|
|
||||||||
Guest Access | Sign In via User Name/Password |
|||||||||
* From the Medizinische Klinik and Institut für Statistik und Epidemiologie (Dr. Ulm), Klinikum rechts der Isar der Technischen Universität München; and the Deutsches Herzzentrum (Drs. Lehmann, Horcher, Dennig, Plewan, and Alt), Klinik an der Technischen Universität München, Munich, Germany.
Correspondence to: Günter Lehmann, MD, Deutsches Herzzentrum München, Klinik an der Technischen Universität, Lazarettstraße 36, D-80636 München, Germany
| Abstract |
|---|
|
|
|---|
Background: Right atrial performance has been shown to normalize before the left atrium after external CV. However, no data on atrial function after internal CV are available.
Patients and interventions: Sixty-three patients with chronic AF were randomized to participate in either external or internal CV.
Measurements: Echocardiographic examinations were carried out before as well as immediately after CV (day 0), and at days 1, 7, and 28 thereafter for the determination of cardiac dimensions, volumes, and transvalvular flow patterns.
Results: After randomized internal CV or external CV, stable sinus rhythm was restored in 59 patients. Irrespective of the mode of CV, the right atrium resumed its mechanical function immediately after CV, whereas the left atrium was stunned beyond day 7. The mode of CV, internal or external, had no influence on the recovery of atrial mechanical function.
Conclusions: The right atrium resumes its normal function immediately after internal as well as external CV, whereas left atrium function is delayed. In contrast to the assumption that low-energy internal CV would impact less on atrial mechanical recovery, the type of method of CV used has no effect on such recovery.
Key Words: atrial fibrillation atrial performance echocardiographic parameters external cardioversion internal cardioversion
| Introduction |
|---|
|
|
|---|
trical CV methods with respect to the time course of resumption of left and right atrial mechanical activity following either internal or external CV of chronic AF. It was also of special interest to determine whether the time course of normalization of atrial performance would be related to atrial dimensions or volumes prior to electrical CV and whether the maintenance of sinus rhythm would be predicted by echocardiographic parameters following CV.
| Materials and Methods |
|---|
|
|
|---|
3 weeks) or evidence of digitalis toxicity, abnormal
electrolyte levels, or hyperthyroidism, in addition to patients with a
history of long QT syndrome, an acute myocardial infarction within the
past 6 weeks, a history of embolism, or either an atrioventricular
valve disease greater than moderate in degree or a mechanical
atrioventricular valve prosthesis.1
2
Clinical
examinations were performed, and medical histories were obtained.
Routine 12-lead ECG; routine laboratory testing comprising of blood
cell count, liver enzymes, serum electrolytes, serum creatinine, urea,
blood coagulation parameters, and analysis of thyroid parameters; and
M-mode and Doppler echocardiography were performed in all patients. For
exclusion of thromboembolic risks (ie, presence of left
atrial thrombi), transesophageal echocardiography was performed in all
patients before CV. Creatine kinase and potassium values were
determined before and at 6 h after each CV attempt. Antiarrhythmic
treatment, other than either sotalol or bisoprolol, was withheld for at
least five half-lives before CV. Patients were then randomized to
undergo either external or internal CV.
Informed Consent and Documentation
The benefits and risks of the study were explained to the
patients. Written informed consent was obtained from all patients based
on the protocol of the study as approved by the Ethics Committee of the
Klinikum rechts der Isar.
Interventions
External CV
: External CV was performed under the supervision
of an anesthetist. Up to a maximum of three R wave-triggered shocks of
increasing energy (200 J, 360 J, and again 360 J) were applied
by an external defibrillator as described
elsewhere.1
2
9
10
Internal CV : Internal CV was performed in the cardiac catheterization laboratory. A single-lead atrial CV catheter (EP Med Systems; Mount Arlington, NJ) was inserted via either the right femoral or brachial venous access as previously reported.9 10 16 Up to a maximum of five R wave-triggered shocks of increasing energy (3, 6, 9, 12, and 15 J) were applied using biphasic shocks.
Follow-up Evaluation
All patients received follow-up evaluations in the outpatient
department. A 12-lead ECG was obtained, and M-mode and Doppler
echocardiography were performed immediately before CV and at days 1, 7,
and 28 after CV. Patients were randomly treated with either sotalol
(n = 28; mean daily dose, 178 ± 37 mg; range, 120 to 240 mg) or
bisoprolol (n = 31; mean daily dose, 6 ± 3 mg; range, 2.5 to 20
mg) after effective CV to sinus rhythm.17
Treatments with
angiotensin-converting enzyme inhibitors, diuretics, and digitalis were
continued based on the clinical status of the patients. Anticoagulation
was continued for 4 weeks after successful CV.
Echocardiographic Evaluation
End-diastolic and end-systolic left and right ventricular
diameters as well as left and right atrial dimensions were measured
from a parasternal long-axis view and apical four-chamber view
according to American Society of Echocardiography
criteria18
19
using the respective longest and shortest
longitudinal and cross-sectional diameters (Sonos 5500; Hewlett
Packard; Palo Alto, CA). Mitral and tricuspid flow velocities were
measured with pulsed Doppler echocardiography to obtain peak early
(passive ventricular filling [E]) and late (active atrial contraction
[A]) flow velocities. Flow velocity across the left ventricular
outflow tract was assessed by pulsed Doppler echocardiography.
Volumetric quantification was performed using automated calculation of
volumes based on the rotational ellipsoid.20
Statistical Analyses
Statistical analyses were performed according to mode of
treatment. Continuous variables are expressed as mean ± SD.
Categorical variables were analyzed using the
2 test. Students t test for
paired or unpaired samples was applied as appropriate. Comparisons of
more than two groups of data were performed with a repeated-measures
analysis of variance, subjected to multiple comparison according to the
Friedman test. Statistical univariate and multivariate analyses were
performed with the Statistical Package for Social Sciences (SPSS;
Chicago, IL) for clinical and echocardiographic parameters, outcome,
and follow-up.1
Statistical significance was assumed at
p < 0.05.
| Results |
|---|
|
|
|---|
|
When comparing both internal and external electrical CV modalities, we found that there were no differences regarding maintenance of sinus rhythm at 28 days or with atrial and ventricular volumes, diameters, or ejection fractions at all points in time. External (Fig 1 , top) and internal CV (Fig 1 , bottom) did not differ regarding peak E, peak A, or the ratio of the amplitude of the waves created by early diastolic filling and atrial contraction (E/A ratio) at any point in time. Thus, in contrast to the assumption that low-energy internal CV would have less impact on atrial mechanical recovery, the method of CV had no effect. Accordingly, the data of patients who received external and internal CV were pooled for the remaining analyses.
|
Because no basal E/A ratio was available for any patient, the values
measured on day 28 after CV were taken as baseline characteristic of
the individual patients. Because there are many variables with the
potential to influence the E/A ratio, a subgroup analysis of patients
in sinus rhythm was performed on day 28. Accordingly, patients were
dichotomized with respect to their E/A ratio (< 1 or
1) on day
28. Subgroups did not differ with respect to clinical parameters or
underlying heart diseases. There was a constancy of E over time in both
subgroups, a constant rise of A, and a subsequent decline in E/A, which
was more rapid in the subgroup of patients with a final E/A ratio
< 1, reflecting a more rapid gain in atrial contractility (Fig 2
).
|
Time Course of Resumption of Atrial Performance in Relation to
Preprocedural Dimensions
On the basis of the assumption that A and the E/A ratio mirror
mechanical atrial function, regression analyses were performed to
evaluate the relation between atrial dimensions or volumes before CV
and time course of normalization of atrial performance, reflected by
the differences of A and E/A between days 0 and 28. Neither the
diameters of the atria and ventricles nor the volumes of the left
atrium and ventricle reliably predicted the resumption of mechanical
atrial performance over the 28 days after electrical CV in a
statistically significant manner. Of note, left atrial volumes were
always larger and left atrial ejection fraction was always smaller than
their right atrial counterparts at all points in time and irrespective
of rhythmic outcome on day 28.
| Discussion |
|---|
|
|
|---|
The higher total energy application with external CV is reflected by higher creatine kinase values (118 U/L vs 37 U/L), especially in patients who required three or more shocks. According to one study,26 elevations of creatine kinase are found in > 50% of patients undergoing external CV, but without concomitant elevation of the creatine kinase-MB fraction or cardiac troponin I. Indeed, there was only one patient in whom the MB fraction was found elevated (reaching 13 U/L). Therefore, the creatine kinase increase with external CV primarily results from muscular contractions that are not found with low-energy internal CV.
The second important finding of the present randomized study is that the resumption of mechanical atrial activity occurs earlier in the right atrium, when compared with the left atrium. There is a constancy in E velocity mirroring the passive ventricular filling across both atrioventricular valves over time; however, normalization of A velocity, reflecting the active mechanical atrial contraction,27 and return of E/A ratio occur almost immediately in the right atrium. In contrast, no change in these parameters was observed in the left atrium within 7 days after CV. This phenomenon had been observed earlier after exclusively external CV5 ; in the present study, a primarily identical course over time was found also for low-energy internal CV. This finding is in contrast to recently published data that inferred atrial stunning from external and internal CV.7 8 28 In these nonrandomized studies, patients were included for electrical CV after failure of pharmacologic attempts. Because both underlying heart disease and AF duration have the potential to lead to structural alterations of both atria, which, in turn, predominate the left atrium,5 15 29 the atria of patients requiring electrical CV were the more seriously affected, rendering nonelectrical measurements as well as low-energy electrical CV less effective. These findings are also in keeping with a report on the rapidity of atrial recovery in association with the duration of AF before CV.30 Accordingly, it is not the procedure, but rather the extent of the organic affection of the atria, the reversibility, and perhaps, the intrinsic differences in electrophysiology between both atria that determine the time-course of mechanical atrial recovery after CV.5 7 12 24 27 30 31 It is not only atherosclerosis, pressure volume overload, or the duration of AF that impact on atrial electrophysiology,32 but also inborn structural differences between both atria that render the left atrium more vulnerable to arrhythmias than the right atrium.31 The coexistence of sinus rhythm in the right atrium and AF emanating from the left have been reported.33 Consequently, the delayed recovery of mechanical and electrical left atrial function after either CV mode forms another basis to continue oral anticoagulation for up to 4 weeks, despite the presence of sinus rhythm.5 7 24 27
There is, however, one study34 inferring an identical and rapid time course of mechanical recovery of both atria, normalizing even within 24 h after chemical CV. Methodologic reasons may explain its conclusions. First, only 31 of 50 patients converted within 24 h of receiving amiodarone and formed the patient group. Because chemical CV is known to be less effective than electrical CV,2 5 8 9 15 we can assume that the 31 patients had relatively little atrial organic alteration. This can be deduced from their AF duration (approximately 4 weeks, on average) and their preserved left ventricular function, which is known to deteriorate substantially in proportion to AF duration.5 Second, mean values of atrial ejection forces were different from that in control subjects, almost twice as high in the left atrium at 24 h and remaining higher on day 7 after CV; however, because of the small patient number, they failed to reach statistical significance. Finally, one half of the patients were receiving various antiarrhythmic treatments with the potential of affecting electrophysiology and contractility, and medical treatment was unknown for 12 patients. Thus, mechanical recovery of both atria also must be regarded as different when treated with chemical CV of AF of a relatively short duration.
In summary, after both internal and external CV of AF with modes and energies as described, there was no evidence of damage to the atrial myocardium. The present study adds to the growing evidence that the atrial stunning process is the result of the reversion to sinus rhythm itself, regardless of the method used. Normalization of left atrial performance takes significantly longer than normalization of the right atrium. Electrical CV mode exerts no influence on the time course of restoration of atrial performance. However, because of the delay in normalization of mechanical function of the left atrium, there is a rationale for continuation of anticoagulation in patients after CV even with stable sinus rhythm.
| Footnotes |
|---|
Received for publication January 31, 2001. Accepted for publication May 10, 2001.
| References |
|---|
|
|
|---|
This article has been cited by other articles:
![]() |
E. Donal, H. Yamada, C. Leclercq, and D. Herpin The Left Atrial Appendage, a Small, Blind-Ended Structure: A Review of Its Echocardiographic Evaluation and Its Clinical Role Chest, September 1, 2005; 128(3): 1853 - 1862. [Abstract] [Full Text] [PDF] |
||||
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |