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Transcript
Europace (2008) 10, 1343–1345
doi:10.1093/europace/eun239
SHORT COMMUNICATION
Idiopathic ventricular tachycardia arising
from the right ventricular apex
Antonio Navarrete*
Department of Clinical Cardiac Electrophysiology, Medical Consultants, Muncie, IN 47304, USA
Received 19 May 2008; accepted after revision 4 August 2008; online publish-ahead-of-print 28 August 2008
KEYWORDS
Idiopathic ventricular
tachycardia;
Ablation;
Non-contact mapping
Idiopathic, focal ventricular tachycardia that originates from the right ventricular apex is presented.
Arrhythmogenic ventricular dysplasia needs to be ruling out prior to making this diagnosis. This is a
rare entity that can be cured with an ablation and therefore it needs to be considered in the differential
diagnosis of idiopathic VTs before implanting a defibrillator.
Case
A 53-year-old Caucasian male presented to the ER complaining of palpitations and mild chest pain lasting for 40 min
that started while he was working at his desktop. Twelvelead ECG showed wide QRS complex tachycardia, left
bundle with left superior axis morphology, late transition
at a cycle length of 230 ms (Figure 1B). The tachycardia
was haemodynamically well tolerated. Following failure to
convert the patient with amiodarone 300 mg intravenously,
a 200 J biphasic synchronized shock restored sinus rhythm.
He had neither past cardiac history nor family history of
sudden death. Twelve-lead ECG in sinus rhythm revealed
no acute coronary ischaemia (Figure 1A) with no evidence
of pre-excitation.
He underwent an echocardiogram, a right and left heart
catheterization, a cardiac CT, and a magnetic resonance
image (MRI) that show no anomalies. Sarcoidosis was ruled
out and he did not have clinical symptoms suggestive of
Myocarditis.
The patient was taken to the electrophysiology laboratory. Typical AVNRT was induced several times, so the slow
pathway was ablated despite no clinical documentation.
After that, Isoproterenol was administered up to 3 mcg/m,
and ventricular tachycardia was induced by ventricular
pacing at 400 ms from the right ventricular apex and introducing ventricular extra stimuli at 230 ms. This tachycardia
was difficult to sustain. High-density mapping showed
normal right ventricular electrograms (Figure 3A). There
was not an epsilon wave or T-wave inversion in the precordial leads (Figure 1A). Right ventriculography was normal
(not shown). This suggests that the ventricular tachycardia
Commentary
The width of the QRS (.160 ms) left superior axis, rS .
100 ms, deep S-wave in V6 (Figure 1B), and fusion beats
(Figure 1A) are all very suggestive of ventricular tachycardia. Atrio-ventricular dissociation (Figure 1C) is diagnostic
of it.1 Arrhythmogenic ventricular dysplasia (ARVD) was suspected but two cardiac MRI performed 6 months apart did
not show the presence of right ventricular fatty infiltration
(Figure 2A).
* Corresponding author. Tel: þ1 7652812000; fax: þ1 3178413185.
E-mail address: [email protected]
Figure 1 (A) Baseline 12-lead electrocardiogram. (B) Wide-QRS
tachycardia. (C ) ECG leads III and AVF are shown. The sinus
P-waves are marked with black arrows follow by fusion beats. Atrioventricular dissociation is presented.
Published on behalf of the European Society of Cardiology. All rights reserved. & The Author 2008.
For permissions please email: [email protected].
1344
A. Navarrete
Figure 2 (A) Magnetic resonance imaging of the heart. (B) Thirty degrees right anterior oblique fluoroscopic image showing the balloonmounted multielectrode array, the ablation catheter, three quadripolar catheters in the right atrium, right ventricle, and inferior vena cava.
Figure 3 (A) Intracardiac ventricular electrograms from three different locations within the right ventricle. (B) Surface leads I, AVF, V1,
intracardiac electrograms from the ablation catheter at the successful site and virtual unipolar electrograms computed by the ESI system
are shown. (C) Isopotential map showed the earliest activation site located near the antero-lateral right ventricular apex. Colour scale
has been set to that white indicates most negative potential and blue indicates least negative potential.
is idiopathic. However, a concealed form of ARVD2 cannot be
completely rule out and additional follow-up is needed.
The Ensite array 64-electrode catheter (St Jude Medical,
St Paul, MN, USA) was placed in the right ventricle. An isopotential map depicted an earliest ventricular impulse site
propagating in a centripetal pattern. This map is compatible with a focal mechanism (abnormal automatism vs. triggered) though micro-re-entry cannot be ruled out.
Induction with programmed stimulation and the absence
of over-drive suppression is indicative of triggered mechanism. The earliest tachycardia break-through was found at
the right anterolateral ventricular apex (Figure 3C). Pace
mapping at that site showed 11 out of 12-pace match.
The ventricular electrogram preceded the QRS by 42 ms
(Figure 3B). A 4 mm tip electrode deflectable catheter
(Sapphire, St Jude Medical) was utilized in a temperature
control mode. One RF application at this site with a
maximum temperature of 55º and maximum power of
50 W terminated the tachycardia within 5 s preceded by
acceleration. During 1 year follow-up, the patient is asymptomatic on no medications.
Tada et al. 3 reported premature ventricular contractions
rising from the mid septum and postero-lateral along the tricuspid valve with similar electrocardiographic appearance
to this case. They both have a predominant R-wave in augmented lead in contrast with the right outflow ventricular
tachycardias because their axis is directed superiorly and
leftwards. Although, this one is unique in that there is a
later transition zone (V5–V6), probably due to a more
sequential activation of both ventricles and the absence of
an atrial electrogram at the ablation site.
Idiopathic monomorphic ventricular tachycardia4 includes
the outflow tract (right and left, aortic cusp VT), fascicular
VT (anterior–posterior fascicular VT), septal VT (right and
left), the pulmonary artery, adrenergic monomorphic VT,
and annular VT-(mitral and tricuspid). To my knowledge,
there are no reports in the medical literature of idiopathic
ventricular tachycardia rising from the apex.
Idiopathic ventricular tachycardia arising from the right ventricular apex
Conflict of interest: A.N. is currently conducting research sponsored by, and is also a consultant for, St Jude Medical.
References
1. Miller JM, Das M et al. Differential diagnosis of wide QRS complex tachycardia. In Zipes DP, Jalife J. (eds.), Cardiac Electrophysiology: From Cell
to Bedside. 4th ed. Philadelphia: WB Saunders; 2004. p747–57.
2. Nava A, Thiene G, Canciani B, Martini B, Daliento L, Buja G et al. Clinical
profile of concealed form of arrhythmogenic right ventricular
1345
cardiomyopathy presenting with apparently idiopathic ventricular
arrhythmias. Int J Cardiol 1992;35:195–206.
3. Tada H, Tadokoro K, Ito S, Naito S, Hashimoto T, Kaseno K et al.
Idiopathic ventricular arrhythmias originating from the tricuspid
annulus: prevalence, electrocardiographic characteristics, and results
of radiofrequency catheter ablation. Heart Rhythm 2007;4:
7–16.
4. Badhwar N, Sheinman M. Idiopathic ventricular tachycardia: diagnosis and
management. Curr Probl Cardiol 2007;32:17–43.