Europace Advance Access originally published online on March 20, 2008
Europace 2008 10(5):558-565; doi:10.1093/europace/eun064
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
CARDIAC RESYNCHRONISATION THERAPY
Cardiac resynchronization therapy in patients with heart failure and atrial fibrillation: importance of new-onset atrial fibrillation and total atrial conduction time
1 Department of Cardiology, Thoraxcenter, University Medical Center Groningen, University of Groningen, Hanzeplein 1, PO Box 30.001, 9700 RB Groningen, The Netherlands; 2 The Interuniversity Cardiology Institute Netherlands, Utrecht, The Netherlands
Manuscript submitted 13 December 2007. Accepted after revision 22 February 2008.
* Corresponding author. Tel: +31 50 361 2355; fax: +31 50 361 4391. E-mail address: i.c.van.gelder{at}thorax.umcg.nl
 |
Abstract |
|---|
 Top Abstract IntroductionMethodsResultsDiscussionConclusionFundingReferences |
|---|
Aims: Cardiac resynchronization therapy (CRT) is an established therapy for patients with heart failure and sinus rhythm (SR), but its value in atrial fibrillation (AF) remains unclear. Furthermore, response to CRT may be difficult to predict in these patients. The aim of our study was to investigate whether predictors for CRT success differ between patients with AF and SR and to study the influence of present or developing AF on response to CRT.
Methods and results: We examined consecutive patients in whom CRT was implanted disregarding the atrial rhythm. Atrial fibrillation was defined as either current or earlier AF, response to CRT was defined as a decrease in the left ventricular end-systolic volume of 
10% after 6 months. Total atrial conduction time (TACT), a measure to predict the risk of developing AF, was determined by echocardiography. We included 114 patients, of whom 56 (49%) were known with AF (23 current AF and 33 earlier AF). The other 58 patients had no history of AF. After 6 months, response in current and earlier AF and that in SR patients was comparable (56, 58 and 55%, respectively). In AF patients, multivariate analysis revealed a shorter TACT at baseline [odds ratio (OR) 16.7 (1.5–185.3), P = 0.02] and an interventricular mechanical delay (IVMD) >40 ms [OR 10.4 (1.0–110.9), P = 0.05] as predictors for response. Non-responders more frequently suffered from new-onset AF (P = 0.02).
Conclusion: Failure to CRT is associated with new-onset AF. Total atrial activation time may be a parameter to predict response in AF patients.
Key Words: Atrial fibrillation, Congestive heart failure, Artificial pacing
|
Introduction |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionConclusionFundingReferences |
|---|
Atrial fibrillation (AF) is the most common sustained cardiac rhythm disorder and often coexists with chronic heart failure.1
,2 In these patients, AF may increase cardiovascular morbidity and mortality.3–6 Randomized clinical trials have demonstrated the beneficial effects of cardiac resynchronization therapy (CRT) in patients with pharmacological refractory heart failure with prolonged QRS, low ejection fraction, and sinus rhythm (SR).7–11 Whether CRT is also effective in patients with AF is still to be elucidated. Only a few studies have assessed this issue.12–15 From these limited data, it is suggested that CRT is also effective in patients with AF. Hereby, it should be noted that in most studies, adequate rate control was performed by atrioventricular (AV) node ablation.12–14
Identification of success of CRT, in general, still is a subject of interest.16 It is unknown whether the same predictors of response are valid in patients with SR and AF. Furthermore, it is not clear which patients need AV-node ablation and which could also be treated with rate control medication alone.17,18
Furthermore, AF may be underestimated because of insufficient documentation. Device therapy can be used to determine the actual AF burden in patients with pacemakers or internal cardioverter defibrillators (ICDs). New-onset AF may influence response to CRT. However, only a few studies reported on the prevalence of new-onset AF during follow-up and its influence on outcome.15,19,20
The aim of this study is to investigate the influence of present or developing AF on response to CRT and to study whether predictors for the success of CRT differ between patients with AF and SR.
|
Methods |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionConclusionFundingReferences |
|---|
Patient population
Between January 2004 and January 2007, 114 consecutive patients with congestive heart failure who met eligibility criteria for CRT were included. The eligibility criteria for CRT were according to the guidelines: New York Health Association (NYHA) functional class III or IV despite optimal pharmacological treatment, left ventricular ejection fraction
35%, a left ventricular end-diastolic diameter 55 mm, and wide QRS complex 130 ms.21 In some patients, the QRS duration differed at acceptance for CRT and actual inclusion.
Atrial fibrillation was defined as a history of documented AF being either present at baseline (current AF) or in the past (earlier AF). Atrial fibrillation during follow-up was defined as any AF documented on an electrocardiogram (ECG), Holter monitoring (>30 s), or detected by the device (duration >30 s). Atrial fibrillation burden was determined by the device and defined as the time the patient was in AF divided by the total time. Successful response to CRT was defined as a decrease in the left ventricular end-systolic volume (LVESV) of 10% or more measured by cardiac ultrasound after 6 months of follow-up.22 Baseline assessment included patient history, physical examination, 12-lead ECG, transthoracic echocardiography, exercise testing, radionuclide scanning, and coronary angiography. Clinical history, AF history, and characteristics were carefully retrieved using patient medical records. Dyssynchrony was determined by tissue Doppler imaging, using Echopac 6.1.3., General Electric Vivid 7® (Sloninge, Germany).16 We evaluated aortic pre-ejection time, IVMD, and septal-to-lateral delay. An IVMD >40 ms was considered indicative of IVMD.16 Intraventricular LV dyssynchrony was measured by calculating the septal-to-lateral delay in peak velocities.16 A mechanical delay >60 ms was considered indicative of intraventricular dyssynchrony.16 Total atrial conduction time (TACT) is the total duration of the atrial activation and may thus serve as a measure of severity of atrial structural remodelling and predictor of AF.23 This was determined by transthoracic echocardiography, the time from initiation of the electrocardiographic P-wave (lead II) to the local lateral left atrial activation time.23 This was measured by placing the sample volume in the left atrial basal portion and measuring the time between initiation of the electrocardiographic P-wave and the peak velocity by tissue velocity imaging (Figure 1). Total atrial conduction time could only be measured in the presence of SR at baseline and was not assessed in patients treated with amiodarone, because it may prolong the TACT, leaving 58 patients with an adequate TACT measurement. Coronary angiography was performed prior to implantation in all patients to exclude causes of heart failure amenable to surgery or intervention. Peak oxygen consumption and the anaerobic threshold were determined at baseline. Glomerular filtration rate was computed using the simplified modification of diet renal disease equation.
|
Follow-up
All patients were routinely seen every 6 months at the outpatient department. At all visits, patient history, medication use, physical examination, ECG, pacemaker interrogation, transthoracic echocardiography, a radionuclide scan, and exercise test were performed. At each CRT interrogation, data were stored both on a computer disc and in a computerized ICD medical record database of the University Medical Center Groningen. A consistent protocol to standardize CRT and ICD programming was used, in which there were no systemic differences in the programming between patients with AF and SR. In most patients, the device was programmed in the DDD-R mode with an AV delay of 110 ms, in the case of permanent AF in the VVI-R mode. The lower rate was programmed at 60 bpm and the upper rate was programmed according to the upper heart rate during exercise testing. Cumulative percentages of ventricular pacing were recorded in the CRT device as the total number of ventricular paced beats in proportion to the total number of beats during the device's life. The duration of follow-up was computed from the time of CRT implantation until death or heart transplantation when applicable, or to the date when the last follow-up data were obtained. Determining whether a patient is a responder or non-responder is based on the LVESV measured by an independent examiner blinded for the clinical response of the patient at 6 months of follow-up.
Atrial fibrillation therapy
Atrial fibrillation was treated according to a rhythm control strategy depending on complaints related to AF and ventricular rate during AF.24 In the case of paroxysmal or persistent AF in the presence of symptoms (worsening of heart failure and palpitations), or too high ventricular rate to allow optimal ventricular pacing, a rhythm control strategy was adopted including electrical cardioversions if required and institution of anti-arrhythmic drugs: sotalol (160–240 mg) daily or amiodarone (200 mg daily after 4 weeks of loading with 600–800 mg daily). If AF was accepted, rate control was carefully instituted aiming at optimal biventricular pacing.
Statistical analysis
Baseline descriptive statistics are presented as the mean ± SD or median (range) for continuous variables and numbers with percentages for categorical variables. Differences between variables in patients who responded vs. those who did not respond were evaluated by Student's t-test or Mann–Whitney U-test, depending on normality of the data, for continuous data and Fisher's exact test or 
2 test for categorical data.
We calculated adjusted odds ratios (ORs) of clinical characteristics, baseline drug therapy, and device characteristics with logistic regression, to identify predictors of CRT response. Linearity of the continuous variables with respect to the response variable was assessed by determining the quartiles of their distribution. Thereafter, OR for each quartile were calculated. In the case of a linear trend in the estimated ORs, the variable was introduced in the model as continuous. If no linearity was shown, the variable was further categorized by taking together the quartiles with ORs similar in magnitude, primarily the median value or otherwise based on clinical relevance. The multivariate analysis was performed using all variables with P < 0.10 in the univariate analysis. A stepwise approach was used. The final model included all variables with P < 0.05, and variables with P 0.05 in the multivariate model were excluded. Interaction was investigated; in all analysis, P < 0.05 was considered statistically significant.
|
Results |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionConclusionFundingReferences |
|---|
Patient characteristics
We included 114 patients of whom 56 (49%) had AF (23 current AF and 33 earlier AF). The other 58 patients had no history of AF. Of the patients with AF, 19 (34%) had earlier paroxysmal AF, 31 (55%) (earlier) persistent AF, and 6 (11%) permanent AF. The patient characteristics at baseline are shown in Table 1. Patients with AF had a higher diastolic blood pressure, a larger right atrium, a more impaired right ventricular function, and more often had undergone previous cardiac surgery.
|
Device characteristics
At random, patients received a Guidant® (St. Paul, MN, USA) or Medtronic® (Minneapolis, MN, USA) CRT-D. The presence of a history of AF or echocardiographic parameters was not taken into account for device selection.
Response to therapy
Median follow-up was 18 months (6–38 months). In the total group, 64 (56%) patients were defined as responders 6 months after implantation. The response rate was comparable between patients with current and earlier AF [n = 19 (58%) vs. n = 13 (56%), respectively] and between patients with and without AF [n = 32 (57%) vs. n = 32 (55%), respectively]. Atrioventricular-junctional ablation was performed in only one patient (prior to implantation). After 6 months of follow-up, the LVESV had decreased significantly in responders (Figure 2A), whereas non-responders showed a significant increase in the LVESV (Figure 2B). There was no significant difference in the amount of decrease or increase in the LVESV between patient with or without AF.
|
Response as measured by improvement in the functional class for heart failure was higher when compared with the defined measure of response: a decrease in the LVESV
10%. After 6 months of follow-up, 82 (72%) patients improved one or more point in the NYHA class, 17 (74%) vs. 21 (64%) of the patients with current and earlier AF, respectively, and 38 (68%) vs. 44 (76%) patients with AF vs. no-AF (all not statistically significant). The median peak VO2 increased during follow-up [from 14.3 (4.2–31.5) mL/min/kg to 15.4 (8.1–35.4) mL/min/kg after 6 months of follow-up, P = ns]. The increase in the percentage of achieved compared with predicted peak VO2 was significantly higher in responders vs. non-responders from baseline to the end of the follow-up. The percentage achieved/predicted peak VO2 increased from 58% (23–145) to 65% (37–109), P = 0.2, in responders vs. from 60% (14–148) to 61% (29–107), P = 0.9, in non-responders. The same figure was found in both AF and no-AF patients. Differences in baseline characteristics between responders and non-responders in the AF group are listed in Table 2. Multivariate analysis revealed that a shorter TACT [OR 16.7 (1.5–185.3), P = 0.02, Figure 3] and an IVMD >40 ms [OR 10.4 (1.0–110.9), P = 0.05] were related to response in CRT patients known with AF. Univariate predictors for response to CRT were left ventricular lead positioning (posterior vs. anterior localization) [OR 3.8 (0.9–15.4), P = 0.06], non-ischaemic cardiomyopathy [OR 2.6 (0.8–7.8), P = 0.09], and a septal-to-lateral delay >60 ms [OR 3.5 (1.0–12.5), P = 0.05].
|
|
Predictors of response in patients without AF were non-ischaemic cardiomyopathy [OR 9.4 (1.6–56.8), P = 0.01], creatinine <113 µmol/L [OR 12.7 (1.7–92.6), P = 0.01], systolic blood pressure [OR 8.1 (1.2–55.3), P = 0.03], and left ventricular lead position (posterior vs. anterior localization) [OR 9.5 (1.6–56.1), P = 0.02].
Atrial fibrillation during follow-up
A total of 35 (62%) patients in the AF group vs. 14 (24%) patients in the no-AF group (P = <0.0001) had AF during follow-up. At the time of implantation of the CRT device, 23 patients had AF. After testing the ICD, 11 of these patients (48%) converted to SR. Nine of the latter patients had a recurrent episode of persistent AF and underwent ECV during follow-up. Only 2 of them remained in SR during follow-up. Of the patients with a history of paroxysmal or persistent AF but SR at baseline, 6 patients developed persistent AF and 8 paroxysmal AF during follow-up. More patients with previous persistent AF developed AF during follow-up [8/19 (47%) vs. 6/19 (32%) patients with persistent vs. paroxysmal AF prior to implantation, respectively]. The AF burden during follow-up was low in patients with prior paroxysmal AF: a median of 0% (0–60). In the non-responders, the AF burden was 0% (0–60) vs. 0% (1–9) in the responders. The AF burden in the patients with prior persistent AF was 2% (0–100) [1% (0–100) vs. 16% (0–100) in responders vs. non-responders].
In the no-AF group, 14 (24%) patients had AF during follow-up. The AF burden as measured by the device was statistically different between patients with a history of AF and those with no history of AF [26% (0–100) vs. 0% (0–64), P < 0.001]. At the end of follow-up, 17 (30%) vs. 3 (5%) patients in the AF vs. no-AF group were in permanent AF (P < 0.0001) (Figure 4).
|
New-onset AF during follow-up (14 of 58 patients with no previous AF) was associated with a lower response [4 (29%) responders vs. 10 (71%) non-responders, respectively, P = 0.02].
In patients with a history of AF and SR at baseline, the TACT was barely longer in those who developed AF during follow-up (173 ± 26 vs. 146 ± 26 ms, respectively, P = 0.05) (Figure 5). This difference was not observed in patients with no history of AF. Total atrial conduction time predicted the success of CRT in patients with a history of AF. In these patients, TACT was significantly higher in non-responders [186 ± 16 vs. 137 ± 20 ms, (P < 0.001)].
|
|
Discussion |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionConclusionFundingReferences |
|---|
Our study demonstrates that response to CRT is comparable between patients with current and earlier AF and SR patients. New-onset AF, however, was associated with failure to CRT. Furthermore, the study shows that predictors for response are different in AF and SR patients. Total atrial conduction time may be a parameter to predict response in patients with a history of AF.
Prevalence of atrial fibrillation in cardiac resynchronization therapy patients
In heart failure patients, the occurrence of co-existent AF is strongly related to the underlying NYHA functional class. The prevalence of AF is 5% for NYHA functional class I, 10–25% for classes II and III, and as high as 50% for class IV.2 For heart failure patients who are still in SR, the annual incidence of AF is 
5%. The development of AF is difficult to predict, but the risk is greatest in those with atrial conduction delay or evidence of atrial mechanical dysfunction, both markers of the presence of a substrate for AF.25,26 In our study, 49% of the patients had either earlier or current AF and another 24% developed new-onset AF during follow-up. These figures are somewhat higher than previously reported, even for NYHA III patients. This may relate to the fact that (i) we also included patients with previous AF but SR at baseline and (ii) new AF was carefully documented by the implanted device. Hoppe et al.19 reported an incidence of AF in 66 of 409 (16%) vs. 58 of 404 (14%) patients who received CRT vs. medical therapy, respectively, during a follow-up of 29 months. These figures are lower than ours. In their study, however, AF was only documented by ECGs and, in contrast to our study, not by the device. It undoubtedly underscores the importance of AF in patients treated with CRT. Unreliable pacing may occur due to the absence of AV-synchrony and too high ventricular rates.
Response to cardiac resynchronization therapy
In the present study, the response to CRT was equal in patients with and without AF and in patients with current and earlier AF. However, only limited evidence is available about the success of CRT in patients with AF. It is suggested that CRT is effective in patients with AF. On an individual basis, however, the response to CRT may be lower in patients with AF when compared with SR patients. Patients who had undergone an AV-node ablation more frequently responded to CRT because the intervention guaranteed successful pacing almost continuously.13–15 In our study, only one patient underwent AV-node ablation.
An important finding is we observed that new-onset AF, in contrast to the presence of AF at baseline, was associated with failure to CRT. It is difficult to determine whether new-onset AF post-CRT is a consequence or a cause of haemodynamic deterioration, i.e. failure to CRT. On the one hand, AF post-CRT may reduce effective biventricular pacing, due to high heart rates during AF, leading to failure of CRT. On the other hand, deterioration of the haemodynamic situation may also induce AF. In addition, we do not know whether new-onset AF patients were, nevertheless, better with CRT as they would have been without CRT. Bax and coworkers13,15 were the first to describe this issue. This finding implies that during follow-up, the presence of AF should be carefully monitored as it either may be a marker of deterioration of the haemodynamic situation due to progression of the disease, or, the other way around, may eventually lead to an impaired haemodynamic situation.27
The response rate in our study was significantly higher when an improvement of one or more NYHA class was evaluated. In accordance with our data, other studies found a poor relation between clinical response and echocardiographic response to CRT.28
Predictors for response
Many studies investigated predictors for response to CRT in SR patients. To a lesser extent, this has been investigated in AF patients. Our data reveal that predictors for successful CRT in AF patients are a shorter duration of the TACT and a long IVMD. Univariately, also typical predictors for the success of CRT, such as septal-to-lateral dyssynchrony and non-ischaemic cardiomyopathy, were associated with response. The finding that TACT influences response to therapy is new and may be used to predict response. Clearly, research has to be performed to assess its definite significance. The risk of AF is greatest in those with atrial conduction delay or evidence of atrial mechanical dysfunction, i.e. in the presence of markers for the presence of a substrate for AF.25,26 TACT is the total duration of the atrial activation and may thus be a measure of severity of structural remodelling, i.e. the presence of a substrate of AF. The technique to assess atrial activation time has recently been introduced by Merckx et al.23 They could demonstrate a good correlation with the golden standard for total atrial activation time and the signal average ECG. Clearly, it may not be concluded from the present findings that the typical predictors for response to CRT are of no value in patients with AF.
In patients with no-AF, predictors for response were different. Non-ischaemic cardiomyopathy, lower creatinine plasma levels, higher systolic blood pressure, and a posterior left ventricular lead position determined success. The TACT did not influence response in no-AF patients. The fact that patients with and without AF have different predictors for response has not been described earlier. Previous studies, especially in SR patients, observed that a more prolonged IVMD, non-ischaemic cardiomyopathy, a smaller left ventricular end-systolic diameter, lower systolic blood pressure, a septal-to-lateral delay of >60 ms, and/or left ventricular and right ventricular lead position were associated with higher response to CRT.16,29–31 Possibly, the TACT plays a more important role in AF patients because these patients are at a greater risk for developing AF burden during the follow-up.
Atrial fibrillation burden during follow-up
Indeed, AF during CRT occurred more frequently in patients known with previous AF. During a mean follow-up of 18 months, 62% of these patients had additional AF episodes. This figure was significantly lower (24% of the patients) in patients without previous AF. Previous studies reported the occurrence of AF between 16 and 38%, depending on the duration of the follow-up and the presence of earlier AF.19,20 This relatively high percentage of AF at least, in part, relates to the definition used (any AF documented on an ECG, Holter monitoring, or detected by the device with a duration >30 s).
Limitations
This is an observational study and is affected by all the limitations of these studies. On the other hand, because of a prospective real-time database implementation, we have minimal missing data, and all our patients are consecutive, which limits possible patient selection bias.
|
Conclusion |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionConclusionFundingReferences |
|---|
The present study notifies that the development of new AF is associated with a lower success of CRT. Furthermore, it signifies that predictors for response to CRT are different between AF and SR patients and introduces a new predictor for response of CRT in AF patients, the total atrial activation time.
|
Funding |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionConclusionFundingReferences |
|---|
D.J.V.V. and I.C.V.G. received financial support for research from Medtronic, Guidant and Biotronik.
Conflict of interest: none declared.
|
References |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionConclusionFundingReferences |
|---|
[1] Wang TJ, Larson MG, Levy D, Vasan RS, Leip EP, Wolf PA, et al. Temporal relations of atrial fibrillation and congestive heart failure and their joint influence on mortality: the Framingham Heart Study. Circulation (2003) 107:2920–5.
[2] Neuberger HR, Mewis C, Van Veldhuisen DJ, Schotten U, Van Gelder IC, Allessie MA, et al. Management of atrial fibrillation in patients with heart failure. Eur Heart J (2007) 28:2568–77.
[3] Dries DL, Exner DV, Gersch BJ, Domanski MJ, Waclawiw MA, Stevenson LW. Atrial fibrillation is associated with an increased risk for mortality and heart failure progression in patients with asymptomatic and symptomatic left ventricular systolic dysfunction: a retrospective analysis of the SOLVD trials. Studies of Left Ventricular Dysfunction. J Am Coll Cardiol (1998) 32:695–703.
[4] Van Veldhuisen DJ, Aass H, El Allaf D, Dunselman PH, Gullestad L, Halinen M, et al. Presence and development of atrial fibrillation in chronic heart failure. Experiences from the MERIT-HF Study. Eur J Heart Fail (2006) 8:539–46.[CrossRef][Web of Science][Medline]
[5] Smit MD, van Dessel PF, Rienstra M, Nieuwland W, Wiesfeld AC, Tan ES, et al. Atrial fibrillation predicts appropriate shocks in primary prevention implantable cardioverter-defibrillator patients. Europace (2006) 8:566–72.
[6] Rienstra M, Smit MD, Nieuwland W, Tan ES, Wiesfeld AC, Anthonio RL, et al. Persistent atrial fibrillation is associated with appropriate shocks and heart failure in patients with left ventricular dysfunction treated with an implantable cardioverter defibrillator. Am Heart J (2007) 153:120–6.[CrossRef][Web of Science][Medline]
[7] Cazeau S, Leclercq C, Lavergne T, Walker S, Varma C, Linde C, et al. Effects of multisite biventricular pacing in patients with heart failure and intraventricular conduction delay. N Engl J Med (2001) 344:873–80.
[8] Auricchio A, Stellbrink C, Sack S, Block M, Vogt J, Bakker P, et al. Long-term clinical effect of hemodynamically optimized cardiac resynchronization therapy in patients with heart failure and ventricular conduction delay. J Am Coll Cardiol (2002) 39:2026–33.
[9] Abraham WT, Fisher WG, Smith AL, Delurgio DB, Leon AR, Loh E, et al. Multicenter InSync Randomized Clinical Evaluation. Cardiac resynchronization in chronic heart failure. N Engl J Med (2002) 346:1845–53.
[10] Bristow MR, Saxon LA, Boehmer J, Krueger S, Kass DA, DeMarco T, et al. Cardiac-resynchronization therapy with or without an implantable defibrillator in advanced chronic heart failure. N Engl J Med (2004) 350:2140–50.
[11] Cleland JG, Daubert JC, Erdmann E, Freemantle N, Gras D, Kappenberger L, et al. The effect of cardiac resynchronization on morbidity and mortality in heart failure. N Engl J Med (2005) 352:1539–49.
[12] Linde C, Leclercq C, Rex S, Garrigue S, Lavergne T, Cazeau S, et al. Long-term benefits of biventricular pacing in congestive heart failure: results from the MUltisite STimulation in cardiomyopathy (MUSTIC) study. J Am Coll Cardiol (2002) 40:111–8.
[13] Molhoek SG, Bax JJ, Bleeker GB, Boersma E, van Erven L, Steendijk P, et al. Comparison of response to cardiac resynchronization therapy in patients with sinus rhythm versus chronic atrial fibrillation. Am J Cardiol (2004) 94:1506–9.[CrossRef][Web of Science][Medline]
[14] Gasparini M, Auricchio A, Regoli F, Fantoni C, Kawabata M, Galimberti P, et al. Four-year efficacy of cardiac resynchronization therapy on exercise tolerance and disease progression: the importance of performing atrioventricular junction ablation in patients with atrial fibrillation. J Am Coll Cardiol (2006) 48:734–43.
[15] Kies P, Leclercq C, Bleeker GB, Crocq C, Molhoek SG, Poulain C, et al. Cardiac resynchronisation therapy in chronic atrial fibrillation: impact on left atrial size and reversal to sinus rhythm. Heart (2006) 92:490–4.
[16] Bax JJ, Abraham T, Barold SS, Breithardt OA, Fung JW, Garrigue S, et al. Cardiac resynchronization therapy: part 1—issues before device implantation. J Am Coll Cardiol (2005) 46:2153–67.
[17] Steinberg JS. Desperately seeking a randomized clinical trial of resynchronization therapy for patients with heart failure and atrial fibrillation. J Am Coll Cardiol (2006) 48:744–6.
[18] Van Gelder IC, Van Veldhuisen DJ, Crijns HJ, Tuininga YS, Tijssen JG, Alings AM, et al. RAte Control Efficacy in permanent atrial fibrillation: a comparison between lenient versus strict rate control in patients with and without heart failure. Background, aims, and design of RACE II. Am Heart J (2006) 152:420–6.[CrossRef][Web of Science][Medline]
[19] Hoppe UC, Casares JM, Eiskjaer H, Hagemann A, Cleland JG, Freemantle N, et al. Effect of cardiac resynchronization on the incidence of atrial fibrillation in patients with severe heart failure. Circulation (2006) 114:18–25.
[20] Hügl B, Bruns HJ, Unterberg-Buchwald C, Grosse A, Stegemann B, Lauer B, et al. Atrial fibrillation burden during the post-implant period after CRT using device-based diagnostics. J Cardiovasc Electrophysiol (2006) 17:813–7.[CrossRef][Web of Science][Medline]
[21] Gregoratos G, Abrams J, Epstein AE, Freedman RA, Hayes DL, Hlatky MA, et al. ACC/AHA/NASPE 2002 Guideline Update for Implantation of Cardiac Pacemakers and Antiarrhythmia Devices—summary article: a report of the American College of Cardiolo/American Heart Association Task Force on Practice Guidelines (ACC/AHA/NASPE Committee to Update the 1998 Pacemaker Guidelines). J Am Coll Cardiol (2002) 40:1703–19.
[22] Yu CM, Bleeker GB, Fung JW, Schalij MJ, Zhang O, van der Wall EE, et al. Left ventricular reverse remodeling but not clinical improvement predicts long-term survival after cardiac resynchronization therapy. Circulation (2005) 13:1580–6.
[23] Merckx KL, De Vos CB, Palmans A, Habets J, Cheriex EC, Crijns HJ, et al. Atrial activation time determined by transthoracic Doppler tissue imaging can be used as an estimate of the total duration of atrial electrical activation. J Am Soc Echocardiogr (2005) 18:940–4.[CrossRef][Web of Science][Medline]
[24] Van Gelder IC, Hagens VE, Bosker HA, Kingma JH, Kamp O, Kingma T, et al. A comparison of rate control and rhythm control in patients with recurrent persistent atrial fibrillation. N Engl J Med (2002) 347:1834–40.
[25] Pozzoli M, Cioffi G, Traversi E, Pinna GD, Cobelli F, Tavazzi L. Predictors of primary atrial fibrillation and concomitant clinical and hemodynamic changes in patients with chronic heart failure: a prospective study in 344 patients with baseline sinus rhythm. J Am Coll Cardiol (1998) 32:197–204.
[26] Sanders P, Morton JB, Davidson NC, Spence SJ, Vohra JK, Sparks PB, et al. Electrical remodelling of the atria in congestive heart failure: electrophysiological and electro anatomic mapping in humans. Circulation (2003) 108:1461–8.
[27] Swedberg K, Olsson LG, Charlesworth A, Cleland J, Hanrath P, Komajda M, et al. Prognostic relevance of atrial fibrillation in patients with chronic heart failure on long-term treatment with beta-blockers: results from COMET. Eur Heart J (2005) 26:1303–8.
[28] Bleeker GB, Bax JJ, Fung JW, van der Wall EE, Zhang Q, Schalij MJ, et al. Clinical versus echocardiographic parameters to assess response to cardiac resynchronization therapy. Am J Cardiol (2006) 97:260–3.[CrossRef][Web of Science][Medline]
[29] Reuter S, Garrigue S, Barold SS, Jais P, Hocini M, Haissaguerre M, et al. Comparison of characteristics in responders versus non responders with biventricular pacing for drug-resistant congestive heart failure. Am J Cardiol (2002) 89:346–50.[CrossRef][Web of Science][Medline]
[30] Gold MR, Auricchio A, Hummel JD, Giudici MC, Ding J, Tockman B, et al. Comparison of stimulation sites within left ventricular veins on the acute hemodynamic effects of cardiac resynchronization therapy. Heart Rhythm (2005) 2:376–81.[CrossRef][Web of Science][Medline]
[31] Richardson M, Freemantle N, Calvert MJ, Cleland JGF, Tavazzi L. Predictors and treatment response with cardiac resynchronization therapy in patients with heart failure characterized by dyssynchrony: a pre-defined analysis from the CARE-HF trial. Eur Heart J (2007) 28:1827–34.
CiteULike 
Connotea 
Del.icio.us What's this?
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||