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European Journal of Heart Failure 2002 4(3):263-267; doi:10.1016/S1388-9842(02)00004-1
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© 2002 European Society of Cardiology

Short-term effects of sinus rhythm restoration in patients with lone atrial fibrillation: a hormonal study

P. Jourdaina,*, M. Bellorinia, F. Funcka, Y. Fullab, N. Guillarda, J. Loireta, B. Thebaulta, N. Sadegd and M. Desnosc

a Service de Cardiologie Hôpital René Dubos, 6 avenue de l'Ile de France, 95300 Pontoise, France
b Service de Médecine Nucléaire Hôpital Cochin, 27 boulevard Saint Jacques, 75014 Paris, France
c Service de cardiologie Hôpital Européen G. Pompidou, Rue Leblanc, 75015 Paris, France
d Service de Biochimie Hôpital René Dubos, 6 avenue de l'Ile de France, 95300 Pontoise, France

* Corresponding author. Tel.: +33-1-30-75-41-86; fax +33-1-30-75-44-28. E-mail address: patrickjourdain{at}hotmail.com


   Abstract
Top
 Abstract
1. Introduction
 2. Methodology
 3. Results
 4. Discussion
 5. Conclusion
 References
 
It is well known that atrial fibrillation can lead to heart failure, and is attributed to rapid ventricular rate (tachycardia-induced cardiomyopathy). Some recent studies suggest the possible existence of an intrinsic left-ventricular factor related to atrial fibrillation, irrespective of other elements. In order to demonstrate the implication of this factor, we measured B-type Natriuretic Peptide, known as a functional marker of left-ventricular dysfunction, in 40 consecutive patients with chronic non-valvular atrial fibrillation, with low ventricular rate and absence of clinical heart failure or echocardiographic left-ventricular dysfunction. In all patients, Brain Natriuretic Peptide (BNP) plasma level was high and dramatically decreased 24 h after external electrical cardioversion (61.4 pg/ml before cardioversion, 23.5 pg/ml 1 day after cardioversion, P<0.002). Our study demonstrates that atrial fibrillation, in absence of high ventricular rate, induces an asymptomatic cardiac alteration that is not detectable by echocardiography.

Key Words: Cardioversion • Natriuretic peptides • Atrial fibrillation

Received January 11, 2001; Revised August 14, 2001; Accepted December 14, 2001


   1. Introduction
Top
 Abstract
 1. Introduction
2. Methodology
 3. Results
 4. Discussion
 5. Conclusion
 References
 
Atrial fibrillation can be responsible for auriculo-ventricular alterations, which can themselves lead to an authentic cardiomyopathy called rhythmic cardiomyopathy. Indeed, left-ventricular dysfunction secondary to rapid atrial fibrillation (AF) is common: animal models and clinical studies have shown that severe cardiac failure can occur after chronic supraventricular tachycardia in patients without underlying cardiac disease [1]. This tachycardia-induced cardiomyopathy induced by rapid ventricular rates is reversible after rate control [2–4]. It has been emphasized that many patients who were initially believed to have idiopathic dilated cardiomyopathy with AF had, in fact, a cardiomyopathy due to AF and showed a normal ventricular function after return to sinus rhythm [5]. The B-type Natriuretic Peptide is a hormone secreted by cardiomyocytes in response to an increased stretching of myocytic fibers. It is a diagnostic and prognostic marker in acute and chronic heart failure. We wanted to find out if the isolated chronic atrial fibrillation and the return in sinusal rhythm influenced the level of BNP of subjects presenting an echographically normal heart.

The purpose of our study was to assess changes in cardiac hormonal activity reflected by the evolution of BNP level in patients with chronic AF, without rapid ventricular rate, without valvular disease or ventricular dilation, with normal ejection fraction, before and after cardioversion.


   2. Methodology
Top
 Abstract
 1. Introduction
 2. Methodology
3. Results
 4. Discussion
 5. Conclusion
 References
 
Forty consecutive patients referred for electrical cardioversion of supra-ventricular arrhythmia were prospectively included in our study. The investigation conformed with the principles outlined in the Declaration of Helsinki.

The inclusion criteria were:

  1. Presence of a supra-ventricular arrhythmia with rest ventricular rate <100/mn for more than 1 month, proved by at least two electrocardiograms.
  2. Absence of clinical, radiological and echocardiographical signs of heart failure during the whole period of arrhythmia.
  3. Patient's information and agreement regarding blood samples.

The exclusion criteria were:

  • Existence of an echocardiographical left-ventricular systolic dysfunction defined as left-ventricular ejection fraction <60% measured using the biapical Simpson's method, as recommended by the American Society of Echocardiography [6].
  • Existence of a left-ventricular dilation defined as telediastolic left-ventricular diameter >60 mm in long axis parasternal view.
  • Existence of renal failure defined as creatinin plasma level >120 µmol/l.
  • Existence of mitral or aortic valve disease.
  • Existence of a ventricular rate at the inclusion >100 beats per minute (bpm).

Patients in whom arrhythmia recurred during the 24 h following cardioversion were retrospectively excluded from the study.

External electrical direct cardioversion was performed by a cardiologist assisted by a nurse. General anesthesia was administered by an anesthetist by means of Diprivan, and patients received oxygen mask ventilation under permanent control of saturation rate.

External electrical shocks were delivered by antero-left lateral electrodes with a Defiguard defibrillator (Brucker). Successive energies used were 200, 300 and 360 J. An electrocardiogram was then performed and the patient awakened. Hospitalization was prolonged 24 h after anesthesia with permanent control of cardiac rhythm by telemetry monitoring (Hewlett Packard).

Plasma BNP measures were performed on peripheral venous blood samples, in special test-tubes containing EDTA and Apronitin in order to minimize protease activity. Each time, we took 5 ml of blood by means of a peripheral venous catheter set up at least 2 h before hand. The sample taking was carried out on patients in dorsal decubitus for at least 30 min. Blood was immediately stored at –4 °C, centrifuged at 2500 rev./min and the supernatant was stored at –20 °C.

Blood samples were taken 1 h before cardioversion (after a 30-min rest), 30 min after return to sinus rhythm and 24 h after cardioversion.

Plasma BNP levels were obtained by radio-immunological test (Cis Bio International under Shionogi license) [7]. This test used an immunofixation technique with two antibodies, one marked as radioactive. Biological measurements and medical data analysis were performed double-blindly by two different teams at two different sites. BNP blood plasma level normal cut off was <10 pg/ml.

All data were stored using Excel 98. Statistical analysis was carried out using Sigmastat 2.0 and Statview 5.0 software. Results are presented as mean±standard deviation. Comparisons between different results used Student's t-test for parametric data and Mann–Whitney test for non-parametric data and the {chi}2 test for the percentages observed. A P-value <0.05 was considered as statistically significant.


   3. Results
Top
 Abstract
 1. Introduction
 2. Methodology
 3. Results
4. Discussion
 5. Conclusion
 References
 
In our initial population, 36 patients referred for a programmed cardioversion returned to sinus rhythm after cardioversion (group A). Four patients could not be put back in sinus rhythm after three attempts of cardioversion (group B).

The mean age was 63±12.5 years; 28% were women. 84% patients had already had preliminary atrial arrhythmia prior to inclusion. The mean duration of current arrhythmia was 7.8±11.5 consecutive months.

Seventy-five percent of the patients had been treated with Amiodarone, 15% with a Vaughan Williams class 2 anti-arrhythmic drug, and 10% did not receive any anti-arrhythmic therapy before cardioversion.

All patients had received anticoagulation therapy for at least 1 month, with INR between 2 and 4.

Return to sinus rhythm was obtained in 76% patients with a single 200 J shock, 13% patients needed a second 300 J shock and 11% patients needed a third 360 J shock.

There was no adverse affect related to cardioversion or anesthesia.

In group A, the mean BNP plasma level fell from 61.4 pg/ml before shock to 46.3 pg/ml 30 min after return to sinus rhythm (P<0.007) and 23.5 pg/ml 24 h after cardioversion (P<0.002) (Fig. 1).


Figure 1
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  		Fig. 1 Variation of BNP plasma levels before and after cardioversion.

 
Systolic and diastolic blood pressures variations among blood samples were not statistically significant (Table 1). Mean ventricular rate decreased from 81.1 bpm before shock to 64.9 bpm 30 min after return to sinus rhythm and 61.6 bpm after 24 h (P<0.05).


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  		Table 1 Evolution of hemodynamic parameters

 
In the same way, the level of creatininemia was not modified by the cardioversion. The variations of the level of BNP are therefore not induced by variations of the afterload or BNP clearance.

In group B, the plasma level of BNP did not vary significantly between the different samples (respectively 52±10, 48±13, 58±7 pg/ml). In this group, there was no significant variation of the arterial pressure or heart rate.


   4. Discussion
Top
 Abstract
 1. Introduction
 2. Methodology
 3. Results
 4. Discussion
5. Conclusion
 References
 
Our study shows that patients with ‘normal’ heart (absence of clinical heart failure and echocardiographic left-ventricular systolic dysfunction) present high BNP levels during chronic atrial fibrillation. Many studies are available on the effects of arrhythmia or atrial enlargement on Atrial Natriuretic Peptide (ANP) plasma levels but specific information about the effects of atrial fibrillation on ventricular neurohormonal activation are lacking.

Many published studies have shown that plasma BNP level is high in systolic and diastolic heart failure. BNP level is indeed correlated to severity of cardiac failure, assessed by NYHA classification and left-ventricular ejection fraction [8–10]. BNP is a 32-amino acid hormone synthesized mainly by ventricular myocytes and is a sensitive and specific marker of left-ventricular dysfunction [7]. Its structure is similar to ANP but its secretion and half-life are very different. Its plasmatic rate accurately reflects its ventricular secretion [11].

In our population, there was no clinical heart failure and no echocardiographic left-ventricular systolic dysfunction. However, we noted a high plasmatic rate of BNP in all patients (normality threshold <10 pg/ml for our kit of dosage). Since this study is preliminary, we did not study the variations of the different echocardiographic parameters parallel to the evolution of the BNP level. However, the variation of these parameters has already been largely analyzed by catheterization, or by trans-thoracic or by trans-oesophageal echocardiography [11–13]. This suggests that the recovery of the echographic auricular function and the recovery of the left-ventricular systolic function in patients presenting an alteration of these parameters caused by the arrhythmia are relatively slow [14,15] and depends on arrhythmia duration [16], compared to the variations that we highlighted relating to the BNP levels.

Impairment of cardiac function in AF has been attributed to the loss of atrial contraction and to rapid ventricular rate. However, some studies suggested that irregularity of the ventricular rhythm, independently of ventricular rate, can contribute to impairment of cardiac function during AF [17]. Furthermore, Van Gelder [18] showed that in patients with chronic AF unassociated with valvular disease, after cardioversion, atrial systole improves after one week and remains unchanged thereafter, whereas ejection fraction improves after one week and then after one month. Restoration of sinus rhythm is associated with a delayed improvement in left-ventricular ejection fraction preceded by an early restoration of atrial contractility and an acute slowing of the heart rate, suggesting that intrinsic left-ventricular cardiomyopathy is present in patients with AF.

It would, nevertheless, be interesting to carry out a study coupling the measurement of BNP and echocardiographic measurements in order to determine which are the parameters best correlated with the variations of BNP. What is sure, is that BNP indicates a very fast correction of cardiac neurohormonal activation induced by the atrial fibrillation isolated on an echographically healthy heart in contrast with ANP (atrial-dependent hormone) which is normalized one month after restoration of sinus rhythm [19].

In this study, we were interested in patients presenting a relatively slow chronic atrial fibrillation. In these patients, one cannot eliminate the existence of rhythmic variations, which were already described as being able to lead to myocyte deterioration. However, it seems that the existence of a high BNP level is in favor of a possible role of an irregularity of RR cycles like that which has been previously described [6]. Indeed, in our study, the heart rate is little modified compared to the BNP by the return in sinus rhythm. The restoration of the sinus rhythm corrects the irregularity of the cycles and normalizes BNP.

The speed of the BNP variations is also a new concept. The mechanisms of BNP secretion are still not very clear. It is known that BNP is partly contained in intra myocytic granules and is partly synthesized in a very fast way starting from various stimuli such as endothelin secretion or volume overload of the left ventricle [20,21]. Its theoretical half-life is 22 min [22]. The fast drop of BNP after return to sinus rhythm is closer to that found by Kazanegra et al. among patients suffering from acute heart failure [23]. Taking into account the half-life of BNP and the duration necessary to stop the proteinic synthesis chain, it is difficult to conceive that only a reduction in the synthesis of BNP comes into play, but the mechanism that underlies this fast drop of BNP still remains unexplained.

The site of BNP secretion is difficult to discern in the absence of selective catheterization coupled with the cardio version. The data currently published are not unequivocal. BNP is secreted mainly by the ventricular myocytes. Catheterization studies have found that the plasma level of BNP measured at the root of the aorta is correlated with the level found in the inter ventricular anterior vein (AIV) [10,24]. According to the same authors, there is no gradient in the secretion of BNP between the coronary sinus and the AIV in patients with chronic heart failure as well as in healthy subjects.

The absence of a difference in the BNP level reported by Rossi et al. [25] between the chronic heart failure patients in AF or in sinus rhythm goes against the assumption of a significant auricular contribution. Other authors were interested in the detection of messenger ARN coding for BNP on the atria [26]. For these authors, there exists indeed messenger ARN coding for BNP in the auricular walls but it is not correlated with the plasma levels of BNP. In a study on patients with mitral stenosis, ANP but not BNP changes after successful percutaneous transvenous mitral valvulotomy [27].

Even if the share of responsibility of the atria cannot formally be eliminated with regard to the rise of BNP found among our patients, we put forth the following assumption that this neurohormonal activation induced by the insulated AF at slow ventricular rate might reflect the existence of an induced cardiac attack. This attack may constitute the first stage of rhythmic cardiomyopathy. Only medium and long term follow-up of patients with good left-ventricular function in slow chronic arrhythmia will confirm this assumption and thus allow to determine precociously the patients who have the most significant repercussion of the AF, even if their traditional parameters of left-ventricular function are normal.


   5. Conclusion
Top
 Abstract
 1. Introduction
 2. Methodology
 3. Results
 4. Discussion
 5. Conclusion
References
 
The lone AF on healthy patients leads to a significant neurohormonal activation highlighted by a rise in the BNP plasma level. This effect is very quickly corrected by the return to sinus rhythm by means of a cardio lateral version. One can consider that high BNP levels reflect a significant repercussion of the AF, which has not been highlighted by echocardiography.


   References
Top
 Abstract
 1. Introduction
 2. Methodology
 3. Results
 4. Discussion
 5. Conclusion
 References
 

  1. Shinbane J.S., Wood M.A., Jensen D.N., et al. Tachycardia-induced cardiomyopathy: a review of animal models and clinical studies. J Am Coll Cardiol (1997) 29(4):709–715.[Abstract]
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  15. Alam M., Thorstrand C. Left ventricular function in patients with atrial fibrillation before and after cardioversion. Am J Cardiol (1991) 69:694–696.[CrossRef][Web of Science]
  16. Manning W.J., Silvermann D.I., Katz S.E., et al. Impaired left atrial mechanical function after cardioversion: relation to the duration of atrial fibrillation. J Am Coll Cardiol (1994) 23:1535–1540.[Abstract]
  17. Daoud E.G., Weiss R., Bahu M., et al. Effect of an irregular ventricular rhythm on cardiac output. Am J Cardiol (1996) 78(12):1433–1436.[CrossRef][Web of Science][Medline]
  18. Van Gelder I.C., Crinjs H.J., Blanksma P.K., et al. Time course of hemodynamic changes and improvement of exercise tolerance after cardioversion of chronic atrial fibrillation unassociated with cardiac valve disease. Am J Cardiol (1993) 72(7):560–566.[CrossRef][Web of Science][Medline]
  19. Berglund H., Boukter S., Theodorsson E., et al. Raised plasma concentrations of atrial natriuretic peptide are independent of left atrial dimensions in patients with chronic atrial fibrillation. Br Heart J (1990) 64:9–13.[Abstract/Free Full Text]
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  23. Kazanegra R., Cheng V., Garcia A., et al. A rapid test for B type Natriuretic peptide correlates with falling wedge pressures in patients treated for decompensated heart failure: a pilot study. J Cardiac Failure (2001) 7:21–29.[CrossRef][Web of Science][Medline]
  24. Sumida H., Yasue H., Yoshimura M., et al. Comparison of secretion pattern between A type and B type Natriuretic peptides in patients with old myocardial infarction. J Am Coll Cardiol (1995) 25:1105–1110.[Abstract]
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