title: [Mechanisms of initiation in atrial fibrillation].
abstract: Atrial fibrillation is the most relevant arrhythmia in daily clinical practice. The pathophysiology is determined by multiple independent reentrant wavelets in both atria. Repetitive triggers and an underlying substrate may favor the initiation and maintenance of atrial fibrillation. Mapping studies in patients with drug-refractory paroxysmal atrial fibrillation identified potentials from the ostia of pulmonary veins as a main source of triggers that initiate atrial fibrillation. In ongoing clinical trials, catheter ablation of pulmonary vein foci is used to eliminate atrial premature beats and thereby prevent the initiation of atrial fibrillation. The autonomic modulation of the heart rate and the occurrence of other supraventricular tachycardias that degenerate into atrial fibrillation are also considered as triggering mechanisms of atrial fibrillation. Since symptomatic bradycardia is associated with an increased incidence of atrial fibrillation, atrial pacing therapies for prevention of atrial fibrillation are another concept. Ongoing clinical trials evaluating the efficacy of pacing in patients with and without a primary pacemaker indication are currently under investigation. To date, data to which extent anatomical and electrophysiological characteristics of the atria influence the initiation and maintenance of atrial fibrillation are still missing. The myocardial adaptation to atrial fibrillation, the so-called "atrial remodeling", includes shortening of the atrial refractory period, slowing of atrial conduction, shortening of the atrial action potential, a progressive reduction of L-type calcium channel expression and microfibrosis of the myocardial tissue. New drug developments target atrial remodeling by modulating ion channel function and receptors of the angiotensin metabolism.
authors.affiliation: Ludwig-Maximilians-Universität Abt. Innere Medizin I Klinikum Grosshadern Marchioninistr. 15 81377 München, Germany.
authors.forename: E
authors.initials: E
authors.lastname: Hoffmann
authors.forename: S
authors.initials: S
authors.lastname: Janko
authors.forename: C
authors.initials: C
authors.lastname: Reithmann
authors.forename: G
authors.initials: G
authors.lastname: Steinbeck
mesh_terms: D000200:Action Potentials; D000465:Algorithms; D000818:Animals; D000889:Anti-Arrhythmia Agents / Q000008:administration & dosage / Q000627:therapeutic use; D001281:Atrial Fibrillation / Q000188:drug therapy / Q000503:physiopathology* / Q000628:therapy*; D002121:Calcium Channel Blockers / Q000008:administration & dosage / Q000627:therapeutic use; D005117:Cardiac Complexes, Premature / Q000503:physiopathology; D002304:Cardiac Pacing, Artificial; D017115:Catheter Ablation; D004195:Disease Models, Animal; D004285:Dogs; D004554:Electric Countershock; D004562:Electrocardiography; D004594:Electrophysiology; D006041:Goats; D006339:Heart Rate; D006801:Humans; D008297:Male; D008875:Middle Aged; D015337:Multicenter Studies as Topic; D011446:Prospective Studies; D016032:Randomized Controlled Trials as Topic; D013997:Time Factors; D014700:Verapamil / Q000008:administration & dosage / Q000627:therapeutic use
chemical_list: D000889:Anti-Arrhythmia Agents; D002121:Calcium Channel Blockers; D014700:Verapamil