2012, Vol. 19, No. 3, pp. 320–322
Copyright © 2012 Via Medica
Sustained monomorphic left ventricular
outflow tract tachycardia early
after aortic valve replacement
Ruzbeh Zaker-Shahrak, David Altmann, Philipp Sommer,
Thomas Gaspar, Robert Schönbauer, Arash Arya
Department of Electrophysiology, University of Leipzig, Heart Center, Leipzig, Germany
Sustained monomorphic ventricular tachycardia (VT) after valve surgery is uncommon. Cases
of focal VT or bundle-branch re-entry after aortic valve surgery have been reported. We present
the case of a 60 year-old patient with an incessant outflow tract VT early after aortic valve
replacement. We suggest the disease process affecting the valve and adjacent area, and/or the
surgical procedure, might somehow relate to VT substrate adjacent to the aortic annulus.
(Cardiol J 2012; 19, 3: 320–322)
Key words: ventricular tachycardia, aortic valve replacement, left ventricular
outflow tract, scar-related-re-entry
Catheter ablation is an established therapy for
ventricular tachycardia (VT) in patients with structural heart disease . Sustained monomorphic VT
after valve surgery is uncommon. Cases of focal VT
or bundle-branch re-entry after aortic valve surgery
have been reported [2, 3]. We present the case of
a 60 year-old patient with incessant VT early after
aortic valve replacement (AVR) and aortocoronary
A 60 year-old patient was referred to our hospital with sustained monomorphic VT one month
after biologic AVR (Medtronic Hancock 29 mm) and
triple aortocoronary bypass surgery due to severe
aortic valve stenosis and three vessel coronary artery disease. The patient had no history of myocardial infarction (MI). The VT was noticed during car-
diac rehabilitation. The patient presented with
shortness of breath and sweating. Initial attempts
to terminate the VT by amiodarone and external
electrical cardioversion were unsuccessful. Thereafter, ajmalin was given, which temporarily halted
the VT. However, frequent premature ventricular
beats with the same morphology as the clinical VT
were still present. Echocardiography showed normal left ventricular ejection fraction (LVEF 65%)
without wall motion abnormality during sinus
rhythm. Coronary angiography was performed
which excluded new coronary artery stenosis and/
/or graft stenosis/closure.
In the electrophysiological study, the clinical
VT (Fig. 1, cycle length: 380 ms) was easily induced
with programmed ventricular stimulation from the
right ventricular (RV) apex and terminated with
overdrive pacing. Based on the VT morphology, activation mapping was begun in the RV outflow tract
using CARTO-3® mapping system (Biosense Webster, Inc, Diamond Bar, California, USA). However,
Address for correspondence: Arash Arya, MD, University of Leipzig, Heart Center, Department of Electrophysiology,
Strümpellstrasse 39, 04289 Leipzig, Germany, tel: +49 341 865 1413, fax: +49 341 865 1460,
e-mail: [email protected]
Ruzbeh Zaker-Shahrak et al., Early VT after valve replacement
Figure 1. Left: 12-lead surface ECG during ventricular tachycardia. Upper panel on the right shows right and left
anterior oblique fluoroscopic projections of the successful ablation site. Lower panel on the right shows activation
mapping in the left ventricular outflow tract (LVOT) in the same projections. Yellow and blue arrows show the earliest
activation sites in the right and left outflow tracts, respectively; ABL — ablation catheter; AV — prosthetic aortic
valve; CS — coronary sinus; LAO — left anterior oblique; RVOT — right ventricular outflow tract.
the earliest site was only 10 ms earlier than the QRS
complex (Fig. 1, right, yellow arrow). A transseptal approach was used to access the LV outflow
tract. Substrate mapping revealed a very small scar
area in the LV outflow tract, inferior to the right coronary cusp. Activation mapping showed the earliest activation in the same region (Fig. 1, –40 ms).
Ablation at this site terminated the VT and rendered
it non-inducible. The patient received an implantable cardioverter-defibrillator at another center.
During the follow-up period of five months, there
was no recurrence of VT.
Sustained monomorphic VT in patients with
ischemic heart disease is almost always due to
macrore-entry in the border zone of a ventricular scar
due to an old MI, which differs from the focal VT in
the setting of a structurally normal heart. In a review
of 496 patients referred within five years for electrophysiological study due to recurrent monomorphic
VT, Eckart et al.  showed that only a small percentage of them (4%, 20 patients) had monomorphic VT
after aortic or mitral valve surgery in the absence of
MI. In 16 (80%) patients, monomorphic VT occurred
5–15 years after the valve surgery. The mechanisms
of VT in these patients were scar-related re-entry in
14 cases and bundle-branch re-entry in the other two.
Those patients with bundle-branch re-entry had
marked systolic LV dysfunction [3, 4]. In four (20%)
patients the VT occurred within a month of cardiac
surgery. Only in one (5%) patient was the underlying
mechanism of the VT due to re-entry .
Scar-related re-entry usually occurs long after
valve surgery . The reproducible induction of VT
Cardiology Journal 2012, Vol. 19, No. 3
with programmed ventricular stimulation and termination through ventricular overdrive pacing supports re-entry as the underlying mechanism of the
clinical VT. Patients with scar-related macrore-entry usually have low-voltage regions, often with low-amplitude, fractionated electrograms. A very small
scar area below the right coronary cusp could be
seen in the voltage mapping of the outflow tract.
Therefore we hypothesized that the mechanism of
the observed VT was most probably due to microreentry close to the prosthetic valve. We speculated
that the disease process affecting the valve and the
adjacent myocardium, and/or the surgical procedure, might somehow explain the observed VT substrate .
considered as a potential mechanism of VT early
after valve surgery. The disease process affecting
the valve and adjacent area, and/or the surgical procedure, might somehow relate to the VT substrate
adjacent to the aortic annulus .
Conflict of interest: none declared
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