therapeutic implications.