Atrial fibrillation (AF) is the most common sustained arrhythmia. Congestive heart failure (CHF), an increasingly frequent cardiovascular disorder affecting millions of people world-wide, has become the most important risk factor of AF in developed countries, as a result of ageing populations. Approximately two thirds of patients with CHF are >65 years of age and likely to have AF as a coexistent complication. Epidemiological surveys and large clinical trials in CHF provide strong evidence that AF is a marker of increased mortality. AF may compromise LV systolic function and worsen CHF through poor rate control, irregularity of ventricular response, and loss of atrial systolic activity. Furthermore, enhanced adrenergic stimulation in the setting of CHF facilitates AV conduction and promotes the progression of cardiomyopathy, and AF may worsen CHF as a consequence of the negative inotropic effects of drugs used to control the heart rate of rhythm, or of the proarrhythmic effects of drugs used to maintain sinus rhythm. This article reviews the putative mechanisms behind atrial remodelling due to long-standing AF, and the role of neuro-hormonal alterations in the atrial electrophysiologic and structural changes which facilitate its perpetuation. It also reviews and discusses various controlled trials of angiotensin-converting enzyme inhibitors and AT-1 receptor blockade in the perspective of AF treatment and prevention. Finally the role of specific antiarrhythmic drugs, the respective advantages and shortcomings of rate versus rhythm control in patients with AF and CHF, and the important issue of chronic anticoagulation are presented in the light of time-tested therapies, as well as new promising therapeutic approaches.