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S118 Abstracts Heart, Lung and Circulation2008;17S:S1–S209

Methods: Mapping was performed in eight sheeps, 60 ± 54weeks post-MI. Twenty multielectrode needles weredeployed at thoracotomy in the left ventricle within andsurrounding scar. Needles were located using EnsiteTM.Endocardial contact (needle) and noncontact unipolarelectrograms were recorded simultaneously during SRand multisite pacing. DSM maps were calculated as aratiometric consensus of peak negative voltage (PNV).ADSM maps were calculated using a root mean squareconsensus of peak–peak voltage (P2PV). Scar was quan-tified histologically and correlated with mapping criteriausing receiver operator curves with 50% scar density cut-off.Results: All modalities could identify scar (symbols†p < 0.001, ‡p < 0.01, §p < 0.05). During SR, decreasedsensitivity in identifying scar was observed with PNV(contact AUC = 0.8†, noncontact AUC = 0.63§) com-pared to P2PV (contact AUC = 0.92†, noncontact 0.68‡).ADSM was more sensitive (AUC = 0.72†) in identi-fying scar than DSM (AUC = 0.68‡) and noncontactSR mapping. Increased pacing threshold (ADSM%,≤2 mA = 61 ± 19%, >2 mA = 29 ± 8%, AUC = 0.93†)and conduction delay (ADSM%, ≤30 ms = 63 ± 19%,>30 ms = 45 ± 23%, AUC = 0.72‡) were associated withdecreased ADSM%. ADSM sensitivity was improved withlimited distance from the array (r < 40 mm, AUC = 0.74†).Conclusions: ADSM is more reliable in detecting scar

p < 0.001); delayed activation in the high-posterior(78 ± 14 ms vs. 46 ± 15 ms, p < 0.05), high-septal (81 ± 27 msvs. 46 ± 7 ms, p < 0.05) and low-septal RA (87 ± 41 ms vs.42 ± 13 ms, p < 0.05); greater proportion of DP/FS (48%vs. 7%, p < 0.001) and lower regional voltage (1.4 ± 0.3 mVvs. 2.1 ± 0.5 mV, p < 0.005) compared to SR. Anatomicalregions of FS correlated with regions of low voltage(r = −0.63, p = 0.01). Septal-paced and SR-maps showedlines of block at: the crista terminalis (10 vs. 11), septum (8vs. 2, p = 0.02), lateral RA (4 vs. 1), eustachian ridge (2 vs.0) and appendage (1 vs. 0). Septal-paced maps identifiedsignificantly more lines (25 vs. 14, p = 0.03) of greaterlength (60 ± 27 mm vs. 43 ± 12 mm, p < 0.05). Additionally,the crista terminalis identified in septal-paced maps wassignificantly longer (80 ± 24 mm vs. 42 ± 10 mm, p < 0.001).Conclusions: Direction-dependent analysis revealed sig-nificant changes in regional conduction velocities, voltageand fractionation. These heterogeneous changes suggestectopy from septal sites may be more likely to initiatearrhythmia by conducting around areas of functional blockto promote re-entry.

doi:10.1016/j.hlc.2008.05.283

283Adenosine–Triphosphate Facilitates Visualisation of theCoronary Sinus during Non-selective Venography of theLow Right Atrium

compared to other noncontact mapping parameters mea-

sured. Areas identified as scar by ADSM had functionalproperties consistent with scar.

doi:10.1016/j.hlc.2008.05.282

282Characterisation of Direction-dependent ConductionAbnormalities Predisposing to Atrial Arrhythmias

Christopher X. Wong ∗, Martin K. Stiles, Bobby John,Anthony G. Brooks, Pawel Kuklik, Dennis H. Lau, HanyDimitri, Ross L. Roberts-Thomson, Scott R. Willoughby,Lorraine Mackenzie, Glenn D. Young, PrashanthanSanders

Cardiovascular Research Centre, Department of Cardiology,Royal Adelaide Hospital and the Disciplines of Medicine andPhysiology, University of Adelaide, Adelaide, Australia

Introduction: Conduction abnormalities in the atria arecritical for the maintenance of atrial arrhythmias. Weaimed to determine the direction-dependent conductionabnormalities that may predispose to atrial arrhythmias.Methods: Twelve patients with paroxysmal atrial flut-ter underwent electroanatomic mapping of the rightatrium (RA) in both sinus-rhythm (SR) and septal-pacingat the coronary sinus. Direction-dependent conductionvelocities, voltage properties and electrogram charac-teristics were evaluated. As previously described, ≥4double-potentials or fractionated-signals (DP/FS) span-ning ≥5 mm was defined as a line of conduction block.Results: Septal-paced maps demonstrated: slower con-duction velocities (0.78 ± 0.19 m/s vs. 1.17 ± 0.16 m/s,

Edmund Lee ∗, Fiona Foo, Barry Mckeown, PradyokSaklani, Andrew Liu

Fremantle Hospital, Perth, WA, Australia

Background: A rate-limiting step in the implantation ofcardiac resynchronisation therapy devices is the visuali-sation and subsequent cannulation of the coronary sinus.By creating transient heart block and ventricular standstill,adenosine–triphosphate has been successfully used to aidvisualisation of the pulmonary veins during non-selectivecontrast venography of the left atrium. We hypothesisedthat adenosine may facilitate visualisation of the coronarysinus (CS) during non-selective contrast venography of theright atrium (RA).Methods: Patients with sinus rhythm undergoing implan-tation of a standard dual chamber pacemaker wereprospectively studied. Following implantation of the rightventricular lead, a Judkins right catheter was advancedto the low RA in proximity to the tricuspid annulus.Non-selective contrast venography was performed beforeand after administration of 12 mg of intravenous adeno-sine. Fluoroscopic images were then compared by threeobservers to determine if the CS os could be identified.Results: Four patients were studied. Non-selective con-trast venography of the RA without adenosine did notresult in visualisation of the CS os in any patients. In onepatient, adenosine failed to induce heart block and theCS could not be identified. In two patients, one borderof the CS could be identified with non-selective con-trast venography of the RA post-adenosine. In one patientclear visualisation of the CS was evident following adeno-

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sine. No patients suffered persistent adverse effects fromadenosine.Conclusion: Adenosine facilitated non-selective venogra-phy of the right atrium shows promise as a technique tofacilitate visualisation of the CS.

doi:10.1016/j.hlc.2008.05.284

284Does Radio-opaque Contrast Use During BiventricularPacemaker Implantation (BiVI) Adversely Affect RenalFunction?

Hany Abed ∗, Neva Bull, Robert Blake, Malcom Barlow,James Leitch, Stuart Turner

The John Hunter Hospital, Newcastle, NSW, Australia

Results and discussion: Thirty patients were studied (21me2fiCpg(4gptCrti

doi:10.1016/j.hlc.2008.05.285

285Effect of Electrical Cardioversion on Atrial FibrillationResistant to Termination

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ale, 66 ± 13 years old, QRS duration; 166 ± 30 ms, LVnd-diastolic diameter; 68 ± 10 mm, LV ejection fraction;6 ± 10% and NYHA; 3.4 ± 0.4). 73% had impaired renalunction before BiVI. A mean volume of 160 ± 49 ml non-onic iso-osmolar contrast was used during implantation.reatinine (Cr) increased in four patients but only oneatient met the criteria for CIN. Mean Cr, for the entireroup, decreased from 140 ± 9 �mol/L to 115 ± 8 �mol/L�Cr −18% [95% C.I.: −12, −36%, p < 0.001]) such that only9% had renal impairment post-BiVI. These findings sug-est the improvement in cardiac function, and hence renalerfusion, as a result of BiVI outweighs any adverse con-

rast effects.onclusion: Contrast load during BiV implantation is

arely associated with contrast-induced nephropathy. Inhe majority of patients, BiVI results in a net improvementn renal function.

hristopher X. Wong ∗, Anthony G. Brooks, Martin K.tiles, Bobby John, Dennis H. Lau, Hany Dimitri, Ross L.oberts-Thomson, Pawel Kuklik, Scott R. Willoughby, Lor-

aine Mackenzie, Glenn D. Young, Prashanthan Sanders

Cardiovascular Research Centre, Department of Cardiology,oyal Adelaide Hospital and the Disciplines of Medicine andhysiology, University of Adelaide, Adelaide, Australia

ntroduction: Electrical cardioversion of atrial fibrillationAF) is commonly unsuccessful and often requires mul-iple attempts before eventual termination. We sought toetermine the characteristics of AF resistant to cardiover-ion and the effect of cardioversion on the fibrillatoryrocess.ethods: Cardioversion was performed following AF

blation in 106 patients (96 M, 55 ± 12 years). AF cycleength (CL) and dominant frequency (DF) were measured

ithin the coronary sinus at baseline prior to ablation, andmmediately before and after unsuccessful cardioversion.esults: There were a total of 40 unsuccessful cardiover-

ions. Cardioversion caused a significant increase in CL,nd fibrillatory activity was observed to markedly slowmmediately following cardioversion, before acceleratingo a plateau slower than that that prior to cardiover-ion (205 ± 32 to 217 ± 41 ms, p < 0.001). Ten patients hadultiple unsuccessful cardioversions during the same

rocedure, the maximum being 5. Of these, those resistanto a greater number of cardioversions before terminationad shorter baseline CL (p < 0.001). Subsequent unsuc-essful cardioversion attempts showed greater baseline toostcardioversion increase in CL (47 ± 79 vs. 58 ± 78 vs.