340

Reversal of Tachycardiomyopathy Due to Left Atrial

Tachycardia by Ivabradine
SHOMU BOHORA, M.D.,∗ YASH LOKHANDWALA, M.D.,† PRITESH PAREKH, M.D.,‡
and APURVA VASAVDA, M.D.‡
From the ∗ Baroda Heart Institute and Research Centre, Vadodara, India; †Arrhythmia Associates, Mumbai, India;
and ‡CARE Hospitals, Surat, India

Reversal of Tachycardiomyopathy. Ivabradine has been shown to be effective in reducing sinus

rate. Here we report of a case where ivabradine reduced the rate of a focal atrial tachycardia relieving
patient’s symptoms and reversing tachycardiomyopathy. (J Cardiovasc Electrophysiol, Vol. 22, pp. 340-342,
March 2011)

ivabradine, atrial tachycardia, cardiomyopathy, catheter ablation, automaticity

Case Report
A 15-year-old girl with history of palpitations was noted
to have atrial tachycardia and tachycardiomyopathy with left
ventricular ejection fraction (LVEF) of 40% at baseline. There
was no relief of symptoms in spite of being on maximum tol-
erated dose of beta-blockers and amiodarone for 3 months. On
presentation to us, she had incessant tachycardia with P wave
characteristics suggestive of a left atrial (LA) origin (P waves
negative in leads I and aVL and positive in inferior limb leads).
No disclosures.
Address for correspondence: Shomu Bohora, M.D., Baroda Heart Institute
and Research Centre, 44 Haribhakti Colony, Old Padra Road, Vadodara
390020, India. Fax: 91-261-23927777; Email: shomubohora@yahoo.com
Manuscript received 12 May 2010; Revised manuscript received 2 June
2010; Accepted for publication 3 June 2010.
doi: 10.1111/j.1540-8167.2010.01860.x
Electrophysiology (EP) study showed presence of early atrial ac-
tivation in the LA appendage by 26 ms as compared to surface P
waves (Fig. 1). Radiofrequency (RF) ablation, however, was not
successful despite prolonged efforts. Patient remained in inces-
sant tachycardia. Though the patient was on maximum dose of
amiodarone and beta-blockers, the heart rate continued to be
150/minute on follow-up (Fig. 2). A repeat mapping and ablation
was planned. Before a repeat procedure was planned, ivabra-
dine 2.5 mg twice daily was started on experimental grounds,
after having fully explained the patient and relatives regarding
the drug. After 2 days of starting ivabradine, the heart rate de-
creased to 90/minute, though with the same P-wave morphology
as the existing tachycardia on electrocardiogram (ECG) (Fig. 3).
The patient’s symptoms resolved completely. Amiodarone and
digoxin were withdrawn. The patient remained in a controlled
rate, as monitored on 24-hour Holter study, after 1 month with
the LVEF becoming 60%.
The patient herself stopped ivabradine after 2 months. She
again developed similar symptoms and LV dysfunction was
noted. A repeat EP study was performed. Mapping showed
earliest signals at the junction of the left superior pulmonary

Figure 1. Intracardiac recording during incessant atrial tachycardia with mapping catheter in left atrial appendage showing activation early than surface
P wave by 26 msec. His = His bundle electrogram; HRAd = high right atrial distal; hraP = high right atrial proximal; MAPD = mapping catheter distal;
MAPP = mapping catheter proximal.

Figure 2. Twelve-lead electrocardiogram 1 month after ablation, showing similar P-wave morphology as the index tachycardia with tachycardia rate of
150/minute.
vein and LA appendage, preceding the P wave onset by 46 ms.
RF ablation at the site was successful. The patient now 1-month
postablation continues to be symptom free.
Discussion
Incessant atrial tachycardia can be disabling and often
difficult to treat. Despite prolonged mapping during the first
EP study, we failed to achieve clinical success. On regular
drug therapy the patient remained symptomatic with inces-
sant tachycardia and tachycardiomyopathy.
Postulating a possibility of the role of I(f) channels in au-
tomatic pacemaker-mediated rhythms, ivabradine was started
after explaining to the patient and relatives the drug and its
effects. Ivabradine, an I(f) channel modulator, has a docu-
mented effect in reducing sinus rate in various studies and
Figure 3. Twelve-lead electrocardiogram on third day of starting ivabradine 2.5 mg twice daily showing similar P-wave morphology as during the index
tachycardia, but with a rate of 90/minute.
Bohora et al. Reversal of Tachycardiomyopathy 341
case reports.1-4 In our patient the symptoms resolved and the
heart rate decreased by the third day of starting ivabradine.
A similar P-wave morphology as the tachycardia on ECG
suggested that the rate of the ectopic atrial tachycardia had
decreased due to the effect of ivabradine. The normalization
of LV function within 1 month of rate control suggested LV
dysfunction mediated due to incessant tachycardia. Stoppage
of ivabradine by the patient, leading to recurrence, reinforced
the hypothesis. Finally, a repeat procedure showed the ori-
gin of tachycardia near the junction of the left superior pul-
monary vein and the LA appendage, which was successfully
treated by RF ablation.
This case report highlights the effect of ivabradine in focal
atrial tachycardia remote from the sinus node. Given the fact
that the patient was a child with no structural heart disease,
the possibility of an automatic focus, and hence the response
342 Journal of Cardiovascular Electrophysiology Vol. 22, No. 3, March 2011
to ivabradine, was more likely. Microreentry-related focal
tachycardias, which may be more common in the elderly or
in patients with structural heart disease, may not respond to
ivabradine.
Molecular mechanisms of abnormal automaticity in hu-
mans are still not clear. The effect of ivabradine in de-
creasing the rate of an atrial tachycardia raises the possible
role of I(f) current in causing automatic atrial tachycar-
dias. Alternatively it is possible that some atrial tachycar-
dias may be due to the presence of sinus nodal-like tissue
in the atrial tissue, which may cause abnormal automatic
rhythms.
Ivabradine possibly can be given as an antiarrhythmic in a
patient having atrial tachycardia resistant to routine drugs in
whom ablation has failed, or as a bridge to ablation therapy.
Further large studies are needed to evaluate the response
of ivabradine in tachycardias, including atrial fibrillation, to
define the subset of patients in whom it might be effective, and
also to understand the molecular mechanisms of automaticity
of tachycardias and other possible antiarrhythmic effects of
ivabradine.
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