European Heart Journal (2003) 24, 801–810

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Clinical and electrophysiological differencesbetween patients with arrhythmogenic right

ventricular dysplasia and right ventricular outflow

tract tachycardia

D. O'Donnella*, D. Coxa, J. Bourkea, L. Mitchellb, S. Furnissa

aDepartment of Cardiology, Freeman Hospital, Newcastle upon Tyne, UK b

Department of Radiology, Freeman Hospital, Newcastle upon Tyne, UK Received 17 August 2002; revised 6 September 2002; accepted 11 September 2002

Aims Radiofrequency catheter ablation is considered first line treatment for sympto-matic patients with right ventricular outflow tract tachycardia (RVOT). The role ofablation in arrhythmogenic right ventricular dysplasia (ARVD) is more limited. As such,differentiating between the two conditions is essential.Methods and results This study compared non-invasive findings, magnetic resonanceimages (MRI), invasive electrophysiological characteristics, results of ablation andlong-term outcome in 50 consecutive patients with RVOT (33) or ARVD (17). Structuralabnormalities were uniform in the ARVD group; in addition 18 (54%) of the RVOT

tachycardia group had MRI abnormalities. At electrophysiological study the tachy-cardia in the ARVD group displayed features of re-entry in over 80%, but behaved witha triggered automatic basis in 97% with RVOT. Ablation was complete or partialsuccess in 12 (71%) patients with ARVD and ventricular tachycardia (VT) recurred ineight (48%). In the RVOT patients, ablation was a complete success in 97% withrecurrent VT in 6%. Long-term success in the RVOT patients was 95% in both patientswith and without MRI abnormalities.Conclusions Electrophysiological characterization can differentiate ARVD from RVOT.The finding of abnormalities on MRI does not have any bearing on arrhythmiamechanism, acute or long-term success of RFA.© 2003 The European Society of Cardiology. Published by Elsevier Science Ltd. All

rights reserved.

KEYWORDS

Ventricular tachycardia;

Catheter ablation;

Cardiomyopathy

Introduction

Right ventricular tachycardia is commonly due toarrhythmogenic right ventricular dysplasia/cardiomyopathy (ARVD) or idiopathic right ven-tricular outflow tract (RVOT) tachycardia.1,2 ARVDis an inherited progressive cardiomyopathy charac-

terized by right ventricular dysfunction due tofibrofatty replacement of myocardium, predispos-ing to ventricular tachycardia and death.3 – 7 Rightventricular outflow tract tachycardia is a benigncondition, traditionally considered to be a primaryelectrical disease in the absence of structural heartdisease.8 – 11 The differentiation between ARVDand RVOT tachycardia is important clinically whendiscussing prognosis and management options.

At the extremes of disease presentation differ-entiating between the two conditions is usuallystraightforward. However, detailed analyses using

* Corresponding author. Department of Cardiology, Austinand Repatriation Medical Center, Studley Road, Heidleberg,Victoria 3084, Australia. Tel.: +61-3-9496-5000; fax:+61-3-9459-0971E-mail address: [email protected] (D. O'Donnell).

European Heart Journal (2003) 24, 801 – 810

0195-668X/03/$ - see front matter © 2003 The European Society of Cardiology. Published by Elsevier Science Ltd. All rights reserved.doi:10.1016/S0195-668X(02)00654-1



magnetic resonance imaging (MRI),12 – 15 signalaveraged electrocardiograms1,11 and endomyo-cardial biopsy1 have detected structural abnormali-ties in patients with RVOT tachycardia, which aresimilar to those seen in the early stages of ARVD.These findings have made the differentiation of

ARVD and RVOT tachycardia at the time of initialdiagnosis more difficult in some patients. It isunclear whether the two conditions representseparate entities or together form a continuousspectrum of disease, with ROVT tachycardia repre-senting a concealed or early form of ARVD. Theclinical and prognostic significance of the structuralabnormalities detected with newer technologies isuncertain.

The aim of this study was to compare the twoconditions with regard to the demographic, elec-trocardiographic, structural and invasive electro-

physiological characteristics, in patients with ARVDor RVOT tachycardia. These findings were alsoanalysed to identify any correlation with the acuteor longer term success of radiofrequency ablation.

Methods

Patients

This study analysed details of 50 consecutivepatients with right ventricular tachycardia, in the

absence of coronary disease, surgical scars or leftventricular dysfunction, who were scheduled toundergo electrophysiological study and radio-frequency ablation. The right ventricular origin wasdetermined by electrocardiographic criteria andconfirmed in all cases at electrophysiological study.The patients were prospectively diagnosed as ARVDor RVOT tachycardia, according to guidelinespublished by the Study Group on ARVD/C of theWorking Group of Myocardial and PericardialDiseases of the European Society of Cardiologyand of the Scientific Council on Cardiomyopathiesof the International Society and Federation of

Cardiology.16 This classification takes account ofgenetic, electrocardiographic depolarization andrepolarization, arrhythmic, structural and histo-logical factors. Based on this classification, thediagnosis of ARVD requires the presence of twomajor criteria or one major and two minor criteriaor four minor criteria.

Electrocardiographic analysis

A standard 12-lead electrocardiogram was recordedduring sinus rhythm free from anti-arrhythmic drug

effects. The QRS/T complex in V1 – 3 was examinedfor the presence of epsilon waves, right bundlebranch block and T wave inversion. QRS andQT measurements were made using a CalcompDigitizer from electrocardiograms recorded at apaper speed of 50 mm s−1.

Signal averaged electrocardiograms were ob-tained using a Marquette MAC VU system. Record-ings were made during sinus rhythm using standardFrank leads X, Y and Z. Two hundred and fifty beatswere averaged to obtain a noise level of <0.3 µV.The signals were amplified, averaged and filteredwith a bidirectional filter at frequencies of 40 – 250 Hz. The duration of the total filtered QRScomplex, the duration of the filtered QRS complexafter the voltage decreased to <40 mV, and the rootmean square of the amplitude of signals in the last40 ms of the filtered QRS complex were measured

by a computer algorithm. Results were deemedabnormal if any two of the following criteria weremet: (1) the filtered QRS duration was ≥120 ms; (2)the duration of the filtered QRS complex after thevoltage decreased to <40 mV, was >40 ms; (3) theroot mean square of the voltage in the last 40 ms ofthe QRS complex was <20 mV.

Ventricular tachycardia morphology was ob-tained either from a 12-lead electrocardiogramrecording during sustained ventricular tachycardiaor from an electrocardiogram with consistentmonomorphic ventricular ectopic beats.

Structural analysis

Transthoracic echocardiography

All patients underwent transthoracic echocardiog-raphy prior to the study, which was reported by acardiologist blinded to the clinical details. Thefocus on the right ventricle included measurementsof overall right ventricular size and function, aswell as a description of localized right ventricularaneurysms, segmental dilatation or regional wallmotion abnormalities.

Magnetic resonance imaging

MRI of the heart was performed according to astandardized technique in all patients. Scans wereperformed either before or a minimum of 12months after the ablation procedure. The MRIwas obtained with a Magnetom Vision (Siemens,Germany) system. Using a breath-hold techniquethe static images were obtained as T1-weightedspin echo and T2-weighted STIR scans. Cine imageswere obtained using cardiac-gated sequences.

802 D. O'Donnell et al.



patients were classified as ARVD and 33 as RVOTtachycardia. The demographic, structural, electro-cardiographic and clinical data is detailed in Tables1 and 2.

There were no significant differences in symp-toms between patients with ARVD and RVOT tachy-cardia. The mode of presentation was syncope orcollapse in 42% and palpitations in the remaining58%. Exercise potentiation of symptoms was re-ported in 26 (79%) of the RVOT tachycardia patientsand in 10 (59%) patients with ARVD. Almost 60% ofpatients with ARVD had a family member with ARVDor a family history of premature sudden cardiacdeath. None of the RVOT tachycardia patients had afamily history of tachycardia.

Electrocardiographic analysis

The routine electrocardiogram was abnormal in 52%of patients with ARVD and in 6% of patients withRVOT tachycardia. Thirty percent of the patientswith ARVD displayed epsilon waves, incompleteright bundle branch block or a localized prolonga-tion of the QRS complex in V1 or V2. T wave inver-

sion in the right precordial leads (V1 – V3) was seen in36% of patients with ARVD and 6% of patients withRVOT tachycardia. Late potentials on the signalaveraged electrocardiogram were not present inany patient with RVOT tachycardia but werepresent in 78% of the patients with ARVD (Figs. 2and 3).

All patients had ventricular tachycardia or re-

peated monomorphic ventricular ectopic beatsdocumented on electrocardiogram. In all cases aleft bundle branch block pattern was present. Allpatients with RVOT tachycardia and nine (53%) ofthe patients with ARVD demonstrated an inferioraxis during tachycardia. The remaining patientswith ARVD demonstrated a normal or superior axisduring tachycardia. Seven patients (42%) with ARVDbut none with RVOT had more than one morphologyof documented clinical tachycardia.

Structural assessments

Transthoracic echocardiograms detected structuralabnormalities in seven (42%) patients with ARVD.Major MRI abnormalities were present in 15 (88%)ARVD patients. All patients with echocardiographicabnormalities also had major abnormalities on MRIscans. The remaining two (12%) ARVD patients dem-onstrated minor abnormalities only on MRI scans.

Fig. 1 (a,b) An example of two different morphologies of ventricular tachycardia that were both seen clinically in a patient withARVD. (c) An example of monomorphic ventricular ectopic beats which were induced with isoprenaline in a patient with RVOTtachycardia.

Table 1 Clinical characteristics of enrolled patients

ARVD RVOT P value

Number 17 33Age 40±10 39±9 nsMale 11 (65%) 11 (33%) nsSyncope 8 (47%) 13 (39%) ns

Exercise potentiation 10 (59%) 26 (79%) nsFamily history 9 (53%) 0 <0.01ECG depolarization 5 (30%) 0 <0.01ECG repolarization 6 (36%) 2 (6%) =0.03Arrhythmias 17 (100%) 33 (100%) nsStructural

Major 7 (41%) 0 >0.01Minor 7 (41%) 1 (3%) <0.01

Number of major criteria 1.2 0.0 <0.01Number of minor criteria 3.0 1.1 <0.01

Family history, ECG depolarization and repolarizationabnormalities, arrhythmias, structural and major andminor criteria are all defined according to the StudyGroup on Arrhythmogenic Right Ventricular Dysplasia/Cardiomyopathy of the Working Groups on Myocardial andPericardial Disease and Arrhythmias of the EuropeanSociety of Cardiology and of the Scientific Council onCardiomyopathies of the World Heart Federation.12

ARVD=arrhythmogenic right ventricular dysplasia; RVOT=right ventricular outflow tract tachycardia; ns=notsignificant.

Table 2 Structural abnormalities

ARVD RVOT P value

TTE—RV dilatation 6 (35%) 0 <0.01TTE—RV RWMA 2 (12%) 0 nsMRI—RV dilatation 8 (47%) 0 <0.01MRI—RV RWMA 11 (65%) 1 (3%) <0.01

MRI—Fat >2 cm2 9 (53%) 1 (3%) <0.01MRI—Fat <2 cm2 7 (41%) 13 (42%) nsMRI—Thinning >2 cm2 10 (59%) 1 (3%) <0.01MRI—Thinning <2 cm2 7 (41%) 11 (33%) nsMajor MRI findings 15 (88%) 2 (6%) <0.01Minor MRI findings 2 (12%) 16 (48%) =0.02No abnormalities 0 15 (45%) <0.01

ARVD=arrhythmogenic right ventricular dysplasia; RVOT=right ventricular outflow tract tachycardia; TTE=transthoracic echocardiogram; RV=right ventricle; RWMA=regional wall motion abnormality; MRI=magnetic resonanceimaging. Major MRI findings=right ventricular wall motionabnormality, right ventricular dilatation, fatty infiltration>2 cm2 or focal thinning >2 cm2. Minor MRI findings=fattyinfiltration <2 cm2 or focal thinning <2 cm2.

Clinical and electrophysiological differences between patients 805



Structural abnormalities were detected on MRIscans in 18 (54%) patients with RVOT tachycardiabut no echocardiographic abnormalities werepresent. The MRI abnormalities were consideredmajor in two (6%) and minor in the remaining 16(48%).

Right ventricular cine angiography was per-formed at the discretion of the cardiologist in 23patients, 11 with ARVD and 12 with RVOT. This wasreported as abnormal in seven patients with ARVD,but none with RVOT.

Electrophysiological study andradiofrequency ablation

Ventricular tachycardia was inducible with pro-grammed electrical stimulation in 14 (82%) patientswith ARVD, but in only one (3%) with RVOT tachy-cardia. All with RVOT tachycardia had ventricular

tachycardia or frequent monomorphic ventricularectopic beats during isoprenaline infusion. Ven-tricular tachycardia was sustained, defined aslasting longer than 30 s, in 12 (71%) of the ARVDpatients and in five (15%) of the RVOT tachycardiagroup.

The ARVD patients had an average of 1.8 mor-phologies of inducible ventricular tachycardia(range 1 – 6), with 12 (71%) demonstrating morethan one morphology (Table 3). At least one ofthe induced morphologies matched the clinicalventricular tachycardia in all patients. All RVOT

Fig. 2 (a) Example of normal electrograms in the right ventricular outflow tract of a patient with ARVD. The recordings are at a paperspeed of 100 mm s−1. The mapping electrodes are recorded with a gain of 1000. (b) Example of fragmented electrograms in the rightventricular free wall of the same patient with ARVD. The recordings are at a paper speed of 100 mm s −1. The mapping electrodes arerecorded with a gain of 2500.

Fig. 3 Kaplan – Meier curve of freedom from ventricular tachy-cardia. Cumulative rates of freedom from ventricular tachy-cardia (VT) recurrence comparing patients with arrhythmogenicright ventricular dysplasia (-%-) and right ventricular outflowtract tachycardia (

——).




tachycardia patients demonstrated only a singlemorphology of ventricular tachycardia or ventricu-lar ectopic beats, which was identical to that re-corded clinically. The mean cycle length ofventricular tachycardia was 360 ms (265 – 440 ms) inthe RVOT patients and 310 ms (230 – 420 ms) in theARVD patients.

Mapping of the right ventricle revealed frag-mented potentials in the majority of patientswith ARVD and only in a single patient with RVOTtachycardia. The sites of the fragmented potentialscorrelated poorly with successful ablation sites.

The successful ablation sites in the RVOTpatients had a mean pre-systolic activation of 28 ms(13 – 48 ms) and this was greater than 30 ms in 18patients. In the ARVD group, concealed entrain-ment was demonstrated for 15 different ventriculartachycardias in 12 patients. Fragmented electro-grams and diastolic potentials guided ablationin the remaining patients. The mean number ofablations per procedure was 10; the number ofablations in the ARVD patients (mean 18, range7 – 38) was significantly greater than in theRVOT tachycardia patients (mean 6, range 1 – 22)(P <0.01).

Acute success

Acute procedural success was achieved in 32 (97%)and failure in one (3%) of the RVOT patients. Acutesuccess was achieved in seven (41%) of the ARVDpatients with a partial success in five (29%) andfailure in five (29%).

There were no significant differences in demo-graphic, electrophysiological or conduct of ablationbetween patients with a procedural success orfailure.

Follow-up

The mean follow-up was 56 months (13 – 92months), and all patients were followed-up for aminimum of 12 months. Recurrence of ventriculartachycardia was documented in eight (47%) of theARVD patients and two (6%) of the RVOT tachy-cardia patients. Recurrence in the RVOT tachy-cardia patients followed a successful procedure inone patient and an unsuccessful procedure in theother. In the ARVD patients, recurrence followed acomplete or partially successful procedure in threepatients and in five patients with an unsuccessful.No patients died during the follow-up period.

Two of the ARVD patients had an implantablecardioverter defibrillator prior to the procedureand an additional six patients received a defibrilla-tor following the procedure. Fifteen of the ARVDpatients, including all patients who were nottreated with an implantable cardioverter defibril-lator, were maintained long-term on sotalol (4) oramiodarone (11). None of the patients with RVOTreceived an implantable cardioverter defibrillatoror class 3 anti-arrhythmic agents. The RVOT patientwho failed ablation was discharged on atenolol.

Outcome in patients with MRI abnormalities

The presence of MRI abnormalities in the patientswith RVOT tachycardia did not have a significanteffect on acute procedural success. The procedurewas successful in 17/18 with MRI abnormalities and15/15 without MRI abnormalities (P ns).

Recurrent ventricular tachycardia was seen intwo RVOT tachycardia patients; one patient withMRI abnormalities and an unsuccessful initialprocedure, and one with asymptomatic recurrence

Table 3 Electrophysiological studies

ARVD RVOT P value

Inducible with PES 14 (82%) 1 (3%) <0.01Inducible with isoprenaline 3 (18%) 27 (81%) <0.01Monomorphic VEBs only 1 (6%) 6 (18%) nsSustained tachycardia 12 (71%) 5 (15%) <0.01

Number of VT morphologies l.8±0.8 1.0±0.1 <0.01Greater than one VT morphology 12 (71%) 0 <0.01Fragmented potentials 14 (82%) 1 (3%) <0.01Number of ablations 15±5 8±3 =0.05Successful procedure 8 (48%) 32 (97%) <0.01Follow-up (months) 58±18 54±17 nsRecurrent VT 8 (48%) 2 (6%) <0.01

ARVD=arrhythmogenic right ventricular dysplasia; RVOT=right ventricular outflow tract tachycardia; VT=ventricular tachycardia;PES=programmed electrical stimulation; VEB=ventricular ectopic beat. Sustained tachycardia >30 s; ns=not significant.




following an initially successful procedure in apatient without MRI abnormalities (Table 4). Thepatient with the initial failed procedure had asuccessful repeat procedure using an irrigatedtip catheter. The patient with an asymptomaticrecurrence declined a further procedure.

DiscussionThis study compared 50 consecutive patients withARVD or RVOT tachycardia, using traditional diag-nostic tools, MRI and invasive electrophysiologicalfeatures and correlated these with proceduralsuccess and long-term outcome following radio-frequency ablation. The major findings of the studyare firstly that ARVD and RVOT tachycardia aredifferent electrophysiological syndromes. Regard-less of results from non-invasive investigations,electrophysiological findings can independentlydifferentiate the two diagnoses on the basis of the

mechanism of induction, the number of ventriculartachycardia morphologies and fragmented electro-grams. And secondly, that in RVOT tachycardia thepresence of minor abnormalities on MRI has noimpact on electrophysiological properties, ablationsuccess or long-term recurrence of ventriculartachycardia.

Invasive electrophysiology study

This report has demonstrated that invasive electro-physiological findings can differentiate ARVD andRVOT tachycardia. In this study ventricular tachy-

cardia was inducible by programmed electricalstimulation in 82% of the patients with ARVD, but inonly 3% of those with RVOT tachycardia. Converselytachycardia was uniformly inducible with isoprena-line and cycle length dependent in the patientswith RVOT tachycardia. Seventy percent of thepatients with ARVD had more than one morphologyof inducible ventricular tachycardia and the major-ity had significant zones of fragmented electro-grams, whereas all RVOT tachycardia patients hadonly a single morphology of ventricular tachycardiaand fragmented electrograms were rarely seen.

These electrophysiological findings suggest sig-nificant differences in underlying disease processbetween ARVD and RVOT patients. Arrhythmia in-duction with programmed electrical stimulationparticularly in the presence of fragmented electro-grams favours re-entry as the predominant mech-anism for tachycardia in ARVD patients. Inductionof ventricular tachycardia by isoprenaline with cy-

cle length dependence is consistent with acyclic—AMP mediated triggered activity being thepredominant mechanism in RVOT tachycardia.21

The more extensive disease process evidencedby zones of fragmented electrograms contributes tothe different ventricular tachycardia morphologiesseen in individual ARVD patients.

The findings at electrophysiological study clearlydifferentiate the two diagnoses on the basis oftheir different arrhythmic mechanisms. This allowsaccurate identification of patients who will becured by ablation and remain free from recurrence

or progression of tachycardia.

Structural information

With advances in technology, non-invasive imaginghas become more sensitive in detecting right ven-tricular structural abnormalities. In this study, MRIdetected twice as many structural abnormalities inthe ARVD patients than a combination of trans-thoracic echocardiography and right ventricularcine angiography. None of the RVOT tachycardiapatients had structural abnormalities on echocardi-

ography or angiography. However, MRI detectedabnormalities in 54%. Similar rates of MRI abnor-malities in patients with RVOT tachycardia havepreviously been reported.12 – 15

The extent of MRI abnormality also differed be-tween patients with ARVD and RVOT tachycardia.Major structural abnormalities were seen on MRI in88% of patients with ARVD but in only 6% of thosewith RVOT tachycardia. Minor abnormalities onlywere detected in the remaining 12% of ARVDpatients and in 48% of patients with RVOTtachycardia.

Table 4 Relationship of MRI findings in patients with right ventricular outflow tract tachycardia to acute and long-term successof radiofrequency ablation

Number Acute success Recurrent VT

Overall 33 32 (97%) 2 (6%)MRI abnormality 18 (54%) 17 (95%) 1 (5%)No MRI abnormality 15 (46%) 15 (100%) 1 (5%)




In this report the electrophysiological character-istics did not correlate with the presence or ab-sence of abnormalities on MRI. Mode of tachycardiainduction, presence of fragmented signals andnumber of ablations in the RVOT tachycardiapatients was similar whether MRI abnormalities

were present or not. The presence of abnormalitieson MRI did not have any bearing on acute or thelonger term success or subsequent recurrence ofventricular tachycardia following ablation.

The finding of a degree of structural abnormalityon MRI has led to speculation that RVOT tachycardiamay be an early form of ARVD with the samepotential for disease progression. However, studiesto date have failed to show evidence of diseaseprogression during follow-up of patients withRVOT tachycardia.16,22 This analysis supports theprevious findings, with no evidence of disease pro-

gression or arrhythmia recurrence during follow-upfollowing ablation.

Previous studies

This analysis supports the conclusions of others thatARVD and RVOT tachycardia are fundamentallydifferent entities that can usually be distinguishedclinically.1,2,6,23 Major abnormalities on standardelectrocardiograms, signal-averaged electrocardio-grams or transthoracic echocardiography arehallmarks of ARVD.

Contrary to previous reports, frequency of symp-toms and history of syncope were similar in ARVDand RVOT tachycardia.1,24 This study enrolled onlypatients referred for electrophysiological evalua-tion and this has introduced selection bias intothe sample. The patients enrolled in the studyprobably represent the more symptomatic end ofthe RVOT tachycardia spectrum. This may haveblunted any expected differences in symptomfrequency between the two groups.

The procedural success rates and ventriculartachycardia recurrence rates in this report are in

keeping with previously published figures. Ablationis rarely curative of all arrhythmias in ARVD; theacute success rate is reported to be less than 40%with high later recurrence rates over time dueto the progressive nature of the disease.25,26 Thesuccess rate of ablation in the ARVD patients in thisstudy was 42% and the recurrence rate 48% over 58months of follow-up. Ablation for RVOT tachy-cardia, on the other hand, is traditionally thoughtto be curative in the majority of patients and theacute success rate of 97% and long-term successrate of 94% in this report is expected.20,22

Clinical implications

The importance of electrophysiological findings inpredicting arrhythmia mechanism and long-termoutcome should assist in recommending ongoingtherapy following radiofrequency ablation. Even in

the presence of minor structural abnormalitiesablation is curative in the majority of patientswith features of RVOT and a focal arrhythmia mech-anism.

Recurrent ventricular tachycardia is seen inalmost half of the patients with ARVD following anablation procedure; 19% after a successful proce-dure and 100% following an unsuccessful procedure.The recurrence of ventricular tachycardia after asuccessful procedure in ARVD is significantly higherthan after successful ablation of RVOT or evenventricular tachycardia associated with ischaemicheart disease.27 The inability of a successful proce-dure to reliably protect against ventricular tachy-cardia recurrence in ARVD patients suggests thatablation should be reserved for patients with highlysymptomatic episodes and considered an adjunct toimplantable cardioverter defibrillators.

This study in part attempted to address the issueof disease progression amongst RVOT tachycardiapatients. Whilst no evidence of disease progressionwas documented, the rate of progression in ARVD isunknown and may be highly variable.28 Thefollow-up in this study may be insufficient andserial evaluations over a longer time frame would

be needed to definitively answer the question ofprogression.

Conclusions

This analysis shows that ARVD and RVOT tachy-cardia can be differentiated clearly on the basisof electrophysiological characteristics. The findingssuggest the two conditions behave as fundamen-tally different entities.

The presence of minor structural abnormalities

on MRI in RVOT tachycardia patients is consistentwith benign natural history, high ablation successrates and low later ventricular tachycardiarecurrence.

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European Heart Journal (2003) 24, 801–810

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