Diastolic dysfunction and risk of atrial fibrillation: a mechanistic appraisal.

Atrial fibrillation (AF) is the most common sustained arrhythmia, and its prevalence in the population is increasing.1 Diastolic dysfunction shares many common risk factors with AF, including age, hypertension,2–5 obesity,6,7 and diabetes.8,9 Like AF, diastolic dysfunction increases with age,10 and patients given the diagnosis of diastolic dysfunction are more likely to have AF at the time.11 Diastolic dysfunction has significant pathological effects on atrial structure and function, many of which are proarrhythmic. However, much remains to be learned about the specific mechanisms through which diastolic dysfunction ultimately promotes AF. Previous reviews have examined the broad association of diastolic dysfunction and AF.12 In this review, we attempt to examine this association on a mechanistic level. We begin with a basic review of the physiology of diastolic function, with particular attention to the complex interaction between the atrium and the ventricle during diastole. We then provide an overview of some of the most common clinical methods to quantify diastolic function and highlight the strengths and weaknesses of these methods with regard to providing an accurate picture of this physiology. We describe how these methods are applied to diagnose diastolic dysfunction, including the development of a widely adopted classification scheme of diastolic dysfunction. We then review the limited clinical data available connecting diastolic dysfunction with the risk of incident, nonvalvular AF, with a focus on studies examining diastolic dysfunction in populations without structural heart disease—ie, with preserved systolic function in the absence of hypertrophic cardiomyopathic disease or congenital heart disease. Finally, we attempt to reconcile the results of these clinical studies with experimental data in both human, animal, and cellular models, to create a mechanistic link between diastolic dysfunction and pathological changes that increase the likelihood of AF.