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European Heart Journal Advance Access originally published online on September 6, 2006
European Heart Journal 2006 27(18):2201-2207; doi:10.1093/eurheartj/ehl098
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© The European Society of Cardiology 2006. All rights reserved. For Permissions, please e-mail: journals.permissions@oxfordjournals.org

Atrial fibrillatory rate and sinus rhythm maintenance in patients undergoing cardioversion of persistent atrial fibrillation

Fredrik Holmqvist1,*, Martin Stridh2, Johan E.P. Waktare3, Leif Sörnmo2, S. Bertil Olsson1 and Carl J. Meurling1

1 Department of Cardiology, Lund University Hospital, Lund, Sweden
2 Department of Electroscience, Lund Institute of Technology, Lund, Sweden
3 The Cardiothoracic Centre, Liverpool, UK

Received 8 February 2006; revised 19 May 2006; accepted 26 May 2006; online publish-ahead-of-print 6 September 2006.

* Corresponding author. Tel: +46 46 17 35 18; fax: +46 46 15 78 57. E-mail address: fredrik.holmqvist{at}med.lu.se


   Abstract
Top
 Abstract
Introduction
 Methods
 Results
 Discussion
 Conclusions
 References
 
Aims The study set out to explore whether an index of atrial electrical electrophysiology can be used to predict atrial fibrillation (AF) relapse, and if the predictive properties differ as a result of arrhythmia duration.

Methods and results The study comprised 175 consecutive patients with persistent AF (median duration 94 days, range 2 to 1044) referred for cardioversion. Twenty-nine patients had arrhythmia duration under 30 days (median 5 days, range 2–26). Atrial fibrillatory rate (AFR) was estimated using a frequency power spectrum analysis of QRST-cancelled ECG. At 1-month follow-up, 56% of the patients had relapsed to AF. The pre-cardioversion mean AFR of those patients was 399±52 fibrillations per minute (fpm) compared with 363±63 fpm among patients maintaining SR (P<0.0001). In patients with short AF duration, the difference was even more pronounced (424±52 vs. 345±65 fpm, P<0.01). In this group, a finding of an AFR above the mean value of the study population predicted AF relapse with high accuracy.

Conclusion In patients undergoing cardioversion of persistent AF, AF relapse is predicted by a higher AFR. A stronger association is seen in patients with short arrhythmia duration, reflecting either rapid remodelling or pre-existing changes in those who relapse to AF.

Key Words: Atrial fibrillation • Electrophysiology • Atrial remodelling


   Introduction
Top
 Abstract
 Introduction
Methods
 Results
 Discussion
 Conclusions
 References
 
Cardioversion of persistent atrial fibrillation (AF) to sinus rhythm (SR) has long been the accepted management strategy. However, studies such as AFFIRM and RACE1,2 have demonstrated that accepting permanent AF, with appropriate rate control and thromboembolic prophylaxis, results in comparable clinical outcome for elderly patients with no or minimal symptomatic impact from AF. The major drawback of the routine cardioversion strategy is the high rate of relapse to AF. Although rates of restoring SR are usually over 90%, as few as 25% of patients remain in SR 1 year post-cardioversion.3 Addition of prophylactic pharmacological anti-arrhythmic therapy increases the proportion maintaining SR, but the rhythm maintenance strategy still fails in approximately half of the patients.3 Numerous studies have aimed at identifying factors predicting SR maintenance following cardioversion,4–8 but virtually no parameter has shown consistent value in this respect. The few exceptions (i.e. arrhythmia duration4,6 and left atrial (LA) size7,8) are not sufficiently powerful predictors of outcome to guide management, and should probably rather be seen as indicators of relapse probability.

Atrial electrical remodelling is known to facilitate the persistence of AF and has been shown to correlate to arrhythmia recurrence in animal models.9 Whether or not this holds true also in man is not known.7,10,11 Two small studies, using an indirect, non-invasive electrophysiological approach, have been reported.7,10 Although both studies estimated atrial fibrillatory rate (AFR)12–16 and both included patients with AF of long duration, the results are conflicting.

The present study was designed to further investigate the question of whether AFR, a non-invasive index of atrial refractory period,12 is clinically useful in predicting the outcome following cardioversion of persistent AF. Furthermore, as electrical remodelling inevitably will be complete9,17 and structural changes probably will become of increasing importance,18,19 we explored if the predictive accuracy of AFR becomes lower as the arrhythmia duration increases.


   Methods
Top
 Abstract
 Introduction
 Methods
Results
 Discussion
 Conclusions
 References
 
Study population
In a retrospective approach, files of consecutive patients with persistent AF referred to our department for cardioversion between 1 January 2003 and 30 June 2005 were screened for inclusion in the study. Exclusion criteria were changes in pharmacological regime (during the study period or less than two weeks prior to study inclusion), or implanted pacemaker active at the time of baseline ECG recording. All patients gave informed consent via an opt-out procedure. The study was approved by the local Ethics Committee and complied with the Declaration of Helsinki.

Data acquisition
A standard 12-lead ECG was acquired prior to cardioversion. The digital signal (sampling frequency 500 Hz, sampling resolution 5 µV) was written to a file and transferred to a central database (Infinity MegaCare, Draeger Medical Systems, Inc., Danvers, MA, USA). After patient identification, it was downloaded for subsequent off-line processing.

The time frequency analysis (TFA) estimates AFR by computerized processing of QRST-subtracted surface-recorded ECG signals.12,16,20 In this study, QRST cancellation (i.e. identification, templating, and removal of ventricular components of the ECG to produce an atrial recording) utilized a spatiotemporal technique.16 The AFR was obtained by averaging the values of the AFR trend over the time interval of interest.

In the present study, AFR was estimated from a 10 s recording instead of as in previous publications, where a 60 s segment was used. The new method was validated, by comparing AFR computed from a 60 s recording and AFR computed from the first 10 s of the same recording, in a subset of the patients.

A standard transthoracic echocardiography was performed in association with the cardioversion.

Study protocol
Patients were considered asymptomatic if AF was diagnosed on routine ECG, without any concomitant symptoms.

Arrhythmia duration was defined as the time elapsed from symptom onset (or in case of asymptomatic AF, from the last-documented SR) until cardioversion. When exploring the impact of arrhythmia duration on the predictive properties of AFR, patients were separated in two sub-groups, using arrhythmia duration of 30 days as the cut-off value.

All patients underwent external DC-cardioversion. Cardioversion was considered successful if AF was abolished followed by at least two sinus beats. All patients successfully cardioverted underwent a 12-lead ECG prior to hospital discharge.

All patients were followed for four weeks. Patients were offered ECG if they suffered from symptoms of arrhythmia recurrence at any time during the study. All patients underwent a final ECG evaluation at four weeks post-cardioversion.

Cardioactive drugs were left unchanged for the duration of the study.

Post-processing analysis and statistics
Normally distributed data are expressed as mean±standard deviation. Median and range are used when normal distribution could not be assumed (i.e. arrhythmia duration).

Secondary analyses were conducted in the pre-specified sub-group of patients with AF of short duration (less than 30 days). When exploring the predictive properties of AFR, mean AFR was used to minimize bias introduction.

Mann–Whitney U test was used for comparison between samples. Fisher's exact test was used for discrete variables. All tests were two-sided and a P<0.05 was considered statistically significant. A multivariable logistic regression model was used including the significant variables from the univariate analysis. One variable at a time was removed, excluding the variable with the highest non-significant P-value.The variable was kept in the model if its exclusion changed the effect estimate of AFR by 10% or more. The multivariable odds ratios (OR) and their corresponding 95% confidence intervals (CI) are given. Model assumptions were checked by residual analysis. All statistical analyses were performed using STATISTICA for Windows version 6.1 (StatSoft, Inc., Tulsa, OK, USA).


   Results
Top
 Abstract
 Introduction
 Methods
 Results
Discussion
 Conclusions
 References
 
Data availability
A total of 314 patient files were screened for inclusion in the study. Five patients were excluded because of changes in pharmacological regime, and eight patients because of implanted pacemaker actively pacing at the time of baseline ECG recording. ECG prior to cardioversion was deficient in 107 of those patients; another 12 patients were excluded because of deficient follow-up ECG. In seven patients, the TFA failed (inadequate signal-to-noise ratio). No differences were observed in age, gender distribution, or outcome following cardioversion, between patients included in and patients excluded from the study (data not shown).

Validation of 10 s TFA
In 61 patients, a standard 5 min recording was obtained for method validation. The mean AFR computed from a 60 s segment (AFR60) in those patients was 376±54 fpm whereas the mean AFR computed from the initial 10 s segment of the same recording (AFR10) was 380±53 fpm. The mean error of AFR10 compared with AFR60 was 3.7±20 fpm. The corresponding 90% limits of agreement was 3.7±34 fpm.

Study population
A total of 175 patients (133 men, mean age 68±10 years) were included in the study. In 37% of the patients, there were no other cardiac or major medical diagnoses (i.e. lone AF), whereas the remaining patients had concomitant heart disease (summarized in Table 1).


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  		Table 1 Clinical characteristics and measured parameters in study population

 
No cardioactive drug was used by 13% of the patients. The distribution of the drug utilization in the remaining patients is shown in detail in Table 1, notably, only 7 and 2% were using sotalol and amiodarone, respectively, and no patients were using class I anti-arrhythmic drugs.

Mean AFR was 383±60 fpm. The median arrhythmia duration was 94 days (range 2–1044). Echocardiography demonstrated a mean LA diameter of 48±7 mm and mean left ventricular ejection fraction (LVEF) was 54±14%.

Eight patients were successfully cardioverted but AF relapsed within 10 s. The remaining 167 patients were in SR at discharge. At follow-up, 77 patients (44%) remained in SR.

Measured parameters in relation to outcome
The presence of congestive heart failure (CHF) was more common (19/98 vs. 6/77, P=0.03) and the LVEF was lower (51±15 vs. 57±13%, P=0.03) among patients relapsing to AF compared with those maintaining SR. Neither the remaining patient characteristics (i.e. gender, age, AF duration, presentation and history, and co-morbidity with the exception of CHF), nor LA diameter showed any definite relationship to SR maintenance. Of the ongoing medications, only digitalis use differed among the two populations, with a higher utilization among patients relapsing to AF (35/98 vs. 15/77, P=0.02). The complete comparison is listed in Table 1.

Average fibrillatory rate was lower among patients maintaining SR compared with those relapsing to AF (363±63 vs. 399±52 fpm, P=0.0004) (Figure 1).


Figure 0981
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  		Figure 1 The difference in AFR in the study population. Average fibrillatory rate was lower among patients maintaining SR compared with those relapsing to AF (363±63 vs. 399±52 fpm, P=0.00005, Student's t-test). Notably there is a large overlap between the two populations, making identification of clinically useful cut-off values difficult.

 
Using multivariable logistic regression, only two parameters proved to be independent predictors of AF relapse within four weeks: AFR>384 fpm (OR=3.2, CI 95% 1.7–6.1, P<0.0001) and digitalis use (OR=2.3, CI 95% 1.1–4.8, P=0.03). R2 for the model was 0.11.

Measured parameters in relation to AF duration
In 29 patients, arrhythmia duration was less than 30 days (median 5.5, range 2–26 days), leaving 146 patients with duration of at least 30 days (median 117, range 32–1044 days) or unknown duration (i.e. asymptomatic AF, without ECG documentation prior to hospital admission). The patients with shorter duration tended to be symptomatic at presentation to a larger extent (28/29 vs. 90/146, P=0.0001) and exhibited a lower use of digitalis (2/29 vs. 48/146, P=0.003) and ß-blockers (13/29 vs. 112/146, P=0.001) compared with the population with longer duration. In parallel, the proportion of patients with lone AF and without cardioactive drugs was higher among patients with short duration (16/29 vs. 49/146 and 8/29 vs. 14/146, P=0.04 and P=0.01, respectively). LA diameter was on an average slightly less in patients with shorter AF duration (46±7 vs. 49±7 mm, P=0.01), and the LVEF was higher in the short duration group (60±9 vs. 52±15%, P=0.009).

There were no differences observed in mean AFR (384±70 vs. 382±58 fpm, P=0.85) between patients with short AF duration and those with longer duration. However, the differences in mean AFR between patients maintaining SR and those relapsing to AF within respective group were markedly different. The complete comparison is listed in Table 2.


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  		Table 2 Clinical characteristics and measured parameters in relation to duration

 
The diagnostic property of AFR in the subset of patients with short arrhythmia duration (less than 30 days) was further explored, using the mean AFR (384 fpm) as cut-off value, resulting in a sensitivity of 79% (CI 95% 49–94) and a specificity of 80% (CI 95% 51–95) (Figure 2). Neither patient characteristics nor echocardiographic parameters differed between patients maintaining SR and those relapsing to AF (Table 3). This was confirmed using multivariable logistic regression; only AFR (AFR<384 fpm) was independently predictive of AF relapse within four weeks (OR=15, CI 95% 2.4–89, P=0.003). R2 for the model was 0.31.


Figure 0982
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  		Figure 2 Scatter plot of individual patients with AF duration less than 30 days. Subjects are grouped according to the rhythm at follow-up. The use of the group mean (384 fpm) as cut-off value resulted in a sensitivity of 79% (CI 95% 49–94) and a specificity of 80% (CI 95% 51–95) when predicting AF relapse within the follow-up period.

 

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  		Table 3 Clinical characteristics and measured parameters in patients with limited AF duration

 
AFR in relation to cardioactive drugs
The majority of patients were on ß-blockers (n=125). These patients exhibited a higher AFR than patients without these drugs (389±54 vs. 368±71 fpm, P=0.04). Neither calcium channel blockers nor digitalis influenced AFR significantly (374±52 vs. 384±61 fpm, P=0.51 and 392±56 vs. 379±62 fpm, P=0.22, respectively).

Only 16 patients were on anti-arrhythmic drugs in the present study (sotalol, n=12; amiodarone, n=4). Neither the median arrhythmia duration of these patients (111 days, range 2–274 vs. 93 days, range 2–1044, P=0.68), nor the other clinical characteristics differed significantly compared with patients without these drugs.

The AFR was lower among patients on anti-arrhythmic drugs compared with the rest of the study population (338±63 vs. 387±58 fpm, P=0.002). Furthermore, among patients on anti-arrhythmic drug therapy, the difference in AFR between those maintaining SR and those relapsing to AF was highly significant (292±53 vs. 382±36 fpm, P=0.002) with an almost complete separation of the groups.


   Discussion
Top
 Abstract
 Introduction
 Methods
 Results
 Discussion
Conclusions
 References
 
In the present study, we demonstrate that AFR differs between patients maintaining SR following cardioversion of persistent AF and those patients who relapse into AF. It is evident from the analyses that the value of AFR as a predictor of SR maintenance is highest in AF of short duration. In fact, if the arrhythmia duration exceeds 30 days, AFR probably does not add value in clinical decision making. AFR also appears to have high predictive accuracy for SR maintenance in patients with ongoing anti-arrhythmic drug treatment.

Data availability and study population
A total of 301 patients were eligible for inclusion into the study. The majority of the exclusions were due to missing ECG. The high frequency of missing ECG reflects insufficient clinical routines, where an ECG was recorded, but not saved in the central database for unknown reasons. However, there were no differences between patients included and those not, suggesting these were random omissions, unlikely to influence the results of the study. Very few patients were lost due to analysis failure (n=7), demonstrating the robustness of the method.

The rate of SR maintenance at 1 month follow-up (44%) is in keeping with previously published studies4,21 where anti-arrhythmic drug usage (9% in this study) is low. In particular, the low usage, in comparison to other descriptive studies,22 is probably largely due to the inclusion criterion of unchanged pharmacological therapy.

The arrhythmia duration was varied in the study population, reflecting typical clinical selection of patients referred for cardioversion of persistent AF, and in keeping with previous trials recruiting consecutive patients.4 The proportion of female patients in the present study is low (24%) and less than reported in the previous studies.23,24 The reason for this is unknown, but if it is not a chance finding, referral bias or treatment bias may have occurred.

Overall, the study population appears to be clinically representative and there is no evidence of an important bias introduced by data collection and analysis.

Methodological issues
The TFA of QRST-cancelled ECG is an established and validated methodology.12,14–16,20 The response of its derived parameter, AFR, to changes in medication and autonomic tone has been explored.25–28 Keeping in mind that the TFA of QRST-cancelled ECG, as performed in the present study, foremost reflects the activity in the right atria (V1 data is used for estimating the spectra),29 and its potential shortcoming when constant conduction velocity cannot be assumed, TFA of QRST-cancelled ECG offers a non-invasively obtained index of atrial refractory period.

The estimation of AFR from two segments of the same recording, with a length of 60 and 10 s, respectively, generated a mean error of less than 1% clearly indicating that AFR10 can be used for group comparisons. Moreover, the relatively narrow span of the 90% limits of agreement indicates that AFR10 could also be used for individual predictions, as the error in a given patient is likely to be neglectable compared with the difference observed between the compared groups.

Traditional factors predicting SR maintenance
Overall, relatively few of the clinical variables differed between patients relapsing to AF and those maintaining SR. For instance, there was minimal difference in median arrhythmia duration compared with those relapsing into AF. This is in contrast to several previously published studies,4,6,8 but it is perhaps noteworthy that none of these studies found arrhythmia duration to be a strong predictor of SR maintenance, and several other studies have failed to find an association.5,7

In the present study, the prevalence of CHF differed between the two groups, with a higher prevalence of CHF in the AF group. This was paralleled by a lower LVEF in the AF group. In a previously published series, no difference in LVEF and NYHA class could be found between patients maintaining SR and those not,6 but the patient population differed in ways that may be important. The arrhythmia duration was longer (median 11 months) and all patients were started on anti-arrhythmic drugs after study inclusion.

The use of digitalis, the only variable besides high AFR, independently predictive of AF relapse was higher among patients relapsing to AF, which may be interpreted in at least two ways. First, digitalis is known to increase intracellular calcium overload30 that is believed to be the key process of atrial remodelling. Hence, digitalis use may augment the electrical remodelling impact.31–33 Second, digitalis is commonly used in CHF, a feature associated with AF relapse in the present study. Neither sotalol nor amiodarone showed any definite relationship to SR maintenance in this study, but numbers on these agents were very small. Furthermore, the use of these agents was clinically determined thus introducing a selection bias with those at the highest risk of relapse being treated with the agents.

AFR and SR maintenance
In the present study, we found a difference in AFR between patients relapsing to AF and those maintaining SR. This finding is definite in spite of the duration being relatively long in the vast majority of the patients studied, i.e. the median duration by far exceeded the believed time frame of electrical remodelling evolution.9,34 AFR was the strongest, independent predictor of AF relapse of all studied parameters. However, although the difference is evident when comparing groups, the inter-individual variation in AFR within each group is extensive. This most likely illustrates the escalating influences of other processes, such as contractile and structural remodelling,35 as the duration increases. Importantly, AFR can only be seen as an index exclusively of remodelling if serial recordings are being analysed from each patient. When employed in the manner as in the present study, AFR reflects electrical remodelling and also any pre-existing change (e.g. hypertension, cardioactive drugs). This probably in part explains the extensive overlap which makes identification of clinically useful cut-off values based on AFR impossible.

Two previous, smaller studies have addressed the same issue as the present.7,10 Both studies included patients with AF of long duration (median 618 months), who were cardioverted and followed for 10 weeks. The demographic and echocardiographic parameters of patients in these two studies were comparable with one major exception. In the study from our group,10 patients on anti-arrhythmic drugs were excluded and no statistically significant difference could be detected between patients relapsing to AF and those maintaining SR. In contrast, in the other study,7 all patients were started on anti-arrhythmic drugs after ECG acquisition and a highly significant difference was found. The present study found that AFR was lower in those treated with anti-arrhythmic drugs irrespective of AF duration, as might be expected. However, it also found that in the subgroup on anti-arrhythmics, AFR was an excellent predictor of outcome. This was a post hoc analysis in a small patient sample and the results must be interpreted with caution, but it does suggest that the confounding effect of anti-arrhythmic drug therapy may explain the difference in the two previous studies. The finding in the present study that AFR was highly predictive of AF relapse in patients treated with anti-arrhythmic drugs irrespective of AF duration warrants further investigation.

AFR in AF of limited duration
Previous studies have illustrated that electrical remodelling develops rapidly, with a time course of 1–6 weeks in experimental models.9,17,34 Subsequently, other factors influence the atria; illustrated by a continuous increase in the persistence of AF even after electrical remodelling has been completed.35 Therefore, although human data are sparse, it is reasonable to assume that the role of electrical remodelling is foremost important in the first few weeks of AF. Consequently, a specific aim of the present study was to explore the predictive properties of AFR in patients with limited arrhythmia duration. If only considering the sub-group of patients with arrhythmia duration less than 30 days, the predictive property of AFR increases dramatically. In this setting, AFR was the only independent predictor of AF relapse with R2 of the model exceeding 30%. By using the mean AFR of these patients as cut-off value, AF relapse could be predicted with high accuracy, with the point-estimate of sensitivity and specificity both being in the 80% range (Figure 2). This corresponds well to the time-frame in which electrical remodelling is likely to have the largest impact on relapse probability.9,34 Although the use of mean AFR as cut-off value was arbitrarily chosen, it is notable that it is in close agreement with previously used cut-off values, suggesting that a true difference in atrial electrophysiology may be seen at those rates.13,36 Inevitably, the utilized method reflects not only the electrical remodelling induced by the arrhythmia, but also any pre-existing change in atrial refractory period. Thus, the predictive properties of AFR originate from its association to atrial refractory period, which in turn is the result of both electrical remodelling and pre-existing changes.

Study limitations
There were a considerable number of exclusions due to deficient ECG. As previously noted, this was most likely random omissions, but is nevertheless a limitation of the study. The present study utilized recordings of shorter duration than used in previous studies. Although the comparison made indicates that the estimates of AFR are similar regardless of recording length, the methodology is not yet as robust as hitherto used. The method used primarily estimates the atrial refractory period of the right atrium (spectra are computed from the V1 lead). Therefore, assumptions regarding LA electrophysiology cannot be made. The patient population was selected to be clinically representative and is consequently, to some extent heterogeneous in terms of baseline characteristics and ongoing medication. The importance and consequences of these parameters in relation to AFR and outcome must therefore be made with caution.


   Conclusions
Top
 Abstract
 Introduction
 Methods
 Results
 Discussion
 Conclusions
References
 
We demonstrated that AFR is higher in patients relapsing to AF than in those maintaining SR for 4 weeks after cardioversion of persistent AF. This implies a role of the degree of atrial electrical remodelling in the recurrence of human AF. The difference in pre-cardioversion AFR is most marked in the subset of patients with arrhythmia duration of less than 30 days. In this group, AFR can be used as a predictor of SR maintenance with sufficient accuracy to be of clinical utility. Although data were limited, this study also suggests that AFR may also be an important predictor of outcome in patients already on anti-arrhythmic drug treatment.

Conflict of interest: none declared.


   References
Top
 Abstract
 Introduction
 Methods
 Results
 Discussion
 Conclusions
 References
 

  1. Wyse DG, Waldo AL, DiMarco JP, Domanski MJ, Rosenberg Y, Schron EB, Kellen JC, Greene HL, Mickel MC, Dalquist JE, Corley SD. (2002) A comparison of rate control and rhythm control in patients with atrial fibrillation. N Engl J Med 347:1825–1833.[Abstract/Free Full Text]
  2. Van Gelder IC, Hagens VE, Bosker HA, Kingma JH, Kamp O, Kingma T, Said SA, Darmanata JI, Timmermans AJ, Tijssen JG, Crijns HJ. (2002) A comparison of rate control and rhythm control in patients with recurrent persistent atrial fibrillation. N Engl J Med 347:1834–1840.[Abstract/Free Full Text]
  3. Lundstrom T and Ryden L. (1988) Chronic atrial fibrillation. Long-term results of direct current conversion. Acta Med Scand 223:53–59.[Web of Science][Medline]
  4. Frick M, Frykman V, Jensen-Urstad M, Ostergren J, Rosenqvist M. (2001) Factors predicting success rate and recurrence of atrial fibrillation after first electrical cardioversion in patients with persistent atrial fibrillation. Clin Cardiol 24:238–244.[Web of Science][Medline]
  5. Antonielli E, Pizzuti A, Palinkas A, Tanga M, Gruber N, Michelassi C, Varga A, Bonzano A, Gandolfo N, Halmai L, Bassignana A, Imran MB, Delnevo F, Csanady M, Picano E. (2002) Clinical value of left atrial appendage flow for prediction of long-term sinus rhythm maintenance in patients with nonvalvular atrial fibrillation. J Am Coll Cardiol 39:1443–1449.[Abstract/Free Full Text]
  6. Biffi M, Boriani G, Bartolotti M, Bacchi Reggiani L, Zannoli R, Branzi A. (2002) Atrial fibrillation recurrence after internal cardioversion: prognostic importance of electrophysiological parameters. Heart 87:443–448.[Abstract/Free Full Text]
  7. Bollmann A, Husser D, Steinert R, Stridh M, Sörnmo L, Olsson SB, Polywka D, Molling J, Geller C, Klein HU. (2003) Echocardiographic and electrocardiographic predictors for atrial fibrillation recurrence following cardioversion. J Cardiovasc Electrophysiol 14:(Suppl. 10), S162–S165.[CrossRef][Web of Science][Medline]
  8. Dittrich HC, Erickson JS, Schneiderman T, Blacky AR, Savides T, Nicod PH. (1989) Echocardiographic and clinical predictors for outcome of elective cardioversion of atrial fibrillation. Am J Cardiol 63:193–197.[CrossRef][Web of Science][Medline]
  9. Wijffels MC, Kirchhof CJ, Dorland R, Allessie MA. (1995) Atrial fibrillation begets atrial fibrillation. A study in awake chronically instrumented goats. Circulation 92:1954–1968.[Abstract/Free Full Text]
  10. Meurling CJ, Roijer A, Waktare JE, Holmqvist F, Lindholm CJ, Ingemansson MP, Carlson J, Stridh M, Sornmo L, Olsson SB. (2006) Prediction of sinus rhythm maintenance following DC-cardioversion of persistent atrial fibrillation - the role of atrial cycle length. BMC Cardiovasc Disord 6:11.[CrossRef][Medline]
  11. Raitt MH, Kusumoto W, Giraud GD, McAnulty JH. (2004) Electrophysiologic predictors of the recurrence of persistent atrial fibrillation within 30 days of cardioversion. Am J Cardiol 93:107–110.[CrossRef][Web of Science][Medline]
  12. Holm M, Pehrson S, Ingemansson M, Sörnmo L, Jahansson R, Sandhall L, Sunemark M, Smideberg B, Olsson C, Olsson SB. (1998) Non-invasive assessment of the atrial cycle length during atrial fibrillation in man: introducing, validating and illustrating a new ECG method. Cardiovasc Res 38:69–81.[Abstract/Free Full Text]
  13. Bollmann A, Kanuru NK, McTeague KK, Walter PF, DeLurgio DB, Langberg JJ. (1998) Frequency analysis of human atrial fibrillation using the surface electrocardiogram and its response to ibutilide. Am J Cardiol 81:1439–1445.[CrossRef][Web of Science][Medline]
  14. Stridh M and Sörnmo L. (2001) Spatiotemporal QRST cancellation techniques for analysis of atrial fibrillation. IEEE Trans Biomed Eng 48:105–111.[CrossRef][Web of Science][Medline]
  15. Stridh M, Sörnmo L, Meurling CJ, Olsson SB. (2001) Characterization of atrial fibrillation using the surface ECG: time-dependent spectral properties. IEEE Trans Biomed Eng 48:19–27.[CrossRef][Web of Science][Medline]
  16. Stridh M, Sörnmo L, Meurling CJ, Olsson SB. (2004) Sequential characterization of atrial tachyarrhythmias based on ECG time-frequency analysis. IEEE Trans Biomed Eng 51:100–114.[CrossRef][Web of Science][Medline]
  17. Goette A, Honeycutt C, Langberg JJ. (1996) Electrical remodelling in atrial fibrillation. Time course and mechanisms. Circulation 94:2968–2974.[Abstract/Free Full Text]
  18. Rubin DN, Katz SE, Riley MF, Douglas PS, Manning WJ. (1996) Evaluation of left atrial appendage anatomy and function in recent-onset atrial fibrillation by transesophageal echocardiography. Am J Cardiol 78:774–778.[CrossRef][Web of Science][Medline]
  19. Schotten U, Duytschaever M, Ausma J, Eijsbouts S, Neuberger HR, Allessie M. (2003) Electrical and contractile remodelling during the first days of atrial fibrillation go hand in hand. Circulation 107:1433–1439.[Abstract/Free Full Text]
  20. Pehrson S, Holm M, Meurling C, Ingemansson M, Smideberg B, Sörnmo L, Olsson SB. (1998) Non-invasive assessment of magnitude and dispersion of atrial cycle length during chronic atrial fibrillation in man. Eur Heart J 19:1836–1844.[Abstract/Free Full Text]
  21. Tieleman RG, Van Gelder IC, Crijns HJ, De Kam PJ, Van Den Berg MP, Haaksma J, Van Der Woude HJ, Allessie MA. (1998) Early recurrences of atrial fibrillation after electrical cardioversion: a result of fibrillation-induced electrical remodelling of the atria? J Am Coll Cardiol 31:167–173.[Abstract/Free Full Text]
  22. Nieuwlaat R, Capucci A, Camm AJ, Olsson SB, Andresen D, Davies DW, Cobbe S, Breithardt G, Le Heuzey JY, Prins MH, Levy S, Crijns HJ. (2005) Atrial fibrillation management: a prospective survey in ESC member countries: the Euro Heart Survey on Atrial Fibrillation. Eur Heart J 26:2422–2434.[Abstract/Free Full Text]
  23. Friberg J, Scharling H, Gadsboll N, Truelsen T, Jensen GB. (2004) Comparison of the impact of atrial fibrillation on the risk of stroke and cardiovascular death in women vs men (The Copenhagen City Heart Study). Am J Cardiol 94:889–894.[CrossRef][Web of Science][Medline]
  24. Go AS, Hylek EM, Phillips KA, Chang Y, Henault LE, Selby JV, Singer DE. (2001) 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 285:2370–2375.[Abstract/Free Full Text]
  25. Holmqvist F, Stridh M, Waktare JE, Brandt J, Sornmo L, Roijer A, Meurling CJ. (2005) Rapid fluctuations in atrial fibrillatory electrophysiology detected during controlled respiration. Am J Physiol Heart Circ Physiol 289:H754–H760.[Abstract/Free Full Text]
  26. Ingemansson MP, Holm M, Olsson SB. (1998) Autonomic modulation of the atrial cycle length by the head up tilt test: non-invasive evaluation in patients with chronic atrial fibrillation. Heart 80:71–76.[Abstract/Free Full Text]
  27. Meurling CJ, Ingemansson MP, Roijer A, Carlson J, Lindholm CJ, Smideberg B, Sörnmo L, Stridh M, Olsson SB. (1999) Attenuation of electrical remodelling in chronic atrial fibrillation following oral treatment with verapamil. Europace 1:234–241.[Abstract/Free Full Text]
  28. Meurling CJ, Waktare JE, Holmqvist F, Hedman A, Camm AJ, Olsson SB, Malik M. (2001) Diurnal variations of the dominant cycle length of chronic atrial fibrillation. Am J Physiol Heart Circ Physiol 280:H401–H406.[Abstract/Free Full Text]
  29. Holm M, Johansson R, Olsson SB, Brandt J, Luhrs C. (1996) A new method for analysis of atrial activation during chronic atrial fibrillation in man. IEEE Trans Biomed Eng 43:198–210.[CrossRef][Web of Science][Medline]
  30. Morgan JP. (1985) The effects of digitalis on intracellular calcium transients in mammalian working myocardium as detected with aequorin. J Mol Cell Cardiol 17:1065–1075.[Web of Science][Medline]
  31. Bosch RF, Scherer CR, Rub N, Wohrl S, Steinmeyer K, Haase H, Busch AE, Seipel L, Kuhlkamp V. (2003) Molecular mechanisms of early electrical remodelling: transcriptional downregulation of ion channel subunits reduces I(Ca,L) and I(to) in rapid atrial pacing in rabbits. J Am Coll Cardiol 41:858–869.[Abstract/Free Full Text]
  32. Bosch RF, Zeng X, Grammer JB, Popovic K, Mewis C, Kuhlkamp V. (1999) Ionic mechanisms of electrical remodelling in human atrial fibrillation. Cardiovasc Res 44:121–131.[Abstract/Free Full Text]
  33. Skasa M, Jungling E, Picht E, Schondube F, Luckhoff A. (2001) L-type calcium currents in atrial myocytes from patients with persistent and non-persistent atrial fibrillation. Basic Res Cardiol 96:151–159.[CrossRef][Web of Science][Medline]
  34. Yue L, Feng J, Gaspo R, Li GR, Wang Z, Nattel S. (1997) Ionic remodelling underlying action potential changes in a canine model of atrial fibrillation. Circ Res 81:512–525.[Abstract/Free Full Text]
  35. Allessie M, Ausma J, Schotten U. (2002) Electrical, contractile and structural remodelling during atrial fibrillation. Cardiovasc Res 54:230–246.[Abstract/Free Full Text]
  36. Stambler BS, Wood MA, Ellenbogen KA. (1997) Antiarrhythmic actions of intravenous ibutilide compared with procainamide during human atrial flutter and fibrillation: electrophysiological determinants of enhanced conversion efficacy. Circulation 96:4298–4306.[Abstract/Free Full Text]

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