Chest ACCP Education Calendar
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

Guest Access | Sign In via User Name/Password
This Article
Right arrow Abstract Freely available
Right arrow Full Text (PDF) Free
Right arrow Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when eLetters are posted
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Article Archive
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via ISI Web of Science (3)
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Azpitarte, J.
Right arrow Articles by Tercedor, L.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Azpitarte, J.
Right arrow Articles by Tercedor, L.
(Chest. 2001;120:132-138.)
© 2001 American College of Chest Physicians

In Patients With Chronic Atrial Fibrillation and Left Ventricular Systolic Dysfunction, Restoration of Sinus Rhythm Confers Substantial Benefit*

José Azpitarte, FESC; Oscar Baún, MD; Eduardo Moreno, MD; Rocío García-Orta, MD; Jesús Sánchez-Ramos, MD and Luis Tercedor, MD

* From the Division of Cardiology, Virgen de las Nieves University Hospital, Granada, Spain.

Correspondence to: José Azpitarte, MD, Division of Cardiology, Virgen de las Nieves University Hospital, Av de las Fuerzas Armadas 2, 18014 Granada, Spain; e-mail: jazpitarte{at}lettera.net


   Abstract
TOP
 Abstract
Introduction
 Materials and Methods
 Results
 Discussion
 References
 
Study objectives: To evaluate the benefit of sinus rhythm (SR) restoration in patients with chronic controlled atrial fibrillation (AF) and left ventricular systolic dysfunction (LVSD).

Design: Prospective case-control study on the short-term outcome (6 to 9 months) of clinical and echocardiographic variables following attempted cardioversion.

Setting: Outpatient clinic of a university hospital.

Patients: Fifteen men and 5 women, ranging in age from 40 to 76 years, who had chronic controlled (mean [± SD] ventricular rate, 82 ± 10 beats/min) AF and left ventricular fractional shortening (LVFS) of < 28% at baseline. Control was provided by retrospective paired echocardiographic examinations of six AF patients, plus the study cases with potentially unsuccessful cardioversion or early recurrence of AF.

Interventions: Attempt to restore SR with amiodarone or electrical countershock.

Measurements and results: Conversion was attained in 17 patients, but AF recurred early in 4 patients, 3 of whom had proven ischemic LVSD. In the 13 patients with sustained SR, LVFS increased from 20 ± 4% to 31 ± 6% (p < 0.0001). In contrast, no changes were detected in the control group (n = 13). This improvement was paralleled by decreases in left ventricular (LV) end-diastolic dimension (from 55 ± 7 to 51 ± 6 mm; p = 0.014), LV mass (from 181 ± 28 to 159 ± 37 g; p = 0.015), and left atrial diameter (from 45 ± 9 mm to 42 ± 7; p = 0.003). A marked decrease in heart rate (from 82 ± 9 to 64 ± 5 beats/min; p < 0.0001) and a reduction in New York Heart Association functional class (from 2.3 ± 0.9 to 1.2 ± 0.4; p = 0.0007) also were observed in patients with sustained SR but not among subjects in the control group.

Conclusions: Even when adequate control of the ventricular rate has been achieved, the LV function of patients with chronic AF greatly improves after restoration and maintenance of SR.

Key Words: amiodarone • atrial fibrillation • case-control study • electrical countershock • heart failure • left ventricular dysfunction


   Introduction
TOP
 Abstract
 Introduction
Materials and Methods
 Results
 Discussion
 References
 
As many as 30% of patients with heart failure have been reported to have concomitant atrial fibrillation (AF).1 In this setting, AF traditionally has been regarded as a mere epiphenomenon, ie, as an innocent bystander of the underlying myocardial disease. However, some reports2 3 4 5 have documented cases of complete resolution of congestive heart failure after conversion to sinus rhythm (SR). Despite the relevance of this fact, which was first reported > 60 years ago,2 it has been largely ignored in clinical practice, perhaps because few studies6 7 8 9 10 have, to our knowledge, addressed this issue in a prospective and comprehensive way. There is also a concern about whether the best therapeutic approach to these patients is to restore SR or simply to adequately control the ventricular rate. Thus, to gain deeper insight into the potential benefit of restoring SR, we conducted a prospective study on patients who had echocardiographic left ventricular systolic dysfunction (LVSD) and a controlled ventricular rate before attempted cardioversion.


   Materials and Methods
TOP
 Abstract
 Introduction
 Materials and Methods
Results
 Discussion
 References
 
Study Patients
One hundred forty-seven consecutive patients with chronic AF were evaluated in the outpatient clinic of our institution and submitted to an echocardiographic examination after a period of pharmacologic treatment aimed at controlling the ventricular heart rate (Fig 1 ). Among the group of 99 patients who underwent a high-quality M-mode echocardiogram, 20 patients (15 men and 5 women) with left ventricular fractional shortening (LVFS) of < 28% constituted the basis of the study.



View larger version (26K):
[in this window]
[in a new window]
[Download PPT slide]
  		Figure 1.. Flow diagram showing the enrollment of patients, their outcomes following cardioversion, and the final composition of the two compared groups. On the left, 13 patients who had sustained SR after conversion. On the right, seven patients with unsuccesful cardioversion (n = 3) or early recurrence of AF (n = 4), plus six historical control subjects in chronic AF. LVFS of < 28% in a high-quality M-mode echocardiogram was a requisite for inclusion. Furthermore, a focus on ventricular rate control was made before echocardiographic examination of the study patients. FS = fractional shortening.

 
History, physical examination, ECG, and chest radiograph were performed before the echocardiography in every case. The mean (± SD) age of the patients was 61 ± 10 years (range, 40 to 76 years). LVSD was considered to be of ischemic origin because of typical angina (one patient, also with an aortic mechanic prosthesis) or history of myocardial infarction (five patients). In the other 14 patients, a definite origin of LVSD could not be established, although nonsevere hypertension was present in 5 patients and 1 patient had undergone an aortic valve replacement. The mean duration of AF, for the 16 patients in whom it could be determined, was 12 ± 9 months (range, 3 to 65 months).

Prior to baseline echocardiography and the attempted cardioversion, all patients received anticoagulation therapy and were treated by digoxin as a first-line therapy for ventricular rate control. The adequacy of the ventricular response, and therefore the need for additional drug therapy, was judged in the usual clinical manner through fortnightly examinations at the outpatient clinic. As a result, 19 of 20 patients received another of the following drugs: low dose of amiodarone, 200 mg daily (9 patients); atenolol (4 patients); diltiazem (2 patients); and verapamil (4 patients). In order to evaluate more accurately the ventricular rate control achieved, a 24-h Holter recording was performed in each patient at the time of the echocardiography. Seventeen patients were also receiving angiotensin-converting enzyme (ACE) inhibitor therapy, and 9 patients were receiving furosemide therapy. After the drug treatment, 2 patients were New York Heart Association functional class I, 12 patients were class II, 4 patients were class III, and 2 patients were class IV.

After the baseline echocardiogram, an ACE inhibitor drug was added to the treatment of three patients who were not already receiving it. The reversion of AF was attempted by an oral loading dose of amiodarone (1g daily until a total dose of 100 mg/kg of weight) followed by a maintenance dose (200 mg daily) in the nine patients who were already receiving it for ventricular rate control. If this therapy was unsuccessful, patients underwent synchronized direct-current external shock, as did those not treated by amiodarone. Following the index cardioversion, all patients who attained SR were placed on low-dose amiodarone therapy. Conversely, amiodarone was withdrawn and replaced by bisoprolol in those patients who did not attain conversion. Finally, patients not receiving amiodarone therapy before failed conversion remained with or were changed to ß-blocker therapy if they previously were taking a calcium channel blocker. The study was approved by the Ethics Committee of the Virgen de las Nieves University Hospital, and written informed consent was obtained from all of the participants.

Echocardiography
A two-dimensionally guided M-mode echocardiogram (model XP 128; Acuson; Mountain View, CA) was performed in each patient by one expert cardiologist. Only recorded echocardiograms that demonstrated optimal visualization of left ventricular (LV) interfaces were used. Measurements for M-mode-guided calculation were taken just below the tip of the mitral valve and were averaged from three cardiac cycles with a preceding RR interval between 750 and 950 ms. LV end-diastolic dimension (LVEDD), LV end-systolic dimension (LVESD), septal thickness (ST), posterior wall thickness (PWT), and left atrial (LA) diameter were measured according to the guidelines of the American Society of Echocardiography.11 LVFS (%), a measure of LV systolic (LVS) function, was calculated as follows: (LVEDD - LVESD) ÷ LVEDD. LV mass (LVM), according to Devereux et al,12 was estimated as follows: 1.04 ([ST + PWT + LVEDD3] - LVEDD3) x 0.8 + 0.6. To avoid interreader differences, allthe echocardiographic measurements were done by the same author (E.M.).

The first examination was performed prior to cardioversion, at a mean of 68 ± 12 days (range, 44 to 92 days) after the beginning of the ventricular rate control therapy. The second examination took place between 6 and 9 months after the index cardioversion. Although every patient in the study provided their own control, we used, for external control purposes, paired echocardiographic examinations performed at least 6 months apart on six patients with chronic AF and LVFS values of < 28% who were randomly selected from our echocardiographic archives. At the time of the echocardiography, all the control subjects were receiving digoxin therapy plus one additional drug (four patients were receiving atenolol, one patient was receiving bisoprolol, and one patient was receiving verapamil), and five patients also received ACE inhibitor therapy. For the purposes of comparison, it was planned to form a group, adding patients with potential failed conversion or early recurrence of AF to the six control examinations.

Statistical Analysis
Values are expressed as mean ± SD. The Student’s t test was used to detect baseline differences between the patients and the control subjects. The same test, for paired data, was used to detect changes after attempted cardioversion in the study patients, and between the first and second examination in the external control group. Comparisons between percentages were made with Fisher’s Exact Test. AF-free survival curves were calculated using the Kaplan-Meier method, and the log-rank test was used for curves comparison. p Values < 0.05 were defined as statistically significant. Statistical analyses were performed with statistical software (GraphPad Prism, version 2.0; GraphPad Software; San Diego, CA).


   Results
TOP
 Abstract
 Introduction
 Materials and Methods
 Results
Discussion
 References
 
Attainment and Maintenance of SR
SR was obtained in 17 patients, 6 by amiodarone therapy and 11 by electrical cardioversion. Two of three patients who were resistant to electrical therapy had LVSD of ischemic origin. Early recurrence of AF occurred in four patients. Thus, two groups of 13 cases each were available for comparison (Fig 1) . Three of the four patients who returned early to AF had ischemic LVSD. The other 13 patients (12 of whom had nonischemic LVSD) were in SR at the time of the second examination. In 12 of these patients, SR has been maintained from the last recording to the date of writing, representing a mean follow-up of 12 ± 7 months. In the remaining patient, who also had ischemic LVSD in addition to an aortic mechanic prosthesis, the AF recurred at month 14 of observation. One patient had a transient episode of AF related to acute pneumonia 14 months after cardioversion. The proportion of patients who were free of AF recurrence was 92% in patients with nonischemic LVSD, whereas none of the four patients with ischemic LVSD were free of recurrence (p = 0.0009 [Fig 2 ]).



View larger version (20K):
[in this window]
[in a new window]
[Download PPT slide]
  		Figure 2.. The proportion of patients remaining free of recurrent AF after successful conversion. Freedom was significantly higher in patients with nonischemic LVSD (p = 0.0009 [log-rank test]). The number of patients in each group is shown in parentheses.

 
Changes in LV Function
There was no significant difference between the baseline echocardiographic data of patients who remained in SR and those of patients who persisted in or returned to AF (Table 1 ). After 6 months, the LVFS increased from 20 ± 4 to 31 ± 6% (p < 0.0001) in the 13 patients who were in SR at this time. By contrast, no changes were noted in the group of 13 patients who were in AF at the follow-up (Table 1) . Figure 3 shows the individual evolution of the LVFS values. Whereas LVFS increased in all patients who had sustained SR, this outcome was rarely observed in patients who were in AF at the second examination. As a consequence, 10 of the 13 patients with SR were at or above the level of 28% at the second examination, whereas this behavior was noted in only 2 of the 13 patients with persisting or recurring AF (p = 0.005). LVEDD (baseline, 55 ± 7 mm; repeat examination, 51 ± 6 mm; p = 0.014), LVM (baseline, 181 ± 28 g; repeat examination, 159 ± 37 g; p = 0.015), and LA diameter (baseline, 45 ± 9 mm; repeat examination, 42 ± 7 mm; p = 0.03) only decreased in the patients with sustained SR.


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

  		Table 1.. Outcome of Echocardiographic and Ventricular Rate Measurements*

 


View larger version (27K):
[in this window]
[in a new window]
[Download PPT slide]
  		Figure 3.. Extent of increase in LVFS over time. Solid boxes connected by lines indicate individual data points for each patient, at baseline and after 6 to 9 months. Solid boxes with deviation bars indicate mean pooled data at each time point. A universal improvement can be observed in patients who were in SR at the second evaluation (left), whereas this kind of response was only occasionally seen in control subjects (right). The number of patients in each group is shown in parentheses.

 
Changes in Ventricular Heart Rate and Functional Class
At baseline, the mean ventricular rate of AF (24-h Holter monitoring) was 82 ± 9 beats/min. After 6 months, the mean heart rate of the 13 patients with sustained SR had decreased to 64 ± 5 beats/min (p < 0.0001; Table 1 ). In spite of these heart rate changes, and because of bias in the cycle selection, the mean RR intervals from which the echocardiographic measures were derived did not differ between before and after cardioversion. The ventricular response of the seven patients with failed conversion or AF recurrence was similar at the first and second examination. Concerning symptomatic evaluation, an improvement in New York Heart Association class (2.3 ± 0.9 at baseline vs 1.2 ± 0.4 at follow-up; p = 0.0007) was observed in the patients with sustained SR but not in the seven patients with unsuccessful conversion or AF recurrence (2.3 ± 0.5 at baseline vs 2.6 ± 0.5 at the second examination; p = 0.36).


   Discussion
TOP
 Abstract
 Introduction
 Materials and Methods
 Results
 Discussion
References
 
To date, research into the outcome of LV function after conversion to SR in patients with AF and LVSD has been sparse.6 7 8 9 10 There is also reasonable doubt as to whether the restoration of SR is the best therapy for these patients or whether similar benefits can be obtained by a simple ventricular rate control. With this in mind, we designed a study using M-mode two-dimensionally guided echocardiography and prospectively enrolled a population that had LVFS of < 28% before cardioversion. Prior to the echocardiographic examination, we focused on controlling the ventricular rate response in order to segregate the possible improvements in LV function intrinsic to the restoration of SR from those induced by a sustained lower ventricular rate. In other words, we wanted to investigate whether a gain in LV function can be achieved even after an adequate control of the ventricular rate has been obtained.

Major Findings
The main study outcome is that, despite previous good control of the ventricular rate, LVS function was greatly improved in patients with restored and sustained SR. In contrast, no changes were detected in those patients who returned to or persisted in AF during the echocardiographic follow-up. In addition, reductions in LVEDD, LVM, and LA diameter were observed only in patients with sustained SR.

It is generally accepted that atrial systole improves LV performance by means of the Frank-Starling mechanism, ie, by increasing LV preload (the end-diastolic fiber length).13 In an experimental model, Linderer et al14 observed that AF causes an upward shift in the end-diastolic pressure-diameter relationship (ie, the end-diastolic volume becomes smaller at a given end-diastolic pressure). According to the Frank-Starling law, this smaller LV end-diastolic volume results in a smaller stroke volume (a downward shift of the conventional ventricular function curve). Interestingly, the opening of the pericardium shifts the end-diastolic pressure-diameter relationship downward and the stroke volume-end-diastolic diameter relation upward; thus, it counters the effect of the withdrawal of the atrial contribution on these curves. Therefore, the primary reaction (an upward shift in the end-diastolic pressure-diameter relationship) on this sequence of events was thought to be caused by an unemptied atrium that compromised the pericardial volume.14

According to these experimental data, the following changes can be expected with the restoration of SR: (1) a better emptying of the LA at LV end-diastole, and thus a removal of the restraining pericardial force; (2) a downward shift in the end-diastolic pressure-diameter relationship; (3) and an improvement (upward shift) of the ventricular function curve. These favorable hemodynamic changes, rather than an improved myocardial intrinsic contractility, may account for the reported improvement in exercise performance after successful cardioversion.10 15 16

In the present study, a decrease rather than an increase in the LVEDD was observed in patients with sustained SR. This finding, suggesting that the improvement in LV function was likely due to a better myocardial contractility and not to the Frank-Starling mechanism, was apparently in conflict with the above-mentioned experimental results. However, the following large differences between the two studies must be pointed out: in the acute experimental work, the data were obtained from animals with normal LV values,14 whereas our patients had chronic AF and marked LVSD. In our view, it is possible that in the chronic setting a remodeling of the LV with regression of the dilation might have occurred after several months of the improved ventricular efficiency afforded by sustained SR.

The Link between AF and LVSD
Despite the small number of patients enrolled in the study, a striking difference was observed in the attainment and maintenance of SR between patients with proven ischemic LVSD and those with LVSD of presumably nonischemic origin. This finding should be taken with reservation because it emerged from an a posteriori analysis. In addition, it should be taken into account that we used only clinical criteria to distinguish between ischemic and nonischemic LVSD. Nevertheless, this finding suggests that AF-LVSD concomitance encompasses a wide physiopathologic spectrum. At one end, AF is a mere epiphenomenon of a profound alteration in LV function (ie, LVSD of ischemic origin), so that a high recurrence rate is likely as long as the primary cause of LVSD persists. However, at the other end of the spectrum, the arrhythmia may be a primary phenomenon that induces insidious myocardial dysfunction, with no expectation of recurrences because of the ensuing improvement in LVS function. Evidently, intermediate situations also can occur when AF is not the primary cause of the LVSD but can contribute to it. Low-dose dobutamine stress echocardiography was proposed to distinguish between idiopathic LVSDwith secondary arrhythmia and tachycardia-induced LVSD,17 in order to predict the recovery of LV function after the restoration of SR. Our study does not contain these kind of data, but the universal improvement of LV function observed among the nonischemic patients suggests that AF-induced LVSD is far more widespread than is currently understood.

To Simply Control Ventricular Rate or to Attempt Conversion to SR?
Reduction of the heart rate is thought to be the principal mechanism implicated in the improvement of LV function.18 19 Tachycardia is an inefficient, energy-wasting mechanism of ventricular contraction,20 and an experimental model of tachycardia-induced heart failure has been studied extensively.21 22 Its clinical counterpart, tachycardia-induced cardiomyopathy, was first described in patients with incessant atrial tachycardia.23 Concerning AF, the best examples of the regression of heart failure have been reported in patients with noncontrolled ventricular responses.4 5 In the present study, we tried to demonstrate that the restoration of SR can improve LV function even after an adequate ventricular response has been achieved. The mean ventricular rate at rest achieved in our patients was well below the range considered to be a good control.24 Despite this, LV function was greatly improved after conversion. There was no difference between before and after cardioversion in the mean RR intervals preceding the cycles from which the echocardiographic measures were taken, which obviously was due to a bias in the selection of cycles. However, it was also evident that the ventricular rate estimated by 24-h Holter recording was significantly lower in SR. Thus, it was not feasible to differentiate between the improvement intrinsic to SR restoration and that achieved by the additional sustained reduction in heart rate provided by SR per se.

While our study was not able to distinguish the origin of improvements, it seems clear that SR is more physiologic and must always be attempted. The achievement of SR not only restores atrial function but also suppresses the variation in RR intervals that adversely affects LV function, regardless of the ventricular rate.25 26 In addition, the heart rate is more stable because the sinus node is much less influenced by sympathetic drive than is the atrioventricular conduction.27 Alternatively, if SR cannot be achieved and an adequate ventricular rate is difficult to obtain, atrioventricular junction ablation and permanent ventricular pacing have been proposed to improve LV function.28 29 However, another study30 was unable to show any benefit of this therapy in terms of improving cardiac performance.

Limitations of the Study
The present study has some limitations that deserve consideration. First, for ethical reasons, it was not a randomized study, and the group constituted for comparison purposes was partially retrospective. Second, the number of patients enrolled was small. Third, the evaluation of symptoms was not performed in a blinded fashion. The estimation of LV function in patients with AF is problematic due to changes from beat to beat. To minimize this difficulty, we selected for M-mode measurement three cycles with predefined RR intervals that were similar. Evidently, M-mode has limitations in evaluating global LV function; however, it is an adequate tool for intrapatient follow-up comparison. In addition, to avoid interreader differences, all of the echocardiographic measurements were performed by the same author.

The most important limitation of the study was the inability to exclude other factors that can improve LV function. For instance, several drugs prescribed for our patients, such as digoxin,31 ACE inhibitors,32 amiodarone,33 or ß-blockers,34 can improve LV performance. However, most patients were taking these drugs before the baseline data were obtained. We cannot rule out the possibility that hidden and reversible conditions played some role in the good outcomes of patients with LVSD, such as concealed alcoholism followed by total abstinence,35 subclinical myocarditis,36 or simply a better control of hypertension.

Clinical Implications
Despite these reservations, we think that the results obtained from the intrapatient comparisons are sufficiently impressive to spell out a clear message on the clinical approach to AF in the setting of LVSD. The independently worse prognosis conferred by AF has been documented.37 The increased risk of embolism is well appreciated,38 but the importance of AF in the progression of heart failure39 40 is poorly understood. Furthermore, there is increasing evidence that patients with heart failure who convert to SR have a lower mortality rate than those who do not.41 All these data, along with our results, suggest that a more vigorous approach to cardioversion should be adopted in patients with AF and LVSD, especially when the latter has no clear origin.

In conclusion, patients with chronic AF and LVSD of nonischemic origin receive considerable medium-term benefits from SR restoration, even when an adequate control of the ventricular rate has been achieved. This finding is of major clinical relevance and should be tested in a larger population.


   Footnotes
 
Abbreviations: ACE = angiotensin-converting enzyme; AF = atrial fibrillation; LA = left atrium; LV = left ventricle, ventricular; LVEDD = left ventricular end-diastolic dimension; LVFS = left ventricular fractional shortening; LVM = left ventricular mass; LVS = left ventricular systolic; LVSD = left ventricular systolic dysfunction; SR = sinus rhythm

Received for publication April 11, 2000. Accepted for publication January 29, 2001.


   References
TOP
 Abstract
 Introduction
 Materials and Methods
 Results
 Discussion
 References
 

  1. Cowie, MR, Wood, DA, Coats, AJS, et al (1999) Incidence and etiology of heart failure: a population-based study. Eur Heart J 20,421-428[Abstract/Free Full Text]
  2. Brill, IC (1937) Auricular fibrillation with congestive heart failure and no other evidence of heart disease. Am Heart J 13,175-182[CrossRef]
  3. Philips, E, Levine, SA (1949) Auricular fibrillation without other evidence of heart disease: a cause of reversible heart failure. Am J Med 7,479-489
  4. Peters, KG, Kienzle, MG (1988) Severe cardiomyopathy due to chronic rapidly conducted atrial fibrillation: complete recovery after restoration of sinus rhythm. Am J Med 85,242-244[ISI][Medline]
  5. Grogan, M, Smith, HC, Gersh, B, et al (1992) Left ventricular dysfunction due to atrial fibrillation in patients initially believed to have idiopathic dilated cardiomyopathy. Am J Cardiol 69,1570-1573[CrossRef][ISI][Medline]
  6. Kieny, JR, Sacrez, A, Facello, A, et al (1992) Increase in radionuclide left ventricular ejection fraction after cardioversion of chronic atrial fibrillation in idiopathic dilated cardiomyopathy. Eur Heart J 13,1290-1295[Abstract/Free Full Text]
  7. Alam, M, Thorstrand, C (1992) Left ventricular function in patients with atrial fibrillation before and after cardioversion. Am J Cardiol 69,694-696[CrossRef][ISI][Medline]
  8. Shite, J, Yokota, Y, Yokoyama, M (1993) Heterogeneity and time course of improvement in cardiac function after cardioversion of chronic atrial fibrillation: assessment of serial echocardiographic indices. Br Heart J 70,154-159[Abstract/Free Full Text]
  9. Van Gelder, IC, Crijns, HJ, Blanksma, PK, et al (1993) Time course of hemodynamic changes and improvement of exercise tolerance after cardioversion of chronic atrial fibrillation unassociated with cardiac valve disease. Am J Cardiol 72,560-566[CrossRef][ISI][Medline]
  10. Xiong, C, Sonnhag, C, Nylander, E, et al (1995) Atrial and ventricular function after cardioversion of atrial fibrillation. Br Heart J 74,254-260[Abstract/Free Full Text]
  11. Sahn, D, DeMaria, A, Kisslo, J, et al (1978) Recommendations regarding quantitation in M-mode echocardiography: results of a survey of echocardiographic measurements. Circulation 58,1072-1083[Abstract/Free Full Text]
  12. Devereux, RB, Alonso, DR, Lutas, EM, et al (1986) Echocardiographic assessment of left ventricular hypertrophy: comparison to necropsy findings. Am J Cardiol 57,450-458[CrossRef][ISI][Medline]
  13. Samet, P, Bernstein, W, Levine, S (1965) Significance of the atrial contribution to ventricular filling. Am J Cardiol 15,195-202[CrossRef][ISI][Medline]
  14. Linderer, T, Chatterjee, K, Parmley, WW, et al (1983) Influence of atrial systole on the Frank-Starling relation and the end-diastolic pressure-diameter relation of the left ventricle. Circulation 67,1045-1053[Abstract/Free Full Text]
  15. Lipkin, DP, Frennaux, M, Stewart, R, et al (1988) Delayed improvement in exercise capacity after cardioversion of atrial fibrillation to SR. Br Heart J 59,572-577[Abstract/Free Full Text]
  16. Ueshima, K, Myers, J, Morris, CK, et al (1993) The effect of cardioversion on exercise capacity in patients with atrial fibrillation. Am Heart J 126,1021-1024[CrossRef][ISI][Medline]
  17. Paelinck, B, Vermeersch, P, Stockman, D, et al (1999) Usefulness of low-dose dobutamine stress echocardiography in predicting recovery of poor left ventricular function in atrial fibrillation dilated cardiomyopathy. Am J Cardiol 83,1668-1671[CrossRef][ISI][Medline]
  18. Shinbane, JS, Wood, MA, Jensen, DN, et al (1997) Tachycardia-induced cardiomyopathy: a review of animal models and clinical studies. J Am Coll Cardiol 29,709-715[Abstract]
  19. Van Den Berg, MP, Tuinenburg, AE, Crijns, HJGM, et al (1997) Heart failure and atrial fibrillation: current concepts and controversies. Heart 77,309-313[Abstract/Free Full Text]
  20. Prabhu, SD, Freeman, GL (1993) Left ventricular energetics in closed-chest dogs. Am J Physiol 265,H1048-H1055[Abstract/Free Full Text]
  21. Moe, GW, Stopps, TP, Howard, RJ, et al (1988) Early recovery from heart failure: insights into the pathogenesis of experimental chronic pacing-induced heart failure. J Lab Clin Med 112,426-432[ISI][Medline]
  22. Perreault, CL, Shannon, RP, Komamura, K, et al (1992) Abnormalities in intracellular calcium regulation and contractile function in myocardium from dogs with pacing-induced heart failure. J Clin Invest 89,932-938
  23. Packer, D, Bardy, G, Worley, S, et al (1986) Tachycardia-induced cardiomyopathy: a reversible form of left ventricular dysfunction. Am J Cardiol 57,563-570[CrossRef][ISI][Medline]
  24. Rawles, JM (1990) What is meant by a "controlled" ventricular rate in atrial fibrillation? Br Heart J 63,157-161[Abstract/Free Full Text]
  25. Daoud, E, Weis, R, Bahu, M, et al (1996) Effect of irregular ventricular rhythm on cardiac output. Am J Cardiol 78,1433-1436[CrossRef][ISI][Medline]
  26. Clark, D, Plumb, V, Epstein, A, et al (1997) Hemodynamic effects of irregular sequence of ventricular cycle lengths during atrial fibrillation. J Am Coll Cardiol 30,1039-1045[Abstract]
  27. Nagayoshi, H, Janota, T, Hnatkova, K, et al (1997) Autonomic modulation of ventricular rate in atrial fibrillation. Am J Physiol 41,H1643-H1649
  28. Heinz, G, Siostrzonek, P, Kreiner, G, et al (1992) Improvement in left ventricular systolic function after successful radiofrequency His bundle ablation for drug refractory, chronic atrial fibrillation and recurrent atrial flutter. Am J Cardiol 69,489-492[CrossRef][ISI][Medline]
  29. Rodriguez, LM, Smeets, J, Xie, B, et al (1993) Improvement in left ventricular systolic function by ablation of atrioventricular nodal conduction in selected patients with lone atrial fibrillation. Am J Cardiol 72,1137-1141[CrossRef][ISI][Medline]
  30. Brignole M, Nenozzi C, Gianfranchi L, et al. Assessment of atrioventricular junction ablation and VVIR pacemaker versus pharmacologic treatment in patients with heart failure and chronic atrial fibrillation: a randomized, controlled study. Circulation 1998; 98:953–960
  31. Gheorghiade, M, St Clair, J, St Clair, C, et al (1987) Hemodynamic effects of intravenous digoxin in patients with severe heart failure initially treated by diuretics and vasodilators. J Am Coll Cardiol 9,849-857[Abstract]
  32. Kramer, BL, Massie, BM, Topic, N (1983) Controlled trial of captopril in chronic heart failure: a rest and exercise hemodynamic study. Circulation 67,807-816[Free Full Text]
  33. Singh, SN, Fletcher, RD, Fisher, SG, et al (1995) Amiodarone in patients with congestive heart failure and asymptomatic ventricular arrhythmias: Survival Trial of Antiarrhythmic Therapy in Congestive Heart Failure. N Engl J Med 333,77-82[Abstract/Free Full Text]
  34. Eichhorn, EJ, Heesch, CM, Barnett, JH, et al (1994) Effect of metoprolol on myocardial function and energetics in patients with nonischemic dilated cardiomyopathy: a randomized, double-blind, placebo-controlled study. J Am Coll Cardiol 24,1310-1320
  35. Guillo, P, Mansourati, J, Maheu, B, et al (1997) Long-term prognosis of patients with alcoholic cardiomyopathy and severe heart failure after total abstinence. Am J Cardiol 79,1276-1278[CrossRef][ISI][Medline]
  36. Smith, SC, Ladenson, JH, Mason, JW, et al (1997) Elevations of cardiac troponin I associated with myocarditis: experimental and clinical correlates. Circulation 95,163-168[Abstract/Free Full Text]
  37. Benjamin, EJ, Wolf, PA, D’Agostino, RB, et al (1998) Impact of atrial fibrillation on the risk of death: the Framingham Heart Study. Circulation 98,946-952[Abstract/Free Full Text]
  38. Brodsky, MA, Chun, JG, Podrid, PJ, et al (1996) Regional attitudes of generalists, specialists, and subspecialists about management of atrial fibrillation. Arch Intern Med 156,2553-2562[Abstract]
  39. Pozzoli, M, Cioffi, G, Traversi, E, et al (1998) Predictors of primary atrial fibrillation and concomitant clinical and hemodynamic changes in patients with chronic heart failure: a prospective study in 344 patients with baseline sinus rhythm. J Am Coll Cardiol 32,197-204[Abstract/Free Full Text]
  40. Dries, DL, Exner, DV, Gersh, BJ, et al (1998) Atrial fibrillation is associated with an increased risk for mortality and heart failure progression in patients with asymptomatic and symptomatic left ventricular dysfunction: a retrospective analysis of the SOLVD trials. J Am Coll Cardiol 32,695-703[Abstract/Free Full Text]
  41. Deedwania, PC, Singh, BM, Ellenbogen, K, et al (1998) Spontaneous conversion and maintenance of sinus rhythm by amiodarone in patients with heart failure and atrial fibrillation: observations form the Veterans Affairs Congestive Heart Failure Survival Trial of Antiarrhythmic Therapy (CHF-STAT). Circulation 98,2574-2579[Abstract/Free Full Text]



This article has been cited by other articles:


Home page
 Eur Heart J SupplHome page
C. Butter, G. Winbeck, M. Schlegl, M. Seifert, A. Wagner, E. Wellnhofer, and E. Fleck
Management of atrial fibrillation in cardiac resynchronization therapy: Clinical practice of CRT: how to improve the success rate
Eur. Heart J. Suppl., August 1, 2004; 6(suppl_D): D106 - D111.
[Abstract] [Full Text] [PDF]

This Article
Right arrow Abstract Freely available
Right arrow Full Text (PDF) Free
Right arrow Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when eLetters are posted
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Article Archive
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via ISI Web of Science (3)
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Azpitarte, J.
Right arrow Articles by Tercedor, L.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Azpitarte, J.
Right arrow Articles by Tercedor, L.

HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS