Subscribe to RSS
DOI: 10.1055/s-0031-1292035
© Georg Thieme Verlag KG Stuttgart · New York
Remodeling durch Vorhofflimmern und klinische Implikationen für die Kardioversion
Remodeling by atrial fibrillation: clinical implications for cardioversionPublication History
eingereicht: 25.3.2011
akzeptiert: 30.6.2011
Publication Date:
18 October 2011 (online)

Zusammenfassung
Vorhofflimmern (VHF) tritt zumeist in vorerkrankten Herzen auf. Es führt jedoch auch selbst zu beträchtlichen Umbauvorgängen („Remodeling“), insbesondere der Herzvorhöfe. Diese Vorgänge geschehen zeitabhängig, und es wurden elektrische, kontraktile, endotheliale und strukturelle Remodeling-Prozesse beschrieben. Die medikamentöse Therapie des VHF umfasst neben einer effektiven Antikoagulation gemäß der aktuellen Risikostratifikations-Systeme (CHADS2 oder CHA2DS2VASc) zunächst eine frequenzkontrollierende Behandlung. Sollten Patienten hiernach weiterhin symptomatisch bleiben, ist eine rhythmuskontrollierende Therapie indiziert. Um den Sinusrhythmus zu re-etablieren, kann eine Kardioversion (elektrisch oder pharmakologisch) durchgeführt werden. Die elektrische Kardioversion ist hoch-effektiv, erfordert jedoch eine Sedierung/Narkose zur Durchführung, pharmakologische Kardioversion sollte nur bei hämodynamisch stabilen Patienten mit kurzanhaltendem (< 48 Stunden) VHF durchgeführt werden. Es stehen verschiedene antiarrhythmische Substanzen (Amiodaron, Flecainid, Propafenon und das jüngst zugelassene vorhofselektive Antiarrhythmikum Vernakalant) zur pharmakologischen Kardioversion zur Verfügung. Während Amiodaron nur eine geringe Effektivität für eine rasche Kardioversion aufweist, kann es bei Patienten mit Herzinsuffizienz oder relevanter struktureller Herzerkrankung eingesetzt werden. Klasse-I-Antiarrhythmika können nur bei Patienten ohne relevante strukturelle Herzkrankheit eingesetzt werden, jedoch ist der Wirkeintritt im Vergleich zu Amiodaron rascher. Vernakalant kann bei stabilen Patienten mit struktureller Herzerkrankung angewandt werden und ist eine neue alternative Therapieoption zur raschen pharmakologischen Kardioversion.
Abstract
Atrial fibrillation (AF) most often occurs in pre-diseased hearts. On the other hand substantial alterations (particularly atrial) are induced by the arrhythmia itself. Such remodeling occurs in a time-dependent manner. Remodeling of electrical, contractile, endothelial and structural properties / components has been reported. Medical treatment of AF importantly comprises anticoagulation according to risk stratification scores (CHADS2 or CHA2DS2VASc) besides rate control measures. In patients who remain syptomatic despite rate control a rhythm control strategy is indicated. In order to re-establish sinus rhythm patients may undergo electrical or pharmacological cardioversion. Electrical cardioversion is highly efficient but requires conscious sedation, pharmacological cardioversion should only be performed in hemodynamically stable patients with recent (< 48 h) onset AF. Several anti-arrhythmic options exist for pharmacological cardioversion (amiodarone, flecainide, propafenone and the recently approved atrial-specific agent vernakalant). While amiodarone has low efficacy for rapid restoration of sinus rhythm, it can be given to patients with heart failure or significant structural heart disease. Class-I substances can only be applied to patients without significant structural heart disease but onset of action is more rapid. Vernakalant can be applied to hemodynamically stable patients with structural heart disease and represents a novel alternative option for rapid pharmacological cardioversion.
Schlüsselwörter
Vorhofflimmern - Kardioversion - vorhofselektive Antiarrhythmika
Keywords
atrial fibrillation - cardioversion - atrial-specific drugs
Literatur
- 1
Alboni P. et al .
Outpatient treatment of recent-onset atrial
fibrillation with the „pill-in-the-pocket“ approach.
N Engl J Med.
2004;
351
2384-2391
MissingFormLabel
- 2
Allessie M A. et al .
Pathophysiology and prevention of atrial
fibrillation.
Circulation.
2001;
103
769-777
MissingFormLabel
- 3
Burstein B, Nattel S.
Atrial fibrosis: mechanisms
and clinical relevance in atrial fibrillation.
J Am Coll
Cardiol.
2008;
51
802-809
MissingFormLabel
- 4
Camm A J. et al .
Guidelines for the management of atrial
fibrillation.
Eur Heart J.
2010;
31
2369-2429
MissingFormLabel
- 5
Chevalier P. et al .
Amiodarone versus placebo and classic drugs
for cardioversion of recent-onset atrial fibrillation.
J
Am Coll Cardiol.
2003;
41
255-262
MissingFormLabel
- 6
Chung M K. et al .
C-reactive protein elevation in patients
with atrial arrhythmias: inflammatory mechanisms and persistence
of atrial fibrillation.
Circulation.
2001;
104
2886-2891
MissingFormLabel
- 7
Coplen S E. et al .
Efficacy and safety of quinidine therapy
for maintenance of sinus rhythm after cardioversion.
Circulation.
1990;
82
1106-1116
MissingFormLabel
- 8
Corley S D. et al .
Relationships between sinus rhythm, treatment,
and survival in the Atrial Fibrillation Follow-Up Investigation
of Rhythm Management (AFFIRM) Study.
Circulation.
2004;
109
1509-1513
MissingFormLabel
- 9
de Denus S. et al .
Rate vs rhythm control in patients with
atrial fibrillation.
Arch Intern Med.
2005;
165
258-262
MissingFormLabel
- 10
Dernellis J, Panaretou M.
Relationship between
C-reactive protein concentrations during glucocorticoid therapy
and recurrent atrial fibrillation.
Eur Heart J.
2004;
25
1100-1107
MissingFormLabel
- 11
Dittrich H C. et al .
Echocardiographic and clinical predictors
for outcome of elective cardioversion of atrial fibrillation.
Am J Cardiol.
1989;
63
193-197
MissingFormLabel
- 12
Dobrev D.
Cardiomyocyte Ca2+ overload in atrial tachycardia:
is blockade of L-type Ca2+ channels a promising approach
to prevent electrical remodeling and arrhythmogenesis?.
Naunyn
Schmiedebergs Arch Pharmacol.
2007;
376
227-230
MissingFormLabel
- 13
Dobrev D.
Atrial Ca2+ signaling in atrial fibrillation as an
antiarrhythmic drug target.
Naunyn Schmiedebergs Arch
Pharmacol.
2010;
381
195-206
MissingFormLabel
- 14
Duggan S T, Scott L J.
Intravenous
vernakalant: a review of its use in the management of recent-onset
atrial fibrillation.
Drugs.
2011;
71
237-252
MissingFormLabel
- 15
Echt D S. et al .
Mortality and morbidity in patients receiving
encainide, felcainide, or placebo.
N Engl J Med.
1991;
324
781-788
MissingFormLabel
- 16
Ehrlich J R. et al .
Atrial-selective approaches for the treatment
of atrial fibrillation.
J Am Coll Cardiol.
2008;
51
787-792
MissingFormLabel
- 17
Ehrlich J R, Hohnloser S H.
Milestones
in the management of atrial fibrillation.
Heart Rhythm.
2009;
6
S62-S67
MissingFormLabel
- 18
Ehrlich J R, Nattel S, Hohnloser S H.
Atrial fibrillation and congestive heart failure: specific considerations
at the intersection of two common and important cardiac disease
sets.
J Cardiovasc Electrophysiol.
2002;
13
399-405
MissingFormLabel
- 19
Fenster P E. et al .
Conversion of atrial fibrillation to sinus
rhythm by acute intravenous procainamide infusion.
Am
Heart J.
1983;
106
501-504
MissingFormLabel
- 20
Fresco C, Proclemer A, for t he
PAFIT 2 Investigators.
Management of recent onset
atrial fibrillation.
Eur Heart J.
1996;
17
41-47
MissingFormLabel
- 21
Goette A, Bukowska A, Lendeckel U.
Non-ion channel blockers as anti-arrhythmic drugs (reversal
of structural remodeling).
Curr Opin Pharmacol.
2007;
7
219-224
MissingFormLabel
- 22
Hammwohner M. et al .
Platelet expression of CD40/CD40
ligand and its relation to inflammatory markers and adhesion molecules
in patients with atrial fibrillation.
Exp Biol Med (Maywood
).
2007;
232
581-589
MissingFormLabel
- 23
Jahangir A. et al .
Long-term progression and outcomes with
aging in patients with lone atrial fibrillation.
Circulation.
2007;
115
3050-3056
MissingFormLabel
- 24
Khan I A.
Single oral loading dose of propafenone for pharmacological
cardioversion of recent-onset atrial fibrillation.
J Am
Coll Cardiol.
2001;
37
542-547
MissingFormLabel
- 25
Kneller J, Leon J, Nattel S.
How do class 1 antiarrhythmic drugs terminate atrial fibrillation?.
Circulation.
2001;
104
5
MissingFormLabel
- 26
Logan W F. et al .
Left atrial activity folowing cardioversion.
Lancet.
1965;
2
471-473
MissingFormLabel
- 27
Nattel S.
New ideas about atrial fibrillation 50 years on.
Nature.
2002;
415
219-226
MissingFormLabel
- 28
Nishida K. et al .
Mechanisms of atrial tachyarrhythmias associated
with coronary artery occlusion in a chronic canine model.
Circulation.
2011;
123
137-146
MissingFormLabel
- 29
Reisinger J. et al .
Prospective comparison of flecainide versus
sotalol for immediate cardioversion of atrial fibrillation.
Am
J Cardiol.
1998;
81
1450-1454
MissingFormLabel
- 30
Roy D. et
al .
Vernakalant hydrochloride for rapid conversion
of atrial fibrillation.
Circulation.
2008;
117
1518-1525
MissingFormLabel
- 31
Roy D. et
al .
Amiodarone to prevent recurrence of atrial fibrillation.
N Engl J Med.
2000;
342
913-920
MissingFormLabel
- 32
Roy D. et
al .
Rhythm control versus rate control for atrial fibrillation
and heart failure.
N Engl J Med.
2008;
358
2667-2677
MissingFormLabel
- 33
Schotten U. et al .
Pathophysiological mechanisms of atrial
fibrillation: a translational appraisal.
Physiol Rev.
2011;
91
265-325
MissingFormLabel
- 34
Singh S N. et al .
Amiodarone in patients with congestive
heart failure and asymptomatic ventricular arrhythmia.
N
Engl J Med.
1995;
333
77-82
MissingFormLabel
- 35
The Atrial Fibrillation Follow-up
Investigation of Rhythm Management (AFFIRM) Investigators .
A Comparison of Rate Control and Rhythm Control in Patients
with Atrial Fibrillation.
New Engl J Med.
2002;
347
1825-1833
MissingFormLabel
- 36
Wijffels M C. et al .
Atrial fibrillation begets atrial fibrillation:
a study in awake chronically instrumented goats.
Circulation.
1995;
92
1954-1968
MissingFormLabel
PD Dr. med. Joachim R. Ehrlich
Abt. für Kardiologie, klinische Elektrophysiologie
Universitätsklinikum
Theodor Stern Kai 7
60590 Frankfurt
Phone: 069/6301-5579
Fax: 069/6301-6517
Email: j.ehrlich@em.uni-frankfurt.de
Professor Dr. med. Andreas Götte
Medizinische Klinik II, Kardiologie und Internistische Intensivmedizin
St. Vincenz-Krankenhaus GmbH
Am Busdorf 2
33098 Paderborn
Phone: 05251/86-1651
Fax: 05251/86-1652
Email: Andreas.Goette@med.ovgu.de