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Abstracts
ABSTRACTS
87 ± 81 vs. 81 ± 80 vs. 121 ± 88 ms, p < 0.001), and greater baseline to postcardiovsersion decrease in DF (1.1 ± 0.9 vs. 1.1 ± 1.1 vs. 1.4 ± 0.8 vs. 0.9 ± 0.8 vs. 2.0 ± 0.5 Hz, p < 0.001) before eventual termination. Conclusions: We found that cardioversion slows the AF process despite lack of termination. Patients resistant to cardioversion often require a number cardioversion attempts. Such patients who require a greater number have a lower baseline CL, and activity after subsequent cardioversions is progressively slower suggesting a cumulative effect of multiple attempts. doi:10.1016/j.hlc.2008.05.286 286 Paroxysmal Lone Atrial Fibrillation is Associated with an Abnormal Substrate: The “Second Factor” Martin Stiles ∗ , Bobby John, Christopher Wong, Pawel Kuklik, Glenn Young, Prashanthan Sanders Cardiovascular Research Centre, Royal Adelaide Hospital and the Disciplines of Medicine and Physiology, University of Adelaide, Adelaide, Australia Introduction: Despite early termination to prevent atrial fibrillation (AF) begetting AF, this disease often progresses. A “second factor” predisposing to AF has been postulated. Methods: Twenty-five patients with lone paroxysmal AF (1 week arrhythmia-free) and 25 age-matched controls were studied. Catheters at the lateral right atrium (RA), crista terminalis, coronary sinus (CS), septal RA and sequentially about the left atrium (LA) determined: effective refractory period (ERP) at 10 sites; conduction time along the lateral RA, inferior LA, LA roof and CS; and conduction characteristics at the CT. Electroanatomical maps created during sinus rhythm determined regional differences in conduction and voltage. Results: Baseline characteristics were comparable between groups. Patients with AF demonstrated the following differences: larger atria (RA 102 ± 21 mL vs. 69 ± 9 mL, p < 0.001; LA 99 ± 19 mL vs. 77 ± 17 mL, p = 0.006); prolonged P-wave (128 ± 8 ms vs. 95 ± 10 ms, p < 0.001); longer bi-atrial activation (128 ± 17 mL vs. 89 ± 10 ms, p < 0.001); delayed activation along the lateral RA (55 ± 14 ms vs. 43 ± 7 ms, p = 0.01) and inferior LA (52 ± 15 ms vs. 40 ± 10 ms, p < 0.05); slower regional conduction (1.3 ± 0.1 m/s vs. 2.1 ± 0.4 m/s, p < 0.001); greater proportion of fractionated electrograms (27 ± 8% vs. 8 ± 5%, p < 0.001); abnormalities along the crista terminalis (double potentials 4.9 ± 1.8 vs. 0.7 ± 0.8, p < 0.001; maximum duration 84 ± 15 ms vs. 52 ± 11 ms, p < 0.001); longer corrected sinus node recovery (265 ± 57 ms vs. 185 ± 60 ms, p = 0.002); and lower voltage (1.7 ± 0.4 mV vs. 3.1 ± 0.5 mV, p < 0.001). Patients with AF demonstrated higher regional ERPs than controls (p < 0.001). Conclusion: Patients with paroxysmal AF demonstrate abnormalities characterised by structural change, conduction abnormalities and sinus node dysfunction. These factors, in the absence of recent arrhythmia, may rep-
Heart, Lung and Circulation 2008;17S:S1–S209
resent the “second factor” predisposing these patients to AF. doi:10.1016/j.hlc.2008.05.287 287 High-density Mapping of Atrial Fibrillation to Characterise the Relationship Between Dominant Frequency and Electrogram Fractionation Martin Stiles ∗ , Anthony Brooks, Pawel Kuklik, Bobby John, Lauren Wilson, Hany Dimitri, Dennis Lau, Christopher Wong, Glenn Young, Prashanthan Sanders Cardiovascular Research Centre, Royal Adelaide Hospital and the Disciplines of Medicine and Physiology, University of Adelaide, Adelaide, Australia Introduction: Sites of complex fractionated atrial electrograms (CFAEs) and high dominant frequency (DF) have been implicated in maintaining atrial fibrillation (AF). Methods: Twenty patients underwent bi-atrial highdensity contact mapping (507 ± 150 points/patient) during AF. CFAEs were characterised by automated algorithm to quantify electrogram complexity (CFE-mean). Spectral analysis determined the frequency with greatest power and sites of high DF. Results: CFE-mean was higher (less fractionated) for right compared to left atria: 103 ms (IQR 76–143) vs. 98 ms (72–139 ms), p < 0.001; and in paroxysmal compared to persistent AF: 117 ms (85–161 ms) vs. 92 ms (70–127 ms), p < 0.001. DF was lower for right compared to left atria: 5.49 Hz (4.91–6.15 Hz) vs. 5.57 Hz (4.91–6.23 Hz), p = 0.02; and in paroxysmal compared to persistent AF: 5.27 Hz (4.69–5.71 Hz) vs. 5.93 Hz (5.35–6.67 Hz), p < 0.001. Significant regional DF variation was observed in paroxysmal (p < 0.001) but not persistent AF. Highest DF points clustered together with 5.2 ± 1.7 clusters/patient. Correlation between CFE-mean and DF was poor point-by-point (r = −0.17, p < 0.001) but moderate on an individual basis (r = −0.50, p = 0.03). High-density exploration of their spatial relationship demonstrated CFAE areas in close proximity (5 mm, IQR 2–10 mm) to high DF sites; 17% superimposed, 63% <10 mm and 10% 10–20 mm. This observation is further supported by simultaneous activation mapping at these sites. Conclusions: Greater fractionation and higher DF are seen in persistent AF and left atria. Preferential high DF areas are observed in paroxysmal but not persistent AF. CFAEs and DF correlate within individuals but not point-by-point. Exploration of their spatial relationship demonstrates CFAEs in areas adjacent to high DF. These parameters may provide complementary information for ablation. doi:10.1016/j.hlc.2008.05.288