Atrial fibrillation: new horizons.
Atrial fibrillation (AF) is the most common cardiac arrhythmia seen in clinical practice. The understanding of the pathophysiology of AF has changed drastically during the last several decades. Recent observations have challenged the concept of the multiple circuit reentry model in favor of single focus or single circuit reentry models. Atrial electrical dysfunction provides a favorable substrate and transmembrane ionic currents are key determinants. Interest has also been generated in the role of angiotensin converting enzyme (ACE) inhibition in reversing the electrical and structural remodeling. Reverting to the sinus rhythm seems to be the best way for reverse remodeling of atria during atrial fibrillation. Antiarrhythmic drugs (AADs) are only modestly effective. Of these amiodarone seems to provide the most benefits. Drugs like verapamil and ACE inhibitors may also help as adjuvant therapies in the reverse remodeling of atria. Nonpharmacological methods have been used to control both rate and rhythm for patients with AF. Recently, there has been a surge in interest to focal ablation of atrial foci. Focal sources of AF are commonly found in pulmonary veins (PV). Ablation in pulmonary veins through identification of the earliest endocardial activation has met with variable success. Anatomical approaches have involved circumferential radiofrequency ablation of pulmonary vein ostia using novel techniques such as balloon based circumferential ultrasound ablation system and circular cryoablation catheter. Most recently the segmental approach is preferred because the myocardial fibers surrounding the PV are not continuous. Segments where musculature is present can be identified using high frequency depolarization signals recorded through multi-electrode loop catheter or even conventional catheters.
Kuo
Chi-Tai
CT
Division of Cardiology, Chang Gung Memorial Hospital, Chang Gung University, Taoyuan, Taiwan. chitai@adm.cgmh.org.tw
Luqman
Nazar
N
Lin
Kuo-Hung
KH
Lee
Ying-Shiung
YS
D001281:Atrial Fibrillation / Q000503:physiopathology / Q000628:therapy*; D006801:Humans