Atrial fibrillation and the pulmonary veins

Atrial fibrillation is a common cardiac arrhythmia that decreases the patient’s quality of life and increases the risks of ischemic stroke and of heart failure. The current therapeutic options have limited success in preventing atrial fibrillation, including ablative pulmonary vein isolation. This thesis focuses on the genesis of atrial fibrillation related to the pulmonary veins, atrial stretch, and ablation scar. It provides evidence for a new concept of atrial fibrillation termed positional atrial fibrillation which occurs in 1 of 5 patients. The left lateral body position is a common atrial fibrillation-triggering position in these patients, and left lateral recumbence increases localized wall stress in the pulmonary veins, but not in the left atrium, of healthy volunteers. Moreover, the thesis demonstrates that even in the absence of arrhythmia-induced remodeling and of co-morbidities, the ovine pulmonary vein myocardium contains structural and functional properties conducive to reentry. The atrial-pulmonary vein transition is subject to ablation in pulmonary vein isolation. A direct effect of ablation energy and subsequent scar formation downsize the dimensions and contractility of the pulmonary veins, thereby attenuating pulmonary vein stretch. When the atrium is stretched, the ablation scar in a single pulmonary vein increases the genesis of atrial fibrillation. Lastly, preliminary data demonstrate that the pro- or antiarrhythmic effect of pulmonary vein ablation depends on changes in pulmonary vein strain and refractoriness. Therefore, modulation of atrial stretch should be part of atrial fibrillation treatment, and ablation therapy with stretch-targeted atrial and pulmonary vein scar formation may constitute such a therapy.