title: The role of pacing mode in the development of atrial fibrillation.
abstract: Asynchronous ventricular pacing has been shown to increase the risk of development of atrial fibrillation (AF) because of various mechanisms: retrograde atrioventricular (AV) conduction with increase in atrial pressure causing acute atrial stretch and reverse flow in the pulmonary veins, mitral regurgitation, reduced coronary blood flow, adverse neuroendocrine reactions, etc. Dual-chamber pacing preserves atrioventricular synchrony. However, in randomized multicentre trials comparing VVI(R) with DDD(R) pacing, AF is only slightly less frequent in the dual-chamber mode. This is most likely due to unnecessary ventricular pacing, which is frequent in dual-chamber pacing. At nominal values, dual-chamber devices usually do not permit intrinsic AV conduction but promote delivery of the ventricular stimulus at an inappropriate time in an inappropriate place. Programming of long AV delays facilitates spontaneous AV conduction but usually cannot completely avoid unnecessary ventricular pacing and causes other problems in the dual-chamber mode. Atrial septal lead placement can improve left-sided AV synchrony and promote spontaneous AV conduction. Programming of the AAI(R) mode is superior to the dual-chamber mode but cannot be used if AV conduction is impaired intermittently or permanently. Therefore, dedicated algorithms enhancing spontaneous AV conduction in the dual-chamber mode are desirable for a large proportion of pacemaker patients.
authors.affiliation: Department of Cardiology, Division of Clinical Electrophysiology, JW Goethe University, Frankfurt, Germany. c.w.israel@em.uni-frankfurt.de
authors.forename: Carsten W
authors.initials: CW
authors.lastname: Israel
mesh_terms: D001281:Atrial Fibrillation / Q000209:etiology* / Q000503:physiopathology*; D002304:Cardiac Pacing, Artificial / Q000009:adverse effects* / Q000379:methods; D003326:Coronary Circulation / Q000502:physiology; D006329:Heart Conduction System / Q000503:physiopathology; D006801:Humans; D009200:Myocardial Contraction / Q000502:physiology; D017725:Ventricular Pressure / Q000502:physiology