1. A pitvari fibrilláció (ablációs) kezelése
Pap Róbert
SZTE

2. Elbocsátási aritmia-diagnózisok

3. The solid curve indicates the projected increase in AF prevalence if no further increase in AF incidence occurs. The dotted curve indicates the increase in AF prevalence if the increase in incidence rate continues to rise to a similar extent as it rose between 1980 and 2000.

4. Prevalencia

6. Nathan H, Eliakim M. The junction between the left atrium and the pulmonary
veins. An anatomic study of human hearts. Circulation 1966;34:412– 422.
Mechanizmus
Jalife J, Berenfeld O, Mansour M. Mother rotors and fibrillatory conduction: a
mechanism of atrial fibrillation. Cardiovasc Res 2002;54:204 –216.
Ectopic foci vs. circus movement activity. Moreover, these investigators estimated that
maintenance of fibrillation in the canine atrium required a
The exact mechanisms underlying AF are still poorly critical number of four to six wavelets. Some support of
understood despite many years of research and speculation. this idea came from the pharmacological experiments of
As early as 1907, Winterberg [11] surmised that AF was Wang and co-workers [17,18] in which termination of
due to multiple rapidly firing foci distributed throughout atrial fibrillation by class IC antiarrhythmic drugs was
the atria. In 1914, Mines [12] advanced the circus move- preceded by a decrease in the mean number of wavelets.
ment theory of reentry. Thereafter, and until the late Subsequent experiments in dogs [19], as well as more
19509s, all of the hypotheses proposed to explain AF were recent intra-operative mapping studies in humans [20],
variations of the circus movement and ectopic focus have provided important insight into the characteristics of
theories [13,14]. However, following publication of the wave front propagation during fibrillation, and have given
multiple wavelet hypothesis by Moe and Abildskov [10], it support to Moe’s idea that multiple wavelets distributed
became generally accepted that AF was the result of the randomly throughout the atria gave rise to the seemingly
random propagation of multiple wavelets across the atria, a chaotic activation patterns observed in the electrocarprocess
that was thought to be independent of the initiating diograms of patients with AF. Finally, the hypothesis was
event. emboldened by the clinical observation that chronic AF
could be cured in some patients by the placement of
2.2. Multiple wavelets vs. circus movement multiple surgical lesions (MAZE) to compartmentalize the
atria into regions presumably unable to sustain the multiple
Moe and Abildskov [10] strongly argued that both the wavelets [21]. Indeed, this theory is virtually universally
ectopic focus and circus movement reentry notions were accepted by most clinical electrophysiologists today.
inadequate descriptions of AF. For them it was hard to However, none of the above-mentioned studies gave
believe that either mechanism could be endowed with the answers to many critical questions about the origin of the
necessary stability to persist for many years as AF turbulent activity that gave rise to the multiple wavelets in
commonly does. Thus, they proposed that the mechanism the experiments. For example, while the computer simulaof
AF, whether occurring spontaneously in man or pro- tions of Moe et al. [15] suggested that 15–30 wavelets
duced experimentally, was fundamentally different from were needed at a given time to keep the fibrillatory process
flutter and from automatic ectopic discharge. In 1964, Moe going, the experiments of Allessie et al. [16] could show
et al. published their classical computer model study on only 4–6 wavelets propagating on the surface of the dog
AF [15]. Based on that numerical study and on their heart. In the presence of such a small number of wavelets,
previous experimental results [10], they postulated that AF one would expect that, at any given time, a large amount
could exist as a stable state, self-sustained and independent of tissue in both atria would be recovered from previous
of its initiating agency, and also that an independent excitation, which would lead to coalescence of wavelets
survival of the arrhythmia was possible only in the and eventual termination of AF. In other words, it is
presence of inhomogeneous atrial repolarization enhanced reasonable to speculate that, in the experiments of Allessie
by adequate vital activity. The idea of Moe et al. was et al. [16], the arrhythmia could have been in fact the result
simple. They considered fibrillation to be a fundamentally of a single (or a small number of) high frequency source
turbulent and self-sustaining process, which takes place in that was (were) hidden from view. Additional questions
a non-homogeneous excitable medium. Such a process include the following: is spontaneously occurring fibrillacould
be initiated by an impulse propagating through the tion the result of a ‘‘mother rotor’’ that breaks and
medium at a time when some of its components have fractionates into multiple independent offspring? What are
recovered while others remain partially or fully refractory the fundamental structural and electrophysiological characas
a result of a preceding activation. Accordingly, some teristics that sustain the wavelets and which enable their
elements in the medium may
Moe GK, Rheinboldt WD, Abildskov JA. A computer model of atrial fibrillation.Am Heart J 1964:200 –220. 6

7. Pitvari fibrilláció kezelése
Frekvencia-kontroll Ritmus-kontroll
- Gyógyszeres (béta-blockoló, Ca-antagonista, digoxin)
- Gyógyszeres
Nem-gyógyszeres:
AV csomó abláció + pacemaker
Nem-gyógyszeres
Anticoaguláns kezelés

9. Frekvencia- vagy ritmus-kontroll?

10. Circulation 2004 Covariates Significantly Associated With Survival pHR
Age at enrollment*
<0.0001
1.06
Coronary artery disease
<0.0001
1.65
Congestive heart failure
<0.0001
1.83
Diabetes
<0.0001
1.56
Stroke or transient ischemic attack
<0.0001
1.54
Smoking
<0.0001
1.75
First episode of atrial fibrillation
0.0067
1.27
Sinus rhythm
<0.0001
0.54
Warfarin use
<0.0001
0.47
Digoxin use
<0.0001
1.50
Rhythm-control drug use
0.0005
1.41
Circulation 2004

11. Patients Without Recurrence (%)
Ritmus-kontroll?
CTAF Study
100
Amiodarone (n = 201) 80 60
Propafenone (n = 101)
Patients Without Recurrence (%) 40
Sotalol (n = 101) 20
0.0
100
200
300
400
500
600
Days of Follow-up
Roy D, et al. New Engl J Med. 2000;342:913–920.

12. Cox maze III.

13. 1998 Haissaguerre NEJM

14. NEJM 1998

16. Fokális abláció

18. Pulmonális véna izoláció

19. Pulmonális véna izoláció

24. Beavatkozás Anticoaguláns terápia TEE
Intracardialis echocardiographia (ICE)

25. ICE

26. ICE

27. CS LS RA
Map/Abl
AF indukció * 27

29. II LS 1,2 LS 2,3 LS 3,4 LS 4,5 LS 5,6 LS 6,7 LS 7,8 LS 8,9 LS 9,10 Abl
CS 9,10
CS 5,6
CS 1,2

30. Katéter-abláció

31. Késői rekurrencia: 24% Nincs rekurrencia Rekurrencia (N=32) (N=10) p
Persist. AF
16%
50%
0,026
Amio
28%
30%
0,909
Hypertonia
63%
0,482
Diabetes
22%
20%
0,900
ISZB 6%
10%
0,688
Valvularis 3%
0,012
Bal pitvar
49 mm
51 mm
0,468
Bal kamra
54 mm
55 mm
0,373 EF
64%
0,813
Életkor
52 év
60 év
0,031
Előzmény
6,25 év
5,8 év
0,831

33. Randomized Trial of Radiofrequency Ablation versus Antiarrhythmic Drugs as First-Line Treatment of Symptomatic Atrial Fibrillation (RAAFT)
JAMA 2005

34. Ablation for Paroxysmal Atrial Fibrillation (APAF) trial
JACC 2006

35. Catheter ablation versus antiarrhythmic drugs for atrial fibrillation: the A4 study.
cca. 40% required a second ablation
Circulation 2008

36. Candidates in whom to consider first-line ablation for atrial fibrillation
From:   Verma: Curr Opin Cardiol, Volume 23(1).January –8

37. dronedarone

40. CHADS2 score Condition Points C Congestive heart failure 1 H
 Hypertension (or treated hypertension)  A
 Age >75 years  D
 Diabetes
 S2
 Prior Stroke or TIA 2

41. CHADS score
Treatment with Coumadin reduces the risk of stroke in atrial fibrillation by about 2/3 (66%,)
and treatment with aspirin reduces the risk by 1/4 (25%). The risk that anticoagulation will
produce a major bleeding episode varies depending on the patient's medical problems and the
care with which the protime or INR (i.e., the "thinness" of the blood) is monitored, but
generally is less than 1 - 2% per year.
Based on all this information, the developers of the CHADS model recommend strongly
considering therapy with Coumadin for anybody whose CHADS score is 1 or higher. Certainly,
most patients with CHADS scores of 2 or higher stand a strong chance of benefitting from
anticoagulation.
Precautions in using the CHADS model
The CHADS model was developed by studying the records of 1733 Medicare beneficiaries aged
65 to 95, and in this age group the model appears very accurate at predicting stroke risk.
How well the CHADS model works for younger patients is not entirely clear, however, since the
data was gathered for elderly patients. The model is not valid at all for individuals with the
valve disease called mitral stenosis - these patients have a very high risk of stroke, and
virtually all of them should take anticoagulation therapy. 41

43. Dabigatran