Skip Navigation


European Heart Journal Advance Access originally published online on August 4, 2006
European Heart Journal 2006 27(17):2062-2068; doi:10.1093/eurheartj/ehl190
This Article
Right arrow Abstract Freely available
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
27/17/2062    most recent
ehl190v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Related articles in EHJ
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
Google Scholar
Right arrow Articles by Dagres, N.
Right arrow Articles by Cokkinos, D. V.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Dagres, N.
Right arrow Articles by Cokkinos, D. V.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

© The European Society of Cardiology 2006. All rights reserved. For Permissions, please e-mail: journals.permissions@oxfordjournals.org

Pre-treatment with Irbesartan attenuates left atrial stunning after electrical cardioversion of atrial fibrillation

Nikolaos Dagres1,2,*, George Karatasakis1, Fotios Panou2, Georgios Athanassopoulos1, Themistoclis Maounis1, Elias Tsougos2, Kallirrhoe Kourea2, Ioannis Malakos1, Dimitrios Th. Kremastinos2 and Dennis V. Cokkinos1

1 First Cardiology Department, Onassis Cardiac Surgery Center, Athens, Greece
2 Second University Cardiology Department, Attikon University Hospital, University of Athens, Rimini 1, Haidari 12462, Athens, Greece

Received 8 November 2005; revised 19 May 2006; accepted 26 May 2006; online publish-ahead-of-print 4 August 2006.

* Corresponding author. Tel: +30 2105832350; fax: +30 2105832351. E-mail address: nikolaosdagres{at}yahoo.de

See page 2034 for the editorial comment on this article (doi:10.1093/eurheartj/ehl019)


   Abstract
Top
 Abstract
Introduction
 Methods
 Results
 Discussion
 Conclusion
 References
 
Aims Left atrial (LA) stunning, the transient impairment of LA function, is responsible for an increased thrombo-embolic risk after cardioversion of atrial fibrillation (AF). Angiotensin receptor blockers (ARBs) attenuate atrial remodelling in AF and could theoretically influence LA stunning. We studied the effect of Irbesartan on LA stunning.

Methods and results We prospectively assigned 50 patients from the outpatient clinic undergoing electrical cardioversion for AF with duration of >4 weeks, into two matched groups: 25 patients were treated with Irbesartan (228±93 mg/day) for at least 2 weeks prior to cardioversion (Irbesartan group); 25 patients did not receive ARBs (control group). The groups did not differ concerning age (64±13 vs. 63±13 years, respectively), AF duration (20±18 vs. 20±19 weeks), underlying disease, LA diameter (46±7 vs. 47±9 mm), left ventricular dimensions, and ejection fraction (47.7±11.6 vs. 49.7±14.5%).

We assessed LA appendage emptying velocities (LAAEV) and LA spontaneous echo contrast (LASEC) by transoesophageal echocardiography before and after cardioversion and at 2 weeks, and the A-wave by transthoracic echocardiography after cardioversion, at 2 and at 4 weeks.

LA stunning was significantly attenuated in the Irbesartan group. The reduction of LAAEV immediately after cardioversion was significantly less in the Irbesartan group (LAAEV reduction of 9±49% from 28±9 cm/s before cardioversion to 25±13 cm/s immediately afterwards) than in the control group (reduction of 48±20% from 34±15 cm/s before cardioversion to 16±6 cm/s afterwards) (P=0.048). New or increased LASEC occurred in eight patients (32%) in the Irbesartan vs. 16 patients (64%) in the control group (P=0.046).

Conclusion Irbesartan significantly attenuates LA stunning after electrical cardioversion of AF. Therefore, ARBs may represent an important pharmacological supplementation in patients being prepared for cardioversion.

Key Words: Atrial stunning • Atrial fibrillation • Electrical cardioversion • Angiotensin receptor blockers


   Introduction
Top
 Abstract
 Introduction
Methods
 Results
 Discussion
 Conclusion
 References
 
Left atrial (LA) stunning is the transient impairment of LA and LA appendage (LAA) mechanical function after successful cardioversion of atrial fibrillation (AF).1–4 This dysfunction may last up to few weeks, is observed after all methods of cardioversion, and is considered to be responsible for the increased incidence of thrombus formation and embolic events after cardioversion, despite restoration of sinus rhythm.1,2,4–7

Thus, attenuation of atrial stunning by pharmacological agents would have substantial clinical importance, as it would decrease the thrombo-embolic risk after cardioversion. Until now, only few agents have been studied in this regard in humans.8–11 The results have not led to the recommendation of the routine use of any medication for protection against the phenomenon of stunning.

Recent studies demonstrated an important role of the renin–angiotensin system (RAS) in AF. During AF, an electrical and structural remodelling of the atria takes place.12–14 Angiotensin II receptor blockers (ARBs) have been found to significantly attenuate these changes.15–17 Thus, these agents could theoretically also affect atrial stunning.

In the present study, we tested the hypothesis that pre-treatment with the ARB Irbesartan attenuates LA stunning observed after electrical cardioversion of AF.


   Methods
Top
 Abstract
 Introduction
 Methods
Results
 Discussion
 Conclusion
 References
 
Study population
We included patients from the oupatient clinic undergoing elective electrical cardioversion of AF with a duration of >4 weeks. AF was defined by the characteristic surface ECG appearance. Duration of AF was defined as the time from the first ECG documentation of the arrhythmia to the time of cardioversion. All patients had at least two 12-lead ECGs in this time period demonstrating AF with no documentation of sinus rhythm.

The design of the study was a non-randomized clinical trial. The patient flow through the selection and recruitment process is given in Figure 1. Patients were prospectively assigned into two groups matched for age ±5 years and duration of AF ±3 weeks. The first group was treated with Irbesartan for at least 2 weeks prior to cardioversion (Irbesartan group). The target dose of Irbesartan was 300 mg/day and could be reduced to 150 or 75 mg/day in case of hypotensive response. The resulting average dose was 228±93 mg/day. The second group did not receive any ARBs (control group). As shown in Figure 1, a total of 50 patients were finally analysed: 25 patients in the Irbesartan group and 25 patients in the control group. Patients were not blinded to the treatment they were given. As shown in Table 1, the two groups did not differ regarding patient characteristics, including the factors known to influence severity and duration of atrial stunning:4 age, gender, underlying heart disease, AF duration, LA diameter, left ventricular (LV) dimensions, and LV function.


Figure 1901
View larger version (20K):
[in this window]
[in a new window]
[Download PowerPoint slide]
  		Figure 1 Patient flow through the selection and recruitment process.

 

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

  		Table 1 Patient characteristics

 
None of the study patients was receiving ACE-inhibitors. Cardiac medication of the patients is given in Table 2 and did not differ in the two groups.


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

  		Table 2 Medical therapy

 
The study complied with the Declaration of Helsinki and was approved by the local Ethics Committee, informed consent was obtained from all patients.

Echocardiographic examination
Serial changes in LA and LAA function were assessed by transoesophageal echocardiography (TEE) and transthoracic echocardiography (TTE). The flow diagram of echocardiographic examinations is shown in Figure 2. TEE and TTE were performed immediately before and immediately after cardioversion. Thus, TEE, as currently recommended for cardioversion, was carried out in the coronary care unit with pre-medication (midazolam). If no thrombi were found, intravenous anesthesia was given, cardioversion was carried out, as subsequently described, and TEE and TTE measurements were repeated immediately after cardioversion. TEE and TTE were also repeated at 2 weeks after cardioversion, if the patient remained in sinus rhythm, and TTE at 4 weeks after cardioversion.


Figure 1902
View larger version (13K):
[in this window]
[in a new window]
[Download PowerPoint slide]
  		Figure 2 Flow diagram of echocardiography protocol. The numbers given in each step indicate the number of patients undergoing the different steps of the protocol in the two groups. TEE at 2 weeks was not performed in 25 of the 50 patients due to recurrence of AF (n=20) or patients' unwillingness (n=5). TTE at 4 weeks was not performed in 28 of the 50 patients due to recurrence of AF (n=23) or patients' unwillingness (n=5).

 
For TEE, commercially available ultrasound systems were used (Philips Sonos 7500, Hewlett-Packard Sonos 2500, and General Electric Vivid 3 and Vivid 7) equipped with 5 MHz multifrequency multiplane phased-array transducers.

LA appendage emptying velocities (LAAEVs) and LA spontaneous echo contrast (LASEC) were assessed by TEE as previously described.2,3,8 LAAEVs were measured using pulsed-wave Doppler echocardiography by placing the sample volume {approx}1 cm into the mouth of the LAA. The LAA was scanned in planes from 0 to 180° and the optimal angle was used for subsequent analyses. Peak flow velocities were measured at end-diastole and averaged over at least six cardiac cycles in AF and three cardiac cycles in sinus rhythm after cardioversion. LASEC was defined as dynamic intracavitary echoes with a characteristic swirling pattern distinct from white noise artifact. Gain settings were reduced in a stepwise manner to distinguish LASEC from white noise artifact. The degree of LASEC was categorized independently by two experienced observers (G.K., F.P., G.A.) as absent, mild, moderate, or severe as previously described.18 Differences were resolved by consensus. The physicians who performed and interpreted the echocardiographic studies were blinded for patient treatment and especially for patient assignment into the Irbesartan or the control group.

TTE was performed for assessment of LA diameter, LV dimensions, and LV function. The peak velocities of the A-wave (atrial filling, in sinus rhythm) were also determined using an average of several cardiac cycles.

The echocardiographic studies were recorded on super VHS tape for offline analysis.

Electrical cardioversion
Transthoracic electrical cardioversion was performed after adequate anesthesia with intravenous administration of midazolam and propofol at an energy of 100 to 360 J using standard methods.19,20

Statistical analysis
A statistical power analysis was performed. The sample size was adequate to evaluate clinical differences ≥10% achieving 80% statistical power at 0.05 significance level. Data are presented as mean±1 SD. To evaluate differences between groups, the {chi}2 test or the Fisher exact test were used for dichotomous variables and the t-test or the Mann–Whitney test for continuous variables, as appropriate. Between-groups comparisons for the change of LAAEV and the A-wave were performed using a generalized linear model for repeated measurements. In particular, we had three repeated measurements for LAAEV (before cardioversion, after cardioversion, and at 2 weeks) and for the A-wave (after cardioversion, at 2 weeks, and at 4 weeks) and a grouping variable that characterized patients to the Irbesartan group or the control group. The LAAEV and the A-wave were considered as the dependent outcome and the grouping variable as the fixed-effects-factor. Moreover, the interaction between time points and group was tested.

Due to multiple comparisons, the Bonferroni rule was applied to account for the inflation of Type I error. A P-value of <0.05 was considered significant. All P-values were derived from two-sided significance tests. Analyses were performed with the software package SPSS version 13.0 (SPSS Inc., Chicago, Ill, USA).


   Results
Top
 Abstract
 Introduction
 Methods
 Results
Discussion
 Conclusion
 References
 
Cardioversion was successful in all cases. Atrial stunning immediately after cardioversion was significantly attenuated in the Irbesartan group. LAAEV prior to cardioversion did not differ in the two groups (28±9 cm/s in the Irbesartan group vs. 34±15 cm/s in the control group, P=0.39). The reduction of LAAEV immediately after cardioversion, as an expression of atrial stunning, was significantly less in the Irbesartan group (LAAEV reduction of 9±49% from 28±9 cm/s before cardioversion to 25±13 cm/s immediately afterwards) than in the control group (reduction of 48±20% from 34±15 cm/s before cardioversion to 16±6 cm/s immediately afterwards) (P=0.048 for the comparison between the change in the Irbesartan group and the change in the control group, Figure 3).


Figure 1903
View larger version (23K):
[in this window]
[in a new window]
[Download PowerPoint slide]
  		Figure 3 LAAEV in the Irbesartan group (left) and in the control group (right) before (pre), immediately after (post) cardioversion, and at 2 weeks (2 wks). Vertical bars indicate mean value±SD. LAAEV before cardioversion did not differ between the two groups (P=0.39). The asterisks indicate the change of LAAEV immediately after cardioversion compared with the values before cardioversion. The reduction of LAAEV immediately after cardioversion, as an expression of atrial stunning, was significantly less in the Irbesartan group than in the control group (reduction of 9±49% vs. 48±20%) (P=0.048). TEE at 2 weeks was not performed in 25 of the 50 patients due to recurrence of AF (n=20) or patients' unwillingness (n=5).

 
In the Irbesartan group, LAAEV after cardioversion showed an increase >20% compared with the values prior to cardioversion in four patients (16%), no significant change (±20%) in 10 patients (40%), and a decrease >20% in 11 patients (44%). In contrast, LAAEV in the control group showed a decrease >20% in 23 of the 25 patients (92%) after cardioversion (P<0.001 compared with the Irbesartan group). Characteristic examples of LAAEV changes are depicted in Figure 4.


Figure 1904
View larger version (53K):
[in this window]
[in a new window]
[Download PowerPoint slide]
  		Figure 4 Representative LAA pulsed Doppler flows before and immediately after cardioversion in a patient of the Irbesartan group (left, showing no significant change of LAAEV) and a patient of the control group (right, showing a significant decrease of LAAEV).

 
The frequency of new or increased LASEC immediately after cardioversion, as another expression of atrial stunning, was significantly lower in the Irbesartan group (n=8, i.e. 32%) than in the control group (n=16, i.e. 64%, P=0.046), as depicted in Figure 5.


Figure 1905
View larger version (10K):
[in this window]
[in a new window]
[Download PowerPoint slide]
  		Figure 5 Frequency of new or increased LASEC in the Irbesartan group (left) and in the control group (right) immediately after cardioversion. New or increased LASEC was detected in eight of the 25 patients (32%) in the Irbesartan group and in 16 of the 25 patients (64%) in the control group (P=0.046).

 
There was no difference between the Irbesartan and the control group with regard to blood pressure at the time of the echocardiographic measurements before cardioversion (systolic blood pressure 136±17 vs. 134±20 mmHg, respectively, P=0.74; diastolic blood pressure 84±13 vs. 85±16 mmHg, P=0.81) and after cardioversion (systolic blood pressure 127±18 vs. 123±11 mmHg, respectively, P=0.38; diastolic blood pressure 75±11 vs. 72±10  mmHg, P=0.55) There was also no difference between the two groups in the heart rate before (83±16 vs. 81±16  bpm, P=0.74) and after cardioversion (71±10 vs. 67±9 bpm, P=0.22).

TEE at 2 weeks was not performed in 25 of the 50 patients due to recurrence of AF (n=20) or patients' unwillingness (n=5). As expected, LAAEV at 2 weeks was increased compared with values before cardioversion (in the Irbesartan group from 28±9 cm/s before cardioversion to 51±20  cm/s at 2 weeks; in the control group from 34±15 before cardioversion to 43±23 cm/s at 2 weeks) (P=0.38 for the comparison between the increase in the two groups, Figure 3).

In both groups, the A-wave at 2 and at 4 weeks showed, as expected, an increase compared with values immediately after cardioversion (in the Irbesartan group, from 33±16 cm/s immediately after cardioversion to 72±27  cm/s at 2 weeks and 70±28 cm/s at 4 weeks; in the control group, from 28±9 after cardioversion to 59±21 cm/s at 2 weeks and 70±30 cm/s at 4 weeks, Figure 6) (P=0.41 for the comparison of the change of the A-wave during the study course between the two groups).


Figure 1906
View larger version (7K):
[in this window]
[in a new window]
[Download PowerPoint slide]
  		Figure 6 Peak velocity of the A-wave in the Irbesartan group (left) and in the control group (right) immediately after cardioversion (post), at 2 weeks (2 wks), and at 4 weeks (4 wks). Vertical bars indicate mean value±SD. As expected, the A-wave at 2 and at 4 weeks showed an increase compared with values immediately after cardioversion.

 
There was no difference between the two groups regarding heart rate at the time of the echocardiographic studies at 2 weeks (71±21 bpm in the Irbesartan group vs. 69±9 bpm in the control group, P=0.73) and at 4 weeks (62±7 vs. 69±10 bpm, respectively, P=0.093).

In the total population of 50 patients, atrial stunning was not a predictor of AF recurrence: 18 of 23 patients (78%) with AF recurrence within the first 4 weeks after cardioversion showed a decrease of LAAEV >20% immediately after cardioversion vs. 16 of 27 patients (59%) remaining in sinus rhythm at 4 weeks (P=0.26). AF recurrences occurred mostly in the first 2 weeks after cardioversion (20 of 23 recurrences). The recurrence rate within the first 4 weeks did not differ between the Irbesartan and the control group (12 of 25 patients, i.e. 48%, vs. 11 of 25 patients, i.e. 44%, respectively, P=0.78).


   Discussion
Top
 Abstract
 Introduction
 Methods
 Results
 Discussion
Conclusion
 References
 
The main finding of the study is that pre-treatment with Irbesartan significantly attenuates atrial stunning in patients undergoing electrical cardioversion for AF. This is important as attenuation of stunning should be expected to result in a reduced risk of thrombus formation and thrombo-embolic events after cardioversion. Thus, ARBs may represent an important pharmacological supplementation in patients prepared for cardioversion.

The exact mechanism of atrial stunning after cardioversion of AF is not clear. Several factors are considered to be involved in its development, such as tachycardia-induced atrial cardiomyopathy, atrial hibernation, and cytosolic calcium alterations with possible interplay of more than one mechanisms.4,9 Recent studies emphasize the role of intracellular calcium homeostasis.8 It is also proposed that the structural remodelling that takes place during AF and which is characterized by progressive structural changes of the atria, resulting in atrial dilation and interstitial fibrosis,13,14 might be a potential mechanism leading to atrial stunning, especially with longer duration of the arrhythmia.8

Previous investigations have reported an increased activity of the atrial angiotensin II system and angiotensin receptor changes in patients with AF.21,22 Several studies have demonstrated that angiotensin II contributes to the development of the remodelling in AF; inhibition of RAS can lead to regression of the changes described earlier. Thus, ARBs have been reported to prevent the electrical remodelling in AF, especially in the short-term.15,16 This effect is thought to be in part mediated by interference with ion currents, stabilization of electrolyte concentrations, a reduction of calcium overload, and a decrease of atrial stretch.15,23 These agents also attenuate the structural remodelling in AF; this is not surprising, as angiotensin II is a stimulator of collagen synthesis and a strong promoter of fibrosis.16,17,24,25 Inhibition of the remodelling process by blockade of angiotensin could possibly explain the attenuation of atrial stunning observed in our study, although we cannot define the exact mechanism.

The study has several limitations: (i) the design was a non-randomized clinical trial. However, as already mentioned, the Irbesartan and the control group did not differ regarding patient characteristics such as age, gender, underlying heart disease, duration of AF, LA diameter, LV dimensions, and LV function; (ii) the number of included patients (n=50) is limited for repeated measurements comparisons; (iii) we used different antiarrhythmic drugs in various dosages. However, the frequency of usage of these drugs did not differ between the Irbesartan and the control group.

We did not perform echocardiographic measurements during follow-up in patients with AF recurrence, as the focus of our investigation was the atrial stunning in patients with successful cardioversion into sinus rhythm. Thus, such measurements during follow-up in patients with AF recurrence would not have been useful for the purpose of the study. Nevertheless, this does not take away the problem of selection bias if the probability of remaining in sinus rhythm is related to treatment with Irbesartan. However, this relation was not present in our study as the recurrence rate of AF during the first 4 weeks was almost identical in the Irbesartan and the control group (48 vs. 44%).


   Conclusion
Top
 Abstract
 Introduction
 Methods
 Results
 Discussion
 Conclusion
References
 
Pre-treatment with Irbesartan significantly attenuates LA stunning after electrical cardioversion of AF. Therefore, ARBs may represent an important pharmacological supplementation in patients being prepared for cardioversion.

Conflict of interest: There are no financial or other interests which might pose a conflict of interest.


   References
Top
 Abstract
 Introduction
 Methods
 Results
 Discussion
 Conclusion
 References
 

  1. Grimm RA, Stewart WJ, Maloney JD, Cohen GI, Pearce GL, Salcedo EE, Klein AL. (1993) Impact of electrical cardioversion of atrial fibrillation on left atrial appendage function and spontaneous echo contrast: characterization by simultaneous transesophageal echocardiography. J Am Coll Cardiol 22:1359–1366.[Abstract]
  2. Fatkin D, Kuchar DL, Thorburn CW, Feneley MP. (1994) Transesophageal echocardiography before and during direct current cardioversion of atrial fibrillation: evidence for ‘atrial stunning’ as a mechanism of thromboembolic complications. J Am Coll Cardiol 23:307–316.[Abstract]
  3. Grimm RA, Stewart WJ, Arheart KL, Thomas JD, Klein AL. (1997) Left atrial appendage ‘stunning’ after electrical cardioversion of atrial flutter: an attenuated response compared with atrial fibrillation as the mechanism for lower susceptibility to thromboembolic events. J Am Coll Cardiol 29:582–589.[Abstract]
  4. Khan IA. (2003) Atrial stunning: determinants and cellular mechanisms. Am Heart J 145:787–794.[CrossRef][ISI][Medline]
  5. Black IW, Fatkin D, Sagar KB, Khandheria BK, Leung DY, Galloway JM, Feneley MP, Walsh WF, Grimm RA, Stollberger C. (1994) Exclusion of atrial thrombus by transesophageal echocardiography does not preclude embolism after cardioversion of atrial fibrillation. A multicenter study. Circulation 89:2509–2513.[Abstract/Free Full Text]
  6. Omran H, Jung W, Rabahieh R, Schimpf R, Wolpert C, Hagendorff A, Fehske W, Lüderitz B. (1997) Left atrial chamber and appendage function after internal atrial defibrillation: a prospective and serial transesophageal echocardiographic study. J Am Coll Cardiol 29:131–138.[Abstract]
  7. Manning WJ, Silverman DI, Katz SE, Riley MF, Come PC, Doherty RM, Munson JT, Douglas PS. (1994) Impaired left atrial mechanical function after cardioversion: relation to the duration of atrial fibrillation. J Am Coll Cardiol 23:1535–1540.[Abstract]
  8. Sanders P, Morton JB, Kistler PM, Vohra JK, Kalman JM, Sparks PB. (2003) Reversal of atrial mechanical dysfunction after cardioversion of atrial fibrillation. Implications for the mechanisms of tachycardia-mediated atrial cardiomyopathy. Circulation 108:1976–1984.[Abstract/Free Full Text]
  9. Daoud EG, Marcovitz P, Knight BP, Goyal R, Ching Man K, Strickberger A, Armstrong WF, Morady F. (1999) Short-term effect of atrial fibrillation on atrial contractile function in humans. Circulation 99:3024–3027.[Abstract/Free Full Text]
  10. Date T, Takahashi A, Iesaka Y, Miyazaki H, Yamane T, Noma K, Nuruiki N, Ishikawa S, Kanae K, Mochizuki S. (2002) Effect of low-dose isoproterenol infusion on left atrial appendage function soon after cardioversion of chronic atrial tachyarrhythmias. Int J Cardiol 84:59–67.[CrossRef][ISI][Medline]
  11. DeCara JM, Pollak A, Dubrey S, Falk RH. (2000) Positive atrial inotropic effect of dofetilide after cardioversion of atrial fibrillation or flutter. Am J Cardiol 86:685–688.[CrossRef][ISI][Medline]
  12. 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]
  13. Ausma J, Wijffels M, Thone F, Wouters L, Allessie M, Borgers M. (1997) Structural changes of atrial myocardium due to sustained atrial fibrillation in the goat. Circulation 96:3157–3163.[Abstract/Free Full Text]
  14. Brundel BJJM, Henning RH, Kampinga HH, van Gelder IC, Crijns HJGM. (2002) Molecular mechanisms of remodeling in human atrial fibrillation. Cardiovasc Res 54:315–324.[Abstract/Free Full Text]
  15. Nakashima H, Kumagai K, Urata H, Gondo N, Ideishi M, Arakawa K. (2000) Angiotensin II antagonist prevents electrical remodeling in atrial fibrillation. Circulation 101:2612–2617.[Abstract/Free Full Text]
  16. Kumagai K, Nakashima H, Urata H, Gondo N, Arakawa K, Saku K. (2003) Effects of angiotensin II type 1 receptor antagonist on electrical and structural remodeling in atrial fibrillation. J Am Coll Cardiol 41:2197–2204.[Abstract/Free Full Text]
  17. Li D, Shinagawa K, Pang L, Leung TK, Cardin S, Wang Z, Nattel S. (2001) Effects of angiotensin-converting enzyme inhibition on the development of the atrial fibrillation substrate in dogs with ventricular tachypacing-induced congestive heart failure. Circulation 104:2608–2614.[Abstract/Free Full Text]
  18. Seidl K, Rameken M, Drögemüller A, Vater M, Brandt A, Schwacke H, Bergmeier C, Zahn R, Senges J. (2002) Embolic events in patients with atrial fibrillation and effective anticoagulation: value of transesophageal echocardiography to guide direct-current cardioversion. J Am Coll Cardiol 39:1836–1842.[Abstract/Free Full Text]
  19. Mittal S, Ayati S, Stein KM, Schwartzman D, Cavlovich D, Tchou PJ, Markowitz SM, Slotwiner DJ, Scheiner MA, Lerman BB. (2000) Transthoracic cardioversion of atrial fibrillation. Comparison of rectilinear biphasic versus damped sine wave monophasic shocks. Circulation 101:1282–1287.[Abstract/Free Full Text]
  20. Kirchhof P, Eckardt L, Loh P, Weber K, Fischer RJ, Seidl KH, Böcker D, Breithardt G, Haverkamp W, Borggrefe M. (2002) Anterior-posterior vs. anterior-lateral electrode positions for external cardioversion of atrial fibrillation: a randomised trial. Lancet 360:1275–1279.[CrossRef][ISI][Medline]
  21. Goette A, Staack T, Röcken C, Arndt M, Geller JC, Huth C, Ansorge S, Klein HU, Lendeckel U. (2000) Increased expression of extracellular signal-regulated kinase and angiotensin-converting enzyme in human atria during atrial fibrillation. J Am Coll Cardiol 35:1669–1677.[Abstract/Free Full Text]
  22. Goette A, Arndt M, Röcken C, Spiess A, Staack T, Geller JC, Huth C, Ansorge S, Klein HU, Lendeckel U. (2000) Regulation of angiotensin II receptor subtypes during atrial fibrillation in humans. Circulation 101:2678–2681.[Abstract/Free Full Text]
  23. Folkeringa RJ, Tieleman RG, Crijns HJGM. (2004) Non-antiarrhythmic drugs to prevent atrial fibrillation. Heart Rhythm 1:516–518.[CrossRef][ISI][Medline]
  24. Sadoshima J and Izumo S. (1993) Molecular characterization of angiotensin II-induced hypertrophy of cardiac myocytes and hyperplasia of cardiac fibroblasts. Critical role of the AT1 receptor subtype. Circ Res 73:413–423.[Abstract/Free Full Text]
  25. Shi Y, Li D, Tardif JC, Nattel S. (2002) Enalapril effects on atrial remodeling and atrial fibrillation in experimental congestive heart failure. Cardiovasc Res 54:456–461.[Abstract/Free Full Text]

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

Related articles in EHJ:

Inhibition of angiotensin II type 1 receptors reduces atrial stunning and spontaneous echo contrast after electrical cardioversion of atrial fibrillation
Andreas Goette and Ulrich Schotten
EHJ 2006 27: 2034-2035. [Extract] [Full Text]  



This article has been cited by other articles:


Home page
 Eur Heart JHome page
A. Goette and U. Schotten
Inhibition of angiotensin II type 1 receptors reduces atrial stunning and spontaneous echo contrast after electrical cardioversion of atrial fibrillation
Eur. Heart J., September 1, 2006; 27(17): 2034 - 2035.
[Full Text] [PDF]

This Article
Right arrow Abstract Freely available
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
27/17/2062    most recent
ehl190v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Related articles in EHJ
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
Google Scholar
Right arrow Articles by Dagres, N.
Right arrow Articles by Cokkinos, D. V.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Dagres, N.
Right arrow Articles by Cokkinos, D. V.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?