Download Welcome to RHYTHM 2007

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Welcome to RHYTHM 2007
Dear Friends and Colleagues,
We are proud to present the RHYTHM 2007 program which has been granted by 14 CME credits by the European Board
for Accreditation in Cardiology (EBAC) and validated by The French Society of Cardiology (SFC).
This program has been made possible thanks to the involvement of all invited faculty experts and through the precious support of the industry. We all share a mutual interest in developing clinical and fundamental research to improve diagnostic, patient
care and follow up in our daily practice.
Scientific sessions begin on Friday, with two live cases in parallel with conferences on Atrial Arrhythmias (Friday morning) and Ventricular Arrhythmias (Friday afternoon).
Those two live cases on radiofrequency ablation by electro-anatomic and non-contact mapping systems, provide unique educational
tips & tricks from key experts (issued from St Joseph Hospital Marseille and CMC Parly 2, Le Chesnay).
On Saturday, conferences on Atrial Arrhythmia, Echocardiography and Ventricular Resynchronisation alternate with
three video cases focusing on AF ablation and the use of new specific leads in Ventricular Resynchronisation. Each attendee has the
opportunity to update his knowledge and debate on the most accurate medical or electrical treatments, diagnostic and device algorhythm.
Medtronic Luncheon Workshops on Friday and Saturday from 12h30 to 13h45, convivially welcome physicians interested in the latest tendencies of AF monitoring, Subcutaneous Diagnostic and Monitoring (SQDM), wireless telemetry or IDC primary prevention, around seated served lunches.
Friday from 18h30 to 19h30, BIOTRONIK presents a Symposium on "Devices follow-up goes Home Monitoring".
During a welcoming cocktail, experts in clinical studies, worldwide routine use of Home Monitoring or remote FU of ICD, present
their latest results. All medical and paramedical specialists are welcome.
The last scientific session on Sunday morning is dedicated to Free Papers oral presentations. To celebrate the end of this
forth RHYTHM edition, a 1000 € prize is offered to one lucky participant, after random selection among the attending audience.
We are also proud to welcome this year, the first RHYTHM Paramedical session dedicated to the Continuing Medical
Education of French technicians and nurses, from Cath-Lab procedures to the patient's room.
Once again, welcome to the RHYTHM congress, we hope you will enjoy the high level of the scientific sessions, live and
video cases, workshops and symposium, for two and a half days of intensive teaching.
The Rhythm Directors
Chers confrères et amis,
Nous sommes heureux de vous présenter le programme du RHYTHM 2007 accrédité par 14 heures de Formation Médicale
Continue par l'European Board for Accreditation in Cardiology (EBAC) et parrainé par la Société Française de Cardiologie (SFC).
Cet événement a été rendu possible grâce à l'implication de tous les experts de la faculté mais également grâce au précieux
soutien de l'industrie. Nous partageons tous un intérêt mutuel à développer la recherche clinique et fondamentale afin d'améliorer le
diagnostic, le soin et le suivi des patients dans notre pratique quotidienne.
Les sessions scientifiques commencent vendredi, avec deux procédures en direct, diffusées en parallèle de conférences sur les
Troubles du Rythme Auriculaire (vendredi matin) et les Troubles du Rythme Ventriculaire (vendredi après midi).
Ces deux procédures " live", sur l'ablation par radiofréquence avec des systèmes de cartographie electro-anatomique et de non contact,
apporteront des astuces techniques uniques grâce à la compétence et à l'expertise des experts intervenants (issus de l'Hôpital St Joseph
- Marseille et du CMC Parly 2 -Le Chesnay).
Samedi, des conférences sur les Troubles du Rythme Auriculaire, l'Echocardiographie et la Resynchronisation
Ventriculaire alterneront avec la présentation de 3 cas vidéo abordant l'ablation de la FA ou l'utilisation de nouvelles sondes spécifiques dans la Resynchronisation Ventriculaire
Chaque participant a ainsi l'opportunité de mettre à jour ses connaissances et de débattre sur les choix les plus appropriés en matière
de traitements médicaux ou électriques, de diagnostics et de programmes de dispositifs implantables.
Les " Luncheon Workshops " MEDTRONIC, vendredi et samedi de 12h30 à 13h45, accueillent en toute convivialité,
autour d'un déjeuner assis, celles et ceux intéressé(e)s par les dernières tendances du monitoring de la FA, les solutions de monitoring et de diagnostic sous cutané, la télémétrie à distance ou encore les indications de prévention primaire du DAI.
Vendredi de 18h30 à 19h30, BIOTRONIK organise un symposium intitulé "Télécardiologie pour le suivi des prothèses
implantables ". Autour d'un cocktail de bienvenue, les experts présentent leurs derniers résultats sur les études cliniques, la télécardiologie au niveau mondial, ou le suivi à distance des DAI. Tous les participants médicaux et paramédicaux sont les bienvenus.
La dernière session scientifique est consacrée aux présentations orales des Communications Libres.
Pour fêter la fin de cette quatrième édition du RHYTHM, un prix de 1000 € sera attribué à un chanceux participant après tirage au
sort parmi l'auditoire présent.
Enfin, nous sommes également très heureux d'accueillir cette année, les premières sessions PARAMEDICALES du
RHYTHM, dédiées à la Formation Médicale Continue des techniciens (nes) et infirmiers (ères) français, intervenant de la salle de
cathétérisation à la chambre du patient.
A nouveau, bienvenue au RHYTHM 2007, nous espérons que vous apprécierez la haute qualité des conférences, retransmissions en direct, cas vidéo, workshops et symposium durant ces deux journées et demi d'enseignement intensif.
Les Directeurs du RHYTHM
Arrhythmias & Heart Failure
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Congress Directors
Patrick Attuel
Cardiologist
Centre Médico-Chirugical de Parly II
Le Chesnay
France
Claude Barnay
Cardiologist
Centre Hospitalier du Pays d'Aix
Aix-en-Provence
France
Cardiologist
Ospedale Civile
Asti
Italy
Cardiologist
Centre Médico-Chirugical de Parly II
Le Chesnay
France
Cardiologist
Hôpital Saint-Joseph
Marseille
France
Fiorenzo Gaita
Jean-François Leclercq
André Pisapia
Guest Faculty
Jean-Pierre Albenque Cardiologist
Clinique Pasteur
Toulouse
France
Cardiologist
Maurits Allessie
Cardiovascular Research Institute Maastricht
The Netherlands
Cardiologist
Giuseppe Augello
Ospedale San Raffaele
Milano
Italy
Cardiologist
Martin Borggrefe
Universitätsklinikum Mannheim Mannheim
Germany
Frieder Braunschweig Cardiologist
Karolinska University Hospital Stockholm
Sweden
Cardiologist
Michel Bremondy
Hôpital Saint-Joseph
Marseille
France
Jean-Pierre Camous Cardiologist
Université de Nice
Nice
France
Cardiologist
Riccardo Cappato
Istituto Policlinico San Donato San Donato Milanese Italy
Cardiologist
Bruno Cauchemez
Hôpital La Riboisière
Paris
France
Cardiologist
Michel Chauvin
Hôpital Hautepierre
Strasbourg
France
Cardiologist
Pascal Defaye
Hôpital Michallon, CHU
Grenoble
France
Jean-Claude Deharo Cardiologist
CHU La Timone
Marseille
France
Cardiologist
Erwan Donal
CHU Rennes
Rennes
France
Cardiologist
Jacques Faure
Hôpital Saint-Joseph
Marseille
France
Cardiologist
Ange Ferracci
Hôpital Saint-Joseph
Marseille
France
Cardiologist
Pierre Fiorello
Centre Médico-chirurgical
de Parly II
Le Chesnay
France
Frédéric Francheschi Cardiologist
CHU Timone
Marseille
France
Cardiologist
Robert Frank
Groupe Hospitalier
Pitié Salpétrière
Paris
France
Cardiologist
Daniel Gras
Nouvelles Cliniques Nantaises Nantes
France
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Franck Halimi
Cardiologist
Centre Médico-chirurgical
de Parly II
Le Chesnay
Cardiologist
Meleze Hocini
CHU Haut Lévèque
Pessac
Paediatric-Cardiologist
Laurence Iserin
Groupe Hospitalier Necker
Paris
Cardiologist
Michiel Janse
Academic Medical Center
Amsterdam
Cardiologist
Luc Jordaens
Erasmus Medical Centre
Rotterdam
Product Manager Tachycardia
Nordine Kamouche
Medtronic
Paris
Cardiologist
Patrick Khanoyan
Hôpital Saint-Joseph
Marseille
Cardiovascular Surgeon
Dominique Lacroix
CHU de Lille
Lille
Cardiologist
Arnaud Lazarus
Inparys ®
St Cloud
Division of Cardiovascular
Bruno Le Grand
Diseases
Centre de Recherche Pierre Fabre Castres
Cardiologist
Jean-Yves Le Heuzey
Hôpital Européen
Georges Pompidou
Paris
Cardiologist
Jean Lefevre
Hôpital Saint-Joseph
Marseille
Cardiologist
Athanasios Manolis
Hellenic Red Cross Hospital
of Athens
Athens
Cardiologist
William Mc Kenna
The Heart Hospital
London
Cardiologist
Goran Milasinovic
Clinical Center of Serbia
Belgrade
Cardiologist
Matthias Paul
Universitäty Hospital
and Medical School of Müenster Müenster
Product Manager SQDM
Christèle Pelade
Medtronic
Paris
Cardiologist
Maxime Pons
Clinique du Millénaire
Montpellier
Cardiologist
Vincent Probst
CHU de Nantes
Nantes
Cardiologist
Jacques Robin
Hôpital Cardio-vasculaire
L. Pradel
Lyon
Cardiologist
Edwards Rowland
St. George's Hospital
Medical School
London
Damian Sanchez-Quintana Prof. of Human Anatomy
Facultad de Medicina
Badajoz
Cardiologist
Claude Scheublé
Centre Cardiologique du Nord Saint-Denis
Cardiologist
Jérôme Taeib
Centre Hospitalier du Pays d'Aix Aix-en-Provence
Product Manager Imaging
Philippe Thomas
Biosense Webster Europe
Waterloo
New Treatments in Heart Fealure
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France
France
France
The Netherlands
The Netherlands
France
France
France
France
France
France
France
Greece
United Kingdom
Serbia
Germany
France
France
France
France
United Kingdom
Spain
France
France
Belgium
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Educational Objectives
The RHYTHM congress aims at providing continuing medical education on pharmacological and non pharmacological therapies of arrhythmias and heart failure (atrial arrhythmias, ventricular arrhythmias, and ventricular asynchronism).
At the end of the course, attendees should:
Have received an updated scientific knowledge
on pharmacological and non pharmacological therapies
Have received the latest scientific trials information
on ablative techniques and prevention of heart failure
Be able to make the most appropriate diagnostic
and therapeutics for each patient
Have observed how cath-lab should be equipped
and how interventional procedures run
Le congrès RHYTHM a pour but de dispenser une formation médicale continue sur les traitements médicamenteux et électriques des troubles du rythme et de l’insuffisance cardiaque (fibrillation auriculaire, arythmies
et asynchronismes ventriculaires).
A la fin de ces enseignements, les participants devraient :
Avoir reçu une mise à jour scientifique
sur les traitements médicamenteux et électriques
Avoir reçu les derniers résultats concernant les essais cliniques
sur les techniques ablatives et la prévention de l’insuffisance cardiaque
Etre à même de faire le meilleur diagnostic et de prescrire le traitement
le plus approprié pour chaque patient
Avoir observé l’équipement nécessaire à un laboratoire
de cathétérisation et comment se déroulent les procédures
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Accreditation for Continuing
Medical Education
Accréditation dans le cadre
de la Formation Médicale Continue
14 CME Credit hours
The RHYTHM 2007 CONGRESS is accredited by the European Board for Accreditation in
Cardiology (EBAC) for 14 hours of External CME credits.
Each participant should claim only those hours of credit that have actually been spent in
the educational activity. EBAC works according to the quality standards of the European
Accreditation Council for Continuing Medical Education (EACCME), which is an institution of the
European Union of Medical Specialists (UEMS).
Information on disclosure policy Information sur la politique de conflits d'intérêts
In compliance with the EBAC/EACCME guidelines, all speakers/chairpersons participating in this
programme have disclosed potential conflicts of interest that might cause a biais in the presentations.The Organizing Committee is responsible for ensuring that all potential conflicts of interest
relevant to the event are declared to the audience prior to the CME activities.
Crédit de 14 heures de FMC
Le congrès RHYTHM 2007 est accrédité par l'European Board for Accreditation in
Cardiology (EBAC) pour 14 heures de crédit de FMC.
Chaque participant devra déclarer uniquement les heures effectivement passées à cette
activité de formation. EBAC travaille en accord avec les normes de l'European Accreditation Council
for Continuing Medical Education (EACCME), qui est une institution de l'Union Européenne des
Médecins Spécialistes (UEMS).
En accord avec les directives de l'EBAC/EACME, tous les orateurs/modérateurs participant à ce programme ont déclaré les conflits d'intérêts potentiels qui pourraient introduire un biais
dans les présentations. Le comité organisateur est responsable de s'assurer que tous les conflits
d'intérets potentiels relatifs à l'évenement sont déclarés aux participant avant le début du congrès.
Arrhythmias & Heart Failure
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Consulting
Employment
in industry
Stockholder of
a healthcare
company
Owner of
a healthcare
company
Other
Yes
Yes
No
No
No
No
G. Augello
No
No
No
No
No
No
C. Barnay
Yes
Yes
No
No
No
No
M. Borggrefe
No
No
No
No
No
No
F. Braunschweig
Yes
Yes
No
No
No
No
M. Bremondy
No
No
No
No
No
No
J-P. Camous
No
Yes
No
No
No
No
R. Cappato
Yes
Yes
No
No
No
No
M. Chauvin
No
No
No
No
No
No
P. Defaye
No
No
No
No
No
No
J-C. Deharo
No
No
No
No
No
No
E. Donal
No
No
No
No
No
No
J. Faure
No
No
No
No
No
No
A. Ferracci
No
No
No
No
No
No
P. Fiorello
No
No
No
No
No
No
R. Frank
No
No
No
No
No
No
F. Halimi
No
No
No
No
No
No
M. Hocini
No
No
No
No
No
No
Not available
Research
Contract
Disclosure of interest
J-P. Albenque
M. Allessie
P. Attuel
B. Cauchemez
F. Gaita
D. Gras
6
Owner of
a healthcare
company
Other
M. Janse
No
No
No
No
No
No
L. Jordaens
Yes
Yes
No
No
No
No
D. Lacroix
No
Yes
No
No
No
No
B. Le Grand
No
No
Yes
No
No
No
J-Y. Le Heuzey
Yes
Yes
No
No
No
No
J-F. Leclercq
No
Yes
No
No
No
No
A. Manolis
No
No
No
No
No
No
W. Mc Kenna
No
No
No
No
No
No
G. Milasinovic
No
No
No
No
No
No
M. Paul
No
No
No
No
No
No
A. Pisapia
Yes
Yes
No
No
No
No
V. Probst
No
No
No
No
No
No
J. Robin
No
Yes
No
No
No
No
D. Sanchez-Quintana No
No
No
No
No
No
C. Scheublé
No
No
No
No
No
No
J. Taeib
No
No
No
No
No
No
P. Thomas
No
No
Yes
No
No
No
Not available
Stockholder of
a healthcare
company
Page 7
Employment
in industry
18:34
Consulting
25/05/2007
Research
Contract
programme-final-RHYTHM2007-K.qxd
L. Iserin
P. Khanoyan
J. Lefèvre
E. Rowland
New Treatments in Heart Fealure
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Industrial Partnerships
Major Sponsors
Medtronic
St. Jude Medical
Sponsors
Biosense Webster
Boston Scientific - Guidant
Educationnal Grants
Biotronik
Sorin Group
3M Santé
Pierre Fabre Médicaments Information
CVx Medical
Flammarion Médecine
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Live Case Center
Saint-Joseph Hospital, Marseille, France
President
Antoine Dubout
General Director
Bernard Monier
Vice Director
Florent Rovello
Medical Director
Marc Dupont
Cardiovascular Executive
Nursing Officer
Brigitte Pelletier
Biomedical Engineer
Pierre Léger
Chief nursing officer
Sylvie Durbec, Caroline Jacquet
26 boulevard de Louvain - 13 285 Marseille Cedex 08, France
Tel
+33 (0) 491 806 500
Fax
+49 (0) 491 806 417
Website
www.hopital-saint-joseph.fr
E-mail
[email protected]
Video Case Centers
CMC (Medical & Surgical Center), Le Chesnay, France
21, rue Moxouris - 78150 Le Chesnay, France
Tel
+33 (0) 139 637 166
Fax
+33 (0) 139 238 618
Website
www.clinique-parly2.com
E-mail
[email protected]
Centre Hospitalier du Pays d’Aix, Aix-en-Pce, France
Service de Cardiologie
Avenue des tamaris - 13616 Aix-en-Provence cedex 1, France
Tel
+33 (0) 442 335 000
Fax
+33 (0) 442 23 51 69
Website
www.ch-aix.fr
E-mail
[email protected]
New Treatments in Heart Fealure
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Local Organizing Committee
Hôpital Les Broussailles, Cannes, France
Interim Director
Jacques Thierry
President of the
Medical Advisory
Board
Dr Thierry Tibi
Vice-President of
the Medical Advisory
Board
Dr Michel Beltran
Communication Dpt Alice Herbert
25, avenue des Broussailles, 06400 Cannes, France
Tel
+33 (0)493 697 001
Fax
+33 (0) 493 697 009
Website
www.hopital-cannes.fr
E-mail
[email protected]
Congress Organization
Com&Co: your local contacts
Majestic Office
04 97 06 86 27
Laurence Curel
Scientific Coordinator
+33 622 053 405
Caroline Bartocci
Faculty Coordinator
+33 618 237 420
Anne Rubin
Registration
& Housing Coordinator
+33 650 737 696
Lionel Vaillat
Industry Manager
+33 617 712 182
Vérane Bergeron
Executive Manager
+33 621 788 716
Philippe Halaburda
Design Manager
+33 620 712 180
40, avenue de Saint-Antoine - 13015 Marseille - France
Tel
Fax
Website
E-mail
10
+33 491 097 053
+33 496 153 308
www.comnco.com
[email protected]
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General Information
Venue of the Meeting
City of Cannes
Tourism Office
Palais des festivals et des Congrès, La Croisette
06400 Cannes, France
Tel
+33 (0) 492 99 84 22
Fax
+33 (0) 492 99 84 23
Web
www.cannes.fr
Majestic Barrière Hotel
10, La Croisette -BP 163
06407 Cannes Cedex, France
Tel
+33 (0) 492 987 700
Fax
+33 (0) 493 389 790
Mail
[email protected]
Web
www.lucienbarriere.com
Registration & Information Desk
Thursday June 14
Friday June 15
Saturday June 16
Sunday June 17
from 14.00 to 18.30
from 07.30 to 18.00
from 08.00 to 18.00
from 08.30 to 11.00
Admission Requirements
Admission to all RHYTHM 2007 scientific events taking place in the congress area requires
a nominative badge.
Registrants will receive badges with their portfolios.
Speakers Preview Room
Speakers are asked to review, arrange and finalize their Power Point presentations and video
cases with the audiovisual department well in advance of their presentation :
- the day before regarding the morning sessions
- at latest 3 hours before the beginning of the afternoon sessions
Materials will be stored in a secure area.
The Preview Lounge is located at the entrance of the auditorium with the technical staff .
No laptop will be allowed in the Auditorium.
Arrhythmias & Heart Failure
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Certificate of attendance
A certificate of attendance including the EBAC CME Credits will be delivered to all the participants, upon request, at
registration desk.
Official Language
The official language of the RHYTHM congress is English. No translation is provided.
Exhibition Hours
Friday June 15
Saturday June 16
from 09.00 to 19.30
from 09.00 to 18.30
Best visiting times are during breakfasts, lunches and breaks.
RHYTHM 2007 Lunch
Complimentary finest buffet lunch is served for registrants on:
- Friday on the Beach Restaurant (limited to 140 seats) of the Majestic Hotel and in the Exhibition Hall
- Saturday in the Exhibition Hall only
Medtronic also welcomes its guests to take part to its luncheon workshops on Friday and Saturday.
Luncheon Workshops
Seated finest lunch will be served.
Friday, June 15
12.30 - 13.45, Medtronic Lounge
See detailed program page 24
Saturday, June 16
12.30 - 13.45, Medtronic Lounge
See detailed program page 26
Biotronik Cocktail Symposium
Friday, June 15
18.30 - 19.30, Auditorium
La télécardiologie pour le suivi des prothèses implantables
Devices follow up goes Home Monitoring
See detailed program page 25
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General Information
Social Events
VIP’s night
Friday June 15
20.30
The VIP’s night, only available to Faculty Members will take place at the
Terrasse Pisani of the Fouquet’s Restaurant. (Majestic Hotel)
Dresscode : chic
Sandy Party
Saturday June 16
20.00 /00.30
Our Gala Diner, “Sandy Party” will illuminate "Z Plage", the Martinez
Hotel private beach.
Seated buffet dinner & live music entertainment.
Dresscode : chic
Participation : 50 €
Travel to Cannes - official partners
CONGRESS : MEET & RHYTHM 2007
Reference to be quoted : AXZE SE61274
Validity from 08/06/2007-22/06/2007
Air France: 3654* or Internet : www.airfrance.com
Airport Shuttles And Taxis
Shuttles every 30 minutes
* a fee is charged for these calls
- Price around 12,5 € (for a single ticket - 50 minutes trip).
- Taxis cost approximately 70 € (for a single ticket - 30 minutes trip).
ALLO TAXIS CANNES 08 90 71 22 27
ALLO TAXIS
04 93 99 90 77
Shuttle Service, Transfer Nice Airport
- Mercedes Classe
- Minibus 8 places
- Mercedes Classe S
157€
157€
192€
Contact : Virginie Vialard
tel:
+33 (0)4 93 43 90 91
mail:
[email protected]
New Treatments in Heart Fealure
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Car rentals
Company
Reservation
Terminal 1
Terminal 2
ADA
AVIS
BUDGET
EUROPCAR
04 93 21 36 47
04 93 21 36 33
04 93 21 36 50
08 25 35 23 52
04 93 21 42 50
04 93 21 42 80
04 93 21 42 51
08 25 81 00 81
HERTZ
08 25 34 23 43
NATIONAL CITER
SIXT
04 93 21 80 90
04 93 21 80 90
04 93 21 63 47
08 20 05 05 05
08 25 00 35 64
08 03 35 23 52
08 25 35 23 52
08 25 36 13 61
08 25 34 23 43
01 44 38 61 61
01 44 38 55 55
04 93 21 42 72
04 93 21 42 52
04 93 21 48 87
Climate
Cannes is located on the French Riviera, and enjoys a mild Mediterranean climate with an average of 300
days of sunshine per year. You can expect warm and sunny spring weather, temperatures between 18
and 28 Celsius degrees. Beware of the sun and do not forget your sunscreen.
Map of Cannes
(Walking distances in minutes)
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Scientific Program
Programme-at-a-Glance
Friday June 15
09.00 - 19.30
Saturday June 16
09.00 - 18.30
Sunday June 17
09.00 - 11.30
New Treatments in Heart Fealure
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Programme at-a-glance
Friday, June 15, morning
09.00
08.30
12.30
10.30
Opening statement,
Discours d’ouverture,
J-F. Leclercq
11.00
Coffee
Break
09.05
Atrial arrhythmias
Welcoming
Coffee
SESSION 1
Troubles du rythme auriculaire
09.05
Broadcast opening
Live Case Demonstration from Saint-Joseph Hospital
Atrial fibrillation Ablation
10.15
11.30
Live update,
Point Live
Live update, Live update,
Point Live
Point Live
12.20
Saturday, June 16, morning
09.00
08.30
12.30
10.50
Coffee
Break
Welcoming
Coffee
Atrial arrhythmias
SESSION 2
Troubles du rythme auriculaire
Sunday, June 17, morning
08.30
09.00
Welcoming
Coffee
11.30
11.00
11.15
Free Papers Session
Session
communications libres
Attendees Adjournment
lottery
statement
Loterie
participants
20
Discours de clôture
A. Pisapia
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Friday, June 15, afternoon
16.00
14.00
09.00
12.30
Lunch
on the Beach
(140 seats)
&
Buffet
(Exhibiton Hall)
Opening statement,
16.30
18.05
Discours d’ouverture,
J-F. Leclercq
13.45
(Medtronic Lounge
60 seats)
19.30
SYMPOSIUM
Ventricular arrhythmias
(Auditorium)
Troubles du rythme ventriculaire
Luncheon
Workshop
18.30
Coffee
Break
09.15
Broadcast
opening
Live Case Demonstration
Broadcast
opening from Saint-Joseph Hospital
Live
Case Demonstration
from
Saint-Joseph
Hospital
Infundibular
Ventricular
Tachycardia
Ablation
14.40
15.05
Live update, Live update,
Point Live
Point Live
15.30
15.55
16.50
Live update, Live update, Live update,
Point Live
Point Live
Point Live
Saturday, June 16, afternoon
12.30
14.00
15.45
16.15
18.30
Coffee
Break
Buffet
(Exhibiton Hall)
Sandy Party
(Martinez Hotel
Z’ Plage)
13.45
Luncheon
Workshop
(Medtronic Lounge
60 seats)
20.00
Echocardiography
Session
Session
Echocardiographique
New Treatments in Heart Fealure
21
Ventricular
resynchronisation
Resynchronisation
Ventriculaire
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Scientific Program
Conferences - Abstracts
Friday June 15
LIVE
SESSION 1
09.05
09.00 - 19.30
Session 1
Atrial arrhythmias,
Troubles du rythme auriculaire...............................24
Atrial fibrillation
Ablation
12.30
Lunch
12.30
Luncheon Workshop
LIVE
SESSION 2
14.00
Ventricular arrhythmias
18.05
Troubles du rythme ventriculaire..........................25
Infundibular
Ventricular
Tachychardia
Ablation
18.30
Cocktail Symposium
La télécardiologie
pour le suivi des prothèses implantables
19.30
Devices follow up goes Home Monitoring
22
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Scientific Program
Conferences - Abstracts
Saturday June 16
09.15
AUDITORIUM
Session 2
Atrial arrhythmias,
Troubles du rythme auriculaire...............................26
12.30
Lunch
12.30
Luncheon Workshop
14.00
Echocardiography Session
13.45
16.15
Ventricular Resynchronisation
18.30
Session Echocardiographique....................................27
Resynchronisation ventriculaire............................27
Samedi Juin 16
SALON DIANE
09.00 - 18.30
09.30
09.30 - 18.30
Session Paramédicale Francophone
Trouble du rhythme
& Insuffisance Cardiaque..................28 & 29
Sunday June 17
09.00
11.00
11.15
09.00 - 11.30
Free Paper Session
Session Communications Libres............................30
Attendees Lottery, Loterie des participants
Adjournment statement, Discours de clôture
Arrhythmias & Heart Failure
23
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Scientific Program
Friday June 15, morning
Auditorium, 09.00 - 13.45
LIVE SESSION
St Joseph Hospital
Marseille, France
Chairman /
Modérateurs:
P. Attuel & J. Faure
Atrial fibrillation
Ablation
by electroanatomic
mapping system
(Cartomerge tm)
08.30
Welcoming Coffee................................................................................................
09.00
Opening statement, Discours d'ouverture
J-F. Leclercq
09.05
Atrial arrhythmias,
Troubles du rythme auriculaire
Chairmen / Modérateurs : F. Gaita & C. Barnay
09.05
09.25
Live Broadcasting, Lancement de la procédure en Live
Perpetuating mechanisms of AF: anatomical aspects.
Mécanismes de perpetuation de la FA : aspects anatomiques.
D. Sanchez Quintana
09.45
New techniques in AF ablation
Nouvelles techniques d'ablation de la FA
G. Augello
10.15
Live update, Point Live
10.30
Coffee break.......................................................................................................
11.00
Complications of AF ablation
Complications de l'ablation de la FA
R. Cappatto
Live update, Point Live
When ICE visualization meets CARTO XP System vision
Quand l’échographie intracardiaque rencontre le système d’imagerie Carto XP
P. Thomas
Surgical ablation of AF
Ablation chirurgicale de la FA
J. Robin
Live update, Point Live
11.30
11.40
12.00
A. Pisapia
M. Bremondy
Session 1
12.20
12.30
Lunch at the Restaurant on the Beach of the Majestic Hotel (140 seats)
& Buffet (Exhibition Hall) ......................................................................................
12.30
Luncheon Workshop (Medtronic Lounge)
How to monitor Atrial Fibrillation ? Benefits and Constraints
Enjeux et problématiques du monitoring de la FA
A. Ferracci
13.45
24
Medtronic SQDM (Subcutaneous Diagnostic and Monitoring) solutions
Les solutions Medtronic SDQM (Subcutaneous Diagnostic and Monitoring)
C. Pelade
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Scientific Program
Friday June 15, afternoon
Auditorium, 14.00 - 19.30
14.00
Troubles du rythme ventriculaire
LIVE SESSION
St Joseph Hospital
Marseille, France
Chairman
Chairman //
Modérateurs:
Modérateurs:
F.
P. Gaita
Attuel&&A.
J. Ferracci
Faure
Infundibular
Atrial fibrillation
Ventricular
Ablation
tachycardia
by electroanatomic
Ablation
mapping system
tm
by
non contact
)
(Cartomerge
mapping system
(Ensite Array tm)
A. Pisapia
M. Bremondy
Chairmen / Modérateurs : D. Lacroix & B.Cauchemez
14.00
Live Broadcasting, Lancement de la procédure en Live
14.15
AICD indications in CHD: Only LVEF and no more arrhythmologic risk stratification?
Indications de DAI chez les coronariens : seulement la FEVG sans stratification du risque rythmique?
M. Borggrefe
Live update, Point Live
Primary prophylaxis of sudden death in non-ischemic
left ventricular diseases (DCM, HCM).
Prophylaxie primaire de la mort subite dans les cardiopathies gauches
non ischémiques (CMD, CMH)
W. Mc Kenna
Live update, Point Live
An AICD without endocardial lead ?
Un DAI sans sonde?
G. Milasinovic
Live update, Point Live
Post AICD implants therapies: drugs and ablative techniques
Traitements après implantation d’un DAI: médicaments et ablation
L. Jordaens
14.40
14.45
15.05
15.10
15.30
15.35
16.00
Coffee break........................................................................................................................
16.30
Risk stratification of sudden death in ARVD
Appréciation du risque de mort subite dans la dysplasie du VD
M. Paul
Live update, Point Live
Risk stratification of sudden death in congenital heart diseases
Appréciation du risque de mort subite dans les cardiopathies congénitales
L. Iserin
Markers of risk of sudden death in chanellopathies
Facteurs pronostiques de mort subite dans les maladies des canaux membranaires
V. Probst
Ablation of Ventricular Arrhythmias: endocardial, epicardial, Purkinje ?
Ablation des TdR ventriculaires: endocarde, épicarde, Purkinje ?
R. Frank
16.50
16.55
17.15
J-F. Leclercq
F. Halimi
Cocktail
Symposium
Ventricular arrhythmias,
17.35
18.05
18.30
19.30
La télécardiologie pour le suivi des prothèses implantables
Devices follow up goes Home Monitoring
Chairmen / Modérateurs : P. Attuel & F. Francheschi
(Auditorium)
Résultats de l'étude ŒDIPE:
OnE Day pacemaker Implantation Program with homE-monitoring
Results of OEDIPE study. F. Halimi
Qu'apprend-t-on de l'utilisation routinière de la télécardiologie au niveau mondial ?
What do we learn from worldwide routine use of Home Monitoring? A. Lazarus
Suivi à distance des défibrillateurs implantables par Télécardiologie
Remote follow-up of ICDs by Home Monitoring, L. Jordaens
Table Ronde, Discussion P. Attuel, F. Franceschi, F. Halimi, A. Lazarus, L. Jordaens & M. Pons
Arrhythmias & Heart Failure
25
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Scientific Program
Saturday June 16, morning
Auditorium, 09.00 - 13.45
08.30
Welcoming Coffee..............................................................................................................
09.00
Session 2
Atrial Arrhythmias
Troubles du rythme auriculaire
09.00
09.20
09.50
10.20
Chairmen / Modérateurs : P. Defaye & M. Chauvin
AF classification attempt: duo from dog to human EP lab
Tentative de classification de la FA : duo à partir du laboratoire expérimental et Clinique
P. Attuel & F. Halimi
Tachycardiomyopathies : who ? and why ?
Tachycardiomyopathies : qui et pourquoi ?
M. Janse
Atrial Fibrillation: experimental effects of drugs
Fibrillation Auriculaire : effets expérimentaux des médicaments
E. Allessie
Can we expect a class V of antiarrhythmic?
Peut-il y avoir une classe V d'antiarythmiques
B. Le Grand
10.50
Coffee break....................................................................................................................
11.20
Advocacy : AF and heart failure.
Playdoyer : FA et insuffisance cardiaque
11.20
Pro-rhythm control therapy by AF ablation of left atrium
Pour une therapie de contrôle du rythme par ablation de FA dans l'oreillette gauche
M. Hocini
11.35
Pro rate-controlled therapy (including AV node ablation and biventricular PM)
Pour un contrôle de la fréquence (incluant l'ablation du noeud AV avec PM biventriculaire)
J-Y. Le Heuzey
AF Ablation with Electro-anatomical mapping system: EnSite NavX tm.
Ablation de FA par système de cartographie électro-anatomique EnSite NavX tm
A. Ferracci
Real words experience in AFIB (ACTIF registry)
Expérience "réelle" de la FA (registre ACTIF)
J-P. Albenque
11.50
12.10
12.30
Buffet (Exhibition Hall)........................................................................................................
12.30
Luncheon Workshop (Medtronic Lounge)
13.45
26
Improved implant and follow up management with Conexus wireless telemetry
Interroger et programmer à distance avec la télémétrie à distance ConexusTM
N. Kamouche
Advanced warning with OptiVol fluid status monitoring : Clinical cases
Anticiper l'apparition d'une surcharge pulmonaire : cas cliniques avec la fonction OptiVol
D. Gras
ICD primary prevention indications in real life
Les indications de prévention primaire du DAI en pratique
P. Fiorello
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Scientific Program
Saturday June 16, afternoon
Auditorium, 14.00 - 18.30
14.00
Echocardiographic Session
Session Echocardiographie
Chairmen / Modérateurs : J. Lefèvre & C. Scheublé
14.00
14.20
14.40
15.15
Echocardiographic criteria for asynchronism
Critères échocardiographiques d'asynchronisme
P. Khanoyan
DTI criteria and setting optimization
Critères DTI et optimisation des réglages
E. Donal
3D criteria.
Critères 3D
C. Scheublé
Responders and non-responders: why ?
Répondeurs et non-répondeurs: pourquoi ?
J. Lefèvre
15.45
Coffee break....................................................................................................................
16.15
Ventricular Resynchronisation
Resynchronisation ventriculaire
Chairmen/Modérateurs: A. Manolis & J-P. Camous
16.15
16.35
16.55
17.15
17.35
17.55
New Treatments in Heart Fealure
27
Prophylactic implantations in heart failure
Indications prophylactiques dans l'insuffisance cardiaque
E. Rowland
Ventricular resynchronisation using ICD
& wireless programming-OTW lead
Resynchronisation ventriculaire avec sonde OTW orientable,
DAI et programmation sans fil
C. Barnay & J. Taieb
How to improve materials to obtain 100% efficacy?
Comment améliorer les matériels pour avoir 100% d'efficacité ?
J-C Deharo
CRT-D implant with the Attain StarFix™ LV lead
Resynchronisation ventriculaire : avec la sonde VG StarFix ®
A. Pisapia
Monitoring of heart failure by the devices
Surveillance de l’insufissance cardiaque par les prothèses
F. Braunschweig
AF and HF patients: which therapy?
Patients en FA et insuffisance cardiaque: quel traitement ?
D. Gras
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Session paramédicale francophone
Troubles du rythme
& Insuffisance Cardiaque
Samedi 16 Juin, matinée
Salon Diane, 09.30 - 13.00
Discours d’ouverture : A. Pisapia
Ablation de FA par radiofréquence
CONFÉRENCES
Modérateurs: A. Ferracci, J. Taieb, Dr P. Fiorello, N. Solans, C. Duboué
M. Gagnant & G. Lemarchand
09.30
09.45
10.00
10.15
Rappels anatomiques : l'oreillette gauche et les veines pulmonaires
Hôpital. St-Joseph, Marseille : Dr A. Ferracci
Définition et diagnostic de la FA : signes cliniques, étiologie, complications
CH Aix-en-Pce : Dr J. Taieb
Traitements de la FA : médicamenteux & techniques d'ablation par RF
(traitements "classiques" et nouveautés)
CMC Parly II : Dr P. Fiorello
Aspects anatomo électriques du Flutter et de la FA
CMC Parly II : Dr C. Bertrand
TABLE RONDE & ECHANGES PRATIQUES
10.30
Ablation de FA par RF
- Prise en en charge du patient en chambre
- La procédure d'ablation
- Bloc, salle de cathétérisme ou salle d' hémodynamique
- Préparation de la salle, du matériel, accueil et induction du patient
- Procédure opératoire, suivi infirmier & complications post-opératoires
- Retour en service et sortie du patient
- Ablation de FA par radiofréquence
ATELIER PRATIQUE
12.15
Prise en charge d'un arrêt cardiaque en chambre :
- Massage cardiaque, CEE, intubation
13.00
CH Haut Lévèque, Bordeaux
IDE Salle Hémodynamique :
C. Duboué, N. Solans
Clinique Pasteur, Toulouse
Equipe IDE Salle Rythmologie
Hôpital St-Joseph, Marseille
Cades de santé cardiologie médicale :
C. Jacquet & V. Rousset-Rouvière
IDE Bloc : G.Lemarchand
IDE SIC : L. Legal, C. Pausé, M-P.
Temporel
Hôpital St-Joseph Marseille
Anesthésie/Réa. : Dr B. Lalanne
Cadre IADE Bloc - SSPI :
S. Gautier- Plaindoux
Cadre de santé cardiologie médicale, HAD :
V. Rousset-Rouvière
Déjeuner (Fouquet’s)................................................................................................................................
28
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Samedi 16 Juin, après-midi
Salon Diane, 14.00 - 18.30
Troubles du rythme ventriculaire
14.00
14.15
14.30
14.45
CONFÉRENCES
Modérateurs: M. Bremondy, B. Lalanne, P. Sbragia, Dr Zhang, M. Zacharenko, A. Ide & R. Ranaivoson
Rappel anatomophysiologique :
Ventricules ECG et réseaux de conduction
Hôpital Nord Marseille : Dr P. Sbragia
Définitions et diagnostics des troubles
du rythme ventriculaires (ESV, TV, FV)
Hôpital Nord Marseille : Dr P. Sbragia
Traitements médicamenteux, autres
Hôpital St-Joseph, Marseille : Dr M. Bremondy
Arrêt cardiaque en chambre : rappels théoriques
Hôpital St-Joseph, Marseille : Dr B. Lalanne
TABLE RONDE & ECHANGES PRATIQUES
15.15
Ablation de tachycardie ventriculaire
- La procédure d'ablation
- Procédure opératoire, suivi infirmier
& complications post-opératoires
- Ablation d'une TV infundibulaire
par cartographie de non contact
16.00
CHU Nancy
IDE Bloc : M. Zacharenko
Résident : Dr Zhang
Hôpital St-Joseph, Marseille
IDE Bloc : A. Ide
IDE SIC : M. Gagnant, R. Ranaivoson
Pause (Hall d’exposition)...........................................................................................................................
Resynchronisation ventriculaire
CONFÉRENCES
Modérateurs: C. Durand, J. Faure, C. Shorijan, B. Collet, V. Anguivel & L. Garcin
16.30
16.45
17.00
Définition, diagnostic et traitements l'Insuffisance Cardiaque (IC)
Hôpital St-Joseph, Marseille : Dr C. Durand
Critères cliniques et para-cliniques du patient IC pour resynchronisation ventriculaire
Hôpital St-Joseph, Marseille : Dr C. Durand
DAI triple chambre : présentation du dispositif
Hôpital St-Joseph, Marseille : Dr J. Faure
TABLE RONDE & ECHANGES PRATIQUES
17.15
Thérapie de resynchronisation cardiaque
- Cas de cathétérismes difficiles au niveau du sinus coronaire
- Suivi et complications post-opératoires
- Implantation d'un DAI triple chambre
New Treatments in Heart Fealure
29
UCL Mont-Godinne, Belgique
Technicien Biomédical Rythmologie :
B. Collet
Hôpital St-Joseph, Marseille
IDE Cardio Médicale :
V. Anguivel, L. Garcin
IDE Bloc : C. Shorjian
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Scientific Program
Sunday June 17, morning
Auditorium, 09.00 - 11.30
08.30
Welcoming Coffee..............................................................................................................
09.00
Free Papers Session,
Session Communications Libres
Chairmen/Modérateurs: J. Faure, A. Ferracci, P Fiorello & F. Halimi
09.00
Does the dor procedure (ventricular reduction) lessen the need for
ICD'S in ischemic cariomuopathy: outcome in 55 consecutive patients
S. R. Gundry
09.15
Ablation of paroxysmal focal atrial fibrillation located
in the coronary sinus
Z. J. Kechida
09.30
Assessment of inducible sustained ventricular tachycardia
in patients with coronary artery disease
L. Chiriac
09.45
Heart Failure and cardiac arrhythmias in children and adults
with obstructive hypertrophic cardiomyopathy
A. Gudkova
10.00
Evaluation of the use of home monitoring follow up service
for patients with implantable cardiac devices
G. McParland
10.15
Atrial bigeminy: a new protocol to test inducibility of atrial flutter
P. Fiorello
10.30
Sympatho-vagal imbalances preceded Common Atrio-Ventricular
Nodal Re-entry Tachycardia induction: an Heart Rate Variability study
P. Vergara
10.45
Prevalence of drug-induced electrocardiographic pattern of the
Brugada syndrome in a healthy European population
C. Bertrand
11.00
Free papers attendees lottery
1000 € Reward by random selection
Loterie pour les participants aux Communications Libres
Prix de 1000 € à gagner par tirage au sort
11.15
30
30
Adjournment statement,
Discours de clôture
A. Pisapia
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Friday, June 15
09.05 - 12.30
SESSION 1
Atrial arrhythmias
Troubles du rythme auriculaire
Chairmen/ Modérateurs: F. Gaita
Ospedale Civile, Asti, Italia
C. Barnay
Centre Hospitalier du Pays d'Aix,
Aix-en-Provence, France
Abstracts of the conferences
Arrhythmias & Heart Failure
33
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Atrial arrhythmias
SESSION 1
Troubles du rythme auriculaire
Perpetuating mechanisms of AF : anatomical aspect
Mécanismes de perpetuation de la FA : aspects anatomiques
D. Sanchez Quintana
Facultad de Medicina. UEX. O6071 Badajoz, Spain
09.25
The rapid development of treatment strategies for atrial fibrillation (AF) has
prompted interest in the complex anatomic substrate underlying the mechanism of this
arrhythmia. For many years it was thought that for AF to take place and be maintained the
existence of several simultaneous wave fronts of activation is necessary with an alteration
in autonomic regulation.
Amongst the mechanisms involved in the pathogenesis of AF might be the
neurohormonal activation as an increase of angiotensin II type I receptor has been observed in patients with paroxysmal and chronic AF. The angiotensin II induced cardiovascular disorders which decrease the production of nitric oxide causes endothelial dysfunction and may represent an associated prethrombotic state during atrial remodelling.
The important role of spontaneous initiation of AF by ectopic foci arising inside
or around the pulmonary veins (PVs) has been recently established. Although the substrate
for atrial fibrillation (AF) is still unclear, it is well accepted that the architecture of the pulmonary vein-atrium junction plays a crucial role as underlying anatomic substrate to initiate and perpetuate AF. Isolation of pulmonary venous triggers can be achieved either by
electrical disconnection targeting focally the electrical continuity between the atrial and
venous myocardial tissue, or by creating circumferential ablation lines around the orifices
of the PVs. Some operators extend these lines from the encircled PV ostial area to involve
the atrial tissue adjacent to the orifices and the posterior wall of the left atrium. Therefore,
the anatomic emphasis for clinical electrophysiologist is now .not only in the myocardial
sleeves of the PVs but also in the anatomic and architectural details of the veno-atrial junctions and their neighboring left atrial landmarks.
The pulmonary venous wall in humans has continuity from the left atrial myocardium (so-called myocardial sleeves) in a fine matrix composed of collagen, elastic fibres and blood vessels. The longer sleeves are found in the right and left superior PVs, and
the distal margins are irregular in most of the veins, specially those of the inferior veins
which tend to have less myocardial coverage than the superior veins. The sleeves are thickest at the veno-atrial junction, with a mean of 1.88±0.45 (range between 1.2 to 2.8 mm)
and they taper toward the lung hilums. But, the sleeves are not uniformly thick circumferentially and neither do they decrease in thickness uniformly. The atrial myocardial sleeves
in the superior veins are thickest inferiorly (at 6 o´clock), and thinnest superiorly (at 12
o´clock), whereas the converse arrangement was the case in the inferior veins. A postmortem morphologic study has described in patients with AF a higher portion of myocardial sleeves with more severe discontinuity, hypertrophy and fibrosis as compared with
patients without AF.
It is still unclear whether initiation and maintenance of human AF depends on
automatic triggered or reentrant mechanism. The rapid advancement of surgical and
catheter-ablation techniques have led to a better understanding of AF mechanism. It is
now well-established that the potential underlying substrate to initiate and perpetuate
various forms of human AF can be categorized into triggers and anatomic substrates
respectively. Although electrical disconnection of the PV venous triggers are effective in
treating paroxysmal AF, additional linear lesions targeting the region of the posterior left
atrial wall, have proven successful in both paroxysmal and chronic AF.
34
Notes :
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Observations from the laboratory of Jalife and collegues demonstrated in the isolated sheep
heart the presence of a small number of stable ongoing circuits generating high frequency
waves and providing a base to generate fibrillatory conduction. Data derived from high resolution optical mapping in this animal model also showed that the focal sources correspond
to single or small number of reentrant rotors discharging at a high frequency and localized
in the PV orifices or at the contiguous posterior left atrial region.
The myocardial architecture revealed by means of carefully dissections of subendocardial and subepicardial myofibers along the full thickness of the left atrium show a complex myoarchitecture of overlapping bands of aligned myocardial fibers. Thus, in most
hearts, there is an abrupt change of subepicardial or subendocardial fibers orientation
(oblique with longitudinal) in the posterior wall of the left atrium at the level of the venoatrial junctions. At these level, the myocardial fibers are usually loop-like extensions from the
longitudinal fibers encircling the veno-atrial junctions especially in the posterior region of the
left atrium. As shown in animal models, changes in myocardial fibers orientation in the posterior wall of the left atrium at the veno-atrial junctions may confer anisotropic properties
that set the scene for activation delay and microreentrant sources.
Specific triggers arising from nonpulmonary vein foci appear less common (1015% of triggers initiating atrial fibrillation) than those that originate within the pulmonary
veins. Foci such as the musculature lining the superior caval vein (SCV), coronary sinus (CS)
and ligament/vein of Marchall.(L/VOM) have been described. The incidence of focal AF in
the musculature of the SCV among patients undergoing radiofrequency catheter ablation for
paroxysmal AF is around 6%. These studies provide evidence that the musculature continuing into the SCV can both initiate and maintain atrial fibrillation. An anatomic feature of
clinical relevance when attempting ablation in the SCV is the close proximity of the right
phrenic nerve and sinus node tissue to the ablation.
The coronary sinus, and its continuation into the great cardiac vein, has it own
muscular wall that increases in thickness closer to its mouth in the right atrium. These muscular sleeves extend 25-52 mm into the wall of the coronary sinus. Frequently, small tongues of fibers extend from the coronary sinus to insert into the posterior wall of the left
atrium. Electrophysiological studies also demonstrated electrical connection between the
right atrium and left atrium through the musculature of the coronary sinus, and focal source of premature despolarization originating within the coronary sinus may trigger atrial
fibrillation. It has been also suggested that electrical disconnection of the two atria targeting
the interatrial connections diminishes the electrophysiological substrate for perpetuation of
atrial fibrillation.
The left atrial oblique vein of Marshal is a tributary vein of the CS. In 60% of
hearts it is a part of the ligament of Marshall (LOM), formed by the venous element with
fibro-fatty tissue, muscular bundle and the autonomic nerves, all forming a vestigial fold.
Histological examinations show myocardial tissue surrounding the vein/ligament of Marshall
at its junction with the CS. In clinical studies, electrical activity originating from the LOM can
be recorded from the endocardial aspect of the LA in or around the orifices of the left PVs.
Several authors have found electrical activity emanating from the ligament of Marshall and
hypothesized that the ligament could play a role in arrythmogenesis.
Finally, the histological features of the atrial tissue in patients with chronic AF are
myolysis of the myocytes and fibrosis. In human with lone AF refractory to conventional antiarrhythmic treatment , myolysis, fibrosis and lymphocyte infiltrates have been observed in
most of the patients (67%). In animal models of chronic AF structural changes revealed that
25% of atrial myocytes were affected by myolysis, accumulation of glycogen, changes in
mitochondrial size and shape. Thus, changes in the myocardium at the cellular level are also
involve in the perpetuation of AF. Whether these are the cause or the effect remain to be
clarified.
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Atrial arrhythmias
Troubles du rythme auriculaire
New techniques in AF ablation
Nouvelles techniques d'ablation de la FA
G. Augello
Ospedale San Raffaele, Milano, Italy
09.45
Abstract Unavailable
Notes :
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Atrial arrhythmias
Troubles du rythme auriculaire
Complications of AF ablation
Complications de l'ablation de la FA
R. Cappatto
Istituto Policlinico San Donato, San Donato Milanese, Italy
11.00
Abstract Unavailable
Notes :
Arrhythmias & Heart Failure
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Atrial arrhythmias
Troubles du rythme auriculaire
SESSION 1
When ICE visualization meets CARTO XP System vision
Quand l’échographie intracardiaque rencontre le système
d’imagerie CARTO XP
P. Thomas
Product Manager Imaging, Biosense Webster Europe, Waterloo, Belgium
11.40
Abstract Unavailable
Notes :
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Atrial arrhythmias
SESSION 1
Troubles du rythme auriculaire
Surgical ablation of AF
Ablation chirurgicale de la FA
J. Robin, MD, PhD, J. Ninet, MD, PhD
Cardiovascular Hospital and Claude Bernard University, Lyon, France
12.00
A simplified alternative to the Cox maze procedure to treat atrial fibrillation with epicardial high-intensity focused ultrasound was developped from 2002
to-date.
The Epicor ® ablation System is designed to deliver HIFU energy to
ablate cardiac tissue. The system consists of the Ablation Control System (ACS)
generator, a family of disposable ablation devices (Ultracinch and Ultrawand) and
a set of accessories.
-The ACS is a microprocessor-based unit that provides acoustic
power to the ultrasound transducers. The proprietary algorithm generated uses a
combination of frequency, power, and duration at which the transducers are activated and powered to generate 3 sequential stages of ablation.
-The transducers are located either on an array (Ultracinch)
positioned around the left atrium in order to create a continuous, circumferential
transmural lesion off-pump on beating heart, or on an handheld ablation device
(Ultrawand) for the epicardial creation of an additional mitral line. The ablation process begins with the deep ablation stage, during which energy is deposited distal
from the transducer in the subendocardial zone, followed by the intermediate stage
in which energy is deposited in the midmyocardial layer, followed by the surface
stage for epicardial energy deposition. Thus the lesion is built up from the endocardium back to the epicardium and is complete within approximately 10 minutes.
This device was evaluated clinically in a prospective European multicenter study from September 2002 to February 2004. All the 103 patients enrolled had
concomitant cardiac operation and the ablation was performed before the procedure. All of them received a circumferential left atrial ablation using the Ultracinch
and an additional mitral line was created in the last 35 (34%) patients using the
Ultrawand.
Atrial Fibrillation duration ranged from 6 to 240 months (mean 44
months). It was permanent is 76 (74%) patients, paroxysmal in 22 (21%) and persistent in 5 (5%).
No complications or deaths were device or procedure related. There were
4 early deaths and 2 late extracardiac deaths. A pacemaker was implanted in 8
patients. The 6 month follow-up was complete in all survivors (93). At the 6-month
visit, freedom for atrial fibrillation was 85% in the entire study group, 80% in
patients with permanent atrial fibrillation, 100% in patients with paroxysmal atrial
fibrillation and 88% in patients who had an additional mitral line. Only the duration
and type of atrial fibrillation increased significantly the risk of recurrence.
Epicor using off-pump epicardial HIFU technology is safe, effective and
easy to use in patient presenting with an atrial fibrillation associated with structural heart disease. A study is running concerning patient with lone atrial fibrillation.
Arrhythmias & Heart Failure
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Friday, June 15
14.00 - 19.30
Ventricular arrhythmias
Troubles du rythme ventriculaire
Chairmen/ Modérateurs: D. Lacroix
CHU Lille, France
B. Cauchemez
Hôpital La Riboisière, Paris, France
Abstracts of the conferences
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Ventricular arrhythmias
Troubles du rythme ventriculaire
AICD indications in CHD:
Only LVEF and no more arrhythmologic risk stratification
Indications de DAI chez les coronariens:
Seulement la FEVG sans stratification du risque rythmique?
M. Borggrefe
Universitätsklinikum Mannheim, Mannheim, Germany
14.15
Abstract Unavailable
Notes :
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Ventricular arrhythmias
Troubles du rythme ventriculaire
Primary prophylaxis of sudden death in non-ischemic
left ventricular diseases (HCM)
Prophylaxie primaire de la mort subite dans les cardiopathies
gauches non ischémiques (CMH)
W. Mc Kenna
The Heart Hospital, University College London Hospital, London, United-Kingdom
14.45
Sudden death remains an uncommon but devastating complication in
young patients with hypertrophic cardiomyopathy. Twenty years ago it was the
commonest cause of sudden death in the young and in athletes. With increased
awareness and the relative simplicity of diagnostic techniques employing ECG and
echocardiography, individuals at risk are being identified and prophylactic treatment initiated. Hypertrophic cardiomyopathy is relatively common affecting at
least 1/500 adults in the population. The majority of these individuals will however not suffer disease related complications. The challenge is to identify the relatively small subset of 10 - 20% who are at risk from sudden death. The profile of
the 'at risk' individual has been established. Unexplained syncope, family history
of premature sudden death, non-sustained ventricular tachycardia on ambulatory
ECG monitoring, abnormal blood pressure response during up-right exercise testing and severe (> 3 cm) left ventricular hypertrophy, all are associated with increased risk from sudden death. The positive predictive accuracy of each of these risks
markers however is relatively low ranging from 10 - 20%. Approximately 25% of
patients seen in a referral institution will have 2 or more risk factors which is associated with annual mortality rates of 3 - 6% and in these patients prophylactic ICD
therapy is warranted. Approximately 50% will have no risk factors and their mortality is sufficiently low (approximately 0.2% pa) to permit appropriate reassurance. Approximately 25% of patients will have a single risk factor but again the majority of these patients will not die suddenly. Further risk analysis of this subset
reveals that the relative risk is greatest in the young. Decisions regarding ICD
should be individualised but in young patients with single risk factor serious consideration for ICD implantation is warranted. Retrospective registries of ICDs in
hypertrophic cardiomyopathy reveals that appropriate charge rates are approximately 5% pa. It is unclear what proportion of such events would have been lethal.
Complications of prophylactic ICD in young patients are much higher than those in
the elderly and the morbidity and mortality associated with ICD needs to be weighed in relation to potential benefit.
Arrhythmias & Heart Failure
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Ventricular arrhythmias
Troubles du rythme ventriculaire
An AICD without endocardial lead ?
Un DAI sans sonde ?
G. Milasinovic 1, S. Raspopovic 1, D. Stamenkovic 2, K. Lopandic 3, M. Ver Heyen 4
1
Clinical Centre of Serbia, Belgrade, Serbia
2
Basic Med d.o.o. Belgrade, Serbia
3
Medtronic B.V, Zagreb, Croatia
4
Medtronic Bakken Research Center, Maastricht, Netherlands
15.10
Subcutaneous Implantable Cardioverter-Defibrillator system (S-ICD) with no transvenous electrode system has been already used to achieve effective defibrillation in pediatric
patients and in patients with anomalous cardiac anatomy, but the defibrillation efficacy with
subcutaneous-only shock vector has not been well studied in general population.
It is expected that S-ICD would have been able to replace "classical" transvenous
ICD in majority of indicated patients, especially for primary prophylaxis. Therefore companies
are developing technologies to better target primary prevention patients and new implanters.
Benefits of S-ICD would be easier implantation technique and predictable faster implantation
time with no fluoroscopy, lower acute and chronic morbidity, less risk with device removal if
necessary, better specificity, and the likelihood to prevent long-term vascular complications with
preserved venous system for future use.
The limitations to the S-ICDs is no bradycardia support (5-10% of prophylactic ICD
patients develop concomitant bradycardia - there was aggressive use of beta blockers in SCDHEFT and the rate of bradycardia development was < 10%).
Patient acceptance of a S-ICD may be influenced by the perceptions of 80 J output, tunneling along rib margin and parasternally, no painless antitachycardia therapies (ATP)
for fast ventricular tachycardia, and some concern regarding potential erosion/migration issues
if the device is heavier/bulkier than existing transvenous system.
Technology challenges include doubling the energy, larger capacitors, different battery systems, completely new integrated circuit designs, completely new lead system design,
and completely new signal detection algorithm.
In this study we concluded that defibrillation with a subcutaneous shock vector is
feasible, although energies in excess of 35 Joules will be needed to achieve uniform implant
success. The failures of 35 Joules did not appear to be correlated with patient weight, body
surface area, shock impedance or LV diameter.
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Ventricular arrhythmias
Troubles du rythme ventriculaire
Post AICD implant therapies: drugs and ablative techniques
Traitements après implantation d'un DAI : médicaments et ablation
Luc Jordaens, Emile Jessurun, Dominic Theuns,
Erasmus Medical Centre Rotterdam, The Netherlands
15.35
Sudden death can be effectively prevented by ICD`s. These data result now in Europe
in increasing implantation numbers, with concomitant problems posed for follow-up. Early observations by our group in 1984 pointed towards 13% inappropriate interventions. It is striking to
observe how this is still confirmed in recent data.
AVID and MADIT II showed an excess for hospitalisation for patients treated with an
ICD, without a clear explanation; the same was observed in DINAMIT. It is clear that early follow-up should be intensified, and that more attention should be spent to programming (without
believing companies that dual chamber algorithms are good) and by understanding data telling
us that pacing should be avoided (Andersen, Wilkoff, Bardy, Theuns…).
We will address some potential policies for follow-up (figure), and present data on
inappropriate therapy, which is most often due to atrial arrhythmias. Dual chamber devices do
not perform significantly better than single chamber devices on a per patient basis, but show nice
electrograms, facilitating interpretation for physicians.
Drug therapy
Multiple shocks are often a reason to continue or initiate antiarrhythmic drugs (AF, fast
conduction over the AV node, incessant VT). While ß-blockers have an effect on events, and postpone events, their replacement by sotalol, or combination with amiodarone is an effective way
of reducing the cumulative rate of interventions (OPTIC). Investigational drugs as azimilide are
promising, but have the potential of torsades the pointes (SHIELD).
The problems with antiarrhythmic drugs are well known in the pacing world, but pose
additional problems in the ICD setting (sensing, pacing threshold, VT rate, excessive pacing, more
dyssynchrony, changes in DFT, proarrhythmia, flutter with aberrancy, impact on antitachycardia
pacing…).
It should not be underestimated that other drug measures are effective as well (lipid
lowering, ARB`s…). Psychological support can prevent problems.
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Ablation therapy
This certainly plays a role in preventing shocks and reducing mortality, but real randomised studies are still not published: improvements are made thanks to electroanatomical
mapping. Atrial arrhythmias can be approached as well. In some settings epicardial ablation and
ablation with hemodynamic support plays a role.
References
1. Andersen HR, Thuesen L, Bagger JP, Vesterlund T, Thomsen PE. Prospective randomised trial of atrial versus ventricular pacing in sick-sinus syndrome. Lancet 1994;344:1523-1528.
2. Wilkoff BL et al.Dual-chamber pacing or ventricular backup pacing in patients with an implantable defibrillator: the Dual Chamber and VVI Implantable Defibrillator (DAVID) Trial. JAMA, 2002;288:3115-23.
3. Theuns DAMJ, Klootwijk APJ, Goedhart DM, Jordaens LJ. Prevention of inappropriate therapy in implantable cardioverter-defibrillators: results of a prospective, randomized study of tachyarrhythmia detection algorithms. J Am Coll Cardiol 2004;44:2362-2367.
4. Bardy GH, et al. . Amiodarone or an implantable cardioverter-defibrillator for congestive heart failure. N
Eng J Med 2005;352:225-37.
5. Theuns DAMJ, Rivero Ayerza M, Boersma E, Jordaens L. Prevention of inappropriate therapy in implantable defibrillators: A meta-analysis of clinical trials comparing single-chamber and dual-chamber arrhythmia discrimination algorithms. Int J Cardiol, 2007.
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Ventricular arrhythmias
Troubles du rythme ventriculaire
Risk stratification of sudden death in ARVD
Appréciation du risque de mort subite dans la dysplasie du VD
M. Paul
Department of Cardiology and Angiology, University Hospital of Münster, Münster, Germany
16.30
Introduction
Arrhythmogenic right ventricular cardiomyopathy/dysplasia (ARVC/D) is a major
cause of ventricular tachyarrhythmias and sudden death in young patients and athletes with
apparently normal hearts. The disease is characterized by localized or diffuse atrophy of predominantly right ventricular myocardium with subsequent replacement by fatty and fibrous
tissue. As a result of these pathomorphological alterations, global and regional right (and
left) ventricular dysfunction and ventricular tachyarrhythmias due to areas of slow conduction and dispersion of refractoriness are the major clinical findings and manifestations of
ARVC/D 1-2. Pedigree analyses suggested a Mendelian pattern of inheritance 3, but only
recently mutations in the gene encoding for Plakophilin-2, an essential morphogenic factor
and architectural component of the heart muscle, were identified as causative for the development of autosomal dominant ARVC 4. Mutations found hereafter in other desmosomal
proteins lead to the recognition of ARVC as a "disease of the desmosome".
Clinical presentation
ARVC/D usually manifests with ventricular tachyarrhythmias with left bundle
branch block morphology in a young population ranging between 15 to 40 years of age. In
contrast, first symptoms of ARVC/D during early childhood or beyond the age of 60 years
are unusual. Men are more frequently and more seriously affected than women. Other
patients present with frequent premature ventricular beats, repetitive ventricular runs, or
nonsustained VT. Associated symptoms span from palpitations and paroxysmal tachycardia
to dizziness, syncope and sudden cardiac arrest. Clinical signs of heart failure are usually
limited to patients with advanced right ventricular dysfunction and/or left ventricular involvement, both mostly occurring in later stages of the disease, and in patients with a long history of ventricular arrhythmias. Diagnostic criteria for ARVC/D were proposed by an international study group 5 and have yet to be validated prospectively.
Risk Stratification
The exact proportion of ARVC/D as the underlying disease in cases of sudden cardiac death victims below 35 years of age is unknown but has been estimated to be 15-25%
6
. These data correspond well with the "natural history" of ARVC/D with mortality rates of
up to 25% after ten years or 2.5% per year on empiric (uncontrolled) antiarrhythmic drug
therapy which does not take into account the widely unknown rate of sudden death as a
primary disease manifestation. Thus, ARVC/D is not a benign disease but requires effective
treatment to reduce symptoms and to prevent sudden cardiac death.
Several clinical variables have been proposed to stratify the risk for sudden death
and recurrent ventricular tachyarrhythmias in ARVC/D. These include a history of cardiac
arrest or syncope, a positive family history of unexplained premature sudden death, severe
right ventricular dysfunction, left ventricular involvement, the inducibility of VT during programmed stimulation, late potentials and ECG features such as right precordial QRS prolongation and dispersion, negative T waves, and epsilon waves. The majority of centres,
however, indicate right ventricular dysfunction and left ventricular involvement as the most
important and independent risk factors for sudden cardiac death and VT recurrences in
ARVC/D.
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Patients with the combination of spontaneous sustained VT, signs of right heart failure
and/or left ventricular dysfunction were found to be at highest risk of sudden death and
demonstrated the worst long-term prognosis 7.
Management of asymptomatic patients and family members
Asymptomatic patients with ARVC/D do not necessarily require specific antiarrhythmic or otherwise cardiac treatment. Yet, they should be followed by regular noninvasive cardiac investigations for an early recognition of ventricular arrhythmias and a potential
progression of the disease. These follow-up visits should include a detailed interview concerning the interim occurrence of arrhythmic symptoms or events, ECG at rest, exercise tests,
Holter monitoring and cardiac imaging by echocardiography and/or magnetic resonance
imaging. Patients with ARVC/D should be advised against participation in competitive sports
since this appears to be associated with accelerated disease progression and increased risk
of sudden death 8. Family members of patients with ARVC/D should visit a cardiologist with
experience in the disease at regular intervals (3 to 5 years or with onset of symptoms)
undergoing the aforementioned noninvasive cardiac tests. If these investigations show signs
suspicious of ARVC/D or if complex ventricular arrhythmias are documented or syncope
occurs, more detailed investigations should be performed to establish the diagnosis, to stratify the risk, and to develop an individualized treatment strategy. Modified diagnostic criteria for family members of affected index patients with ARVC/D were recently proposed but
are not prospectively validated 9. Asymptomatic relatives of genotyped index patients with
ARVC/D may undergo genetic testing after detailed and careful counseling concerning the
potential current and future consequences of a positive test result (10). The major advantage of a negative test is that the individual can be reassured and no follow-up investigations are necessary. In affected but asymptomatic family members of ARVC/D patients,
there is no general indication for prophylactic antiarrhythmic therapy. As an exception, prophylactic treatment with conventional ß-blockers has been recommended by several groups.
However, in selected patients with multiple risk factors, familial sudden death, or inducible
VT during programmed stimulation, the prophylactic implantation of an ICD for primary prevention of sudden death may be discussed. Given the paucity of data available so far, this
approach is currently controversial and requires an individual decision based on the constellation of risk and the patient's preference.
Management of symptomatic patients
In patients with ARVC/D and no history of syncope or cardiac arrest, premature
ventricular beats, couplets or short ventricular runs are usually not associated with an increased arrhythmic risk and therefore do not require specific antiarrhythmic treatment. In many
cases, reassurance of the patient results in an improvement of symptoms. However, should
a patient still suffer severe symptoms from palpitations, treatment with conventional ß-blockers may be considered. Specific antiarrhythmic drugs or catheter ablation should be limited to patients with significant symptoms refractory to these measures. Patients with VT,
syncope or a survived episode of sudden cardiac arrest should undergo a detailed noninvasive and invasive diagnostic work-up including, among others, right ventricular angiography
and programmed ventricular stimulation. In low-risk patients, antiarrhythmic drug therapy
(preferentially sotalol) may be considered and should be guided by serial electrophysiologic
study. Catheter ablation may be an alternative in patients with localized ARVC/D and a single morphology of a hemodynamically well tolerated VT refractory to antiarrhythmic drugs.
In patients with drug-refractory frequent or incessant VT, catheter ablation may be the only
treatment option available, however with a rather palliative claim. Although antiarrhythmic
drug therapy and catheter ablation may reduce VT recurrences, there is no proof from prospective or randomized studies, that they are also effective in the prevention of sudden
death. Therefore, more effective protection is required in individuals at a higher risk of sudden death. In patients with survived cardiac arrest or hemodynamically intolerable fast VT,
and those with risk factors such as extensive right ventricular dysfunction, advanced stages
of ARVC/D, left ventricular involvement, pleomorphic VT and others, ICD implantation is
considered the most appropriate therapeutic option to prevent life-threatening VT recurrences and sudden death 11.
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A proposal for current therapeutic management directed toward an improvement of symptoms and prognosis in patients with ARVC/D is depicted below (adapted from 12):
Notes :
Figure 1. AAD antiarrhythmic drugs (preference: sotalol), EPS electrophysiological study, fam.
Hx family history, ICD implantable cardioverter defibrillator, SD sudden death, VT ventricular tachycardia.
In the future, ongoing multicenter European 13 and North American 14 ARVC/D
registries will provide important data on risk stratification and treatment efficacy which may
refine the management strategies and thereby further improve the long-term prognosis of
patients with ARVC/D.
References
1. Marcus FI, Fontaine GH, Guiraudon G et al. Right ventricular dysplasia: A report of 24 cases. Circulation.
1982;65:384-398.
2. Thiene G, Nava A, Corrado D et al. Right ventricular cardiomyopathy and sudden death in young people.
N Engl J Med. 1988;318:129-133.
3. Paul M, Schulze-Bahr E, Breithardt G, et al. Genetics of arrhythmogenic right ventricular cardiomyopathy
- status quo and future perspectives. Z Kardiol. 2003;92:128-36.
4. Gerull B, Heuser A, Wichter T et al. Mutations in the desmosomal protein plakophilin-2 are common in
arrhythmogenic right ventricular cardiomyopathy. Nat Genet. 2004;36:1162-64.
5. McKenna WJ, Thiene G, Nava A. Diagnosis of arrhythmogenic right ventricular dysplasia/cardiomyopathy.
Br Heart J. 1994;71:215-218.
6. Corrado D, Basso C, Thiene G. Pathological findings in victims of sport-related sudden cardiac death.
Sports Exerc Injury. 1996;2:78-86.
7. Hulot S, Jouven X, Empana JP et al. Natural history and risk stratification of arrhythmogenic right ventricular dysplasia/cardiomyopathy. Circulation. 2004;110:1879-1884.
8. Pelliccia A, Corrado D; Bjornstad HH et al. Recommendations for participation in competitive sport and
leisure-time physical activity in individuals with cardiomyopathies, myocarditis and pericarditis. Eur J
Cardiovasc Prev Rehabil. 2006;13:876-85.
9. Hamid MS, Norman M, Quraishi A et al. Prospective evaluation of relatives for familial arrhythmogenic
right ventricular cardiomyopathy/dysplasia reveals a need to broaden diagnostic criteria. J Am Coll Cardiol.
2002;40:1445-1450.
10. Wichter T, Breithardt G. Implantable cardioverter-defibrillator therapy in arrhythmogenic right ventricular cardiomyopathy: a role for genotyping in decision-making? J Am Coll Cardiol. 2005;45:409-411.
11. Wichter T, Paul M, Wollmann C et al. Implantable cardioverter-defibrillator therapy in arrhythmogenic
right ventricular cardiomyopathy: single-center experience of long-term follow-up and complications in 60
patients. Circulation. 2004;109:1503-1508.
12. Wichter T, Paul M, Eckardt L et al. Arrhythmogenic right ventricular cardiomyopathy: antiarrhythmic
drugs, catheter ablation, or ICD. Herz - Cardiovasc Dis 2005;30:91-101.
13. Basso C, Wichter T, Danieli GA et al. Arrhythmogenic right ventricular cardiomyopathy: clinical registry
and database, evaluation of therapies, pathology registry, DNA banking. Eur Heart J. 2004;25:531-534.
14. Marcus FI, Towbin JA, Zareba W et al. Arrhythmogenic right ventricular dysplasia / cardiomyopathy
(ARVD/C): A multidisciplinary study - design and protocol. Circulation. 2003; 107:2975-2978.
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Ventricular arrhythmias
Troubles du rythme ventriculaire
Risk stratification of sudden death
in congenital heart diseases
Appréciation du risque de mort subite
dans les cardiopathies congénitales
L. Iserin
Pole cardiovasculaire, Hôpital Européen Georges Pompidou et Service de Cardiologie Pédiatrique,
Hôpital Necker, Paris, France
16.55
An increasing number of patients with congenital heart disease (CHD) are entering adulthood.
Sudden death (SD) is a rare event in the paediatric population but frequency increases
during the second decade and after. The majority of the population has been operated in
infancy. Native diseases are less frequent but can lead to SD.
In a cross-sectional study performed on a population of 2,609 consecutive adults
assessed at a CHD specialty clinic, 199 deaths occurred. Mean age at death is 37 +/- 15
years . Sudden death (26%) is the most common cause of death followed by progressive
heart failure (21%) and perioperative death (18%).
Operated congenital defect at risk for sudden death are tetralogy of Fallot,
atrial switch of transposition of the great arteries ,aortic stenosis, and aortic coarctation.
In operated tetralogy of Fallot, sudden death is due to ventricular arrhythmias .
Infundibular scarr and right ventricular dilatation due to pulmonary insufficiency are the
underlying conditions for these arrhythmias . Identified risk factors for sudden death un
this population are numerous.
Electrocardiographic markers (QRS duration, QRS rate of change ) are significantly greater in groups of patients who experienced sustained ventricular tachycardia and
sudden-death. Older age at repair is associated with a higher risk of sudden death .
Pulmonary regurgitation is the main underlying haemodynamic lesion for patients with ventricular tachycardia and sudden death. . MRI Measurements of right ventricle are now crucial for planning pulmonary valve replacement. Fibrosis detected by late gadolinium
enhancement (LGE) by cardiovascular magnetic resonance (CMR) is related to adverse clinical markers, including ventricular dysfunction, exercise intolerance, and neurohormonal
activation. RV LGE is significantly associated with clinical arrhythmia. Usefulness of electrophysiology studies to predict the development of clinical ventricular tachycardia is still
questionable.
Pulmonary valve replacement should be performed before the development of
irreversible right ventricular dysfunction and an increased risk of ventricular tachycardia or
sudden cardiac death . Although various risk factors for sudden death are identified , primary prevention of ventricular arrhythmia in this group is not well defined, haemodynamic
correction of residual lesions is the first step for the patients who did not experienced
rhythm disturbances .
In atrial switch for transposition of the great arteries(Senning or Mustard operation) SD is a major concern. Presence of symptoms of arrhythmia or heart failure, history of documented atrial arrhythmia increase the risk of SD. Electrocardiogram (ECG), chest
X-ray, and Holter ECG findings are not predictive of SD. Neither medication nor pacing are
protective. Most SD events occur during exercise. Evaluation of cardiac right ventricular
systemic function is difficult . MRI estimation of RVEF is helpful. Some patient have evidence of right ventricle desynchronisation . For these patients , surgical resynchronisation
for symptomatic patient is still experimental.
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Aortic stenosis operated in infancy carries a risk of sudden death. Mecanism of
these SD remain unclear. Long standing LV dysfunction is rare , but fibrosis within the LV
is frequent in neonatal aortic stenosis. Although nearly normal valvular function can be
achieved by surgery, rhythm disturbances are no well known especially in adulthood, due
to the different modes of surgery, and the non specific follow up of these adult patients.
In unoperated lesions mortality is high among cyanotic patients , specially with
Eisenmenger syndrome, but sudden death is not always due to arrhythmias (massive haemoptysis, pulmonary hypertension) .
Corrected transposition can be diagnosed in adulthood. Complete AV block can
occur suddenly, but usually SD is related to ventricular tachycardia occuring on a failing
systemic right ventricle, with concomitant atrio-ventricular valve regurgitation.
Like in LV systemic ventricle estimation of RV function is a key for establishing
prognosis in these patients.
Conclusions : patients with known congenital heart defect need lifelong follow-up .Residua and sequelae of their complex anomalies must be evaluated by different
methods. Evaluation of RV function is crucial for establishing risk factors in this "new"
population.
References
Silka MJ, Hardy BG, Menashe VD, Morris CD. A population-based prospective evaluation of risk of sudden
cardiac death after peration for common congenital heart defects.J Am Coll Cardiol. 1998 Jul;32(1):245-51.
Oechslin EN, Harrison DA, Connelly MS, Webb GD, Siu SC. Mode of death in adults with congenital heart
disease. Am J Cardiol. 2000 Nov 15;86(10):1111-6.
Gatzoulis MA, Balaji S, Webber SA, et al. Risk factors for arrhythmia and sudden cardiac death late after repair
of tetralogy of Fallot: a multicentre study. Lancet 2000;356:975- 81.
Khairy P, Landzberg MJ, Gatzoulis MA, et al. Value of programmed ventricular stimulation after tetralogy of
Fallot repair: a multicenter study. Circulation 2004;109:1994 -2000.
Therrien JP, Siu SC, Harris L, et al. Impact of pulmonary valve replacement on arrhythmia propensity late
after repair of tetralogy of Fallot. Circulation 2001;103:2489 -94.
Therrien J, Siu S, McGlaughlin PR, et al. Pulmonary valve replacement n adults late after repair of tetralogy
of Fallot : are we operating oo late? J Am Coll Cardiol 2000;36:1670 -5.
Kammeraad JA, van Deurzen CH, Sreeram N, Bink-Boelkens MT, Ottenkamp J, Helbing WA, Lam J, SobotkaPlojhar MA, Daniels O, Balaji S. Predictors of sudden cardiac death after Mustard or Senning repair for
transposition of the great arteries. J Am Coll Cardiol. 2004 Sep 1;44(5):1095-102.
Warnes CA. Bicuspid aortic valve and coarctation: two villains part of a diffuse problem. Heart 2003;89:965- 6.
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Ventricular arrhythmias
Troubles du rythme ventriculaire
Markers of risk of sudden death in chanellopathies
Facteurs pronostiques de mort subite dans les maladies
des canaux membranaires
V. Probst
L’Institut du thorax, Nantes, France
17.15
Channelopathies are a group of hereditary diseases characterized by the absence of structural abnormalities of the heart but a risk of sudden cardiac death due to ventricular fibrillation occurring frequently in young patients.
Several diseases are related to ion channel disease like long QT syndrome, short
QT syndrome, catecholaminergic ventricular tachycardia and Brugada syndrome. The common point of these different diseases is the usual autosomic dominant transmission mode of
the disease and then the risk for a patient to transmit the disease to the half of his descent.
That means that for all these diseases a familial screening of all the first degree relatives of
all the affected members of the family is a crucial point to avoid sudden death. Another important point for all these diseases is that the severity of the disease is not directly related to the
mutation. That means that a patient affected by a minor form of the disease with a low risk
of sudden death could transmit a severe form of the disease to his descent.
Long QT syndrome.
The long QT syndrome is characterized by a prolongation of the QT interval and
a risk of sudden cardiac death due to torsade de pointes and ventricular fibrillation. Long
QT syndrome is genetically and phenotypically heterogeneous with, to date 8 different
genes and 6 different forms of the disease that have been described. The evaluation of the
risk of sudden death have essentially been evaluated in the three main forms of the diseases (LQT1, LQT2 and LQT3). For this pathology, the risk of sudden death will be related to
the presence of symptoms especially if the symptoms occurred early in life, the duration of
the QT interval, the type of long QT syndrome and the sex of the patient.
Among the asymptomatic patients the higher risk (risk over 50%) will be found
in patients carrier of a LQT1 or LQT2 mutation and a QTc longer than 500 ms and in the
male patient affected by a LQT3 syndrome with QTc longer than 500 ms. On the contrary,
male sex patients carrier of a LQT1 or LQT2 mutations with a QTc duration lower than 500
ms carry a low risk of sudden death (risk<30%).
In any case, for all the patients affected by a long QT syndrome, the risk has to
be individually evaluated regarding to the previously described factors but also to the presence of symptoms, the presence of arrhythmias during Holter recording or exercise test
and also to the compliance to the beta blocker therapy.
The cardiologist and the general practitioner in charge of the patient has also to always keep
in mind that one of the main reason for the occurrence of sudden death in the long QT
patients is the introduction of drugs that affect the QTc duration and it is then essential to
provide to all the patients a list of the drugs to avoid.
Brugada syndrome.
The Brugada syndrome is a genetically inherited arrhythmogenic disorder characterized by an ECG pattern of ST-segment elevation in the right precordial leads and an
increased risk of sudden cardiac death resulting from episodes of polymorphic ventricular
tachyarrhythmias and fibrillation.
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For the Brugada syndrome ventricular fibrillation occurs essentially at rest and
while the patients are asleep. It has also to be note, that the ventricular fibrillations frequently occur during a febrile episode.
For the Brugada syndrome, several risk factors are clearly demonstrated. The risk
of sudden death is higher in male than in female, in previously symptomatic patients, especially in a patient who has already experienced sudden cardiac death. The risk is also higher
in patients who had a spontaneous type I ECG compare to patients in whom the pattern of
Brugada syndrome appears only after the injection of a sodium channel blockers. On the
contrary, the evaluation of the risk in asymptomatic patients is much more difficult. To date,
the evaluation of this risk is essentially based on the capacity to introduce ventricular fibrillation during a ventricular stimulation. However, some authors consider that the prognosis
value of this test is good whereas these results have not been confirm by others. Then, the
indication for the implantation of an ICD in asymptomatic Brugada syndrome patients is not
clear.
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Ventricular arrhythmias
Troubles du rythme ventriculaire
Ablation of Ventricular Arrhythmias :
endocardial, epicardial, Purkinje ?
Ablation des TdR ventriculaires :
endocarde, épicarde, Purkinje ?
R. Frank
CH Pitié Salpétrière Paris, France
17.35
Endocardial catheter VT ablation for drug resistant VT is an effective procedure
to prevent VT recurrence, with a success rate depending of the underlying pathology, from
50 to 70% in cardiopathies, and more than 90% in idiopathic VT. Failures are explained by
large arrhythmogenic substrate, or inaccessible site of origin, mainly deep intraseptal. It can
be also explained by an epicardial origin. Epicardial transcatheter ablation has been initiated
by Dr Sosa from Brazil in 1996 in Chagas disease, using a subxyphoidal approach, and then
expanded to all kind of cardiopathies. Several hundred of patients have been successfully
ablated in the world by this method, mainly indicated when endocardial mapping could not
find an appropriate site to ablate VT.
Our series consists of 35 interventions in 32 patients between 1998 and 2007,
out of 227 VT ablations procedures, with the same criteria of inability to find an appropriate endocardial ablation site. Six patients had a normal heart, and the others had cardiomyopathies (ARVD, DCM), or myocardial scar. In 4 patients epicardial approach was not feasible, due to pericardial adherences, and in 2 others, no arrhythmogenic epicardial substrate could be found. Epicardial Rf ablation was ineffective in 7, and effective in 22, 6 remaining with previously ineffective antiarrhythmic therapy. There was one per operative death
by tearing a dilated right ventriocular wall while trying to force pericardial adherences in an
end stage cardiomyopathy. Complications were mainly inflammatory pericardial effusions,
needing to leave a pigtail drain for 24 hours.
The main unsolved problem is how to recognize an epicardial origin from the surface ECG. Berruezo suggested in 2004 that a wide QRS with a large initial psoedo delta wave
can be indicative of such an origin. It has been confirmed in our series mainly in patients
with so called idiopathic VT.
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Welcome
Abstract Unavailable
Saturday, June 16
09.00 - 12.30
SESSION 2
Atrial arrhythmias
Troubles du rythme auriculaire
Chairmen/ Modérateurs: P. Defaye
Hôpital Michalon, CHU Grenoble, France
M. Chauvin
Hôpital Hautepierre, Strasbourg, France
Abstracts of the conferences
New Treatments
Arrhythmiasin&Heart
HeartFealure
Failure
57
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Atrial arrhythmias
SESSION 2
Troubles du rythme auriculaire
AF classification attempt: duo from dog to human EP lab.
Tentative de classification de la FA :
duo à partir du laboratoire expérimental et Clinique
P. Attuel & F. Halimi
CMC Parly II, Paris, France
09.00
Understanding atrial fibrillation process has been a challenging study subject for
generations of scientists and physicians and is still in 2007 a major topic of interest.
One has to differentiate three distinct components of AF before trying to rationally classify and cure this arrhythmia: initiation, perpetuation and termination of the fibrillatory process.
Initiation appears to be mainly due to rapid focal firing in the atrium. Description
of pulmonary vein foci initiating AF has been a major progress but the exact mechanism of
this automatic activation is still under discussion as well as the modulation role of the autonomic nervous system (atrial ganglionated plexi).
AF perpetuation stays a very controversial subject. It may be due to a permanent
firing from the active pulmonary veins with no participation of the atrial substrate, but may
also be sustained by the atrial substrate itself. In this latter case two mechanisms have been
described: multiple reentrant wavelets with random functional reentry and more recently the
mother rotor theory, a stable spiral wave with daughter wavelets. The influence of the autonomic system has to be underlined as well as the exact role of area of fragmented potentials (functional fragmentation or active critical zones of perpetuation).
Termination of the arrhythmia may result from pulmonary vein disconnection
when the substrate is not able to perpetuate the fibrillation anymore (simple trigger disconnection and/or reduction of atrial critical mass after antrum exclusion and/or foci and
atrial denervation). When the substrate is still fibrillating after PV disconnection additional
lesions have to be performed: left and right atrial lines of compartmentalization and/or
defragmentation of the atrial tissue.
The respective responsibility of trigger exclusion, atrial compartmentalization with
mass reduction, denervation, and destruction of elective areas of perpetuation has to be
evaluated and may be different in each patient depending on the fibrillation form and the
electrical and anatomical atrial substrate remodeling. Further understanding of these
mechanisms is necessary before proposing a new AF classification.
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Atrial arrhythmias
SESSION 2
Troubles du rythme auriculaire
Tachycardiomyopathies : who ? and why ?
Tachycardiomyopathies : qui et pourquoi ?
M. Janse
Experimental and Molecular Cardiology Group, Academic Medical Center, K 2-105, 1105 AZ Amsterdam, The Netherlands
09.20
There is a complex relationship between atrial fibrillation and heart failure. As
Camm and Yusuf formulated it"dilated cardiomyopathy begets atrial fibrillation, which
begets atrial fibrillation, which begets dilated cardiomyopathy "1. In 1914 Sir James
Mackenzie reported that atrial fibrillation was present in 80-90 % of patients with
congestive heart failure ("dropsy") 2. Nowadays, this figure is between 10 and 30% 3,4.
Dilated cardiomyopathy and atrial fibrillation are two of the most common cardiac disorders, affecting 5 and 2.5 million people respectively in the US 1. The two disorders form
a "viscious electromechanical cycle"3.
Why would atrial fibrillation beget cardiomyopathy?
A number of factors play a role: short intervals for passive ventricular filling,
no atrial contribution to filling, worsening of mitral and tricuspid regurgitation, rapid heart
rates, irregular heart rates 5,6,7. Rapid heart rates lead to a reduced contractility, a diminished cardiac sympathetic responsiveness due to a reduced beta1-receptor density, and
abnormalities in cellular calcium handling 6. Upon restoration of a normal heart rate,
there is a dramatic recovery, indicating that cardiomyopathy caused by rapid heart rates
is largely reversible 6. When heart failure is already present, rapid heart rates are deleterious because the force-frequency relationship is reversed 8. In normal hearts an
increase in heart rate leads to an increased contractility, in heart failure to a diminished
contractility.
Although the name "tachycardiomyopathy" implies that rapid heart rates are
essential for the induction of heart failure, there are reports indicating that cardiomyopathy with atrial fibrillation may occur with well controlled ventricular rates 9,10. Thus,
pulmonary vein isolation did improve the left ventricular ejection fraction in patients with
paroxysmal atrial fibrillation, or persistent atrial fibrillation with well controlled ventricular rates 9,10. An editorial stated:" the data compel us to explore the possibility that atrial
fibrillation can cause cardiomyopathy even when ventricular rates are well controlled"11.
It could be that the irregularity of the ventricular responses in atrial fibrillation is a factor in causing heart failure. An irregular sequence of RR intervals has been shown to produce adverse hemodynamic effects that were independent of heart rate 7. The mechanisms responsible for the reduction in cardiac output during an irregular sequence of
paced cycle lengths as compared with regular pacing at the same average rates are
incompletely understood 7, but the data point to the importance of atrioventricular synchrony.
Why would atrial fibrillation beget atrial fibrillation?
In the landmark study of Wijffels et al 12 it was shown that in conscious goats
burst pacing caused episodes of atrial fibrillation that initially lasted only a few seconds,
but with repetitive induction became longer and longer, until finally the arrhythmia became chronic, lasting more than 24 hours. The atrial refractory period shortened in the
course of a few days and the normal rate adaptation was abolished, or even reversed.
The main cause for this electrical remodelling is a reduced L-type calcium current 13.
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Why would cardiomyopathy beget atrial fibrillation?
In a canine model of heart failure, caused by long periods of rapid ventricular
pacing, atrial electrical remodelling occurred: the atrial transient outward current, Ito, the
slow delayed rectifier IKs and the L-type calcium current ICa,L were downregulated and the
Na-Ca exchange current was upregulated 14.
Atrial fibrillation lasted much longer in dogs with heart failure than in controls. The
action potential changes were different from those in which rapid atrial pacing, or repeated
induction of atrial fibrillation caused chronic atrial fibrillation: the action potential duration
was unchanged at slow rates (in contrast to the short action potentials following rapid atrial
pacing) and paradoxically lengthened at rapid rates. The propensity for delayed afterdepolarizations, caused by the upregulated NaCa exchanger, was enhanced. Heart failure also
caused structural remodelling. Atrial fibrous tissue increased from from about 2% in controls
to about 10% 15. Interestingly, when rapid ventricular pacing was stopped, and heart failure reversed, the ionic remodelling completely recovered, but the structural changes remained, as did the ability to induce prolonged episodes of atrial fibrillation 15. Similar findings
were observed in patients with congestive heart failure 16.
There was an increase in atrial refractory periods, and slowing of conduction, with
greater number and duration of electrograms with fractionation or double potentials along
the crista terminalis, associated with areas of low voltage and electrical silence. These findings point to increased fibrosis in the atria. Patients with congestive heart failure had a
greater propensity for atrial fibrillation induced by single extra stimuli, and atrial fibrillation
was more often sustained. The atria of the heart failure patients were significantly enlarged.
In the above I have tried to answer the "Why?" in the title by describing the
various factors that are involved in the "viscious electromechanical cycle" of cardiomyopathy and atrial fibrillation 3.
The "Who?"is difficult to answer. Patients with structural heart disease and left
ventricular dysfunction will undergo increased hemodynamic deterioration and increased
mortality when atrial fibrillation occurs 3. In patients without structural heart disease atrial
fibrillation can cause left ventricular dysfunction that is reversible. In both conditions restoration of sinus rhythm is desirable, certainly in view of the possibility that tachycardiomyopathy may occur with well controlled ventricular rates.
References
1. Camm AJ, Yusuf S. Atrial fibrillation and dilated cardiomyopathy. In: Cardiac Mechano-Electric Feedback
& Arrhythmias. From pipette to patient Edited by P. Kohl. F Sachs and MR Franz. Elsevier Saunders,
Philadelphia, 2005, pp229-239.
2. Mackenzie J.Diseases of the Heart. , 3d edition.Oxford medical Publications, London 1914
3. Cha Y-M, Redfield MM, Shen W-K, Gersh BJ. Atrial fibrillation and ventricular dysfunction. A vicious electromechanical cycle. Circulation 2004;109: 2839-2943.
4. Stevenson WG, Stevenson LW. Atrial fibrillation in heart failure. N Engl J Med 1999; 341: 910-911.
5. Naccarelli GV, Hynes BJ, Wolbrette DL, Bhatta L, Khan M, Samii S, Luck JC. Atrial fibrillation in heart failure: prognostic significance and management. J Cardiovasc Electrophysiol 2003; 14: S281-S286.
6. Shinbane JS, Wood MA, Jensen DN, Ellenbogen KA, Fitzpatrick AP, Scheinman MM. Tachycardia-induced
cardiomyopathy: a review of animal models and clinical studies.
7.Clark DM, Plumb VJ, Epstein AE, Kay GN. Hemodynamic effects of an irregular sequence of ventricular
cycle lengths during atrial fibrillation. J Am Coll Cardiol 1997; 30: 1039-1045.
8. Mulien LA, Hasenfuss G, Leavitt BJ, Allen PD, Alpert NR. Altered myocardial force-frequency relation in
human heart failure. Circulation 1992; 85: 1743-1750.
9. Hsu LF, Jais P, Sanders P, Garrigue S, Hocini M, Sacher F, Takahashi Y, Rotter M, Pasquie JL, Scavee C,
Bordachar P, Clementy J, Haissaguerre M. Catheter ablation for atrial fibrillation in congestive heart failure.
N Engl J Med 2004; 351: 2373-2383.
10. Gentlesk PJ, Sauer WH, Gerstenfeld EP, Lin D, Dixit SZado E, Pa C, Callans D, Marchlinski FE.
Reversal of left ventriclar dysfunction following ablation of atrial fibrillation. J cardiovasc Electrophysiol
2007; 18: 9-14.
11. Asirvatham SJ. Tachycardi-induced cardiomyopathy without the tachycardia: yet another reason to ablate atrial fibrillation! J Cardiovasc Electrophysiol 2007; 18: 15-17.
12. Wijffels MCEF, Kirchhof CJHJ, Dorland R, Allessie MA. Atrial fibrillation begets atrial fibrillation: a study
in awake chronically instrumented goats. Circulation 1995; 92: 1954-1968.
13.Yue L, Feng J, Gaspo R, Li GR, Wang Z, Nattel S. Ionoic remodelling underlying action potential changes
in a canine model of atrial fibrillation. Circ Res 1997; 81: 512-525.
14. Li D, melnyk P, Feng JL, Wang Z, Petracca K, Shrier A, Nattel S. Effects of experimental heart failure on
atrial cellular and ionic electrophysiology. Circulation 2000; 101: 2631-2638.
15. Cha T-J, Ehrlich JR, Zhang L, Shi Y-F, Tardif J-C, Leung TK, Nattel S.Dissociation between ionic remodelling and ability to sustain atrial fibrillation during recovery from experimental heart failure. Circulation
2004; 109: 412-418.
16. Sanders P, Morton JB, Davidson NC, Spence SJ, Vohra JK, Sparks PB, Kalman JM. Electricla remodelling of the atria in congestive heart failure. Electrophysiological and electroanatomic mapping in humans.
Circulation 2003; 108: 1461-1468.
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Atrial arrhythmias
Troubles du rythme auriculaire
SESSION 2
Atrial Fibrillation: experimental effects of drugs.
Fibrillation Auriculaire : effets expérimentaux des médicaments
E. Allessie
Department of Physiology, Cardiovascular Research Institute Maastricht,, Maastricht University, The Netherlands
09.50
Numerous clinical investigations as well as recent experimental studies have
demonstrated that atrial fibrillation (AF) is a progressive arrhythmia. With time, paroxysmal AF will become persistent and within the first week of persistent AF the success rate
of pharmacological cardioversion quickly declines. Electrical remodeling (shortening of atrial
refractoriness) develops within the first days of AF and contributes to the increased stability of the arrhythmia. Voltage clamp studies have shown that this is mainly due to downregulation of the L-type Ca++ current which causes a loss of the plateau phase of the atrial
action potential. Recently, in our goat model of persistent AF, we have found that electrical remodeling has important consequences for the action of class III drugs. The efficacy
of IKr blockers like d-sotalol, dofetilide and ibutilide clearly decreased during the process of
electrical remodeling. This can be explained by the fact that, due to the loss of the plateau
phase of the action potential, the contribution of the delayed activated inward rectifying
current to repolarization becomes less. In electrically remodeled atria, most of the repolarizing current is carried by early activated K+ currents like Ito and IKur. We studied the
effects of administration of AVE 0118, a blocker of Ito, IKur and IKAch in chronically instrumented goats, both before and after AF-induced electrical remodeling. In contrast to 'late'
class III drugs (d-sotalol, dofetilide and ibutilide), blockade of the early activated potassium
currents exerted an enhanced class III effect in electrically remodeled atria. After a couple
of days of atrial fibrillation, both the duration of the atrial refractory period and the median
atrial AF cycle length were significantly more prolonged than during control. Infusion of
AVE 0118 during persistent AF caused a strong, dose dependent, increase of the AF cycle
length from 90±8 ms to more than 180 ms. In 7 of 7 goats with persistent AF, sinus rhythm
could be restored by infusion of AVE 0118. Right atrial MAP recordings during pharmacological cardioversion showed that the prolongation of AF cycle length and termination of
AF was associated with a marked prolongation of the plateau phase of the action potentials. In contrast, the corrected QT interval was not prolonged. Mapping of the free wall of
the right and left atrium during administration of AVE0118 alone or in combination with
dofetilide or ibutilide (Ikr blockers), showed that the conduction velocity of the fibrillation
waves did not decrease. In fact the slowing of the rate of AF was associated with a slight
increase in conduction velocity of the fibrillation waves. As a result the average pathlength
of intra-atrial reentry during AF increased from 5-6cm during control to > 12cm due to
blockade of Ito, IKur, IKAch, and IKr. This about 2.5 fold lengthening of the pathway required for reentry led to fusion of fibrillation waves and finally termination of AF.
More recently we have evaluated the efficacy of the combination of AVE0118
and an IKr blocker (dofetilide and ibutilide).7 We hypothesized that restoration of the plateau phase of the remodeled action potential by AVE0118 would restore the original contribution of IKr to atrial repolarization. This in turn would reinstitute the original antiarrhythmic action of IKr-blockers. Such a synergistic action between 'early' and 'late' class III drugs
was expected to exert still only a limited effect on the ventricles (QT-time). We found that
AVE0118 completely restored the loss of action of IKr-blockers in electrically remodeled
atria. The combination of AVE0118 with dofetilide or ibutilide thus exerted a larger effect
on atrial refractoriness than the sum of their separate effects (synergism). The class III
action of dofetilide and ibutilide on AERP was increased 3-fold by pre-treatment with
AVE0118 (3mg/kg/h).
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During persistent AF, the combined administration of AVE0118 and IKr-blockers prolonged the AFCL to a larger extent than expected from their separate effects.
The combined blockade of IKur/Ito/IKAch and IKr offered a strong antiarrhythmic effect
which could cardiovert persistent AF in up to 100% of the animals, without excessive
QT-prolongation. The combined administration of AVE0118 and an IKr-blocker, almost
doubled the average pathlength of the fibrillation waves. This not only demonstrates a
very powerful and effective class III effect during persistent AF, but it also offers a logical explanation for termination of the arrhythmia. Lengthening of the required intra-atrial
pathways for reentry will allow less fibrillation waves to be present simultaneously in the
available atrial tissue mass. When the number of fibrillation waves is reduced below a
certain critical value, the chance that all fibrillation waves will die out at the same time
becomes so high that AF can no longer perpetuate itself.
The high efficacy in remodeled atria and the atrial specificity provides hope
that atrial specific 'early' class III drugs can be used effectively and safely for cardioversion of persistent AF in humans. Pending the results of larger clinical trials, we can only
speculate on the clinical efficacy and the potential impact of atrial specific antiarrhythmic drugs for the management of AF.
References
1. Wijffels MCEF, Kirchhof CJHJ, Dorland R, Allessie MA. Atrial Fibrillation Begets Atrial
Fibrillation. A study in Awake Chronically Instrumented Goats. Circulation. 1995;92:1954-1968.
2. Allessie MA. Atrial electrophysiologic remodeling: Another vicious circle? J. Cardiovasc.
Electrophysiol. 1998;9:1378-1393.
3. Allessie MA, Boyden PA, Camm AJ, Kleber AG, M.J. L, Legato MJ, Rosen MR, Schwartz PJ, Spooner
PM, Van Wagoner DR, Waldo AL. Pathophysiology and prevention of atrial fibrillation. Circulation.
2001;103:769-777
4. Allessie MA, Ausma J, Schotten U. Electrical, contractile and structural remodeling during atrial
fibrillation. Facts and possible implications. Cardiovasc. Res. 2002;54:230-46.
5. Blaauw Y, Gogelein H, Tieleman RG, van Hunnik A, Schotten U, Allessie MA. "Early" class III drugs
for the treatment of atrial fibrillation: efficacy and atrial selectivity of AVE0118 in remodeled atria of
the goat. Circulation. 2004;110:1717-24.
6. Duytschaever M, Blaauw Y, Allessie M. Consequences of atrial electrical remodeling for the antiarrhythmic action of class IC and class III drugs. Cardiovasc. Res. 2005;67:69-76.
7. Blaauw Y, Schotten U, van Hunnik, A, Neuberger, HR, Allessie MA. Cardioversion of persistent atrial
fibrillation by a combination of atrial specific and non-specific class III drugs in the goat. Cardiovasc.
Res. 2007; in press Pratt CM, Moye LA. Am J Cardiol 1990, 65, 20 Waldo AL, Camm AJ DeRuyter H,
Friedman PL, Mac Neil DJ, Pauls JF, Pitt B, Pratt CM, Schwartz PJ, Veltri EP. Lancet 1996, 348, 7.
Xiao YF, Ma L, Wang SY, Josephson ME, Wang GK, Morgan JP, Leaf A. Am J Physiol 2006, 290:362.
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Atrial arrhythmias
SESSION 2
Troubles du rythme auriculaire
Can we expect a class V of antiarrhythmic?
Peut-il y avoir une classe V d'antiarythmiques?
B. Le Grand
Division of Cardiovascular Diseases, Centre de Recherche Pierre Fabre, 81106 Castres Cedex, France.
10.20
The present available antiarrhythmics of classe I (sodium channel blockers such as
flecainide, Brendel and Peukert, 2002) and III (potassium channel blockers such as d-sotalol,
Kannel et al, 1998) can terminate atrial fibrillation and reduce its recurrence, but in the end
may increase mortality due to a variety of adverse effects including potentially lethal ventricular proarrhythmia. Several clinical trials had to be terminated due to increased mortality in the
treated patient groups (flecainide: CAST-trial, Pratt et al, 1990; d-sotalol: Sword-trial, Waldo et
al, 1996). The gold standard of antiarrhythmic therapy, amiodarone, a very unselective drug,
is hampered by many non-cardiac side effects. Therefore, there is a great medical need for
the development of safer and more efficient drugs for the treatment of atrial arrhythmias.
Most of the clinically available class III antiarrhythmics are blockers of IKr (e.g. dsotalol, dofetilide or ibutilide), while a new antiarrhythmic agent, azimilide), is a combined bloker of both IKr and IKs. However, since IKr and IKs are present in both atrium and ventricle,
undesired ventricular effects can be observed for these drugs, which limit their use for the
treatment of atrial arrhythmias.
Observational, clinical, and experimental studies have demonstrated that long-chain
n-3 polyunsaturated fatty acid (n-3 PUFA) supplementation, including docosahexanenoic acid
(DHA) and eicosapentaenoic acid (EPA), reduces the risk of heart diseases including cardiac
arrhythmias. The risk reductions in sudden death by PUFAs have been demonstrated by several randomized controlled trials. GISSI IV prevenzione study (Marchioli et al, 2002), a randomized clinical trial investigated the effects of PUFAs supplementation in the secondary prevention of myocardial infarction. Treatment with PUFAs lowered total and cardiovascular mortality by 20% and 30%, and sudden cardiac death was reduced by 45%. Several mechanisms
by which n-3 PUFA prevent arrhythmias have been proposed. Thus, it is now well-established
that for the ventricular stage, the antiarrhythmic effects of the n-3 PUFAs are related to blocking effects on late sodium current known to be a potent trigger of ventricular tachycardia and
ventricular fibrillation during ischemia and reperfusion (Xiao et al, 2006). Thus, the late sodium
current is exclusively observed and increased under pathological conditions such as cardiac
hypoxia/ischemia. In addition to its role on action potential and arrhythmias, this increase in
late sodium current results in an elevated [Na+]i. This, in turn, activates the Na+/Ca2+
exchanger in its reverse-mode promoting Ca2+ overload, a well described feature of ischaemic/hypoxic cardiac cells. This increase in [Ca2+]i is a well-known trigger of ischemia induced abnormal ectopic activities. Therefore blockade of late sodium current may have powerful beneficial effects in reducing ischaemic arrhythmias due to [Ca2+]i overload. Both EPA and
DHA have been shown to concentration-dependently fasten the late sodium-current inactivation which render these compounds highly selective for the prevention of cardiac ventricular
arrhythmias induced by ischaemic diseases.
On the other hand, Calo et al (2005) have recently demonstrated that short term
n-3 PUFAs administration in patients undergoing coronary artery bypass graft (CABG) substantially reduced the incidence of postoperative atrial fibrillation and was associated with a
shorter hospital stay. This acute protective mechanism against atrial fibrillation remained unknown and cannot be explained by an interaction with the late sodium channel (which has no
functional relevance in atrial tissue).
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In contrast to IKr and IKs, the ultra-rapid delayed rectifier IKur has been found
only in human atrial cells but not in ventricles (Li et al, 1996). Comparison of the biophysical and pharmaceutical properties of this native current with currents obtained by expression of cloned K-channels provided first evidence that Kv1.5 is the molecular basis for IKur.
In addition, a study with antisense oligonucleotides directed against Kv1.5 mRNA demonstrated specific reduction of IKur density in human atrial myocytes , confirming the involvement of Kv1.5 in this current (Feng et al, 1997). However, it should be noted that the Kv1.5
channel protein was detected by immunohistochemical techniques in both human atrium
and ventricle, contrary to the functional current IKur which only exists in atrial myocytes.
This apparent discrepancy might be explained by different -subunit compositions that might
render the ventricular channel non-functional.
Due to the selectivity of the functional IKur to the atrium, the Kv1.5 channel should
be a promising target for the development of new atrial selective antiarrhythmic drugs.
Because EPA and DHA have been shown to specifically fasten the channel inactivation (see late sodium current), experimental investigations were conducted in cell line
transfected with hKv1.5 channel to evaluate whether these n-3 PUFAs could accelerate the
apparent inactivation process of IKur. The figure1 shows typical patch-clamp recordings of
IKur obtained in absence (left panel) and presence of DHA (10 µM, right panel). DHA markedly abolished the sustained component of the IKur with only weak effects on the peak
current (Pignier et al, 2006) .
Figure 1
This result suggests that DHA fastened the apparent inactivation of IKur (in the
same way as that observed on the late sodium current in the ventricular myocytes). In addition, DHA blocked the sustained component in a concentration manner with an IC50 value of
6.8 µM and in a reversible manner which is in agreement with a typical open channel blockade effect that affords an use-dependent blockade of IKur.
Finally, atrial fibrillation produce electrical remodelling of the human atrium, resulting in a shortening of atrial action potential duration (APD) which in turn enhances the substrate for more recurrent and persistent re-entrant atrial arrhythmia. This shortening of atrial
APD is known to be linked to an extensive activation of Kv1.5 channels during chronic atrial
fibrillation. Therefore, the DHA-induced blockade of Kv1.5 constitutes probably the key mechanism of atrial antiarrhythmic effects of n-3 PUFAs. Thus , by a selective blockade of the sustained component of IKur, n-3 PUFA reversed the atrial fibrillation-induced shortening of atrial
refractoriness without any effect on both normal atrial and ventricular refractoriness. These
observations support the approach of atrial selective modulation of refractoriness through
blockade of IKur for the development of potentially safer and more effective atrial antiarrhythmic agents.
Collectively, the n-3 PUFAs by fastening the sustained inactivation component of
sodium and potassium currents have a high affinity for the pathological state of the myocardium with only moderate effects in normal situation. Indeed, n-3 PUFAs constitute a new and
safer class of antiarrhythmic agent. Finally, blockade of the sustained component of IKur by
DHA is an alternative treatment for the prevention of incidence of atrial fibrillation without any
worsened effects on ventricular repolarisation.
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References
Brendel J, Peukert S. Expert Opin Ther Patents, 2002,12, 1589.
Calo L, Bianconi L, Colivicchi F, Lamberti F, Loricchio ML, De Ruvo E, Meo A, Pandozi C, Staibano M,
Santini, M. J Am Coll Cardiol 2005, 45,1723.
Feng J, Wible B, Li GR, Wang Z, Nattel S. Circ Res 1997, 80, 572.
Kannel WB, Wolf PA, Benjamin EJ, Levy D. Am J Cardiol 1998, 82, 2N
Li GR, Feng J, Yue L, Carrier M, Nattel S. Circ Res 1996, 78, 689.
Marchioli R, Barzi F, Bomba E, Chieffo C, Di Gregorio D, Mascio R. Cir 2002, 105, 1897.
Pignier C, Revenaz C, Rauly-Lestienne I, Cussac D, Gardette J, Delhon A, Le Grand B. World Congress of
Cardiology, Barcelona 2006.
Pratt CM, Moye LA. Am J Cardiol 1990, 65, 20
Waldo AL, Camm AJ DeRuyter H, Friedman PL, Mac Neil DJ, Pauls JF, Pitt B, Pratt CM, Schwartz PJ, Veltri
EP. Lancet 1996, 348, 7.
Xiao YF, Ma L, Wang SY, Josephson ME, Wang GK, Morgan JP, Leaf A. Am J Physiol 2006, 290:362.
New Treatments in Heart Fealure
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Atrial arrhythmias
Troubles du rythme auriculaire
SESSION 2
Advocacy : AF and heart failure
Playdoyer : FA et insuffisance cardiaque
Pro-rhythm control therapy by AF ablation of left atrium
Pour une therapie de contrôle du rythme par ablation de FA
dans l'oreillette gauche
M. Hocini
CHU Haut Lévèque, Pessac, France
11.20
Abstract Unavailable
Notes :
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Atrial arrhythmias
SESSION 2
Troubles du rythme auriculaire
Advocacy : AF and heart failure
Playdoyer : FA et insuffisance cardiaque
Pro rate-controlled therapy
(including AV node ablation and biventricular PM).
Pour un contrôle de la fréquence
(incluant l'ablation du noeud AV avec PM biventriculaire)
J-Y. Le Heuzey
Hôpital Européen George Pompidou, Paris, France
11.35
Heart failure and atrial fibrillation are two new "epidemics". The treatment of
atrial fibrillation is complex, and this complexity is increased in case of heart failure. The
problem of the choice between the two strategies, rhythm or rate control is also present
in patients with heart failure. In the AFFIRM trial it has been demonstrated that rate control
can be proposed in some patients as a first choice therapy and not only in case of failure
of the rhythm control strategy. But, in fact very few patients had a low ejection fraction
and heart failure in AFFIRM (less than 25 %).
If rate control is chosen it can be made by pharmacological means. Digitalis can
be used but the toxicity is often present in patients with heart failure. Beta blockers can be
used but there is no specific study conducted in this peculiar category of patients. It is possible to use beta blockers which have demonstrated an efficacy in heart failure : Carvedilol,
Bisoprolol, Metoprolol, Nebivolol. It is necessary to avoid calcium antagonists which have
an inotropic effect. Finally it's possible to use Amiodarone but the adverse effects are often
a limitation to its use as a rate controlling drug.
If the pharmacological option is not preferred it is possible to propose the "ablate and pace" strategy. In fact very few patients, to date, can be proposed for such therapy. It is a strategy which is efficient for decreasing symptoms, for improving quality of life,
for improving the performances during exercise and for increasing left ventricular function.
In fact the rare cases in which this technique is used concern patients for whom it has been
decided to implant a resynchronisation pacemaker, i.e. with a patent dyssynchrony, and
some very rare elderly patients for whom it is not possible to propose an isolation of the
pulmonary veins. The PABA-CHF trial has demonstrated the superiority of pulmonary vein
ablation versus AV node plus pacing ablation but this trial has a very large number of
methodological limitations.
Finally it will be interesting to analyse the results of the AF-CHF trial which is
ongoing. This trial has a design which is very close to the design of AFFIRM, but it concerns
only patients with heart failure. The enrolment is completed, the patients are followed till
the end of this month, June 2007. The results will be presented at the next meeting of
American Heart Association in November 2007.
New Treatments in Heart Fealure
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Atrial arrhythmias
SESSION 2
Troubles du rythme auriculaire
AF Ablation with Electro-anatomical mapping system:
EnSite NavX tm.
Ablation de FA par système de cartographie électro-anatomique :
EnSite NavX tm
A. Ferracci
11.50
OPERATOR:
SPONSOR:
PATIENT INITIALS:
SEXE:
AGE:
INDICATIONS:
RISK FACTORS:
MEDICAL HISTORY:
PROCEDURE:
PROCEDURE
LASTING:
DEVICE:
Dr A Ferracci, Hôpital Saint Joseph Marseille
ST JUDE MEDICAL
DEB GEN
Female
63
Paroxystic Atrial Fibrillation
NO
Atrial Fibrillation since 2004
Ablation lines:
-Lines around the Left and Right Pulmonary Veins
- Roof lines on the Left Atrium (catching up LPV and RPV lines)
- Coronary Sinus ablation line
Notes :
4 h10 - Scopy lasting : 35 mn
Mapping system : Ensite NavX tm, Catheter : IBI (with L1 bending)
Fusion between scanner and mapping system
Pulmonary veins ablation lines
Roofline + PV isolation lines
Voltage mapping after ablation
VIDEO AVAILABLE
ON THE RHYTHM DVD
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Atrial arrhythmias
SESSION 2
Troubles du rythme auriculaire
Real words experience in AFIB (ACTIF registry).
Expérience "réelle" de la FA (registre actif)
JP Albenque 1, A. Pisapia 2, B. Cauchemez 3, N. Saoudi 4, P. Lagrange 5, G. Atallah 6, JP Cebron 7, H. Mansour 8
Clinique Pasteur, Toulouse 1; Hôpital St Joseph, Marseille 2; Hôpital Ambroise Paré, Paris 3; Hôpital Princesse Grâce,
Monaco 4; Clinique Saint Pierre, Perpignan 5; Clinique Rillieux, Lyon-Nord 6; Nouvelles Cliniques Nantaises, Nantes 7;
CHU Clermont-Ferrand 8
12.10
AIM OF THE REGISTRY
To provide efficacy data in an open, prospective, non-randomized multicenter registry on percutaneous radiofrequency ablation in 500 patients with atrial
fibrillation.
1. INCLUSION CRITERIA
All consecutive patients with atrial fibrillation (AF) referred for radiofrequency
ablation and accessible for follow-up until 6 months after the procedure are included at 8
participating centers.
2. EXCLUSION CRITERIA
Patients with any contraindication to radiofrequency ablation are excluded.
3. ENDPOINTS
1. Number of serious procedure- and/or device related adverse events
2. Freedom of AF recurrences as seen on 24 hour Holter monitoring, ECG and
patient symptoms at 3 and 6 months follow-up with and without anti-arrhythmic drugs for
paroxysmal and chronic atrial fibrillation
3. Procedural success
4. Number of patients stopping anti arrhythmic drugs at 3 months and
6 months follow-up
5. Number of patients stopping anticoagulation at 3 months and 6 months follow-up
6. Procedural data (procedure time, fluoroscopy time, ablation approach)
4. ASSESMENTS
Screening
AAD
AE
ECG
TTE
TEE
Holter
SCAN
Ablation
X
X
X
X
X
X
Post
X
X
X
Abl
X
X
X
X
3MFU
X
X
X
X
6MFU
X
X
X
X
X
X
X
X
X
AAD: number of anti-arrhythmic drugs taken
AE: absence of serious procedure- and/or device related adverse events
TTE: Trans Thoracic Echocardiogram
TEE: Trans Esophageal Echocardiogram
New Treatments in Heart Fealure
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5. FLOW CHART
Notes :
6. STUDY PERIOD
Start enrollment: March 2005
End of enrollment: December 31st 2006
End of follow-up: June 30th 2007
7. INTERIM ANALYSES
148 patients finished 6-month follow-up at time of interim analysis (presented at
ISCAT Paris by J.P. Albenque on October 13 2006). 500 patients have been enrolled by
December 31st 2006. Data are entered using an electronic data entry system.
8. INTERIM RESULTS (148 pts) (part 1)
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8. INTERIM RESULTS (148 pts) (part2)
Notes :
9. PRELIMINARY CONCLUSIONS
• 2/3rd of treated patients have paroxysmal AF
• Complication rate is low (4 %)
• 70% of patients are free of AF recurrences at 6 months
New Treatments
Arrhythmiasin&Heart
HeartFealure
Failure
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Saturday, June 16
14.00 - 15.45
Echocardiography Session
Session Echocardiographique
Chairmen/ Modérateurs: J. Lefèvre
Hôpital Saint-Joseph, Marseille, France
& C. Scheublé
Centre Cardiologique du Nord, Saint-Denis, France
Abstracts of the conferences
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Echocardiographic Session
Session Echocardiographie
Echocardiographic criteria for asynchronism
Critères échocardiographiques d'asynchronism
P. Khanoyan
Hôpital Saint-Joseph, Marseille, France
14.00
Abstract Unavailable
Notes :
Arrhythmias & Heart Failure
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Echocardiographic Session
Session Echocardiographie
DTI criteria and setting optimization.
Critères DTI et optimisation des réglages
E. Donal
CHU Rennes, France
14.20
Recent practice guidelines issued by the ESC or the ACC/AHA for the diagnosis
and treatment of chronic heart failure (HF) state that "Resynchronization therapy using biventricular pacing can be considered in patients with reduced LV-ejection fraction and ventricular dyssynchrony (DYS), manifest as a QRS-duration =120 ms, who remain symptomatic (NYHA III-IV) despite optimal medical therapy to improve symptoms, hospitalizations
and mortality. However, among all recipients of cardiac resynchronization therapy (CRT)
systems, up to 30% do not respond to treatment. Furthermore, some patients with QRS
duration <120 ms who have distinct mechanical DYS might respond to CRT. Therefore, the
substitution, or addition, of indices of mechanical DYS has been proposed to select candidates for CRT with greater accuracy. Assessment of mechanical dyssynchrony has consequently become a matter of great interest. Several imaging techniques and methods have
been proposed to characterize and measure mechanical DYS, mainly Doppler-echocardiography using M-mode, 2- or 3-dimensional imaging, and, above all, tissue Doppler imaging
(TDI). These techniques have important technical limitations, remain difficult to apply
widely in daily practice, and have not been validated in randomized prospective trials for
the selection of CRT candidates. We would like, nevertheless, demonstrate that, DTI or 2Dstrain techniques could be use and could improve our understanding of DYS before and
after CRT-device implantation. We can probably, after a learning curve, demonstrate the
presence of a mechanical DYS of motion but also of contraction. Furthermore, the DTI or
2D-S tools that we use before implantation can be use afterward to best pace the patient
using the optimal AV delay but also sometimes VV delay.
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Echocardiographic Session
Session Echocardiographie
3D criteria.
Critères 3D
C. Scheublé
Centre Cardiologique du Nord, Saint-Denis, France
14.40
Abstract Unavailable
Notes :
Arrhythmias & Heart Failure
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Echocardiographic Session
Session Echocardiographie
Responders and non-responders: why ?
Répondeurs et non-répondeurs: pourquoi ?
J. Lefèvre
Hôpital Saint-Joseph, Marseille, France
15.05
Abstract Unavailable
Notes :
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Saturday, June 16
16.15 - 18.30
Ventricular
Resynchronisation
Resynchronisation ventriculaire
Chairmen/ Modérateurs: A. Manolis
Hellenic Red Cross Hospital of Athens, Greece
& J-P. Camous
Université de Nice, France
Abstracts of the conferences
Arrhythmias & Heart Failure
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Ventricular Resynchronisation
Resynchronisation ventriculaire
Prophylactic implantations in heart failure.
Indications prophylactiques dans l'insuffisance cardiaque
E. Rowland
St. George's Hospital Medical School, London, United-Kingdom
16.15
Abstract Unavailable
Notes :
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Ventricular Resynchronisation
Resynchronisation ventriculaire
Ventricular resynchronisation using ICD
& wireless programming-OTW lead.
Resynchronisation ventriculaire avec sonde OTW orientable,
DAI et programmation sans fil
C. Barnay & J. Taieb
16.35
OPERATORS :
Dr C. Barnay & Dr J. Taieb, Hospital Center Aix-en-Provence, France
SPONSOR :
Boston Scientific
PATIENT INITIALS : CHA HEN
AGE :
67
RISK FACTORS : Ischemic cardiomyopathy
MEDICAL HISTORY: Coronaropathy (Myocardial Infraction)
INDICATION :
Heart Failure
NYHA St III
LVEF 0.25
LVEDD 61 mm (35 mm/m2)
PROCEDURE &
DEVICE :
IDC : GUIDANT CONTAK RENEWAL 4 RF REF H230
LEADS:
RA : CAPSURE FIX MEDTRONIC 5076
RV GUIDANT ENDOTAK RELIANCE GUIDANT
CS : ACUITY STEERABLE 4554
Coronary sinus angiography is observed by
the operators
Folowing the positioning of the coronary
sinus electrode on the video screen
Notes :
" Quick check " screen
of the programmator
VIDEO AVAILABLE
ON THE RHYTHM DVD
Final position of the electrodes
Arrhythmias & Heart Failure
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Ventricular Resynchronisation
Resynchronisation ventriculaire
How to improve materials to obtain 100% efficay?
Comment améliorer les matériels pour avoir 100% d’efficacité?
J-C. Deharo
CHU La Timone, Marseille, France
16.55
Abstract Unavailable
Notes :
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Ventricular Resynchronisation
Resynchronisation ventriculaire
CRT-D implant with the Attain StarFix™ LV lead
Resynchronisation ventriculaire : avec la sonde VG StarFix ®
A. Pisapia
17.15
OPERATORS :
Dr A. Pisapia, Saint-Joseph Hospital, Marseille
SPONSOR :
Medtronic
PATIENT INITIALS : GAR JEA
SEXE :
Male
AGE :
63
RISK FACTORS : Arterial Hypertension
NIDD (Diabetes type II),
Hypercholesterolemia,
Past smoker
MEDICAL HISTORY: Coronaropathy (Myocardial Infraction)
INDICATION :
Diladed cardiomyopathy with coronary origin,
EF (LV) < 30%
DEVICE :
ICD : Medtronic INSYNC SENTRY - 7298
RA Lead : Medtronic Fix Novus 5076-52 cm
RV Lead : Medtronic Sprint Fidelis 6949-65 cm
LV - CS Lead : Medtronic Starfix lead 4195
Notes :
StarFix lead
ICD Medtronic INSYNC SENTRY - 7298
VIDEO AVAILABLE
ON THE RHYTHM DVD
Patient rhythm control on the screen
New Treatments in Heart Fealure
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Ventricular Resynchronisation
Resynchronisation ventriculaire
Monitoring of heart failure by the devices.
Surveillance de l'insufissance cardiaque par les prothèses
F. Braunschweig
Karolinska University Hospital, Stockholm, Sweden
17.35
Following the evidence from large-scale trials and recent guideline recommendations, the number
of heart failure patients being implanted with an electrical device for CRT and/or ICD therapy has
rapidly increased. Characterized by advanced NYHA functional status, unsatisfactory response to
standard pharmacological treatment and, many times, a history of frequent heart failure hospitalizations, these patients put a particular high demand on specialized outpatient care.
In this context, electrical devices offer a unique possibility to collect critical diagnostic information with a potential to improve the management of heart failure patients. Of particular interest,
recent studies suggest that continuous monitoring of intrathoracic impedance and right ventricular
pressures are sensitive tools to detect changes in volume load prior to the onset of clinically overt
symptoms.
Intrathoracic electrical impedance, measured between a right ventricular lead and the
pacemaker, reflects the fluid content in the interpositioned pulmonary tissue. In the MID-HeFT trial,
Yu and co-workers showed that impedance was inversely correlated with the pulmonary capillary
wedge pressure and the patient's fluid balance. Analysing 24 hospitalizations for volume-overloadheart-failure, impedance dropped in all patients mean 18 days prior to hospital admission and 15
before clinical symptoms occurred. A fluid detection algorithm, computing the difference between
actual patient impedance and an auto-calibrated reference, had a sensitivity of 77% for early detection of hospitalization for decompensated heart failure. This technology is currently available in biventricular and dual chamber ICDs (Medtronic. Inc) and subject to evaluation in several registries. A
large controlled clinical trial (DOT-HF) has recently be launched to evaluate the clinical safety and
effectiveness of impedance monitoring and device alerts based on the fluid detection algorithm.
Elevated cardiac filling pressures are critically involved in the pathophysiology of decompensated heart failure and correlate with disease severity and prognosis. Data from studies using
continuous monitoring of right ventricular pressures demonstrated that volume overload exacerbations are often preceded by a gradual increase in right ventricular pressures over several days or
weeks. Therefore, an implantable hemodynamic monitor has been proposed to record central
hemodynamic trends over time. Work by Ohlsson and Magalski et al established the safety and longterm accuracy of the device. Importantly, Adamson and co-workers showed that the IHM is able to
detect significant changes in right ventricular pressures prior to clinical volume exacerbation with a
possible effect on hospitalization for heart failure. The concept of IHM-guided heart failure treatment
was recently evaluated in the COMPASS-HF including 274 patients. The study showed a reduction
in the cumulative number of hospitalizations for heart failure by 22% that did not reach statistical
significance.
However, the traditional time-to-event analysis and a pre-specified sub-analysis of the
group of NYHA-class III patients, representing 85% of the study population, showed a significant
decrease in heart failure-related hospitalizations by 37% and 41%, respectively. Considering these
patients were recruited from state-of-the-art heart failure programs with a high degree of background therapy, these results are certainly promising. While COMPASS-HF investigated the IHM as
a lone standing diagnostic monitoring device, the integration of the hemodynamic sensor into CRT
or ICD platforms appears as a more attractive future option.
Device-based monitoring has the potential to improve the surveillance of patients at risk
by providing early warning of imminent cardiac decompensation and to guide treatment interventions. The integration of this diagnostic information into routine and clinical practice calls for novel
concepts in heart failure outpatient care with the need for a close collaboration between heart-failure and electrophysiology subspecialties. The clinical usefulness of these novel diagnostic features
can be further enhanced by modern telecommunication technology facilitating remote monitoring
of patients in their daily living environment.
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Ventricular Resynchronisation
Resynchronisation ventriculaire
AF and HF patients: which therapy?
Patients en FA et insuffisance cardiaque: quel traitement ?
D. Gras
Nouvelles Cliniques Nantaises, Nantes, France
17.55
Abstract Unavailable
Notes :
New Treatments in Heart Fealure
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Notes :
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Sunday, June 17
09.00 - 11.00
Free Papers Session
Session Communications Libres
Chairmen/ Modérateurs: J. Faure, A. Ferracci
Saint-Joseph Hospital, Marseille, France
P. Fiorello, F. Halimi
CMC Parly II, Le Chesnay, France
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Free Papers Session
Communications Libres
Does the dor procedure (ventricular reduction) lessen
the need for ICD'S in ischemic cariomyopathy :
outcome in 55 consecutive patients.
Steven R. Gundry, MD and Walter J Ehrman, MD
The International Heart and Lung Institute, Palm Springs, California, USA
09.00
Low ejection fraction and ischemic cardiomyopathy are considered reasons for
implanting internal cardiac defibrillators (ICD's). The Dor Procedure, unlike traditional
left ventricular aneursymectomy procedures, does not routinely resect scarred and
potentially arrhythmogenic tissue, which potentially could serve as a foci for subsequent
ventricular arrhythmias. Conversely, by restoring normal ventricular geometry and lessening cardiac wall stress, the Dor Procedure could potentially lessen the potential for
ventricular arrhythmias.
We studied 55 patients who underwent the Dor Procedure for ischemic cardiomyopathy at out institution. All patients underwent from 1 to 5 concommittent coronary artery bypasses. 50/55 pts had mitral valve repair. Two patients had additional plication of simultaneously occurring inferior wall aneursym tissue.
There were 2 post operative deaths (4%), both from sepsis. There were no
episodes of V-tach or V-Fib in the peri-operative period. All patients were discharged
home on 3 months of Amiodarone therapy.
Two patients presented in V-tach to the emergency room in the second postoperative month. Each had stopped Amiodarone. Both survived without incident after
defibrillation in the emergency department.
All other patients are alive and well, without ICD's, up to 5 years post-op.
We conclude that the Dor Procedure, probably by normalizing ventricular geometry and wall stress, appears to obviate the need for ICD's. However, our experience
suggests that early amiodarone therapy is important in achieving these good results, and
should be given for at least 3 months post-operatively.
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Free Papers Session
Communications Libres
Ablation of paroxysmal focal atrial fibrillation located
in the coronary sinus.
Z. Kechida, L. Abid, M. Ait Said, B. Cauchemez
Hôpital La Riboisière, Paris, France
09.15
Introduction:
The paroxysmal atrial fibrillation (AF) can originates in the pulmonary veins but
may arise elsewhere. Different factors are involved in the induction or the maintenance of
AF. A strategy of ablation consisting in the isolation of pulmonary veins with the realization
of segmentation lines can be insufficient. It is necessary to search other substrates in the
left atrium that could be the foci of initiating and maintenance of the atrial fibrillation.
Case report:
We report a case of paroxysmal AF ablation in a 66 year-old-man. This arrhythmia was evolving since three years and was resistant to antiarrhythmic drugs (amiodarone,
flecainide). The longer episode of AF lengthened 30 minutes. During the procedure of radiofrequency ablation and after the large electrical pulmonary vein isolation, frequent salvos of
atrial fibrillation reappeared. Electrophysiological exploration shows an activity in the middle coronary sinus: a potential localized on the electrode 5/6 of a catheter placed in the coronary sinus (tracing 1), this last proved very probably a potential of Marshall Ligament. The
ablation of this focus immediately stopped the arrhythmia. After a three months follow-up,
the patient was asymptomatic without arrhythmia.
Conclusion:
The muscular strips located around the coronary sinus can play a role in the genesis of reentry circuits. This represents 25% of cases of atypical atrial flutter after AF ablation. The coronary sinus can generate therefore focal atrial arrhythmias playing a role in the
triggering and the maintenance of the AF. The ablation in the coronary sinus of these
arrhythmias is curative for these patients.
Tracing 1:
a potential localized on the electrode 5/6 of the catheter placed in the coronary sinus
Arrhythmias & Heart Failure
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Free Papers Session
Communications Libres
Ablation of paroxysmal focal atrial fibrillation located
in the coronary sinus.
L. Chiriac, Al. Campeanu, G. Cristian, R. Bolohan, F. Pinte, M. Iacob, V. Goleanu, I. Tintoiu
Army's Clinical Center for Cardiovascular Disease, Bucharest Romania
09.30
Introduction :
This study was performed to determine the relation between inducible sustained
ventricular tachycardia (ISVT) by programmed electrical stimulation and angiographic, clinical
and echographic data in patients with stable coronary artery disease (CAD). The aim of this
study was to explore if these patients with ISVT are associated with any specific "arrhythmogenic" pattern of coronary artery disease.
Methods and results :
To study the relationship between extent of CAD and ISVT, 129 consecutive patients
with coronary artery disease and inducible sustained monomorphic ventricular tachycardia
were evaluated by left ventriculography and coronary arteriography by standard techniques.
Left ventriculography was performed in the 30º RAO projection.
For wall motion analysis, the ventricle was divided in 17 segments A numerical score
0 to 4 is applied to each of these segments (0 - hyperdynamic; 1 - normal; 2 - hypokinetic; 3
- akinetic; 4 - dyskinetic; 5 - aneurismal) and the total score is divided by the number of segments evaluated to create a wall motion score index. The global score was subdivided into
anterior score representing the distribution of the LAD and posterior score representing the
RCA and LCX territories.
The mean age of the patients was 46 years (range 21 - 72 years), 75% of them
were male. Each patient was matched with two control patients with angina pectoris, but not
ISVT, respecting to age, sex, type and duration of ischemic syndrome and prior myocardial
infarction.
The left ventricular ejection fraction was similar in booth groups. A significant stenosis of the main left coronary artery (>50%) appeared more frequent in arrhythmic patients
(31% in ISVT patients vs 10% of the controls, p<0.01). Also proximal left anterior descending
artery stenosis (>75%) was more frequent in the arrhythmia patients (48% compared to 31%
of the matched controls, p<0.01). The difference was even greater for the subgroup with proximal LAD high-grade stenosis >95% (45 % from case patients vs 20% in control patients,
p<0.01).Three-vessel involvement was more frequent in case group (44% vs 22%, p<0.01).
"Main left equivalent" lesions, was significantly more frequent among ISVT patients.
The wall motion abnormalities were similar in both groups with a difference between groups in anterior wall motion score (2.4 in ISVT patients vs. 1.8 of the controls, p<0.01)
and number of segments with contractility abnormalities (9 in ISVT patients vs 5 in control
patients, p<0.05).
Conclusions :
The logistic regression analysis suggest that ISVT with CAD are associated with a
specific "arrhythmogenic pattern" consisting of some predictive independent factors: LAD
(=95%), TPS (=75%), anterior wall motion score and number of segments with contractility
abnormalities. These findings suggest that the obstruction not involving the proximal LAD did
not appear to have such an arrhythmogenic potential. In ISVT group the incidence was higher
in patients with multivessel coronary artery disease compared to those with single-vessel coronary artery disease. Using the quantitative wall motion analysis, a strong relationship was
found between the subgroup of anterior wall motion score and ISVT.
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Heart Failure and cardiac arrhythmias in children and
adults with obstructive hypertrophic cardiomyopathy.
A. Gudkova, E.Semernin, E.Shlyakhto
Pavlov State Medical University, Saint-Petersburg. Russia.
09.45
Peculiarities of heart failure and cardiac arrhythmias in adults and children with
obstructive hypertrophic cardiomyopathy have been not enough investigated.
Aim:
To evaluate severity of cardiac arrhythmias in adults and children with obstructive hypertrophic cardiomyopathy (HCMP).
Material and methods:
There have been examined 66 patients (19 children and 47 adults) with obstructive hypertrophic cardiomyopathy. Holter ECG monitoring has been performed in 44
patients (9 children and 35 adults) of this group. Morphometric analysis of the myocardium stromal part was performed by using intraoperative biopsies and autopsy cases.
Results:
In children group, 2 patients (22%) presented Grade II arrhythmia, 7 (78%)
presented Grade III, according to Lown classification of ventricular arrhythmia. In adult
group, 22 patients (63%) presented Grade III, 10 (28.5%) presented Grade VI and 3
(8.5%) presented Grade V. According these data, severity of ventricular arrhythmias was
higher in adults than in children (3.45±0.12 vs. 2.8±0.18, p=0.014).
Wolff-Parkinson-White (WPW) syndrome was detected in 7 of 66 patients.
Frequency of WPW syndrome revelation was much higher in children with obstructive
hypertrophic cardiomyopathy (5 of 19 patients, 26.3%), than in adult group (2 of 47
patients, 4.25%). ?hildren with obstructive HCMP had heart failure(HF) NYHA I-III
(1.89±0.20). It was much lower compared to adults with obstructive HCMP. Heart failure in adults group varied from II-IV class NYHA (3.14± 0.14; p = 0.038). The stromal
part of the right part of IVS in adults group varied from 2.12 to 10.60% (5.36±0.34).
The stromal part in children varied from 1.08 to 6.67% (3.62±0.30) and it was obviously lower (p<0.005) compared to adults.
Conclusion:
Severity of heart failure, the stromal part and ventricular arrhythmias in
patients with obstructive hypertrophic cardiomyopathy was obviously higher in adults
than in children. Frequency of WPW syndrome revelation in patients with obstructive
hypertrophic cardiomyopathy was much higher in children than in adults.
.
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Evaluation of the use of home monitoring follow up
service for patients with implantable cardiac devices.
G. McParland, E. Coleman, Lisa Finley, Barry O'Keeffe, Eng Wooi Chew.
Cardiac Department, Belfast City Hospital, N. Ireland
10.00
Aim:
To evaluate home monitoring follow up for the management of patients with
implanted Cardiac Rhythm Management (CRM) devices.
Method:
58 patients implanted with CRM devices volunteered to transfer from hospital
out patient to home monitoring follow up. Each was educated on the use of the home
monitor and subsequent follow up was performed using the home monitoring system.
Data was collected to evaluate the benefits of the system.
Results:
58 patients were recruited into the study. 43 were males with age ranging
from 23-87 years. 29 (50%) were aged 65 years or more. Over a 6 month period 185
transmissions were made. 166 were scheduled follow up and the rest were made as
urgent reviews. 21,004 miles of travel which would have generated C02 emissions of
6091.6 kg/mile was avoided. 21 (41%) of patients would have had to drive themselves
to hospital, 11 (19%) pts having to take time from with 3 (5.1%) losing income. 2 unnecessary hospital admissions were prevented. € 1188 was saved on ambulance and other
travel claims. 26 carers were relieved from accompanying these patients, 16 (26%) avoiding loss of pay. 47 patients (81%) and 11 carers transmitted with 100% reporting easy
usage. 51 (88%) felt more secure having the system at home. 56 pts (97%) preferred
follow up this way. Time taken to perform the follow ups was 15.4 hours (2 working
days) compared with 77 hours (11 working days) of hospital visits. This resulted in 9
working days saved.
Conclusion:
Home monitoring reduced the burden of follow up for the patient and carer,
the environment and financial saving to the health care service. Patients and hospital
staff benefit from a flexible time when transmission and follow up can be done.
Unnecessary hospital admissions can be avoided whilst providing safety and reassurance to the patient.
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Atrial bigeminy:
a new protocol to test inductibility of atrial flutter.
Pierre Fiorello, Franck Halimi, Cathy Bertrand, Jean-François Leclercq, and Patrick Attuel.
Clinic of Parly II. Le Chesnay. France.
10.15
Objectives:
Patients with atrial tachycardias even in a paroxysmal form can benefit from radiofrequency applications. Because precise activation maps are now required to determine the
anatomical target, inducibility testing may play an important role in such a procedure.
As previously reported, bigeminy pacing protocol is able to unmask atrial substrate vulnerability in patients with atrial fibrillation (AF) but little is known on its value
in organized atrial tachycardias such as atrial flutter (AFL).
Methods and results:
We studied 27 Patients (pts) of 64.2±17.3 yrs divided in two groups: Group 1
included 15 pts, with documented sustained atrial arrhythmias, 12 with isolated AFL, 4
pts with both AFL and AF. Group 2 included 12 pts evaluated for syncope without atrial
arrhythmia. We first evaluated effective and functional refractory periods (ERP, FRP),
then a bigeminy pacing was performed during 4 minutes at the right lateral free wall.
The coupling interval S1-S2 was programmed to a mean value of 261.2± 25.0 ms, i.e.
10% longer than the basic ERP. The S1-S1 interval was fixed 10% shorter than sinus
cycle length.
The group 2 pts were older (56.5±16.0 vs 72.9±14.6 yrs, p=0.01), had lesser antiarrhythmic drugs (0.4±0.6 vs 0 per pt), but no difference was observed in terms
of basic pacing rate during bigeminy pacing nor in the premature coupling interval S1S2. Values of ERP and FRP were similar (233.2±47 vs 234.6±14 and 275.0±4 vs
293.2±21 ms respectively, p NS).
During bigeminy application 10/15 pts of group 1 developed a common right
AFL and none of the 12 pts of the group 2. Sensitivity, specificity, negative and positive
predictive values were 70%, 92%, 92% and 73% respectively. Chi square test = 9.64.
Conclusion:
Atrial bigeminy pacing protocol has a high sensibility and specificity for induction of AFL. This test could be used routinely for the diagnosis of undocumented episodes. Further studies are needed to determine if it is able to validate the efficacy of a
radiofrequency ablation procedure.
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Sympatho-vagal imbalances preceded Common AtrioVentricular Nodal Re-entry Tachycardia induction:
an Heart Rate Variability study.
P. Vergara, G. Nigro, E. Ammendola, A. de Chiara, E. Pezzullo, A. Rago, D. Manfredi, R. Chianese, G. Arena, R. Calabrò
Cardiology Department, Second University of Naples, Italy
10.30
Background:
Atrioventricular Nodal Reentry Tachicardia (AVNRT) is a frequent supraventricular arrhythmia due to a re-entry mechanism.
Aim of the Study was to evaluate the autonomic tone in the hour preceding
the AVNRT induction by HRV analysis.
METHODS:
SDNN, HF, LF and VLF in the hour preceding AVNRT spontaneous onset (-pre)
and mean 24 hours (-24h) values were analyzed in 32 pts (13M+19F; 30±21 years) on
Holter recordings. AVNRT diagnosis was confirmed by electrophysiologic study. Number
of premature supraventricular (PSVC) and ventricular (PVC) complexes in the hour preceding AVNRT (-pre) and mean rate per hour (-mean) were scrutinized.
RESULTS:
Eighty episodes of AVNRT were recorded in 32 pts. SDNN-pre, HF-pre, LF-pre
were respectively lower than SDNN-24h, HF-24h, LF-24h (56±34 vs 115±28, p<0.01;
2.78±1.29 vs 3.16±1.76, p<0.01; 3.66±1.53 vs 4.26±1.12, p<0.01); there were no statistical differences between VLF-pre and VLF-24h (5.50±1.38 versus 5.57±0.96). PSVCpre and PVC-pre did not respectively differ from PSVC-mean and PVC-mean.
CONCLUSIONS:
During the hour preceding AVNRT episodes, there is a high sympathetic discharge. AVNRT onset is correlated to modifications of refractory periods of slow and fastpathways of the AV node and not to an increase in ectopic beats.
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Prevalence of drug-induced electrocardiographic
pattern of the Brugada syndrome in a healthy
European population.
C. Bertrand, J-S. Hermida, A. Otmani, J-L. Rey, J-F. Leclercq, P. Attuel, F. Halimi, P. Fiorello
Departements of arrythmology, CHU d'Amiens and CMC Parly 2, 78150 Le Chesnay.
10.45
Aim:
To determine the prevalence of drug- induced type 1 ("coved" ) electrocardiographic (ECG) pattern of the Brugada syndrome in a healthy European population, a
channel sodium blockade test was performed in asymptomatic subjects with an ECG pattern (type 2 and type 3 "saddleback" ) compatible with the diagnosis of Brugada syndrome (BS).
Methods:
Out of 1,000 healthy asymptomatic subjects, only one had a spontaneous typical (type 1) BS ECG. Sixty subjects (6%) had compatible BS ECGS and were tested with
a channel sodium blocker (ajmaline or flecainide), whereas the remaining 939 subjects
had a first normal ECG. We re-studied 10% of this population (i.e. 94 subjects) and recorded a second ECG because of the well described variability of BS ECG. A channel sodium
blockade challenge was performed in subjects with a second compatible BS ECGs.
Results:
One subject (0, 1%) had a spontaneous typical BS ECG. Out of 60 first ECG
compatible with BS, 2 channel sodium blockade tests were positives. In the group of 94
second ECG recorded, 7 subjects had a compatible BS ECG, and 3 channel sodium blockade tests were positives. Thus, the prevalence of typical drug-induced BS ECGs was 5
per 1,000 subjects compared with a prevalence of typical spontaneous BS ECG of 1 per
1,000.
Conclusions:
The prevalence of drug-induced BS ECGs was at least fivefold greater than the
reported prevalence of spontaneous BS ECGs in the healthy population. Together, they
represent 0.6% of the general population.
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