Q J Med 2003; 96: 881-892
© Association of Physicians 2003; all rights reserved.
Review |
Rate or rhythm control in persistent atrial fibrillation?
From the 1Department of Cardiology, Portsmouth Hospitals NHS Trust, Portsmouth, UK, 2Department of Internal Medicine II, Klinikum Lippe, Detmold, Germany, and 3Department of Cardiology, Victoria Hospital, Blackpool, UK
 |
Summary |
|---|
 Top Summary IntroductionRate versus rhythm control:...Patterns of atrial fibrillationOptions for rhythm controlOptions for rate controlTrials of rate versus...ConclusionReferences |
|---|
Atrial fibrillation (AF) is the most common sustained tachyarrhythmia encountered in clinical practice, with the majority of patients aged > 65 years. With an increasingly ageing population, the burden of AF in society continues to rise. One of the principal controversies in AF management is whether to control the ventricular rate and accept the underlying rhythm, or to attempt to achieve sinus rhythm. Until recently there were no clinical trial data directly comparing a rate versus rhythm strategy, and most physicians have opted for rhythm control, based on its theoretical benefits. We present an up-to-date evidence-based overview of the relative merits of rate versus rhythm control in AF, including data from five recent randomized trials. We draw conclusions from these studies and present evidence-based guidance on when to adopt which approach in routine clinical practice.
|
Introduction |
|---|
|
TopSummaryIntroductionRate versus rhythm control:...Patterns of atrial fibrillationOptions for rhythm controlOptions for rate controlTrials of rate versus...ConclusionReferences |
|---|
Atrial fibrillation is the most common sustained tachyarrhythmia encountered in clinical practice,1 with an incidence that doubles with every decade after 55 years of age.2 With an ageing population and improved survival of patients with cardiac disease, its prevalence continues to rise to epidemic proportions.3 Currently about 70% of patients with atrial fibrillation are aged between 65 and 85 years,4 with a population prevalence of 5% in individuals aged > 65 years,5 rising to 9% in those aged > 80 years.6 Atrial fibrillation is associated with a doubling of overall morbidity and mortality from cardiovascular disease6 and is the most common cause of embolic stroke. Three basic principles have formed the cornerstone of treatment for persistent atrial fibrillation: rate control, rhythm control with restoration and maintenance of sinus rhythm, and the prevention of stroke.
|
Rate versus rhythm control: the dilemma |
|---|
|
TopSummaryIntroductionRate versus rhythm control:...Patterns of atrial fibrillationOptions for rhythm controlOptions for rate controlTrials of rate versus...ConclusionReferences |
|---|
In any given patient with persistent atrial fibrillation, the basic therapeutic yet highly controversial question is whether to try to establish sinus rhythm or to leave the patient in atrial fibrillation and control the rate.7 Most physicians have traditionally opted for rhythm control with cardioversion and anti-arrhythmic drug therapy, despite a paucity of evidence to support this strategy.8
Sinus rhythm holds several theoretical advantages: reduced risk of thromboembolism and the need for chronic anticoagulation; improved haemodynamics (with restoration of ‘atrial kick’) and patient quality of life;9 the prevention of persistently rapid ventricular rates leading to tachycardia-mediated cardiomyopathy;10 and finally prevention of atrial structural remodelling (with increased atrial size) and consequent atrial cardiomyopathy.11 However, currently available anti-arrhythmic drugs often have a high side-effect profile, with limited efficacy both for chemical cardioversion and maintaining patients in sinus rhythm after successful electrical cardioversion.12–14
In this review we address the current treatment options aimed at both rate and rhythm control. In addition we present data from five recent randomized trials comparing these two strategies.15–19 Several evidence-based conclusions are drawn, and guidance given to direct AF management in the light of this new evidence.
|
Patterns of atrial fibrillation |
|---|
|
TopSummaryIntroductionRate versus rhythm control:...Patterns of atrial fibrillationOptions for rhythm controlOptions for rate controlTrials of rate versus...ConclusionReferences |
|---|
Atrial fibrillation (AF) is most commonly classified according to its temporal pattern (Figure 1).14,20 Faced with a first detected episode of atrial fibrillation, three recognized patterns may develop. (1) Persistent AF, which is the main focus of this article, describes an episode of sustained AF (usually > 7 days) that does not convert to sinus rhythm without medical intervention, with the promise of achieving sinus rhythm either by pharmacological or electrical cardioversion. (2) Paroxysmal atrial fibrillation (PAF) refers to self-terminating episodes of AF, usually lasting < 48 h. Both paroxysmal and persistent AF may be recurrent. (3) The term ‘permanent AF’ is reserved for episodes of persistent AF, (usually > 1 year) in which cardioversion is not attempted or is unsuccessful, with AF accepted as the long-term rhythm for that patient.
|
|
Options for rhythm control |
|---|
|
TopSummaryIntroductionRate versus rhythm control:...Patterns of atrial fibrillationOptions for rhythm controlOptions for rate controlTrials of rate versus...ConclusionReferences |
|---|
A. Pharmacological cardioversion for persistent atrial fibrillation
Pharmacological cardioversion is most effective when used within 7 days of the onset of AF, and hence is much less effective in patients with persistent AF.21–23 Anti-arrhythmic drugs have a high side-effect profile, and hospital admission is frequently necessary for their initiation. Defetilide, a class III anti-arrhythmic, is the most recently approved anti-arrhythmic drug (1999) and is among the most rigorously studied. The Symptomatic Atrial Fibrillation Investigative Research on Dofetilide (SAFIRE-D)24 and the European and Austrialian Multicenter Evaluative Research in Atrial Fibrillation (EMERALD)25 studies found dofetilide to be superior to placebo (SAFIRE-D) and to low-dose sotalol (EMERALD) in converting patients with persistent AF to sinus rhythm. However, conversion rates were still relatively low (approximately 30%). Furthermore, torsade de pointe is a serious but infrequent (< 3%) side–effect of dofetilide therapy (most episodes occur within 72 h of initiation of therapy). Other than dofetilide, amiodarone is the only anti-arrhythmic that has been found safe and effective in patients with moderate to severe left ventricular dysfunction. Like dofetilide, it is a first-line agent for patients with AF and structural heart disease. In the recent First Antiarrhythmic Drug Sub study of the AFFIRM study, amiodarone was found to be more effective at one year than either sotalol or class I agents for the strategy of maintenance of sinus rhythm without cardioversion.26
Further data supporting the efficacy of amiodarone to convert persistent AF sinus rhythm comes from a recent metanalysis.27 Because of its potential for organ toxicity, amiodarone should generally be used as second- or third-line agent for other types of patients with AF.28 Dronedarone, a benzofuran derivative structurally similar to amiodarone but with a markedly improved side-effect profile has great future promise as a replacement for amiodarone.29
B. Direct-current electrical cardioversion
Although direct-current electrical cardioversion for persistent AF has a very high initial success rate of 80–96%,30,31 as few as 23% of patients remain in sinus rhythm at 1 year, and 16% at 2 years.32 In a recent study, the use of anti-arrhythmics and serial electrical cardioversion for early relapse reported sinus rhythm in 53% of patients at 1 year.33 In a similar study only 25% of the patients remained in sinus rhythm at 5 years.34 Amiodarone is the most effective agent at preventing relapse after successful cardioversion, with 69% of patients in sinus rhythm at 1 year in the Canadian Trial of Atrial Fibrillation (CTAF).35 However, in this study amiodarone was discontinued in 25% of patients due to presumed side-effects. Most recurrences of AF occur within 3 months of cardioversion for a first episode of AF,36 particularly within the first 5 days.37 Several factors have been defined which predict both lack of success or recurrence of atrial fibrillation after cardioversion. These include increased patient body weight, prolonged duration of AF (> 1–2 years), age > 75 years, heart failure and reduced ejection fraction, increased left atrial dimension, rheumatic heart disease and absence of anti-arrhythmic medication.38–44
Current guidelines recommend that patients who have AF of unknown duration or > 48 h be given warfarin for 3 weeks before and 4 weeks after cardioversion, maintaining an INR of 2.0–3.0.14,45 A comparable strategy is the use of transoesophageal echocardiography guided cardioversion (TEE). Data from the ACUTE trial (Assessment of Cardioversion Using Transoesophageal Echocardiography Investigators) showed that patients who had undergone TEE-guided cardioversion had a risk of stroke comparable to the standard management strategy of anticoagulation.46
C. Radiofrequency ablation
The limitations of pharmacological and electrical cardioversion have led to the search for other strategies, including radiofrequency ablation. The majority of AF is initiated by ectopic foci found primarily within the pulmonary veins (PV).47,48 Mapping of this ectopic activity localized it to sleeves of atrial tissue that invest the proximal portions of the pulmonary veins. Further research also showed that catheter-based ablation of these ectopic foci could eradicate episodes of AF.49–52 These findings have catalysed a flood of research interest in this area, with the prospect of a ‘true’ cure for atrial fibrillation. Two primary strategies for the ablation of PV foci have now emerged: (i) electrically-guided focal ablation of PV triggers; and (ii) electrical isolation of the pulmonary vein from the left atrium by way of either segmental or circumferential lesions at the PV ostium.53 At present, circumferential PV isolation (the anatomical approach) appears to offer the greatest success rates with lower procedure times and lower complication rates.54,55 The advent of intracardiac echocardiography has revolutionized radiofrequency ablation by allowing real-time imaging of the highly variable PV ostial anatomy and confirmation of correct catheter position at the PV ostium (thus limiting the risk of pulmonary stenosis). The success rates for radiofrequency ablation are highly variable, but are now approaching 80–90% at one year follow-up in the best centres.56
Further positive data was provided by a recent non-randomized trial of symptomatic AF patients comprising 589 circumferentially ablated patients who were compared with 582 patients who received anti-arrhythmic medications for SR control.57 After a median follow-up of 900 days, there was a significant improvement in mortality, assessment of morbidity, and QoL in ablated patients, compared with those treated with medical therapy. There was no apparent difference in success rates for patients in persistent AF versus those with paroxysmal AF, unlike in previous reports, which had shown much higher success rates for PAF compared with persistent AF.
Limitations of current techniques include a relatively long procedure time, presence of non-PV foci, a high rate of recurrence (leading to the need for repeat procedures), coupled with the risk of symptomatic pulmonary vein stenosis from ablation within the pulmonary veins.58–60 Consequently, at present, given the large patient numbers, limited resources and potential complications, radiofrequency ablation is not the therapy of choice for the majority of patients with AF. Patients should however be considered for PV ablation if they have drug-refractory atrial fibrillation or poor tolerance of drugs.
D. Pacing therapy
Device-based therapy involving specific sites of stimulation combined with overdrive pacing algorithms shows some promise for reducing the incidence of PAF and delaying the development of persistent AF. However, with a myriad of trials of differing design and endpoints, no consensus is currently possible.
E. Surgical treatment
On the basis of the findings that a finite mass of atrial tissue is needed to sustain atrial fibrillation, and that atrial fibrillation is an arrhythmia with multiple re-entrant wavelets, the Maze operation was devised.61,62 In this procedure the atria are dissected into segments, which are then rejoined by suturing, thereby reducing the confluent atrial tissue in which atrial fibrillation wavelets can propagate. Initial mortality rates were high, but with refinement of techniques, recent reports suggest late freedom from AF in 90–98% of patients, with a < 1% risk of thromboembolic events, and excellent quality of life.63–66
|
Options for rate control |
|---|
|
TopSummaryIntroductionRate versus rhythm control:...Patterns of atrial fibrillationOptions for rhythm controlOptions for rate controlTrials of rate versus...ConclusionReferences |
|---|
Definition of adequate rate control
The adequacy of rate control during AF may be judged from clinical symptoms and ECG recordings. The rate has generally been considered controlled when the ventricular response ranges between 60 and 80 bpm at rest and between 90 and 115 bpm during moderate exercise.14,67,68
A. Medical therapy
Digoxin may be acceptable as sole therapy in elderly, sedentary patients.69 However, digoxin is less effective than other agents at controlling ventricular rates, especially during critical illness, exercise or acute AF.70–72 Beta-blockers, verapamil and diltiazem are more effective, and there is synergy between these drugs and digoxin.73,74 In patients with both AF and coronary disease, beta-blockers are the drugs of choice, and they may also be valuable when systolic dysfunction is present. Verapamil may elevate serum digoxin levels into the toxic range, so the dose of digoxin should be reduced if it is used with verapamil.75 Amiodarone is a highly effective rate-controlling agent, however its use is limited by concerns over its long-term side-effect profile. Hence, it should be reserved for patients unable to tolerate the above agents, or where rate control with these agents remains inadequate.76
B. Atrioventricular nodal ablation
Ablation of the atrioventricular (AV) node and implantation of a permanent pacemaker is still a last resort for patients with atrial fibrillation refractory to other treatments. By elimination of AV conduction, the ventricular rate can be completely controlled and regular ventricular contraction restored, both of which might help improve cardiac haemodynamics.77 Since the atria continue to fibrillate, however, atrial contraction and AV synchrony are not restored, and the risk of stroke and need for anticoagulation persist.
In controlled studies of patients with chronic atrial fibrillation and heart failure, ablation of the AV node and insertion of a permanent pacemaker proved more effective than drug treatment in control of palpitations, and improvement of dyspnoea and quality of life, but not cardiac performance.78,79 Mortality was unaffected by the procedure.80 An alternative to complete ablation is modification of the AV node, which is sometimes efficacious in relieving of symptoms and controlling ventricular rate.
|
Trials of rate versus rhythm control |
|---|
|
TopSummaryIntroductionRate versus rhythm control:...Patterns of atrial fibrillationOptions for rhythm controlOptions for rate controlTrials of rate versus...ConclusionReferences |
|---|
Five recent randomized trials have attempted to address the fundamental issue of rate versus rhythm control strategies for optimal management of atrial fibrillation (Table 1).15–19 The results of the ongoing AF-CHF trial are not due to be reported before 2005.81 Important differences between the trials (excluding HOT CAFÉ), as well as differences in the rate versus rhythm control groups are presented for comparison in Tables 1 and 2.
|
|
The PIAF study15
Patients
The PIAF (Pharmacological Intervention in Atrial Fibrillation trial) trial was a multi-centre, randomized trial of 252 patients (aged 18–75 years) with symptomatic atrial fibrillation of between 7 days and 360 days duration.
Treatments
The trial compared rate control (diltiazem was the principle agent used) with rhythm control (amiodarone as the sole pharmacological agent and if necessary electrical cardioversion). All patients received anticoagulation with warfarin, aiming for an INR of 2.0–3.0 throughout the entire study period.
Endpoints
Over the short (1 year) observation period, a similar proportion of patients reported improvement in symptoms (primary endpoint) in both groups (76 responders vs. 70 responders respectively, p = 0.32). Assessment of quality of life, using the Medical Outcomes Study short-form health survey (SF-36) questionnaire82 at baseline and after 12 months, showed no differences between groups. However, there was a higher incidence of hospital admissions (p = 0.001) and adverse drug effects (p = 0.036) in the rhythm control group.
Limitations
This study was small (252 patients), included only symptomatic younger patients (mean age 60 years) and had a short follow-up period (1 year).
The RACE study16
Patients
This larger multi-centre study included 522 patients in persistent atrial fibrillation (
1 year) who had undergone 1–2 electrical cardioversions during the previous 2 years. The patients were on average older than in the PIAF study (mean age 68 years).
Treatments
Patients were randomly assigned (on an intention-to-treat basis) to receive treatment aimed at rate control (target resting heart rate < 100 bpm) or rhythm-control (serial cardioversions and anti-arrhythmic drugs). Ninety percent of the patients in both groups had one or more risk factors for stroke.83–86 Anticoagulation could be stopped or converted to aspirin if patients remained in sinus rhythm > 1 month after cardioversion. In the rate control group, patients < 65 years and without risk factors for stroke could be maintained on aspirin. All other patients were required to remain on warfarin, aiming for an INR of 2.5–3.5.
Endpoints
After a mean (± SD) of 2.3 ± 0.6 years, there was no difference (p = 0.4) in the primary composite endpoint of death from cardiovascular causes, heart failure, thromboembolic complications, bleeding, implantation of a pacemaker, and severe adverse effects of drugs between the rate-control group (44 patients, 17.2%) and the rhythm-control group (60 patients, 22.6%). The distribution of the various components of the primary end point was similar in the rate-control and rhythm-control groups.
Subgroup analysis (not pre-defined) suggested a higher incidence of events (absolute difference) in the rhythm control group for women (21.5%) and hypertensive patients (13.5%). In the rhythm-control group, 103/266 patients (39%) had sinus rhythm, compared with 26/256 patients (10%) in the rate-control group. The majority of patients with thromboembolic events (73%) had atrial fibrillation at the time of the event, and 66% (23/35 patients) of the thromboembolic complications occurred in under-anticoagulated patients (INR < 2).
Limitations
No objective or subjective assessment was carried out of exercise tolerance for the two patient groups.
The AFFIRM study17
Patients
The landmark AFFIRM study is the largest multi-centre, randomized study to date, comparing rate-control with rhythm control (on an intention-to-treat basis) in patients with atrial fibrillation ( 1 year). The inclusion criteria for this study were patients 
65 years of age or < 65 years plus one or more clinical risk factors for stroke: hypertension, diabetes, congestive cardiac failure, transient ischaemic attack, prior cerebrovascular accident or systemic embolism, left atrium 50 mm, shortening fraction < 25%, or left ventricular ejection fraction < 0.40. Cardioversion was allowed prior to randomization, but if the cardioversion was unsuccessful, the patient was excluded.
Treatments
After pharmacological trials of at least two agents in each group, patients were allowed to undergo non-pharmacological therapies. Anticoagulation could be stopped in the rhythm control group if the patient remained in sinus rhythm for a minimum of 4 weeks (preferably 3 months). The target heart rate was < 80 bpm at rest or < 110 bpm after a 6-min walk test.
Endpoints
The primary endpoint was overall mortality. A total of 4060 patients (mean ± SD age 69.7 ± 9.0 years) were enrolled in the study; 70.8% had a history of hypertension, and 38.2% had coronary artery disease. At the 3.5-year study endpoint 60% of patients in the rhythm arm were in sinus rhythm, while rate control (resting heart rate 80 bpm) was achieved in 80% of rate controlled patients, with 85% on warfarin in the rate control group and 70% in the rhythm control group.
There were 356 deaths (primary endpoint) among the patients assigned to rhythm-control therapy and 310 deaths among those assigned to rate-control therapy (mortality at 5 years 23.8% and 21.3%, respectively; p = 0.08), suggesting a trend towards increased mortality with a rhythm control strategy. The survival curves did appear to separate at around 1.5–2 years in favour of the rate control group. There was no difference in the composite secondary endpoint of death, disabling stroke, disabling anoxic encephalopathy, major bleeding and cardiac arrest. In the rhythm-control group, there was a higher rate of patient hospitalization (p < 0.001), and more adverse drug effects. In both groups, the majority of strokes occurred after warfarin had been stopped or when the international normalized ratio was sub-therapeutic, in general agreement with previously reported observations.86 The crossover rate was significantly (p < 0.001) greater among the patients initially assigned to rhythm control (594 patients, actual crossover rate of 37.5% at 5 years) than among patients assigned to rate control (248, actual crossover rate of 14.9% after 5 years), in keeping with the fact that drug therapies aimed at achieving rhythm control are frequently unsuccessful.87–89
Limitations
The high prevalence of sinus rhythm seen in this study compared to the other studies reflects the inclusion of patients with PAF. Also this is the only study to include patients after (rather than before as in the other studies) successful cardioversion with 54% of patients in sinus rhythm at inclusion.
The STAF pilot study18
Patients
The STAF pilot study randomized 200 patients (intention-to-treat basis) with AF of 2 years duration to rate control or rhythm control.
Treatments
The STAF trial was aimed at patients at moderate-to-high risk of AF recurrence. Oral anticoagulation was prescribed in both treatment strategies, according to the guidelines of the American College of Chest Physicians.90
Endpoints
The primary endpoint was a composite of death, stroke or transient ischaemic attack, cardiopulmonary resuscitation, or systemic embolism. After 19.6 ± 8.9 months, there was no difference between the two treatment groups in terms of the primary endpoint (p = 0.99). With the exception of increased hospitalization in the rhythm control group (p < 0.001), there was no difference in the other secondary endpoints of syncope, bleeding (requiring hospitalization/transfusion or both), quality of life (assessed by SF-36), echocardiographic parameters (left ventricular end-systolic diameter, left ventricle end-diastolic diameter, left ventricle ejection fraction, left atrial diameter), resting heart rate and maintenance of sinus rhythm at follow up. After 3 years follow-up, only a minority (23%) of this group of patients at increased risk of AF recurrence remained in sinus rhythm in the rhythm control group, in-spite of up to four cardioversions per patient and up to four anti-arrhythmic drugs.
Limitations
This was a small study (200 patients), but had a long follow-up period.
The HOT CAFÉ study19
Patients
In the recently presented HOT CAFÉ study, 205 patients (aged 50–75 years) in persistent AF ( 2 years) were randomized to either rate or rhythm control.
Treatments
The treatment goal in the rate control group was medical rate control (monitored by 24-h holter) with rhythm control achieved by the use of DC cardioversion with serial anti-arrhythmic use.
Endpoints
At the 1 year endpoint there was a higher incidence of hospital admission in the rhythm-control arm (12% vs. 74%; p < 0.0001), despite a measurably significant improvement in exercise tolerance, as assessed by maximal workload during a treadmill test (5.2 ± 5.1 vs. 7.6 ± 3.3 MET; p < 0.0001). As in the other trials, there was a tendency for higher stroke rates with rhythm control than with rate control (three vs. no cases). After 12 months, 75% of patients were in sinus rhythm in the rhythm control group.
Limitations
This is a small study with a short follow-up period, and has not yet been published in full.
Conclusions from these five studies
Consensus
The five recently reported studies consistently show little difference in clinical outcomes between a rate and rhythm control strategy for patients, either in persistent atrial fibrillation or at a high risk of recurrence. However, a rate control strategy is associated with fewer hospitalizations and less adverse drug effects, compared to a rhythm control strategy. Despite unavailability of individual cost analysis comparing the two different treatment strategies, it is likely that a rate control strategy will prove more cost-effective. Sinus rhythm was difficult to maintain in the long term in all five studies, and crossover rates were high, particularly among patients initially randomized to a rhythm control strategy.
Limitations
It is important to be aware that the results of these recent studies are only directly applicable to AF cases where initially either a rate or rhythm control strategy was felt appropriate. These studies do not therefore close the debate on AF management. Furthermore, these studies have tended to exclude several subgroups of AF patients, including younger patients (< 65 years) in persistent AF, patients without structural heart disease and patients with severe heart failure. In these patients, a primary rhythm control strategy may still be appropriate. In addition, for patients who remain markedly symptomatic despite adequate rate control, or where adequate rate control cannot be adequately achieved, a rhythm control approach including PV ablation should be considered.91
Anticoagulation
At present warfarin is the most consistent therapy that has been shown to improve survival of patients in atrial fibrillation. Adjusted-dose oral anticoagulation is more efficacious than aspirin for prevention of stroke in patients with AF, as suggested by indirect comparisons and by a 33% reduction in a meta-analysis of five randomized trials.92 Data from the rate versus rhythm control studies further stress the importance of maintaining therapeutic anticoagulation long after the restoration of sinus rhythm. This is important for several reasons: current strategies to maintain sinus rhythm are successful only in a minority of patients;93–95 sinus rhythm itself does not guarantee freedom from stroke, as the majority of AF patients, whether in sinus rhythm or not, have at least one additional risk factor for stroke; and finally the subclinical burden of AF is not known for patients who appear to be in sinus rhythm but are at high risk of AF recurrence.
Data from the AFFIRM study provide additional support for recommending long term warfarin therapy to the following patients with AF, even if sinus rhythm is restored: patients 65 years of age or < 65 years plus one or more clinical risk factors for stroke: hypertension, diabetes, congestive cardiac failure, transient ischaemic attack, prior cerebrovascular accident or systemic embolism, left atrium 50 mm, shortening fraction < 25%, or left ventricular ejection fraction < 0.40.
To those for whom the prospect of long-term warfarin therapy seems unappealing, the new oral anticoagulant Ximelagatran shows significant potential. With Ximelagatran there is no need for INR monitoring or dose adjustment, and preliminary data from the recent SPORTIF studies are promising.96,97
Cost analysis
A very recent retrospective cost analysis performed on patients entered into the HOT CAFÉ study has shown that rhythm control is significantly more costly than ventricular control.98
|
Conclusion |
|---|
|
TopSummaryIntroductionRate versus rhythm control:...Patterns of atrial fibrillationOptions for rhythm controlOptions for rate controlTrials of rate versus...ConclusionReferences |
|---|
At present a primary rate control strategy represents an acceptable evidence-based treatment option for a broad group of patients in persistent AF. Rate control may involve non-pharmacological interventions, such as AV node ablation with pacemaker insertion, in a minority of patients. The available data, particularly from AFFIRM, have allowed us to provide evidence-based guidance on which patients should be considered for a rate control strategy (Table 3).
|
|
Footnotes |
|---|
Address correspondence to Dr C.J. Boos, Department of Cardiology, Portsmouth Hospitals NHS Trust, Milton Rd, Portsmouth, Hampshire PO3 AD. e-mail: christopherboos{at}hotmail.com
|
References |
|---|
|
TopSummaryIntroductionRate versus rhythm control:...Patterns of atrial fibrillationOptions for rhythm controlOptions for rate controlTrials of rate versus...ConclusionReferences |
|---|
1. Prystowsky EN, Benson DW Jr, Fuster V, Hart RG, Kay GN, Myerburg RJ, Naccarelli GV, Wyse DG. Management of patients with atrial fibrillation. A Statement for Healthcare Professionals. From the Subcommittee on Electrocardiography and Electrophysiology, American Heart Association. Circulation 1996; 6:1262–77.
2. Benjamin EJ, Levy D, Vaziri SM, D’Agostino RB, Belanger AJ, Wolf PA. Independent risk factors for atrial fibrillation in a population-based cohort. The Framingham Heart Study. JAMA 1994; 271:840–4.
3. Braunwald E. Shattuck lecture- Cardiovascular medicine at the turn of the millennium: triumphs, concerns, and opportunities. N Engl J Med 1997; 337:1360–9.
4. Feinberg WM, Blackshear JL, Laupacis A, Kronmal R, Hart RG. Prevalence, age distribution, and gender of patients with atrial fibrillation. Analysis and implications. Arch Intern Med 1995; 155:469–3.
5. Kannel WB, Wolf PA, Benjamin EJ, Levy D. Prevalence, incidence, prognosis, and predisposing conditions for atrial fibrillation: population-based estimates. Am J Cardiol 1998; 82:2N.[CrossRef][Web of Science][Medline]
6. Go AS, Hylek EM, Phillips KA, Chang Y, Henault LE, Selby JV, Singer DE. Prevalence of diagnosed atrial fibrillation in adults: national implications for rhythm management and stroke prevention: the AnTicoagulation and Risk Factors in Atrial Fibrillation (ATRIA) Study. JAMA 2001; 285:2370–5.
7. Carlsson J, Neuzner J, Rosenberg YD. Therapy of atrial fibrillation: Rhythm control versus rate control. Pacing Clin Electrophysiol 2000; 23:891–903.[CrossRef][Medline]
8. Brodsky MA, Chun JG, Podrid PJ, Douban S, Allen BJ, Cygan R. Regional attitudes of generalists, specialists, and sub specialists about management of atrial fibrillation. Arch Intern Med 1996; 156:2553–62.
9. Donahue TP, Conti JB. Atrial fibrillation: rate control versus maintenance of sinus rhythm. Curr Opin Cardiol 2001; 16:46–53.[CrossRef][Web of Science][Medline]
10. Redfield MM, Kay GN, Jenkins LS, Mianulli M, Jensen DN, Ellenbogen KA. Tachycardia-related cardiomyopathy: a common cause of ventricular dysfunction in patients with atrial fibrillation referred for atrioventricular ablation. Mayo Clin Proc 2000; 75:790–5.[Abstract]
11. Petersen P, Kastrup J, Brinch K, Godtfredsen J, Boysen G. Relation between left atrial dimension and duration of atrial fibrillation. Am J Cardiol 1987; 60:382–4.[CrossRef][Web of Science][Medline]
12. Aronow WS. Atrial fibrillation. Heart Dis 2002; 4:91–101.[CrossRef][Medline]
13. Brodsky MA, Allen BJ, Walker CJ 3rd, Casey TP, Luckett CR, Henry WL. Amiodarone for maintenance of sinus rhythm after cardioversion of atrial fibrillation in the setting of a dilated left atrium. Am J Cardiol 1987; 60:572–5.[CrossRef][Web of Science][Medline]
14. Fuster V, Ryden LE, Asinger RW, et al. ACC/AHA/ESC guidelines for the management of patients with atrial fibrillation. A report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines and the European Society of Cardiology Committee for Practice Guidelines and Policy Conferences (Committee to develop guidelines for the management of patients with atrial fibrillation) developed in collaboration with the North American Society of Pacing and Electrophysiology. Eur Heart J 2001; 22:1852–923.
15. Hohnloser SH, Kuck KH, Lilienthal J. Rhythm or rate control in atrial fibrillation-Pharmacological Intervention in Atrial Fibrillation (PIAF): a randomised trial. Lancet 2000; 356:1789–94.[CrossRef][Web of Science][Medline]
16. Van Gelder IC, Hagens VE, Bosker HA, et al. Rate Control versus Electrical Cardioversion for Persistent Atrial Fibrillation (RACE) Study Group. N Engl J Med 2002; 347:1834–40.
17. Wyse DG, Waldo AL, DiMarco JP, Domanski MJ, Rosenberg Y, Schron EB, Kellen JC, Greene HL, Mickel MC, Dalquist JE, Corley SD. The Atrial Fibrillation Follow-up Investigation of Rhythm Management (AFFIRM) Investigators. A comparison of rate control and rhythm control in patients with atrial fibrillation. N Engl J Med 2002; 347:825–33.
18. Carlsson J, Miketic S, Windeler J, Cuneo A, Haun S, Micus S, Walter S, Tebbe U. STAF Investigators. Randomised trial of rate-control versus rhythm-control in persistent atrial fibrillations: STAF (Strategies of Treatment of Atrial Fibrillation) study. J Am Coll Cardiol 2003; 41:1690–6.
19. Opolski G, Torbicki A, Kosior D, Szulc M, Zawadzka M, Pierscinska M, Kolodziej P, Stopinski M, Achremczyk P, Wozakowska-Kaplon B, Rabczenko D. Rhythm control versus rate control in patients with persistent arial fibrillation. Results of the HOT CAFÉ Polish study. Kardiol Pol 2003; 59:1–16.
20. Gallagher MM, Camm AJ. Classification of atrial fibrillation. Pacing Clin Electrophysiol 1997; 20:1603–5.[CrossRef][Medline]
21. Borgeat A, Goy JJ, Maendly R, Kaufmann U, Grbic M, Sigwart U. Flecainide versus quinidine for conversion of atrial fibrillation to sinus rhythm. Am J Cardiol 1986; 58:496–8.[CrossRef][Web of Science][Medline]
22. Suttorp MJ, Kingma JH, Lie-A-Huen L, Mast EG. Intravenous flecainide versus verapamil for acute cardioversion of paroxysmal atrial fibrillation or flutter to sinus rhythm. Am J Cardiol 1989; 63:93–6.
23. Suttorp MJ, Kingma JH, Jessurun ER, et al. The value of class IC antiarrhythmic drugs for acute cardioversion of paroxysmal atrial fibrillation or flutter to sinus rhythm. Am J Cardiol 1990; 16:1722–7.
24. Singh S, Zoble RG, Yellen L, Brodsky MA, Feld GK, Berk M, Billing CB Jr. Efficacy and safety of oral dofetilide in converting to and maintaining sinus rhythm in patients with chronic atrial fibrillation or atrial flutter: the symptomatic atrial fibrillation investigative research on dofetilide (SAFIRE-D) study. Circulation 2000; 102:2385–90.
25. Greenbaum R, Campbell TJ, Channer KS. Conversion of atrial fibrillation and maintenance of sinus rhythm by dofetelide the EMERALD study. Circulation 1998; 989 (suppl. I):1–633.
26. Maintenance of sinus rhythm in patients with atrial fibrillation: an AFFIRM substudy of the first antiarrhythmic drug. AFFIRM First Antiarrhythmic Drug Substudy Investigators. J Am Coll Cardiol 2003; 42:20–9.
27. Letelier LM, Udol K, Ena J, Weaver B, Guyatt GH. Effectiveness of amiodarone for conversion of atrial fibrillation to sinus rhythm. Arch Intern Med 2003; 163:777–85.
28. Martin DO. Managing chronic atrial fibrillation: strategies to control symptoms and prevent embolism. Cleve Clin J Med 2003; 70 Suppl 3:S30–3.[Medline]
29. Touboul P, Brugada J, Capucci A, Crijns HJ, Edvardsson N, Hohnloser SH. Dronedarone for prevention of atrial fibrillation: A dose-ranging study. Eur Heart J 2003; 24:1481–7.
30. Dalzell GW, Anderson J, Adgey AA. Factors determining success and energy requirements for cardioversion of atrial fibrillation. Q J Med 1990; 76:903–13.[Web of Science][Medline]
31. Boos C, Thomas M, Jones A, Clarke E, Wilbourne G, More R. Higher Energy Monophasic DC Cardioversion for Persistent Atrial Fibrillation: Is it Time to Start at 360 Joules? Ann Noninvasive Electrocardiol 2003; 8:121–126.[CrossRef][Web of Science][Medline]
32. Lundstrom T, Ryden L. Chronic atrial fibrillation. Long-term results of direct current cardioversion. Acta Med Scand 1988; 223:53–9.[Web of Science][Medline]
33. Bertaglia E, D’Este D, Zerbo F, Zoppo F, Delise P, Pascotto P. Success of serial external electrical cardioversion of persistent atrial fibrillation in maintaining sinus rhythm. A randomized study. Eur Heart J 2002; 23:1522–8.
34. Van Gelder IC, Crijns HJ, Tieleman RG, Brugemann J, De Kam PJ, Gosselink AT, Verheugt FW, Lie KI. Chronic atrial fibrillation. Success of serial cardioversion therapy and safety of oral anticoagulation. Arch Intern Med 1996; 156:2585–92.
35. Roy D, Talajic M, Dorian P, Connolly S, Eisenberg MJ, Green M, Kus T, Lambert J, Dubuc M, Gagne P, Nattel S, Thibault B. Amiodarone to prevent recurrence of atrial fibrillation. Canadian Trial of atrial Fibrillation Investigators. N Engl J Med 2000; 342:913–20.
36. Van Gelder IC, Crijns HJ, Van Gilst WH, Verwer R, Lie KI. Prediction of uneventful cardioversion and maintenance of sinus rhythm from direct-current electrical cardioversion of chronic atrial fibrillation and flutter. Am J Cardol 1991; 68:41–6.
37. Tieleman RG, Van Gelder IC, Crijns HJ, De Kam PJ, Van Den Berg MP, Haaksma J, Van Der Woude HJ, Allessie MA. Early recurrences of atrial fibrillation after electrical cardioversion: a result of fibrillation-induced electrical remodeling of the atria. J Am Coll Cardiol 1998; 31:167–73.
38. Frick M, Frykman V, Jensen-Urstad M, Ostergren J, Rosenqvist M. Factors predicting success rate and recurrence of atrial fibrillation after first electrical cardioversion in patients with persistent atrial fibrillation. Clin Cardiol 2001; 24:238–44.[Web of Science][Medline]
39. Dittrich HC, Erickson JS, Schneiderman T, Blacky AR, Savides T, Nicod PH. Echocardiographic and clinical predictors for outcome of elective cardioversion of atrial fibrillation. Am J Cardiol 1989; 63:193–7.[CrossRef][Web of Science][Medline]
40. Coro L, Delise P, Bertaglia E, Mozzato MG, Fantinel M, Bilardo G, D’Este D, Pascotto P. The duration of atrial fibrillation influences the long-term efficacy of low-energy internal cardioversion. Ital Heart J 2001; 2:388–93.[Medline]
41. Duytschaever M, Haerynck F, Tavernier R, et al. Factors influencing long term persistence of sinus rhythm after a first electrical cardioversion for atrial fibrillation. Pacing Clin Electrophysiol 1998; 21(1 Pt 2):284–7.[CrossRef][Medline]
42. Di Pasquale G, Biancoli S, Sassone B, et al. Atrial Fibrillation. Always Cardioversion? No. Ital Heart J 2002; 3(1 suppl):81–90.[Medline]
43. Houghton AR, Sharman A, Pohl JE. Determinants of successful direct current cardioversion for atrial fibrillation and flutter: the importance of rapid referral. Br J Gen Pract 2000; 50:710–11.[Web of Science][Medline]
44. Okcun B, Yigit Z, Kucukoglu MS, Mutlu H, Sansoy V, Guzelsoy D, Uner S. Predictors for maintenance of sinus rhythm after cardioversion in patients with nonvalvular atrial fibrillation. Echocardiography 2002; 19:351–7.[CrossRef][Web of Science][Medline]
45. Hylek EM, Skates SJ, Sheehan MA and Singer DE. An analysis of the lowest effective intensity of prophylactic anticoagulation in for patients with nonrheumatic atrial fibrillation. N Engl J Med 1996; 335:540–6.
46. Asher CR, Klein AL. The ACUTE trial. Transesophageal echocardiography to guide electrical cardioversion in atrial fibrillation. Assessment of Cardioversion Using Transesophageal Echocardiography. Cleve Clin J Med 2002; 69:713–18.
47. Haissaguerre M, Jais P, Shah DC, Takahashi A, Hocini M, Quiniou G, Garrigue S, Le Mouroux A, Le Metayer P, Clementy J. Spontaneous initiation of atrial fibrillation by ectopic beats originating in the pulmonary veins. N Engl J Med 1998; 339:659–66.
48. Chen SA, Tai CT, Tsai CF, Hsieh MH, Ding YA, Chang MS. Radiofrequency catheter ablation of atrial fibrillation initiated by pulmonary vein ectopic beats. Cardiovasc Electrophysiol 2000; 11:218–27.
49. Lau CP, Tse HF, Ayers GM. Defibrillation-guided radiofrequency ablation of atrial fibrillation secondary to an atrial focus. J Am Coll Cardiol 1999; 33:1217–26.
50. Haissaguerre M, Jais P, Shah DC, Garrigue S, Takahashi A, Lavergne T, Hocini M, Peng JT, Roudaut R, Clementy J. Electrophysiological end point for catheter ablation of atrial fibrillation initiated from multiple pulmonary venous foci. Circulation 2000; 101:1409–17.
51. Haissaguerre M, Shah DC, Jais P, Hocini M, Yamane T, Deisenhofer I, Chauvin M, Garrigue S, Clementy J. Electrophysiological breakthroughs from the left atrium to the pulmonary veins. Circulation 2000; 102:2463–5.
52. Macle L, Jais P, Weerasooriya R, Hocini M, Shah DC, Choi KJ, Scavee C, Raybaud F, Clementy J, Haissaguerre M. Irrigated-Tip Catheter Ablation of Pulmonary Veins for Treatment of Atrial Fibrillation. J Cardiovasc Electrophysiol 2002; 13:1067–73.[CrossRef][Web of Science][Medline]
53. Martin DO, Saliba W, McCarthy PM, Gillinov AM, Belden W, Marrouche NF, Natale A. Approaches to restoring and maintaining normal sinus. Cleve Clin J Med 2003l; 70 Suppl 3:S12–29.
54. Marrouche NF, Dresing T, Cole C, Bash D, Saad E, Balaban K, Pavia SV, Schweikert R, Saliba W, Abdul-Karim A, Pisano E, Fanelli R, Tchou P, Natale A. Circular mapping and ablation of the pulmonary vein for treatment of atrial fibrillation: impact of different catheter technologies. Am Coll Cardiol 2002; 40:464–74.
55. Ng FS, Camm AJ. Catheter ablation of atrial fibrillation. Clin Cardiol 2002; 25:384–94.[Web of Science][Medline]
56. Marrouche NF, Martin DO, Wazni O, Gillinov AM, Klein A, Bhargava M, Saad E, Bash D, Yamada H, Jaber W, Schweikert R, Tchou P, Abdul-Karim A, Saliba W, Natale A. Phased-array intracardiac echocardiography monitoring during pulmonary vein isolation in patients with atrial fibrillation: impact on outcome and complications. Circulation 2003; 107:2710–16.
57. Pappone C, Rosanio S, Augello G, Gallus G, Vicedomini G, Mazzone P, Gulletta S, Gugliotta F, Pappone A, Santinelli V, Tortoriello V, Sala S, Zangrillo A, Crescenzi G, Benussi S, Alfieri O. Mortality, morbidity, and quality of life after circumferential pulmonary vein ablation for atrial fibrillation: outcomes from a controlled nonrandomized long-term study. J Am Coll Cardiol 2003; 42:185–97.
58. Arentz T, Jander N, von Rosenthal J, Blum T, Furmaier R, Gornandt L, Josef Neumann F, Kalusche D. Incidence of pulmonary vein stenosis 2 years after radiofrequency catheter ablation of refractory atrial fibrillation. Eur Heart J 2003; 24:963–9.
59. Pappone C. Pulmonary vein stenosis after catheter ablation for atrial fibrillation. J Cardiovasc Electrophysiol 2003; 14:165–7.[Web of Science][Medline]
60. Saad EB, Marrouche NF, Saad CP, Ha E, Bash D, White RD, Rhodes J, Prieto L, Martin DO, Saliba WI, Schweikert RA, Natale A. Pulmonary vein stenosis after catheter ablation of atrial fibrillation: emergence of a new clinical syndrome. Ann Intern Med 2003; 138:634–8.
61. Moe GK. On the multiple wavelet hypothesis of atrial fibrillation. Arch Int Pharmacodyn Ther 1962; 140:183–8.[Web of Science]
62. Cox JL, Schuessler RB, Cain ME, Corr PB, Stone CM, D’Agostino HJ Jr, Harada A, Chang BC, Smith PK, Boineau JP. Surgery for atrial fibrillation. Semin Thorac Cardiovasc Surg 1989; 1:67–73.[Medline]
63. Cox JL, Ad N, Palazzo T, Fitzpatrick S, Suyderhoud JP, DeGroot KW, Pirovic EA, Lou HC, Duvall WZ, Kim YD. Current status of the Maze procedure for the treatment of atrial fibrillation. Semin Thorac Cardiovasc Surg 2000; 12:15–9.[Medline]
64. Cox JL, Ad N, Palazzo T. Impact of the maze procedure on the stroke rate in patients with atrial fibrillation. J Thorac Cardiovasc Surg 1999; 118:833–40.
65. McCarthy PM, Gillinov AM, Castle L, Chung M, Cosgrove D 3rd. The Cox-Maze procedure: the Cleveland Clinic experience. Semin Thorac Cardiovasc Surg 2000; 12:25–9.[Medline]
66. Lonnerholm S, Blomstrom P, Nilsson L, Oxelbark S, Jideus L, Blomstrom-Lundqvist C. Effects of the maze operation on health-related quality of life in patients with atrial fibrillation. Circulation. 2000; 101:2607–11.
67. Rawles JM. What is meant by a ‘controlled’ ventricular rate in atrial fibrillation? Br Heart J 1990; 63:157–61.
68. Resnekov L, Mc Donald L. Electroversion of lone atrial fibrillation and flutter including haemodynamic studies at rest and exercise. Br Heart J 1971; 33:339–50.
69. Rodney H, Falk MD. Atrial Fibrillation. N Engl J Med 2001; 344:1067–78.
70. Schreck DM, Rivera AR, Tricarico VJ. Emergency management of atrial fibrillation: intravenous diltiazem versus intravenous digoxin. Ann Emerg Med 1997; 29:135–40.[CrossRef][Web of Science][Medline]
71. Botker HE, Toft P, Klitgaard NA, Simonsen EE. Influence of physical exercise on serum digoxin concentration and heart rate in patients with atrial fibrillation. Br Heart J 1991; 65:337–41.
72. Goldman S, Probst P, Selzer A, Cohn K. Inefficiency of ‘therapeutic’ serum levels of digoxin in controlling the ventricular rate in atrial fibrillation. Am J Cardiol 1975; 35:651–55.[CrossRef][Web of Science][Medline]
73. Farshi R, Kistner D, Sarma JSM, et al. Ventricular rate control in chronic atrial fibrillation during daily activity and programmed exercise: a crossover open-label study of five drug regimens. J Am Coll Cardiol 1999; 33:304–10.
74. Roth A, Harrison E, Mitani G, et al. Efficacy and safety of medium and high-dose diltiazem alone or in combination with digoxin for control of heart rate at rest and during exercise in patients with chronic atrial fibrillation. Circulation 1986; 73:316–24.
75. Pnadis IP, Morganroth J, Baessler C. Effectiveness and safety of oral verapamil to control exercise-induced tachycardia in patients with atrial fibrillation receiving digitalis. Am J Cardiol 1983; 52:1197–201.[CrossRef][Web of Science][Medline]
76. Clemo HF, Wood MA, Gilligan DM, Ellenbogen KA. Intravenous amiodarone for acute heart rate control in the critically ill patient with atrial tachyarrhythmia. Am J Cardiol 1998; 81:594–8.[CrossRef][Web of Science][Medline]
77. Daoud EG, Weiss R, Bahu M, Knight BP, Bogun F, Goyal R, Harvey M, Strickberger SA, Man KC, Morady F. Effect of irregular ventricular rhythm on cardiac output. Am J Cardiol 1996; 78:1433–36.
78. Brignole M, Menozzi C, Gianfranchi L, Musso G, Mureddu R, Bottoni N, Lolli G. Assessment of atrioventricular junction ablation and VVIR pacemaker versus pharmacological treatment in patients with heart failure and chronic atrial fibrillation: a randomized controlled study. Circulation 1998; 98:953–60.
79. Weerasooriya R, Davis M, Powell A, Szili-Torok T, Shah C, Whalley D, Kanagaratnam L, Heddle W, Leitch J, Perks A, Ferguson L, Bulsara M. The Australian Intervention Randomized Control of Rate in Atrial Fibrillation Trial (AIRCRAFT). J Am Coll Cardiol 2003; 41:1697–702.
80. Ozcan C, Jahangir A, Friedman PA, Patel PJ, Munger TM, Rea RF, Lloyd MA, Packer DL, Hodge DO, Gersh BJ, Hammill SC, Shen WK. Long-term survival after ablation of the atrioventricular node and implantation of a permanent pacemaker in patients with atrial fibrillation. N Engl J Med 2001; 3441:1043–51.
81. The AF-CHF-Investigators. Rationale and design of a study assessing treatment strategies of atrial fibrillation in patients with heart failure: The atrial fibrillation and congestive heart failure (AF-CHF) trial. Am Heart J 2002; 144:597–607.[Web of Science][Medline]
82. McHorney CA, Ware JE, Raczek AE. The MOS 36-item short-form health survey (SF-36), II: psychometric and clinical tests validity in measuring physical and mental health constructs. Med Care 1993; 31:247–63.[Web of Science][Medline]
83. The Stroke Prevention in Atrial Fibrillation Investigators. Predictors of thromboembolism in atrial fibrillation. I Clinical features of patients at risk. Ann Intern Med 1992; 116:1–5.
84. Predictors of thromboembolism in atrial fibrillation. II. Echocardiographic features of patients at risk. Ann Intern Med 1992; 116:6–12.
85. Hart RG, Halperin JL. Atrial fibrillation and thromboembolism: a decade of progress in stroke prevention. Ann Intern Med 1999; 131:688–95.
86. Stroke Prevention in Atrial Fibrillation Study: final results. Circulation 1991; 84:527–39.
87. The National Heart, Lung and Blood Institute Working Group on Atrial Fibrillation: current understandings and research perspectives. J Am Coll Cardiol 1993; 22:1830–4.[Abstract]
88. Waldo AL. Management of atrial fibrillation and the need for AFFIRMative action. Am J Cardiol 1999; 84:698–700.[CrossRef][Web of Science][Medline]
89. Crijns HJ, Van Gelder IC, Van Gilst WH, Hillege H, Gosselink AM, Lie KI. Serial antiarrhythmic drug treatments to maintain sinus rhythm after electrical cardioversion for chronic atrial fibrillation or atrial flutter. Am J Cardiol 1991; 68:335–41.[CrossRef][Web of Science][Medline]
90. Laupacis A, Albers G, Dalen J, Dunn MI, Jacobson AK, Singer DE. Antithrombotic treatment in atrial fibrillation. Chest 1998; 114:579–89S.[CrossRef]
91. Boos CJ, More RS, Carlsson J. Persistent atrial fibrillation: rate control or rhythm control. Rate control is not inferior to rhythm control. Br Med J 2003; 326:1411–12.
92. Hart RG, Benavente O, McBride R, Pearce LA. Antithrombotic treatment to prevent stroke in patients with atrial fibrillation: a meta-analysis. Ann Intern Med 1999; 131:492–501.
93. Adjusted-dose warfarin versus low-intensity, fixed-dose warfarin plus aspirin for high-risk patients with atrial fibrillation : Stroke Prevention in Atrial Fibrillation III randomised clinical trial. Lancet 1996; 348:633–8.[CrossRef][Web of Science][Medline]
94. Hylek EM, Skates SJ, Sheehan MA, Singer DE. An analysis of the lowest effective intensity of prophylactic anticoagulation for patients with nonrheumatic atrial fibrillation. N Engl J Med 1996; 335:540–6
95. The European Atrial Fibrillation Trial Study Group. Optimal oral anticoagulant therapy in patients with nonrheumatic atrial fibrillation and recent cerebral ischaemia. N Engl J Med 1995; 333:5–10.
96. Petersen P, Grind M, Adler J; SPORTIF II Investigators. Ximelagatran versus warfarin for stroke prevention in patients with nonvalvular atrial fibrillation. SPORTIF II: a dose-guiding, tolerability, and safety study. J Am Coll Cardiol 2003; 41:1445–51.
97. Halperin JL; Executive Steering Committee, SPORTIF III and V Study Investigators. Ximelagatran compared with warfarin for prevention of thromboembolism in patients with nonvalvular atrial fibrillation: Rationale, objectives, and design of a pair of clinical studies and baseline patient characteristics (SPORTIF III and V). Am Heart J 2003; 146:431–8.[CrossRef][Web of Science][Medline]
98. Pietrsik A, Kosior D, Niewada M, Rabczenko D, Opolski G. One-year cost-effectiveness of rhythm and rate-control strategy in persistent atrial fibrillation. Eur Heart J 2003; 368:1999 (abstract Suppl).
CiteULike 
Connotea 
Del.icio.us What's this?
This article has been cited by other articles:
|
|
 |
|
  S. A. Hunt, W. T. Abraham, M. H. Chin, A. M. Feldman, G. S. Francis, T. G. Ganiats, M. Jessup, M. A. Konstam, D. M. Mancini, K. Michl, et al. 2009 Focused Update Incorporated Into the ACC/AHA 2005 Guidelines for the Diagnosis and Management of Heart Failure in Adults: A Report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines Developed in Collaboration With the International Society for Heart and Lung Transplantation J. Am. Coll. Cardiol., April 14, 2009; 53(15): e1 - e90. [Full Text] [PDF]
|
|
|
|
 |
|
 2009 WRITING GROUP TO REVIEW NEW EVIDENCE AND UPDA, M. Jessup, W. T. Abraham, D. E. Casey, A. M. Feldman, G. S. Francis, T. G. Ganiats, M. A. Konstam, D. M. Mancini, P. S. Rahko, et al. 2009 Focused Update: ACCF/AHA Guidelines for the Diagnosis and Management of Heart Failure in Adults: A Report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines: Developed in Collaboration With the International Society for Heart and Lung Transplantation Circulation, April 14, 2009; 119(14): 1977 - 2016. [Full Text] [PDF]
|
|
|
|
|
|
2005 WRITING COMMITTEE MEMBERS, S. A. Hunt, W. T. Abraham, M. H. Chin, A. M. Feldman, G. S. Francis, T. G. Ganiats, M. Jessup, M. A. Konstam, D. M. Mancini, et al. 2009 Focused Update Incorporated Into the ACC/AHA 2005 Guidelines for the Diagnosis and Management of Heart Failure in Adults: A Report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines: Developed in Collaboration With the International Society for Heart and Lung Transplantation Circulation, April 14, 2009; 119(14): e391 - e479. [Full Text] [PDF]
|
|
|
|
 |
|
 C. J. Boos, R. A. Anderson, and G. Y.H. Lip Is atrial fibrillation an inflammatory disorder? Eur. Heart J., January 2, 2006; 27(2): 136 - 149. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
Developed in Collaboration With the American Colle, Endorsed by the Heart Rhythm Society, S. A. Hunt, W. T. Abraham, M. H. Chin, A. M. Feldman, G. S. Francis, T. G. Ganiats, M. Jessup, M. A. Konstam, et al. ACC/AHA 2005 Guideline Update for the Diagnosis and Management of Chronic Heart Failure in the Adult--Summary Article: A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Update the 2001 Guidelines for the Evaluation and Management of Heart Failure) J. Am. Coll. Cardiol., September 20, 2005; 46(6): 1116 - 1143. [Full Text] [PDF]
|
|
|
|
|
|
S. A. Hunt, W. T. Abraham, M. H. Chin, A. M. Feldman, G. S. Francis, T. G. Ganiats, M. Jessup, M. A. Konstam, D. M. Mancini, K. Michl, et al. ACC/AHA 2005 Guideline Update for the Diagnosis and Management of Chronic Heart Failure in the Adult--Summary Article: A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Update the 2001 Guidelines for the Evaluation and Management of Heart Failure): Developed in Collaboration With the American College of Chest Physicians and the International Society for Heart and Lung Transplantation: Endorsed by the Heart Rhythm Society Circulation, September 20, 2005; 112(12): 1825 - 1852. [Full Text] [PDF]
|
|
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||