identical changes in heart rate (see figure). In addition, the range of APDschanges vs. DI were smaller in pacing as compared to sympathetic stim-ulation (paired t-test, P � 0.05), exposing the effects of beta-adrenergicactivation and cellular signaling processes on RK. Although their signifi-cance remains unclear, RK curves derived from physiological sympatheticactivity of the autonomic nervous system are shown for the first time todiffer from standard restitution curves derived from direct pacing of themyocardium.

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ROLE OF INTRAMURAL VIRTUAL ELECTRODES IN ELECTRICSHOCK-INDUCED TRANSMURAL ACTIVATION OF PORCINELEFT VENTRICLE ASSESSED OPTICALLY FROM INTACTEPICARDIAL SURFACEOleg F. Sharifov, MD, PhD and Vladimir G. Fast, PhD.University of Alabama at Birmingham, Birmingham, AL.

Background: It is believed that defibrillation shocks directly excite the bulkof ventricular myocardium in excitable state due to intramural virtualelectrodes (IVE) but this hypothesis was not examined in intact myocar-dium. Here, the role of IVE in activation was determined using opticalrecordings of shock-induced Vm changes (Vm) from the intact epicardialheart surface.Methods: Isolated porcine left ventricles (n�3) were sequentially stainedwith a Vm-sensitive dye by two Methods: 1) surface staining (SS); 2) globalstaining (GS) via coronary perfusion. Shocks ( E�2-20 V/cm, 10 ms) wereapplied across the wall in epicardial-to-endocardial direction during thediastole via transparent mesh electrodes; shock-induced Vm were mea-sured optically from the same epicardial locations after SS and GS.Results: During cathodal shocks, both GS- and SS-Vm demonstratedmake activation (Panels A,B). At stronger shocks, GS action potentialupstrokes (GS-APU) exhibited negative deflection (Panel D), likely due toelectrotonic influence from sub-epicardial virtual anodes. During weakanodal shocks, both GS- and SS-Vm exhibited make activation (PanelsA,B) reflecting the presence of sub-epicardial virtual cathodes. SS-Vm

exhibited negative polarizations (Panels A,C), which were absent (Panel B)or diminished (Panel D) in GS-Vm due to spatial averaging. Duringstronger anodal shocks ( E��10V/cm), SS-Vm exhibited break activa-tion (Panel C), whereas GS-Vm showed make activation (Panel D) re-flecting sub-epicardial IVE.Conclusions: Make activation of epicardial surface by anodal shockssupports the role of IVE in shock-induced activation of ventricular myo-cardium. Contribution of sub-epicardial IVE to optical signals can explainthe differences in the shape and polarity of SS- and GS-Vm.

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HEART FAILURE RESULTS IN REDUCED RATE ANDINCREASED VARIABILITY OF WAVE PATTERNS AT THEPOSTERIOR WALL OF THE FIBRILLATING LEFT ATRIUM OFTHE SHEEP HEARTKazuhiko Tanaka, MD, Jerome Kalifa, MD, David Auerbach,MS, Javier Moreno, MD, Mark Warren, PhD, RaviVaidyanathan, BS, Alexey V. Zaitsev, PhD, Omer Berenfeld,PhD, Gerard M. Guiraudon, MD and Jose Jalife, MD.Institute for Cardiovascular Research, SUNY UpstateMedical University, Syracuse, NY and Canadian Surgery

Technologies and Advanced Robotics, University of WesternOntario, London, Ontario, Canada.

Atrial fibrillation and atrial tachycardia (AF-AT) are associated with heartfailure (HF). Whether these arrhythmias involve complex patterns of ac-tivation at the pulmonary veins-posterior left atrial wall junction(PVPJ) inthe setting of HF is not known. We hypothesized that the rate and orga-nization of electrical waves at PVPJ during AF in HF are different fromthat in normal (N) hearts.Methods: We induced HF by right ventricular pacing at 220 bpm (6-7weeks). AF-AT episodes were induced by burst pacing in isolated HF (n �4) and N (n � 4) hearts at baseline and in the presence of 4 �M ofacetylcholine (ACh). Optical mapping (Di-4-ANEPPS, 300 fr/sec) of theendocardial surface of PVPJ was carried out through an opening in the leftatrial appendage. At the PVPJ, we measured the distribution of dominantfrequencies (DFs), the number and patterns of spatio-temporal periodicwaves (more than 4 consecutive wavefronts with the same frequency anddirection: STPs) and of rotating and colliding waves.Results: During baseline only AT was inducible in HF. ACh allowed AF andAT induction in 3 and 1 HF hearts, respectively. However, DFMax at the PVPJin HF was significantly lower than N (mean�SEM: 9.0�2.6 vs. 20.6�1.4 Hz,p�0.05). Relative to the DFMax value, the number of STPs was similar in bothgroups of hearts. However, the number of different wave patterns was signif-icantly higher in HF (0.7�0.3 vs. 0.2�0.1 patterns/sec, p�0.05) and thetransitions from one pattern to another tended to be more frequent in HF thanN (1.2�0.4 vs. 0.7�0.3 transitions/sec, p�0.11). In HF STPs, rotating andcolliding waves formed preferentially in the vicinity of the left side of PVPJwhereas in N they formed also in the middle of the PVPJ area. The totalnumber of rotating and colliding waves/movie was comparable between the 2groups (2.7�2.4 vs. 3.5�1.8, p�0.38).Conclusion: The spatio-temporal organization of waves during AF-AT atthe endocardial PVPJ in the failing sheep heart is different from that innormal hearts. Activity in HF is characterized by a slower than normal ratebut higher variability in the excitation patterns.

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PHENOTYPES OF VENTRICULAR FIBRILLATION DURINGGLOBAL ISCHEMIA IN ISOLATED RABBIT HEARTSTsu-Juey Wu, MD, PhD, Shien-Fong Lin, PhD, Yu-ChengHsieh, MD and Chih-Tai Ting, MD, PhD. Taichung VeteransGeneral Hospital, Taichung, Taiwan Republic of China andCedars-Sinai Medical Center and David Geffen School ofMedicine at UCLA, Los Angeles, CA.

It has been reported that, in well-perfused guinea pig ventricles, the highestdominant frequency (DF) during ventricular fibrillation (VF) is on the anteriorleft ventricular (LV) wall, suggesting the presence of a mother rotor driving theventricles into VF via fibrillatory conduction. It is unclear if the same mech-anism is applicable to VF during global ischemia or in other animal models.By using a dual-camera optical mapping system, activation patterns of VFwere studied in 11 Langendorff-perfused rabbit hearts at baseline, during 10min of no-flow global ischemia, and during 10 min of reperfusion. Fast Fouriertransform analyses of pseudo ECG (pECG) and local optical recordings wereused to determine the DF. Type 1 (fast) VF is defined as VF with multiplewandering wavelets and a broad frequency spectrum. Type 2 (slow) VF isdefined as VF with local spatiotemporal periodicity (STP) and a narrowfrequency distribution. The results show that the mean DFs on pECG were18.7�1.5, 12.3�2.1, and 20.7�2.9 Hz (p�0.0001), respectively, for baselineVF, VF during 10-min global ischemia, and VF during 10-min reperfusion. Nosignificant DF gradient was observed between LV and right ventricle (RV) atbaseline and during reperfusion. However, after 10-min global ischemia, thehighest local DF of RV was higher than that of LV (13.0�1.9, 10.6�2.3 Hz,p�0.0039). Optical mapping showed type 1 VF at baseline. However, at5.0�1.0 min after the onset of ischemia, focal activities with local STPconsistently occurred. Among 31 VF episodes during global ischemia, therewere 43 sites with local STP (1-4 sites/episode). These sites were locatedmostly at RV (n�26), following by interventricular septum (n�9) and LV(n�8). The highest local DF at these focal activities (14.1�2.5 Hz) correlated

S258 Heart Rhythm, Vol 2, No 5, May Supplement 2005