pathologic studies showed myocardial fibers within the ER, thus AFLactivation wavefront may pass through ER. The purpose: of this study wasto demonstrate the role of ER in the typical AFL using the high densitynoncontact mappng.Methods and Results: A total of 34 patients (mean age 62 � 17 yrs, M/F �26/8) with typical AFL underwent electrophysiological study and detailedmapping of atrial activation using the non-contact mapping system (Ensite3000). The ER was located between IVC and coronary sinus ostium (CSO).Conduction block in the ER was defined as wavefront propagation alongthe one side of the ER, turning around the CSO, and traveling along to theother side of the ER. Twenty-two patients (Group I, 65%) had a completeline of block in the ER and 12 patients (Group II, 35%) had conductionthrough the ER during typical AFL. The virtual unipolar electrogram on theER showed widely split double potentials (97 � 13 ms) in the Group Ipatients. Among the Group II, 6 (II A) passed through a gap in the ER withnarrowly split double potentials (45 � 4 ms) (5 from the upper gapbetween CS and ER, one from the lower gap between ER and IVC), and theother 6 (II B) had conduction with a broad wavefront underneath the ER.Conclusion: The ER is not always a posterior barrier during typical CCWRAFL. Radiofrequency ablation from the CSO to TA would not cure theAFL with ER gap.

ABSTRACT SESSION 11: NONINVASIVE EVALUATION II: NoninvasiveAssessment of Right Ventricular TachycardiaThursday, May 20, 20044:30 p.m.–6:00 p.m.

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A new electrocardiographical approach for differentialdiagnosis between ARVC and Brugada syndromeKenji Yodogawa, MD, Norishige Morita, Toshihiko Ohara,Katsuhiko Tateoka, Hiroshi Taniguchi, Atsushi Ueno, TsutomuHorie, Yasuhiro Hirasawa, Junko Abe, MD, Yuki Iwasaki,Mitsunori Maruyama, Hideo Takayama, Yasushi Miyauchi, MD,Yoshiyuki Hirayama, Yoshinori Kobayashi, Takao Katoh andTeruo Takano. Nippon Medical School, Tokyo, Japan.

Background: Brugada syndrome and arrhythmogenic right ventricular cardiomy-opathy (ARVC) are both associated with fatal ventricular arrhythmias. However,their standard ECGs mimic each other. Late potential (LP) by signal averagedelectrocardiogram (SAECG) is often positive in both diseases. Therefore a newapproach is expected for discriminating between these 2 diseases.Methods: This study was comprised of 30patients (10 Brugada patients39.5 � 16.0y.o., 10 ARVC patients 43.4 � 16.7y.o., and 10 normalsubjects 40.4 � 14.2y.o.). Brugada syndrome was diagnosed by its typicalelectrocardiograms and pilsicainide challenge test (all patients changed tothe coved type of ST segment) and electrophysiologic study (ventricullarfibrillation was induced in all patients). Diagnosis of ARVC was made bythe diagnostic standard of McKenna. Time-frequency analysis using wave-let transform was performed for QRS complex of each electrocardiogram,and power value at 10-200Hz was assesed against time course. LP was alsoevaluated by SAECG.Results: LP was positive in 7 (70%) of Brugada patients, 9 (90%) ofARVC patients, and none of normal subjects. Wavelet transformed QRS innormal subjects was mainly composed of low frequency (10-50Hz) com-ponents with high power, and high frequency (80-150Hz) components withlow power. On the other hand, in all of Brugada patients, high frequencycomponents had high power at the middle of QRS complex, and theabnormal signal was mainly developed at 80Hz. In ARVC patients, highfrequency components with substantial power was developed at the termi-

nal portion of QRS complex, but it mainly developed at 150Hz. In com-parison of the high frequency components between two diseases, thefrequency level showing the greatest power was significantly higher inARVC patients than that in Brugada patients (149.1 � 15.2Hz vs 80.4 �20.4Hz, p � 0.005).Conclusion: The frequency levels with high power by wavelet transformanalysis obviously differs between ARVC and Brugada syndrome. Wavelettransform analysis of QRS complex may be a novel tool for differentialdiagnosis between these two diseases.

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Exercise induced ST-segment elevation in arrhythmogenicright ventricular dysplasiaKalpana R. Prakasa, MD, Darshan Dalal, MBBS, ChandraBomma, MD, Mary Corretti, MD and Hugh Calkins, MD.Johns Hopkins Univ School of Medicine, Baltimore, MD.

Background: Arrhythmogenic Right Ventricular Dysplasia (ARVD) ischaracterized by local and diffuse wall motion abnormalities of rightventricle (RV) due to replacement of myocardium with fibrofatty tissue. Ithas been well documented in the literature that patients with Q waveinfarction may have exercise induced ST-segment elevation which corre-sponds to the site of left ventricle (LV) wall motion abnormality. Wesought to test the hypothesis that exercise induced ST-segment elevationmay appear in leads corresponding to the site of RV wall motion abnor-mality in ARVD.Methods and Results: We enrolled 18 ARVD patients (mean age 36 �13yrs, 8 men) with (11 patients) and without (7 patients) RV wall motionabnormalities by conventional Echocardiography (ECHO). All patients hadnormal LV systolic function by ECHO (Ejection Fraction 58% � 8).Organic coronary lesions were ruled out in all of them by cardiac cathe-terization. Clinical ARVD diagnosis was made based on Task Force cri-teria. All patients underwent a symptom limited or sub maximal ExerciseTreadmill Test according to Modified Bruce Protocol. Inter group meanswere compared using Student’s t test. They achieved a maximum predictedheart rate of 91% � 12 and metabolic equivalents of 14 � 4. None of themhad angina during exercise. Eleven out of 18 patients had prematureventricular contractions (61%) during exercise. The development of0.10mv (1mm) or greater of J point elevation, persistently elevated greaterthan 0.10mv at 60-80msec after the J point in three consecutive beats witha stable baseline, was considered an abnormal response. ST-segment ele-vation in leads II, III, AVF and V1-V3 was found in 10 out of 11 patientswith RV wall motion abnormality, while only one patient in the groupwithout RV wall motion abnormality had ST-segment elevation (p � 0.05).Conclusion: Exercise induced ST-segment elevation in leads correspond-ing to the RV wall motion abnormality may add to the diagnosis of ARVD.The absence of organic coronary lesions could suggest the role of mechan-ical factors in the genesis of exercise induced ST-segment elevation.

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Electrocardiographic evidence of progression ofarrhythmogenic right ventricular dysplasiaJonathan P. Piccini, MD, Khurram Nassir, MD, ChandraBomma, MD, Darshan Dalal, MBBS, Harikrishna Tandri,MD, Crystal Tichnell, Cynthia James, PhD and HughCalkins, MD. Johns Hopkins Hosp, Baltimore, MD and JohnsHopkins Univ School of Medicine, Baltimore, MD.

Background: ARVD is a hereditary cardiomyopathy characterized by fi-brous fatty infiltration of the right ventricular free wall which predisposesto abnormal repolarization and sudden death. Accurate diagnosis of ARVDis challenging and is based upon the International Task Force Criteria(TFC). The 12 lead electrocardiogram (ecg) is an essential component inthe diagnosis of ARVD, and has several characteristics germane to ARVD,including precordial T-wave inversion, epsilon waves, and right bundlebranch block. Recently, we have found that prolongation of the S waveupstroke in leads V1, V2, and V3 is the most prevalent ecg abnormality in

S20 Heart Rhythm, Vol 1, No 1, May Supplement 2004

patients with ARVD. The purpose of this study was to determine whetherthere are progressive ecg changes in ARVD over time.Methods and Results: A total of 35 patients (15 males; mean age 36 � 14)diagnosed with ARVD had repeat ecg’s (mean time between tracings 59.1months, median 43 months). Precordial QRS duration, QT duration, andT-wave inversion were measured in all precordial leads. S wave upstroke(defined as the nadir of the S wave until union with the isoelectric line) wasrecorded in leads V1 through V3.Among the 35 patients, 31 (88.6 %) had evidence of ecg progression.Thirteen patients (37 %) had new T-wave inversion in one or more leads.Four patients (11.4%) had interval development of RBBB or IVCD. Ninepatients (25.7 %) had more than a 10 mm increase in QT dispersion.Among all of the parameters, S wave prolongation greater than 10 msecwas the most prevalent ecg marker of progression. 24 patients (68.6 %) hadS wave prolongation in lead V1, V2, or V3, 12 patients (34.3 %) had Swave prolongation in 2 of these leads, and 4 patients (11.4 %) had S waveprolongation in all three leads.Conclusion: Over a median of 43 months, almost 90 % of the ARVD studypopulation had evidence of progression on repeat ecg. S wave upstrokeprolongation, a marker of delayed precordial activation, is the most prev-alent ecg finding of disease progression in ARVD. Future studies shouldinvestigate whether or not these ecg changes correlate with clinical phe-notype and overall prognosis.

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Tissue tracking imaging as a new modality for identifyingthe precise tachycardia origin in idiopathic outflow tracttachycardiaHiroshi Tada, MD, Hiroyuki Toide, BS, Shigeto Naito, MD,Kenji Kurosaki, MD, Sachiko Ito, MD, Goro Shinbo, MD,Shigeru Oshima, MD, Koichi Taniguchi, MD and AkihikoNogami, MD. Gunma Prefectural Cardiovascular Ctr,Maebashi Gunma, Japan and Yokohama Rosai Hosp,Yokohama, Japan.

Background: Tissue tracking imaging (TTI) is a new ultrasonographictechnique that measures the longitudinal myocardial motion amplitude ineach region during systole, demonstrating regional myocardial displace-ment on the basis of myocardial velocities using color Doppler myocardialimaging principles.Methods: Twenty-three patients (pts) with idiopathic ventricular tachycar-dia (8) or premature ventricular contractions (15; I-VT) underwent TTI.The tachycardia origin was defined as the site where the earliest color-coded spot appeared on the myocardium during premature ventricularcontractions or the 1st beat of VT among all images obtained. The VTorigins were validated at the time of the radiofrequency ablation (RFA).Results: 1) I-VT was successfully eliminated in 20 pts. The successfulRFA sites were the septal and free wall aspects of the right ventricularoutflow tract (RVOT) in 13 and 4 pts, respectively. Three I-VTs could beablated from the left sinus of Valsalva (LSV). In these 20 pts, each I-VTorigin determined by TTI corresponded exactly with the site at which theearliest ventricular activation was recorded during RFCA. 2) I-VTs origi-nating from the RVOT free wall (FW-VT) could be visually differentiatedfrom the septal aspect of the RVOT (Sep-VT) by TTI. In these VTsoriginating from the RVOT (RVOT-VT), the earliest color-coded spotappeared at the myocardium below or at the pulmonary valve (PV).However, in 3 I-VTs which could be ablated from the LSV (LSV-VT), itappeared at the septum above the PV. 3) In the remaining 3 pts, the I-VTcould not be ablated from either the RVOT or LSV, and the interval fromthe onset of the QRS complex to the onset of the earliest myocardialdisplacement measured from the quantitative tissue displacement-timecurve (QRS-D) was longer than in pts with successful RFA (76 � 7 vs.35 � 17 ms; p � 0.01).Conclusions: 1) TTI is useful for differentiating between Sep-VTs andFW-VTs or between RVOT-VTs and LSV-VTs. 2) A relatively longQRS-D interval at the earliest color-coded spot may indicate that the actualVT origin is away from the earliest color-coded spot, and RFA at that sitemay result in failure.

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Non-invasive detection of myocardial fibrosis inarrhythmogenic right ventricular cardiomyopathy usingdelayed enhancement MR imaging: Correlation withhistopthologyHarikrishna Tandri, MD, *Manoj Saranathan, PhD, ReneRodriguez, MD, Chandra Bomma, MD, Khurram Nasir, MD,Boaz Rosen, MD, Hugh Calkins, MD, Joao A. C. Lima, MDand David A. Bluemke, MD, PhD. Johns Hopkins UnivSchool of Medicine, Baltimore, MD and Johns Hopkins HospUniv School of Medicine, Baltimore, MD.

Introduction: The most striking morphologic feature of arrhythmogenicright ventricular cardiomyopathy (ARVC) is replacement of right ventric-ular (RV) myocardium by fibrofatty tissue. Endomyocardial biopsy lackssensitivity, and carries a risk of perforation and tamponade. We evaluatedthe role of myocardial delayed enhancement magnetic resonance imaging(MDE-MRI) in non-invasive detection of fibrosis in ARVC.Methods: The study population included 30 consecutive patients who wereevaluated for ARVC. Electrophysiologic testing, right ventriculographyand endomyocardial biopsy were performed when clinically indicated.MRI was performed on a 1.5-T scanner and included cine images inshort-axis and axial plane. Ten minutes after IV administration of 0.2mmol/kg of gadopentate dimeglumine, MDE-MR images were obtained inthe axial, short-axis and the four-chamber view. Diagnosis of ARVC wasmade blinded to the MR data, and based upon the Task Force criteria.Results: Thirteen (45 %) of the 30 patients met the Task Force criteria forARVC. Eight (61%) of the 13 ARVC patients demonstrated delayedenhancement compared to none (0%) of the 17 patients without ARVC(P � 0.001). Ten of the 13 ARVC patients had endomyocardial biopsy, andseven had fibro-fatty changes consistent with the diagnosis of ARVC. Eachof these seven patients had delayed hyperenhancement on MDE-MRI.Three ARVC patients had normal biopsies and only one had evidence ofdelayed enhancement. Endomyocardial biopsy was also performed in 8(47%) of the 17 patients who did not meet the Task Force criteria. None ofthese patients had any abnormalities on histopathology. Also none of thesepatients showed delayed enhancement on MDE-MRI.Conclusions: Non-invasive detection of RV myocardial fibrosis is possibleby MDE-MRI and shows an excellent correlation with histopatholo-gy.MDE-MRI may have a role in evaluation and diagnosis of patients withsuspected ARVC.

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Diagnostic value of tissue Doppler imaging inarrhythmogenic right ventricular dysplasiaKalpana R. Prakasa, MD, Harikrishna Tandri, MD, DarshanDalal, MBBS, Chandra Bomma, MD, Boaz Rosen, MD, ThorEdvardsen, MD, Mary Corretti, MD, Hugh Calkins, MD andTheodore P. Abraham, MD. Johns Hopkins Univ School ofMedicine, Baltimore, MD.

Background: Tissue Doppler echocardiography (TDE) allows real-timequantitative assessment of global and regional, left and right ventricularfunction. The objective of our study was to examine right ventricular (RV)systolic and diastolic function in patients with Arrhythmogenic RightVentricular Dysplasia (ARVD) using conventional echocardiography(ECHO) and TDE. We hypothesized that TDE would detect abnormal RVfunction in ARVD patients with normal RV ejection fraction by ECHO.Methods and Results: This prospective, case-control study enrolled 12ARVD patients (mean age 40 � 13yrs, 7 men) and 18 age-matched familymembers (mean age 34 � 16yrs, 10 men) without ARVD (controls).ECHO and TDE were performed using a GE Vingmed System 5 ultrasoundmachine with a 3.5MHz transducer over a period of one year (8/2002-7/2003). A standard apical 4 chamber view was used to image the RV.Clinical ARVD diagnosis was made based on Task Force criteria. ECHORV function assessment included visual assessment of wall motion, andmeasurements of RV basal short axis diameter and ejection fraction. Online

S21Session 11

electronic tools were used to generate tissue velocity traces from thetricuspid annulus. Peak systolic and early and late diastolic tissue velocitieswere measured and averaged over 3 cardiac cycles to yield a final value.Inter group means were compared using the Student’s t test. Tricuspidannular systolic velocity (Sa; 11.7 � 2.48 cm/s versus 14.64 � 2.34cm/s,p � 0.05) and tricuspid annular early diastolic velocity (Ea; 11.13 �4.28cm/s versus 15.71 � 4.04cm/s, p � 0.05) were significantly lower inARVD patients compared to controls, respectively. Using mean-2SD as thecutoff for normal, ECHO detected abnormal RV systolic function in 3/12(25%) patients whereas TDE identified abnormal function in 7/12 (58%).Conclusion: TDE identified RV systolic dysfunction in ARVD patientswith normal RV function by ECHO. Low tricuspid Ea velocities suggestabnormal RV diastolic function. TDE is a sensitive, quantitative techniquethat may be useful in RV function assessment in ARVD.

ABSTRACT SESSION 12: DEVICES-VENTRICULARFUNCTION/RESYNCHRONIZATION THERAPY II: Clinical Insights intothe Hemodynamics of Cardiac PacingThursday, May 20, 20044:30 p.m.–6:00 p.m.

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Pacing increases Connexin43 expression in patients withhypertrophic obstructive cardiomyopathyPravina M. Patel, Wajid Hussain, MRCP, Cecilia Linde, MD,PhD, Fredrik Gadler, MD, PhD, Lennart Bergfeldt, MD,PhD, Michael R. Rosen, MD and Nicholas S. Peters, MD.Imperial College, St. Mary’s Hosp, London, United Kingdom,Karolinska Inst at Karolinska Hosp, Stockholm, Sweden,Karolinska Hosp, Stockholm, Sweden and Columbia Univ,New York, NY.

Background: We have previously shown that ventricular Cx43 expressionis altered in reactive left ventricular hypertrophy and failure of the humanheart, and is also modified by pacing in an animal model. Pacing remodelsthe ventricles in patients with hypertrophic obstructive cardiomyopathy(HOCM), and we hypothesised that pacing would alter Cx43 expressionand distribution in HOCM.Method: Adult patients (n � 3) with symptomatic HOCM underwent DDDpacing. Endomyocardial biopsies were taken before implantation of apacemaker and again after a mean duration of 12 months. Quantitativeconfocal immunodetection of Cx43 and Cx40 in 6 randomly selectedhighly confocal (�1�m) slices was performed.Results: The distribution of Cx43 retained the normal pattern seen in adultmyocardium, principally localised to the terminal intercalated disks. Thiswas unchanged after pacing. However, there was a 54% increase in Cx43expression following pacing (unpaced 0.0085 � 0.0002 �m2 /�m2 vspaced 0.0132 � 0.002�m2 /�m2; P � 0.05). Cx40 remained undetectablein ventricular myocytes and was only found in conducting tissue.Conclusion: This is the first report of Cx43 changes associated with cardiacpacing in humans. In some clinical settings, pacing appears to modifyarrhythmic tendency, and these changes in Cx43 may provide the mecha-nism, conferring arrhythmic protection in patients with HOCM.

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The extent of myocardial viability predicts improvementin ventricular function, remodeling, and clinical status sixmonths after biventricular pacingJames P. Hummel, MD, J. Todd Belcik, BS, John D.Ferguson, BSc, *J. Michael Mangrum, MD, John P.Dimarco, MD, PhD, Jonathan R. Lindner, MD and *J. PaulMounsey, MD, PhD. Univ of Virginia, Charlottesville, VA.

Biventricular pacing can improve mechanical synchronization in heartfailure patients, resulting in improvements in ventricular function, exercisetolerance, symptoms, and mortality. In patients with ischemic cardiomy-opathy we have reported a close correlation between preimplantation

myocardial viability and acute improvement in left ventricular performanceafter biventricular pacing. We hypothesized that viability would also bepredictive of clinical benefit at 6 months.Fourteen patients with ischemic cardiomyopathy (LVEF 21 � 5%) andstandard indications for CRT underwent biventricular ICD implanta-tion. Transthoracic contrast echocardiography and clinical data werecollected at implantation and at 6 months. Segmental myocardial per-fusion (based on a 17-segment model) was scored by a reader blindedto clinical data as 0 (no perfusion), 1 (partial perfusion), or 2 (normalperfusion). A perfusion score index (PSI), reflecting the extent ofviability, was calculated by dividing summed scores by the number ofsegments analyzed.At 6 months there were improvements in 6 minute walk distance(median, 76m [range, �13 to 187]), Minnesota Living With HeartFailure quality of life score (17pts [�4 to 38]), NYHA Class (1 [0 to2]), and LVEF (7.6 [�6.0 to 13.5]), and a reduction in LV end-diastolicdimension (0.5cm [�0.7 to 1.3]). The global PSI correlated closely withthis 6 month functional improvement (6 minute walk distance [r � 0.75,p �0.03], quality of life score [r � 0.59,p � 0.04], NYHA Class [p � 0.08]), andincrease in LVEF (r � 0.53,p � 0.08); change in left ventricular end-diastolicdimension was inversely correlated (p � 0.006, r � �0.82). The reduction inend-diastolic dimension was not dependent on baseline diastolic dimensionand only occurred in patients with good viability (PSI � 1.0).We conclude in patients with ischemic cardiomyopathy, the degree of myo-cardial viability closely correlates with six month improvement in LVEF andfunctional status. Significant remodeling and reduction in end diastolic dimen-sion did not occur in the absence of good viability.

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Effect of right ventricular pacing site on hemodynamic functionduring bi-ventricular pacing for heart failure patients with atrialfibrillation after atrioventricular node ablation*Angelo Auricchio, MD, PhD, *Christoph Geller, MD,*Michael Kloss, MD, *Helmut U. Klein, MD, *ShelleyCazares, *Yinghong Yu, *Annette Doelger and *EtienneHuvelle, MD. Univ Hosp Magdeburg, Magdeburg, Germanyand Guidant CRM, St. Paul, MN.

Introduction: This study assessed the effects of different right ventricular(RV) pacing sites during bi-ventricular (BV) pacing on systolic function inpatients with heart failure and chronic atrial fibrillation after atrioventric-ular (AV) node ablation.Methods: 13 patients (pts) were enrolled in the PATH-CAF study(PAcing THerapy for heart failure patients with Concomitant AtrialFibrillation). All pts were NYHA Class III. QRS duration was 143 �23ms. After AV node ablation, the pts were acutely paced VVI at 70bpm at various pacing site combinations while recording LV and RVpressure. The baseline mode was RV apex pacing. BV modes werepacing at the LV free wall and RV apex (LV � RVa) and pacing at theLV free wall and RV outflow tract (LV � RVot). Each mode wasrepeated randomly 3 times in a 14-baseline-beat/6-BV-beat sequence.For each pt, the response to each BV mode was evaluated by calculatingthe percent change from baseline in maximum LV � dP/dt and RV �dP/dt. These results were then combined across the patient group tocompare improvements in LV and RV function between modes LV �RVa and LV � RVot.Results: Data was successfully recorded from 8 pts. The median andinter-quartile range (IQR, shown as range on plots) of the improvementfrom baseline in maximum RV � dP/dt was 0.99 (median) and 6.12 (IQR)for mode LV � RVa and 8.36 (median) and 19.31 (IQR) for mode LV �RVot. Corresponding values for LV � dP/dt were 12.23 (median) and12.85 (IQR) for mode LV � RVa and 10.42 (median) and 10.52 (IQR) formode LV � RVot.Conclusions: LV systolic function appears to improve with BV pacingindependent of RV pacing site for this patient group. RV outflow tract

S22 Heart Rhythm, Vol 1, No 1, May Supplement 2004