European Journal of Heart Failure 2002 4(4):485-488; doi:10.1016/S1388-9842(02)00095-8
© 2002 European Society of Cardiology
Reversal of tachycardiomyopathy by the atrial defibrillator
Andrew R.J. Mitchell*,
Philip A.R. Spurrell,
Huseyin Ahmet,
Mike Higson and
Neil Sulke
Department of Cardiology Eastbourne General Hospital, Kings Drive, BN21 2UD, Eastbourne, UK
* Corresponding author. Tel.: +44-1323-417400; fax: +44-1323-414993 E-mail address: mitcharj{at}doctors.org.uk
Key Words: Atrial fibrillation • Atrial defibrillator • Tachycardiomyopathy
Received September 28, 2001; Revised November 15, 2001; Accepted February 4, 2002
 |
1. Introduction
|
|---|
It is increasingly recognized that the long-term consequences
of atrial fibrillation (AF) are not benign. Chronic AF is associated
with an increased mortality and a reduced life expectancy, believed
to be as a consequence of thromboembolic disease (particularly
stroke) and the onset of heart failure
[1,
2]. AF can result
in both rapid and irregular ventricular rates and the development
of atrial fibrillation-induced tachycardiomyopathy
[3]. The
evolution of the patient activated atrial defibrillator has
empowered patients to ‘take charge’ of their condition
and deliver an endocardial synchronised shock to restore sinus
rhythm soon after the onset of arrhythmia
[4]. We report a case
of a patient with recurrent AF who presented with mild heart
failure and reduced ejection fraction (EF) in whom normal left
ventricular function returned and was maintained after repeated
use of the atrial defibrillator.
|
2. Report
|
|---|
We implanted an atrial defibrillator in a 66-year-old male retired
physiotherapist. He had an 18-month history of recurrent persistent
AF and had been cardioverted twice back to sinus rhythm. AF
recurred 4 weeks after the first cardioversion and 2 weeks after
the second. He declined antiarrhythmic drugs due to the perceived
side effects but was anticoagulated with warfarin. After 1 year
of persistent AF he was referred for consideration of an atrial
defibrillator.
During sinus rhythm the patient was extremely well with an unlimited exercise capacity, but when he reverted to AF he immediately noticed a slight reduction in his exercise capacity with mild dyspnoea on exertion (NYHA Class 1). He was a life-long non-smoker, with minimal alcohol intake (less than 10 units per week) and he drank caffeine-free beverages only. There was no history of hypertension or ischaemic heart disease. On physical examination the radial pulse rate was 90 bpm in AF, the jugular venous pressure was elevated 2 cm and there were a few scattered bibasal crepitations. Abdominal examination was normal. His ECG showed AF with a ventricular rate of over 100 bpm and t-wave abnormalities in leads V5–V6 (Fig. 1). His chest X-ray (Fig. 2) revealed cardiomegaly (cardiothoracic ratio 18:33). Routine biochemical screening, including liver, kidney and thyroid function testing, was normal.
Pre-implant transthoracic echocardiography revealed a dilated
left ventricle with left-ventricular end-diastolic dimension
59 mm (normal range 35–56 mm), end-systolic dimension
53 mm (normal range 25–41 mm) and globally poor contraction.
The estimated ejection fraction was 25% and fractional shortening
was 9% (normal range 28–44%). There was mild mitral regurgitation
into a dilated left atrium of 48 mm (normal range 15–44
mm). Exercise testing was performed to document exercise capacity
and during 10 min of a full Bruce protocol, his heart rate accelerated
rapidly to 173 bpm in stage 1, 180 bpm in stage 2, 187 bpm in
stage 3 and 190 bpm at peak workload. Coronary angiography revealed
normal epicardial coronary arteries.
The patient underwent implantation with a 3-lead Medtronic (Minneapolis, USA) Jewel® AF atrial defibrillator. The device was programmed to patient activation using a hand-held activator (Fig. 3) after the patient had taken sedation. He was encouraged to activate the device as soon as possible following the recognised onset of AF. The day following implantation he had a recurrence of AF that was successfully terminated using the manual activator. He was discharged home on long-term treatment with aspirin 75 mg alone.
Over the next month he had five episodes of symptomatic AF that
were all successfully treated by patient activated cardioversion
within 8 h of arrhythmia onset (mean AF duration 2.8 h, total
AF duration 14.2 h). One hour before activating the defibrillator,
the patient took dextromoramide 10 mg and lorazepam 4 mg orally
to reduce the discomfort from the shock. The device was activated
with the patient lying down on his bed with his partner present
in the room. The shock process was extremely well tolerated.
At 1-year follow-up he was symptom free with no recurrence of
AF. Transthoracic echocardiography in sinus rhythm revealed
a normalisation of left ventricular function with a left ventricular
diastolic dimension of 52 mm, systolic dimension of 34 mm, a
calculated EF of 71% and FS 34%. Left atrial size had reduced
to 35 mm. Over the subsequent 2-years of follow-up he has remained
extremely well with no limitation in exercise capacity, no recurrence
of AF and no need for anti-arrhythmic medication. Chest X-ray
at 3 years following implant (
Fig. 4) revealed a normal cardiac
size (cardiothoracic ratio 15:32).
|
3. Discussion
|
|---|
Sustained, poorly controlled AF is associated with the development
of left ventricular dysfunction and can result in marked increase
in left ventricular end-systolic diameter and a corresponding
reduction in fractional shortening and ejection fraction
[5,
6].
These changes have been termed tachycardiomyopathy and may represent
a frequently unrecognised and potentially curable form of heart
failure
[7,
8]. It is often difficult to determine if AF is causing
ventricular dysfunction directly or whether left ventricular
dysfunction causes AF
[9]. Reports of rate and rhythm control
in AF have suggested that the changes of tachycardiomyopathy
are reversible
[8,
10–
12].
The patient reported had persistent AF for at least a year before implantation of his device and exercise testing revealed that during moderate exercise he developed quite rapid ventricular rates. It is likely therefore that he had a significant tachycardia for considerable periods of the day. After implantation of the device the patient had five episodes of persistent AF but cardioverted himself quickly so that his total AF burden was just 14 h. He then had no recurrence of arrhythmia and echocardiography at long-term follow-up revealed that his left ventricular volumes and left atrial size had returned to normal, in spite of no drug treatment. It is likely therefore, that the changes of tachycardiomyopathy and those of atrial electrical and structural remodelling had been reversed, reducing the likelihood of the patient returning to AF and preventing the cycle of changes [13].
|
4. Conclusion
|
|---|
Tachycardiomyopathy due to persistent AF can be reversed by
use of the atrial defibrillator. An improvement in left ventricular
function and a reduction in left atrial size may lead to longer
periods of SR between episodes of AF with ‘sinus rhythm
begetting sinus rhythm’
[14].
|
References
|
|---|
- Stewart S., Hart C., Hole D., McMurray J. Epidemiological features of atrial fibrillation in 25 765 middle-aged men and women: a population-based study [abstr]. Eur Heart J (2000) 21:215.
- Wyse D.G., Love J.C., Yao Q., et al. Atrial fibrillation: a risk factor for increased mortality-an avid registry analysis. J Interv Card Electrophysiol (2001) 5:267–273.[CrossRef][Web of Science][Medline]
- Phillips E., Levine S. Auricular fibrillation without evidence of heart disease: a cause of reversible heart failure. Am J Med (1949) 7:478–489.[CrossRef][Web of Science][Medline]
- Mitchell A.R.J., Sulke N. ‘The patient takes charge.’ Device therapy for atrial fibrillation. Cardiol News (2000) 4:6–9.
- Heinz G., Siostrzonek P., Kreiner G., Gossinger H. 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 (1992) 69:489–492.[CrossRef][Web of Science][Medline]
- Cleland J.G., Thygesen K., Uretsky B.F., et al. Cardiovascular critical event pathways for the progression of heart failure; a report from the ATLAS study. Eur Heart J (2001) 22:1601–1612.[Abstract/Free Full Text]
- Fenelon G., Wijns W., Andries E., Brugada P. Tachycardiomyopathy: mechanisms and clinical implications. Pacing Clin Electrophysiol (1996) 19:95–106.[CrossRef][Medline]
- Schumacher B., Luderitz B. Rate issues in atrial fibrillation: consequences of tachycardia and therapy for rate control. Am J Cardiol (1998) 82:29N–36N.[CrossRef][Web of Science][Medline]
- Gallagher J.J. Tachycardia and cardiomyopathy: the chicken-egg dilemma revisited. J Am Coll Cardiol (1985) 6:1172–1173.[Web of Science][Medline]
- Lemery R., Brugada P., Cheriex E., Wellens H.J. Reversibility of tachycardia-induced left ventricular dysfunction after closed-chest catheter ablation of the atrioventricular junction for intractable atrial fibrillation. Am J Cardiol (1987) 60:1406–1408.[CrossRef][Web of Science][Medline]
- Kieny J.R., Sacrez A., Facello A., et al. Increase in radionuclide left ventricular ejection fraction after cardioversion of chronic atrial fibrillation in idiopathic dilated cardiomyopathy. Eur Heart J (1992) 13:1290–1295.[Abstract/Free Full Text]
- Grogan M., Smith H.C., Gersh B.J., Wood D.L. Left ventricular dysfunction due to atrial fibrillation in patients initially believed to have idiopathic dilated cardiomyopathy. Am J Cardiol (1992) 69:1570–1573.[CrossRef][Web of Science][Medline]
- Pandozi C., Santini M. Update on atrial remodelling owing to rate; does atrial fibrillation always ‘beget’ atrial fibrillation? Eur Heart J (2001) 22:541–553.[Free Full Text]
- Spurrell P.A.R., Mitchell A.R.J., Kamalvand K., Topham A., Sulke N. The impact of atrial defibrillators on the natural history of persistent atrial fibrillation. Does sinus rhythm beget more sinus rhythm? [abstr]. J Am Coll Cardiol (2001) 37:95A.
CiteULike 
Connotea 
Del.icio.us What's this?
Top
1. Introduction
2. Report
