Volume 27, Issue 4 pp. 447-452

Impact of Premature Atrial Contractions in Atrial Fibrillation

THOMAS J. JENSEN

THOMAS J. JENSEN

Department of Cardiology, Gentofte University Hospital, Copenhagen

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JENS HAARBO

JENS HAARBO

Department of Cardiology, Gentofte University Hospital, Copenhagen

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STEEN M. PEHRSON

STEEN M. PEHRSON

Department of Cardiology, Rigshospitalet, Copenhagen, Denmark

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BLOCH THOMSEN

BLOCH THOMSEN

Department of Cardiology, Gentofte University Hospital, Copenhagen

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First published: 14 April 2004
Citations: 28
Address for reprints: Thomas Jon Jensen, M.D., Dept. of Cardiology, Gentofte University Hospital, Niels Andersensvej 65, Post 163, DK-2900 Hellerup, Denmark. Fax: +45 3975 1802; e-mail: [email protected]

Financial support from Medtronic-Vicare, Denmark and The Kai Houmann Nielsen Foundation is gratefully acknowledged.

Abstract

In spite of the increasing knowledge about paroxysmal atrial fibrillation (PAF), details on mode of initiation in unselected patients are scarce. This paper focuses on trigger mechanisms of spontaneous onset of AF in consecutive patients with PAF. One hundred eight consecutive patients with two or more ECG documented AF episodes within the previous year had a 24-hours Holter recording performed. All AF episodes (n = 157) were reviewed and, within the last 10 beats prior to AF initiation. PP intervals were measured on 25 mm/s paper printouts and premature atrial contractions (PACs) were counted. Additionally, randomly selected coupling intervals (PP′) for PACs not triggering AF were measured and compared to AF triggering intervals and to PP′ intervals from healthy controls. PACs preceded all AF episodes. AF initiation displayed a wide variety in terms of PP coupling intervals and number of PACs prior to initiation within and between subjects. In episodes with PACs within the last 10 beats prior to initiation, we observed a long-short PP sequence at the time of initiation. Mean PP′ interval (± SE) for AF triggering PACs was 403 ± 9 ms, significantly shorter, P < 0.0001, than PP′ for nontriggering PACs (584 ± 8 ms) and PACs in healthy controls (589 ± 6 ms). However, a large proportion of nontriggering PACs had short PP′ coupling intervals without triggering AF. These observations highlight the importance of other factors than the trigger per se, such as the arrhythmogenic substrate, and suggest that therapeutic maneuvers aimed at curing PAF should target these as well as the trigger mechanisms. (PACE 2004; 27:447–452)

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