Skip Navigation

Cardiovascular Research 2002 53(4):944-951; doi:10.1016/S0008-6363(01)00559-4
© 2002 by European Society of Cardiology
This Article
Right arrow Abstract Freely available
Right arrow FREE Full Text (PDF) Freely available
Right arrow E-letters: Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when E-letters are posted
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrowRequest Permissions
Right arrow Disclaimer
Google Scholar
Right arrow Articles by Korte, T.
Right arrow Articles by Tebbenjohanns, J.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Korte, T.
Right arrow Articles by Tebbenjohanns, J.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

Copyright © 2002, European Society of Cardiology

Significant prolongation of atrial monophasic action potential duration: short-term reverse electrophysiological changes after internal cardioversion of atrial fibrillation

Thomas Korte*, Michael Niehaus, Gabriele Borchert and Jürgen Tebbenjohanns

Department of Cardiology, Medical School Hannover, Carl-Neuberg-Strasse 1, 30625 Hannover, Germany

korte.thomas{at}mh-hannover.de

* Corresponding author. Tel.: +49-511-532-3817; fax: +49-511-532-8475

Received 18 July 2001; accepted 2 November 2001


   Abstract
Top
 Abstract
1. Introduction
 2. Methods
 3. Results
 4. Discussion
 5. Conclusions
 References
 
Objective: Since short action potentials and short refractory periods facilitate the induction of atrial reentry, this maladaptation has been proposed as the pathophysiological basis of the frequent immediate recurrences of atrial fibrillation (IRAF) after internal cardioversion. However, short-term reverse electrophysiological changes of the atria after cardioversion have not been studied in humans. Methods: Thirty-seven patients with chronic atrial fibrillation of 16±19 months and ten patients with an atrial fibrillation duration ≤48 h underwent internal cardioversion. Antiarrhythmic medication was only continued in 10 patients (21%), who were on amiodarone before cardioversion. Atrial monophasic action potential duration at 90% repolarization (APD90), sinus rate, P wave duration and interatrial conduction times between high right atrium and coronary sinus were recorded at min 0, 1, 3, 5, 10, 15 and 20 after cardioversion. Results: Internal cardioversion was successful in all patients, but twelve of the patients with chronic AF (32%) and three of the patients with intermittent AF (30%) had one to four episodes of IRAF after 16±28 s. There was a significant 52±30 ms APD90 prolongation, 83% of which occurred in min 0–3 (P<0.0001) and 17% in min 3–20 (P<0.05) after internal cardioversion. There was no significant temporal change in sinus rate, P-wave and interatrial conduction time during the time studied. APD90 prolongation and its time dependence did not show a detectable difference in subgroups with chronic AF, IRAF, left atrial size >40 mm and treatment with amiodarone. Conclusions: There is a significant prolongation of action potential duration in min 0–3 after internal cardioversion of atrial fibrillation, whereas sinus rate and intra- and interatrial conduction time remain unchanged. APD90 prolongation in min 0–3 shows a temporal relationship to the high rate of immediate recurrences of atrial fibrillation during this time interval. The data imply that there is a transient recovery of atrial refractoriness after cardioversion and suggest a mechanism of the high rate of early recurrences of atrial fibrillation.

KEYWORDS Arrhythmia (mechanisms); Defibrillation; Ion channels; Remodeling; Supraventr. arrhythmia


   1. Introduction
Top
 Abstract
 1. Introduction
2. Methods
 3. Results
 4. Discussion
 5. Conclusions
 References
 
Immediate recurrence of atrial fibrillation (IRAF) within the first seconds and minutes after cardioversion remains as high as 13–29% [1–3] and is one factor determining unsuccessful electrical cardioversion.

The two components of wavelength, conduction velocity and atrial refractoriness, are basic determinants of AF onset and perpetuation. Wijffels et al. [4] have demonstrated in healthy goats that the artificial maintenance of AF by rapid atrial pacing induced progressive shortening of the atrial refractory period and that rate-related shortening of the effective refractory period was inverted, resulting in shorter refractoriness at lower rates. It was postulated that the loss of the normal increase in refractoriness with a decrease in rate could be an important factor favoring AF and might facilitate the induction of the arrhythmia by premature atrial beats during sinus rhythm. Allessie et al. [5] have proposed to differentiate between long-term reverse electrophysiological remodeling of the atria with alteration of gene expression, hibernation and irreversible structural changes, and short-term reverse electrophysiological (metabolic) changes with altered ion concentration, ion pump activity and phosphorylation of ion channels. A number of animal and humans studies have referred to long-term electrophysiological remodeling caused by atrial fibrillation and its correlation to AF recurrence [6–14]. The short-term reverse electrophysiological changes have been postulated as cause of immediate recurrence of AF but have not been studied after internal cardioversion in humans.

It was the aim of this study to analyze the short-term (metabolic) electrophysiologic changes of the atria in the first minutes after internal cardioversion of atrial fibrillation as potential mechanisms of immediate AF reinitiation and to look for predictors of AF reinitiation in a cohort of consecutive patients with chronic AF, and AF of recent onset.


   2. Methods
Top
 Abstract
 1. Introduction
 2. Methods
3. Results
 4. Discussion
 5. Conclusions
 References
 
2.1. Study population
Low-energy internal cardioversion of AF was performed in consecutive patients with either chronic AF or AF of recent onset ≤48 h. Cardioversion to sinus rhythm was performed for a clinically indicated restoration of sinus rhythm or indicated during an ablation procedure. Evaluation of the patients included clinical history, physical examination, routine laboratory (including T3, T4 and TSH), 12-lead ECG, and transthoracic and transesophageal echocardiography. Class I antiarrhythmic drugs and Sotalol were interrupted five half-times before cardioversion. If patients were on amiodarone, medication was continued. The investigation conforms with the principles outlined in the Declaration of Helsinki, all patients gave informed consent.

2.2. Internal cardioversion protocol
Internal cardioversion was performed by placement of a newly designed steerable cardioversion electrode (TC3+1DT, 7-French, VascoMed) in the coronary sinus and one cardioversion electrode in the anterolateral right atrium (TC2+1JO, 7-French, VascoMed) with insertion in the right femoral vein, respectively (Fig. 1). In eight patients (17%) the coronary sinus could only be cannulated using a specially designed 8-French introduction sheath (SL1, Daig). A quadripolar 6-French electrode (Josephson, Bard) was placed in the right ventricle for triggering shock delivery to the R-wave. Using the coronary sinus catheter as the anode and the right atrial catheter as the cathode, a biphasic cardioversion shock was delivered from an external defibrillator (Ventak ECD, CPI Guidant). Shocks were delivered starting at 15 J, following a 5-J step-up protocol until cardioversion of AF was successful. The time interval between shocks was 3 min. Intravenous application of hypnomidate (0.5 mg/kg) was used for sedation. If no sinus rhythm was achieved with a maximum 35-J shock for internal cardioversion or >4 IRAF occurred cardioversion was declared unsuccessful.


Figure 1
View larger version (117K):
[in this window]
[in a new window]
[Download PowerPoint slide]
  		Fig. 1 Right oblique fluoroscopic projection of the position of the defibrillation electrodes in the anterolateral right atrium (RA) and coronary sinus (CS) and the catheter for recording of monophasic action potentials in the right atrial appendage (RAA). A quadripolar electrode is positioned at the right ventricular apex (RV) for synchronized shock delivery.

 
2.3. Electrophysiological parameters
A 12-lead surface ECG, endocardial recordings of monophasic action potentials at the right atrial appendage, and endocardial signals at the coronary sinus, the high right atrium and the right ventricular apex were acquired continuously in digital format using a Prucka electrophysiology system (CardiaLab, Prucka Engineering). An example of the simultaneous recordings at internal cardioversion is shown in Fig. 2.


Figure 2
View larger version (22K):
[in this window]
[in a new window]
[Download PowerPoint slide]
  		Fig. 2 Original recording: three-lead surface ECG shown with the endocardial recordings of the monophasic action potential at the right atrial appendage (RAA), the coronary sinus (CS), the high right atrium (HRA) and the right ventricular apex (RV).

 
At min 0, 1, 3, 5, 10, 15 and 20 after internal cardioversion of AF monophasic action potential duration at 90% repolarization (APD90) during sinus rhythm, sinus rate and P-wave duration were determined.

Monophasic action potentials were recorded at the right atrial appendage with a 6-French fractually coated, steerable electrode (MAPCath, Biotronik). Measurements of APD90 were performed by two independent observers manually (T.K., G.B.) at a paper speed of 200 mm/s according to the standard method [15]. Mean APD90, derived from the first three signals of sinus beats at min 0, 1, 3, 5, 10, 15 and 20 after cardioversion was determined. Intra- and interobserver variations were <5%. In patients with immediate recurrence of atrial fibrillation measurements were performed after successful cardioversion and persistence of sinus rhythm so that temporal changes could be evaluated. Patients with incomplete MAP recordings or a signal amplitude <10 mV were considered a dropout. A representative example of MAP recording at min 0, 1 and 3 after cardioversion is given in Fig. 3.


Figure 3
View larger version (16K):
[in this window]
[in a new window]
[Download PowerPoint slide]
  		Fig. 3 Original recording: lead I (surface ECG) and monophasic action potentials (from the right atrial appendage) recorded during sinus rhythm at min 0 (A), min 1 (B) and min 3 (C) after cardioversion. Notice the progressive prolongation of APD90 mainly due to a change in plateau length. Sinus rate did not significantly change.

 
Interatrial conduction times were measured at min 1, 3, 5, 10, 15 and 20 by pacing from the right atrial and the coronary sinus cardioversion electrodes for 5 beats at a cycle length of 500 ms, respectively.

2.4. Predictor analysis
In case of significant temporal changes of the measured electrophysiological parameters (APD90, sinus rate, P-wave duration and interatrial conduction times) additional subgroup analysis of patients with chronic AF vs. AF of recent onset, occurrence vs. no occurrence of IRAF, left atrium >40 vs. ≤40 mm and treatment with vs. without amiodarone was performed.

2.5. Definitions
AF has been described before [16,17]. IRAF was defined as the resumption of AF within 3 min after an internal defibrillation shock that resulted in sinus rhythm for at least one beat [1]. Chronic AF was defined as an AF duration of >48 h, and AF of recent onset as an AF duration of ≤48 h.

2.6. Statistical analysis
Continuous variables are expressed as mean±S.D. To assess differences in the course of APD90, sinus rate, P-wave duration and conduction time between right atrium and coronary sinus in min 0–20, a multivariate repeated measures analysis of variance was used. For comparison of APD90 prolongation in min 0–3 and min 3–20, the paired Student's t-test was performed. For the subgroup comparison of APD90 prolongation in min 0–3, the unpaired Student's t-test was used. Nominal values were evaluated by the {chi}2 test. P<0.05 was considered statistically significant.


   3. Results
Top
 Abstract
 1. Introduction
 2. Methods
 3. Results
4. Discussion
 5. Conclusions
 References
 
3.1. Clinical characteristics and acute results of internal cardioversion
Internal cardioversion was performed in thirty-seven patients with chronic AF of 16±19 (1–84) months and ten patients with AF of recent onset and a duration of 10±16 (0.1–48) h. Internal cardioversion was successful in all patients after an application of 21±8 (15–35) J. Table 1 shows the characteristics of the study group. No significant difference was found between the groups with chronic AF vs. AF of recent onset with regard to gender, age, heart disease, left atrial diameter, left ventricular ejection fraction and internal shock delivery. No thrombi were detectable during TEE and T3, T4 and TSH were in the normal range in all of the patients studied.


View this table:
[in this window]
[in a new window]

  		Table 1 Patient characteristics

 
3.2. Patients with IRAF
Fifteen patients (32%) had 1.1±2.0 (1–4) episodes of IRAF after delivery of 25±12 J. The time interval between the termination of AF and reinitiation was 16±28 (3–128) s. The earliest atrial endocardial activation time recorded from the defibrillation catheters was always after the beginning of the P wave of the initiating atrial premature beat. Thus, these atrial premature beats did not seem to originate from the defibrillation catheters. There was no significant difference in the clinical characteristics of the patients with and without IRAF (Table 1).

3.3. Electrophysiological parameters after cardioversion
The electrophysiological study protocol was completed in thirty patients. Seventeen patients were dropouts because of low quality or incomplete MAP recordings. Of the thirty patients with completed electrophysiological protocol, twenty-one (70%) had chronic atrial fibrillation, ten patients (33%) had at least one episode of IRAF, six patients (20%) were on amiodarone at cardioversion and twenty-two patients (73%) had an atrial size >40 mm.

3.3.1. Monophasic action potentials
Fig. 4 demonstrates the temporal changes of APD90 in min 0–20 after internal cardioversion with a APD90 prolongation of 52±33 ms (0–118). Of this APD 90 prolongation 83% occurred in min 0–3 with 44±25 ms (2–100). The temporal effect was highly significant in min 0–3 (P<0.0001) and much less pronounced in min 3–20 (P=0.046). The return cycle to the first sinus beat after successful cardioversion was 1279±530 ms (265–2510) and had no significant effect on APD90 at min 0.


Figure 4
View larger version (9K):
[in this window]
[in a new window]
[Download PowerPoint slide]
  		Fig. 4 Temporal changes in the action potential duration at 90% repolarization (APD90) during min 0–20 after internal cardioversion. The data plotted are derived from the thirty patients with completed electrophysiological study protocol.

 
3.3.2. Sinus rate and intra- and interatrial conduction times
Fig. 5a–c shows the temporal changes in sinus rate, intra- and interatrial conduction time from the high right atrium to the coronary sinus and from the coronary sinus to the high right atrium at a pacing cycle length of 500 ms after cardioversion. No significant temporal changes could be found for sinus rate (P=0.199), P-wave duration (P=0.922) and conduction time from high right atrium to coronary sinus (P=0.769) and from coronary sinus to high right atrium (P=0.769).


Figure 5
View larger version (12K):
[in this window]
[in a new window]
[Download PowerPoint slide]
  		Fig. 5 Temporal changes in sinus cycle length (a), P-wave duration (b) and interatrial conduction times (c) between high right atrium (HRA) and coronary sinus (CS) at a pacing cycle length of 500 ms. The data plotted are derived from the thirty patients after successful internal cardioversion of atrial fibrillation and complete electrophysiological study protocol.

 
3.3.3. Variables with potential influence on prolongation of monophasic action potentials
The influence of four clinical variables on the prolongation of APD90 was analyzed (Fig. 6). APD90 prolongation in min 0–3 was not significantly different in patients with chronic AF vs. patients with AF of recent onset (P=0.948), patients with vs. patients without IRAF (P=0.731), patients with vs. patients without amiodarone at cardioversion (P=0.567) and patients with a left atrial size >40 mm vs. patients with normal atrial size (P=0.304) (due to a low patient number in the studied subgroups and a high common standard deviation, power <20%, respectively).


Figure 6
View larger version (14K):
[in this window]
[in a new window]
[Download PowerPoint slide]
  		Fig. 6 Percent increase in action potential duration at 90% repolarization (APD90) in min 0–3 versus min 3–20 after internal cardioversion for all patients and patients with chronic atrial fibrillation (cAF), immediate recurrence of atrial fibrillation (IRAF), amiodarone treatment (Amio) and a left atrial size >40 mm (LA>40). The significant APD90 increase in min 0–3 was not different between subgroups (P>0.05).

 

   4. Discussion
Top
 Abstract
 1. Introduction
 2. Methods
 3. Results
 4. Discussion
5. Conclusions
 References
 
4.1. Main findings
The main finding of the study is that there is a significant right atrial prolongation of APD90 after internal cardioversion in patients with both chronic AF and AF of recent onset, and that most of the temporal recovery of APD90 prolongation occurs within 3 min. There is a temporal relationship between the changes in action potential prolongation and the high rate of immediate recurrence of AF in min 0–3 after internal cardioversion. APD90 prolongation in min 0–3 is independent of sinus rate, which does not show a significant temporal change during the studied time period. In addition, there is no significant change in intra- and interatrial conduction time as measured by the P wave duration and conduction between high right atrium and coronary sinus.

4.2. Atrial refractoriness and its temporal recovery after termination of atrial fibrillation
High-density mapping studies of AF in humans suggest that a determinant of AF is the presence of a critical number of wandering reentrant atrial wavelets [18,19]. The two components of wavelength, conduction velocity and atrial refractoriness, are thus basic determinants of AF onset and perpetuation. In AF, if the atrial wavelength is long, reentry may not be maintained and AF may self-terminate. However, if atrial wavelength is relatively short because of short refractroy period or depressed conduction, or both, then a greater number of wave fronts can circulate through the atria and AF may be sustained [20–22]. Daoud et al. [23] and others [24] have demonstrated that brief episodes of pacing-induced AF shorten the atrial refractory period following spontaneous AF termination, thereby shortening the wavelength. Temporal changes recovered within 5–10 min after spontaneous AF termination. No information is given about changes in atrial conduction velocity and the influence of rate on refractoriness after AF termination.

As demonstrated in this study, similar short-term changes of atrial refractoriness as measured by action potential duration, occur in min 0–3 after internal cardioversion of both chronic AF and AF of recent onset. In contrast to the study by Daoud et al. [23] we did not perform repeated ERP measurements and measured action potentials during sinus rhythm to exclude possible effects of extensive pacing on the temporal changes in refractoriness. This method also enabled us to monitor sinus rate which showed no significant change during the time analyzed. Thus the temporal changes in refractoriness seem to be independent of sinus node recovery after cardioversion. Furthermore, we demonstrate that the early changes in refractoriness are not accompanied by a temporal change in intra- and interatrial conduction time.

4.3. Occurrence of IRAF
In their study Daoud et al. [23] report on frequent induction of secondary episodes of AF after a primary episode of pacing-induced AF supporting the hypothesis that the AF-induced shortening of the atrial ERP promotes perpetuation of AF. As other investigators [1] we found a high rate (32%) of immediate recurrences of AF within min 0–3 after cardioversion. Thus, there also is a clear temporal relationship between the changes of atrial refractoriness and the propensity for reinduction of AF after internal cardioversion. Consistent with others [1], we could not find a clinical parameter (AF duration, amiodarone treatment, atrial size) predicting IRAF, suggesting that the short-term changes in refractoriness and the propensity of very early AF reinitiation is independent of these variables. Furthermore, this study was not able to demonstrate a direct relationship between the extent of APD90 prolongation and AF duration, occurrence of IRAF, amiodarone treatment and atrial size. This might be explained by the small patient number studied in the subgroups. In particular, the impact of APD90 prolongation on the occurrence of IRAF has to be studied in greater patient cohorts. Other early changes in atrial electrophysiology such as dispersion of repolarization may also faciliate the induction of secondary episodes of AF immediately after cardioversion.

4.4. Mechanisms of prolongation of atrial refractoriness after AF termination
Allessie et al. [5] have proposed to differentiate between long-term reverse electrophysiological remodeling of the atria with alteration of gene expression, hibernation and irreversible structural changes, and short-term reverse electrophysiological (metabolic) changes, demonstrated in this study, with altered ion concentration, ion pump activity and phosphorylation of ion channels.

One likely short-term mechanism for AF-induced shortening of atrial refractoriness is the physiological, rate-dependent shortening of the action potential duration [23]. Activation and deactivation of gated outward potassium current during the action potential plateau phase can result in beat-to-beat potassium accumulation and shortening of the action potential duration and the ERP [25–29]. The reverse mechanism may occur after restoration of sinus rhythm. A second mechanism for shortening of the atrial ERP after AF might be ‘cardiac memory’, which has been described for T-wave changes after rapid ventricular pacing. It has been suggested that cardiac memory is also caused by changes in potassium current, i.e. the transient outward potassium channel [30–32]. A similar alteration in potassium current may occur as a result of AF, and might explain the alteration of post-AF atrial repolarization and its short-term reversal. As a third mechanism of the changes in atrial properties, anisotropic capacitive coupling has been proposed [32–33]. As cause of AF changes in cellular coupling and thus action potential duration may occur. After resumption of isotropic conduction during sinus rhythm, these coupling changes may persist and be reversible after a few minutes. Further studies are needed to more clearly define the ionic mechanisms and signal transduction pathways involved in the short-term electrophysiological changes after AF termination.

4.5. Prevention of IRAF by influencing early electrophysiological changes after AF
Prevention strategies of IRAF have only been studied in a few animal and human studies. Timmermanns et al. [1] reported on atropin or a type Ic antiarrhythmic drug to prevent further IRAF in three of five patients. Tieleman et al. [34] reported on significantly less shortening of the atrial effective refractory period after rapid atrial pacing in goats treated with verapamil. But there was only a minimal reduction in inducibility of AF. Daoud et al. [3] found a reduced recurrence of IRAF in patients with external cardioversion and intravenous administration of verapamil. Tieleman et al. [35] reported that digoxin aggravates tachycardia-induced atrial electrical remodeling in goats with a prolonged shortening of the atrial refractory period. Nakashima et al. [36] showed a complete inhibition of shortening of the atrial effective refractory period after rapid atrial pacing in dogs with angiotensin II antagonist treatment. Tse et al. [2] reported on the efficacy of right atrial pacing in 42% and administration of sotalol in 71% of patients with IRAF. Although our study was not able to show a correlation between the extent of prolongation of monophasic action potentials and IRAF occurrence it might be postulated that influencing the very early electrophysiological changes after internal cardioversion, i.e. atrial refractoriness due to the sudden rate drop might significantly reduce the number of IRAF occurrences.

4.6. Limitations
Atrial refractoriness could not be directly measured, because the short period of 20 min analyzed after cardioversion of atrial fibrillation did not allow extensive pacing protocols. Only monophasic action potentials from the right atrium were recorded to avoid transseptal puncture, and therefore changes of MAP potentials from the left atrium could not be analyzed.


   5. Conclusions
Top
 Abstract
 1. Introduction
 2. Methods
 3. Results
 4. Discussion
 5. Conclusions
References
 
Monophasic action potential duration at 90% repolarization significantly prolongs in min 0–3 after internal cardioversion of atrial fibrillation. Other electrophysiological parameters such as sinus rate and intra- and interatrial conduction time remain constant. APD90 prolongation in min 0–3 shows a temporal relationship to the high rate of immediate recurrences of atrial fibrillation during this time interval. These data suggest recovery of atrial refractoriness as a mechanism of the high rate of early recurrences of AF after cardioversion.

Time for primary review 4 days.


   Acknowledgements
 
We thank H. Herrmann, Ph.D., from the Institute of Biometry of the Medical School Hannover for his support with the statistical analysis.


   References
Top
 Abstract
 1. Introduction
 2. Methods
 3. Results
 4. Discussion
 5. Conclusions
 References
 

  1. Timmermans C, Rodriguez L.M, Smeets J, Wellens H. Immediate reinitiation of atrial fibrillation following internal atrial defibrillation. J Cardiovasc Electrophysiol (1998) 9:122–128.[Web of Science][Medline]
  2. Tse H.F, Lau C.P, Ayers G.M. Atrial pacing for suppression of early reinitiation of atrial fibrillation after successful internal cardioversion. Eur Heart J (2000) 21:1167–1176.[Abstract/Free Full Text]
  3. Daoud E.G, Hummel J.D, Augostini R, Williams S, Kalbfleisch S.J. Effect of verapamil on immediate recurrence of atrial fibrillation. J Cardiovasc Electrophysiol (2000) 11:1231–1237.[CrossRef][Web of Science][Medline]
  4. Wijffels M.C.E.F, Kirchhof C.J.H.J, Dorland R, Allessie M.A. Atrial fibrillation begets atrial fibrillation. A study in awake chronically instrumented goats. Circulation (1995) 92:1954–1968.[Abstract/Free Full Text]
  5. Allessie M.A. Atrial electrophysiologic remodeling: another vicious circle. J Cardiovasc Electrophysiol (1998) 9:1378–1393.[Web of Science][Medline]
  6. Morillo C.A, Klein G.J, Jones D.L. Chronic rapid atrial pacing: structural, functional and electrophysiologic characteristics of a new model of sustained atrial fibrillation. Circulation (1995) 91:1588–1595.[Abstract/Free Full Text]
  7. Franz M.R, Karasik P.L, Li C, Moubarak J, Chavez M. Electrical remodeling of the human atrium: similar effects in patients with chronic atrial fibrillation and atrial flutter. J Am Coll Cardiol (1997) 30:1785–1790.[Abstract]
  8. Sparks P.B, Jayaprakash S, Vohra J, Kalman J.M. Electrical remodeling of the atria associated with paroxysmal and chronic atrial flutter. Circulation (2000) 102:1807–1813.[Abstract/Free Full Text]
  9. Pandozi C, Bianconi L, Villani M, et al. Electrophysiological characteristics of the human atria after cardioversion of persistent atrial fibrillation. Circulation (1998) 98:2860–2865.[Abstract/Free Full Text]
  10. Hobbs W.J.C, Fynn S, Todd D.M, et al. Reversal of atrial electrical remodelling after cardioversion of persistent atrial fibrillation in humans. Circulation (2000) 101:1145–1151.[Abstract/Free Full Text]
  11. Yu W.C, Lee S.H, Tai C.T, et al. Reversal of atrial electrical remodeling following cardioversion long-standing atrial fibrillation in man. Cardiovasc Res (1999) 42:470–476.[Abstract/Free Full Text]
  12. Manios E.G, Kanoupakis E.M, Chlouverakis G.I, et al. Changes in atrial electrical properties following cardioversion of chronic atrial fibrillation: relation with recurrence. Cardiovasc Res (2000) 47:244–253.[Abstract/Free Full Text]
  13. Bosch R.F, Zeng X, Grammer J.B, et al. Ionic mechanisms of electrical remodeling in human atrial fibrillation. Cardiovasc Res (1999) 44:121–131.[Abstract/Free Full Text]
  14. Yue L, Melnyk P, Gaspo R, Wang Z, Nattel S. Molecular mechanisms underlying ionic remodeling in a dog model of atrial fibrillation. Circ Res (1999) 84:776–784.[Abstract/Free Full Text]
  15. Franz M.R. Method and theory of monophasic action potential recording. Prog Cardiovasc Dis (1991) 33:347–368.[CrossRef][Web of Science][Medline]
  16. Lammers W.J.E.P, Ravelli F, Disertori M, Antolini R, Allessie M.A. Variations in human atrial flutter cycle length induced by ventricular beats: evidence of a re-entrant circuit with a partially excitable gap. J Cardiovasc Electrophysiol (1991) 2:375–387.[CrossRef]
  17. Ravelli F, Disertori M, Cozzi F, Antolini R, Allessie M.A. Ventricular beats induce variations in cycle length of rapid (type 2) atrial flutter in man: evidence of leading circle re-entry. Circulation (1994) 89:2107–2116.[Abstract/Free Full Text]
  18. Konings K.T.S, Kirchhof C.J.H.J, Smeets J.R.L.M, et al. High-density mapping of electrically induced atrial fibrillation in humans. Circulation (1994) 89:1665–1680.[Abstract/Free Full Text]
  19. Cox J.L, Canavan T.E, Schuessler R.B, et al. The surgical treatment of atrial fibrillation: intraoperative electrophysiologic mapping and description of the electrophysiologic basis of atrial flutter and atrial fibrillation. J Thorac Cardiovasc Surg (1991) 101:406–426.[Abstract]
  20. Rensma P.L, Allessie M.A, Lammers W.J.E.P, Bonke F.I.M, Schalij M.J. The length of the excitation wave as an index for the susceptibility to reentrant atrial arrhythmias. Circ Res (1988) 62:395–410.[Abstract/Free Full Text]
  21. Michelucci A, Padeletti L, Fradella G.A. Atrial refractoriness and spontaneous or induced atrial fibrillation. Acta Cardiol (1982) 5:333–344.
  22. Smeets J.L.R.M, Allessie M.A, Lammers W.J.E.P, Bonke F.I.M, Hollen J. The wavelength of the cardiac impulse and reentrant arrhythmias in isolated rabbit atrium. Circ Res (1986) 58:96–108.[Abstract/Free Full Text]
  23. Daoud E.G, Bogun F, Goyal R, et al. Effect of atrial fibrillation on atrial refractoriness in humans. Circulation (1996) 94:1600–1606.[Abstract/Free Full Text]
  24. Lubinski A, Kempa M, Lewicka-Nowak E, et al. Electrical atrial remodelling assessed by monophasic action potential and atrial refractoriness in patients with structural heart disease. PACE (1998) 21:2440–2444.[Medline]
  25. Kline R.P, Kupersmith J. Effects of extracellular potassium accumulation and sodium pump activation on autonomic canine Purkinje fibers. J Physiol (1982) 324:507–533.[Abstract/Free Full Text]
  26. Hauswirth O, Noble D, Tsien R.W. The dependence of plateau currents in cardiac Purkinje fibers on the interval between action potentials. J Physiol (1972) 222:22–49.
  27. Noble D, Tsien R.W. Outward membrane currents activated in the plateau range of potentials in cardiac Purkinje fibers. J Physiol (1969) 200:205–231.[Abstract/Free Full Text]
  28. Colatsky T.J, Hogan P.M. Effects of external calcium, calcium channel-blocking agents, and stimulation frequency on cycle length-dependent changes in canine cardiac action potential duration. Circ Res (1980) 46:543–552.[Free Full Text]
  29. Boycott M.R, Jewell B.R. Analysis of the effect of rate and rhythm upon electrical activity in the heart. Prog Biopsy Mol Biol (1980) 361:1–52.
  30. Gelled J.C, Rosen M.R. Persistent T-wave changes after alteration of the ventricular activation sequence: new insights into cellular mechanisms of cardiac memory. Circulation (1993) 88:1811–1819.[Abstract/Free Full Text]
  31. Del Blaze U, Rosen M.R. T-wave changes persisting after ventricular pacing in canine heart are altered by 4-aminopyridine but not by lidocaine: implications with respect to phenomenon of cardiac memory. Circulation (1992) 85:1464–1472.[Abstract/Free Full Text]
  32. Goyal R, Vikstrom B, Hero A, Morady F. Simulation of cardiac memory in a computer model utilizing capacitive coupling. J Electrocardiol (1995) 28:180–183.[CrossRef][Web of Science][Medline]
  33. Spach M.S, Dolber P.C, Heidlage J.F, Kootse J.M, Johnson E.A. Propagating depolarization in anisotropic human and canine cardiac muscle: apparent directional differences in membrane capacitance. Circ Res (1987) 60:206–219.[Abstract/Free Full Text]
  34. Tieleman R.G, de Langen C.D.J, van Gelder I.C, et al. Verapamil reduces tachycardia-induced electrical remodeling of the atria. Circulation (1997) 95:1945–1953.[Abstract/Free Full Text]
  35. Tieleman R.G, Blaauw Y, Van Gelder I, et al. Digoxin delays recovery from tachycardia-induced electrical remodeling of the atria. Circulation (1999) 100:1836–1842.[Abstract/Free Full Text]
  36. Nakashima H, Kumagai K, Urata H, et al. Angiotensin II antagonist prevents electrical remodeling in atrial fibrillation. Circulation (2000) 101:2612–2617.[Abstract/Free Full Text]

Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?



This Article
Right arrow Abstract Freely available
Right arrow FREE Full Text (PDF) Freely available
Right arrow E-letters: Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when E-letters are posted
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrowRequest Permissions
Right arrow Disclaimer
Google Scholar
Right arrow Articles by Korte, T.
Right arrow Articles by Tebbenjohanns, J.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Korte, T.
Right arrow Articles by Tebbenjohanns, J.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?