Key result
WPW syndrome without prior AF is linked to increased atrial fragmentation and ~14% AF inducibility.
Why the study?
Do patients with Wolff-Parkinson-White syndrome without prior paroxysmal atrial fibrillation exhibit greater atrial electrophysiologic abnormalities compared to controls?
Observational (n=76)
Do patients with Wolff-Parkinson-White syndrome without prior paroxysmal atrial fibrillation exhibit greater atrial electrophysiologic abnormalities compared to controls?
Absolute Event Rate: 154% vs 137%
p-value: p=<0.05
Patients with WPW syndrome without prior atrial fibrillation exhibit significant atrial conduction delays and electrophysiologic abnormalities that may increase their vulnerability to developing atrial fibrillation.
May signal elevated AF vulnerability in WPW without prior AF; hypothesis-generating and requires prospective validation before practice change.
BACKGROUND: Paroxysmal atrial fibrillation (PAF) frequently occurs in patients with Wolff-Parkinson-White (WPW) syndrome. HYPOTHESIS: The purpose of this study was to analyze the atrial electrophysiologic abnormalities and vulnerability to develop atrial fibrillation (AF) in patients with WPW syndrome but with no previous history of PAF. METHODS: We investigated atrial electrophysiologic abnormalities and vulnerability to AF in patients with WPW syndrome but without PAF. An electrophysiologic study was performed in 28 patients with WPW syndrome, 23 with atrioventricular nodal reentrant tachycardia (AVNRT) and 25 with other arrhythmias (control), all of whom had no history of PAF. The following atrial excitability parameters were assessed: effective refractory period (ERP), spontaneous or paced (A1) and extrastimulated (A2) atrial electrogram widths, percent maximum atrial fragmentation (%MAF; A2/A1 x 100), wavelength index (WLI; ERP/A2), and inducibility of AF. RESULTS: The ERP tended to be shorter in patients with WPW syndrome and in those with AVNRT than in the control group. The %MAF increased (154 +/- 33 vs. 137 +/- 23%, p < 0.05) and WLI decreased (2.7 +/- 0.8 vs. 3.4 +/- 1.0, p < 0.05) significantly in patients with WPW syndrome compared with the control group; however, these parameters in patients with AVNRT showed intermediate values. Atrial fibrillation was more inducible in patients with WPW syndrome (4/28 [14.3%]) than in those with AVNRT (4.3% [1/23]) and the control group (0/25 [0%]). With respect to patients with WPW syndrome and with and without inducible AF, the %MAF increased (195 +/- 23 vs. 148 +/- 30%, p < 0.01) and the WLI decreased (2.2 +/- 0.3 vs. 2.9 +/- 0.9, p < 0.05) in subjects with inducible AF. CONCLUSIONS: Atrial electrophysiologic abnormalities, especially atrial conduction delays, are more prominent in patients with WPW syndrome, even if they had no previous history of PAF. These abnormalities may play an important role in determining the vulnerability to AF.
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Sakabe et al. (2004) conducted an observational in Wolff-Parkinson-White (WPW) syndrome without paroxysmal atrial fibrillation (n=76). Wolff-Parkinson-White (WPW) syndrome vs. Control group (other arrhythmias) was evaluated on Percent maximum atrial fragmentation (%MAF) (p=<0.05). WPW syndrome in patients without prior paroxysmal atrial fibrillation was associated with increased percent maximum atrial fragmentation (154% vs 137%, p<0.05) and higher AF inducibility (14.3% vs 0%).
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