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Atrial fibrillation (AF) affects approximately two million patients in the USA and an equal number in Europe and increases morbidity and mortality in affected patients and population worldwide. Although acute conversion of AF to sinus rhythm can be achieved in almost all patients, therapeutic options to maintain sinus rhythm (repeated cardioversions, anti-arrhythmic drugs, catheter ablation, or surgical procedures) are often ineffective. Understanding the different mechanisms that contribute to AF may guide us towards a more effective ‘rhythm control’ therapy.Arterial hypertension, found in 65–70% of AF patients1,2 but only in 25–50% of the population,3 is the most common co-morbidity found in AF registries in Germany and Europe. Although this suggests a causal link between hypertension and AF, the mechanisms by which hypertension predisposes to AF are not well understood. Electrical, structural, and ultrastructural changes usually concur in the atria before AF develops. Some of the electrical changes that precipitate AF, shortening of the atrial action potential and refractory period and/or local conduction disturbances, have been delineated in detail during the past decade. The underlying pathophysiological concept of electrical remodelling (AF-induced shortening of atrial refractoriness) stems from studies in … *Corresponding author: Medizinische Klinik und Poliklinik C, Kardiologie und Angiologie, Universitatsklinikum Munster, D-48129 Munster, Germany. Tel: +49 251 8345185; fax: +49 251 8347864. E-mail address : kirchhp{at}uni-muenster.de

Hypertension begets hypertrophy begets atrial fibrillation? Insights from yet another sheep model