Urgent VT Ablation in a Patient with Presumed ARVC

Mr Alex Cambridge, Chief Cardiac Physiologist, St. Barts Hospital, London UK

The patient, a 52 year-old male, attended the ICD clinic without an appointment complaining of palpitations but with no associated dizziness or syncope. Upon interrogation of his ICD he was found to be in ventricular tachycardia at 140bpm and admitted. Later that day he underwent an emergency VT ablation.

Patient Background
Single-chamber abdominal ICD implanted in 1991 following VT consistent with an RVOT origin (LBBB precordial morphology and inferior axis) and inducible VT & VF at EPS. At the time his resting ECG showed a prolonged pr interval of 240ms with normal QRS duration. There was T wave inversion in the inferior leads only and no evidence of depolarisation abnormalities. Holter monitoring performed in the same year demonstrated 2672 ventricular extrasystoles. Echocardiography demonstrated moderate LV dilatation and mild RV dilatation. His family history is unclear and coronary angiography was normal.

In 2002, he was diagnosed with arrhythmogenic right ventricular cardiomyopathy (ARVC) on the basis of RV angiography, which showed a reduced RV ejection fraction and RV dyskinesia. Since then his conduction disease has progressed distally, with the development of left bundle branch block. This has been accompanied by paroxysmal atrial fibrillation and severe deterioration in left ventricular systolic function. He is untroubled by heart failure symptoms.

Ablation Procedure
The patient was brought into the lab in VT (figure 1).

This was of a left bundle precordial morphology and inferior axis and a cycle length of 420ms. Carto 3 and Bard were used. RFA and RFV access was established and an F curve Smarttouch catheter advanced into the RVOT. During mapping tachycardia terminated spontaneously. Pace-mapping was performed in the RVOT with no good matches. Triple-sensed ventricular extrastimuli induced a stable VT2 (figure 2) with a similar cycle length to VT 1.

The ECG morphology was suggestive of a basolateral epicardial origin- ‘QS’ complexes can be see in leads I and avL, there is positive precordial concordance and a delayed intrisicoid deflection (Berruezo et al, Circulation, 2004). Epicardial access was established, however no early signals were found. Coronary sinus mapping was performed and an early signal identified however ablation was not possible due to high impedance. From the map signal we can see the sinus rate at this point is approximately 70bpm (figure 3).

The endocardial LV was then mapped using a retrograde approach. Near the mitral annulus a pre-QRS signal was found and ablation was considered (Figure 4). However is the signal a true diastolic potential?

Closer inspection reveals the sharp component of the map signal is dissociated from the QRS complexes. In fact the patient is now in a dual tachycardia- Atach + VT. The ablation catheter is recording a far field signal from the LA. 
Further mapping revealed a true diastolic potential at the aorto-mitral continuity (figure 5).

Ablation here first accelerated, then slowed and finally changed the tachycardia (figure 6), but to what?

Remember the patient has LBBB- VT has terminated but the rate remains fast due to conduction of the atrial tachycardia.  Further ablation was performed in the left coronary cusp adjacent to the successful site. Images 1 and 2 show RV, LV and epicardial maps with ablation sites in red. Flecainide was given in an attempt to chemically cardiovert however this was unsuccessful.

Image 1

Image 2

Withdrawing the map catheter to the atrium at the end of the procedure shows clearly the atrial activity with intrinsic left bundle branch block (figure 7), a feature typical of dilated cardiomyopathy (Bayes-Genis et al, Eur J Heart Failure, 2003).

The following day internal cardioversion was performed through the ICD. The patient was discharged. A week later he presented to the ICD clinic again complaining of palpitations. 12-lead ECG showed a regular wide complex tachycardia again at 140bpm. However close comparison with previous ECGs revealed this was an atrial tachycardia conducting to the ventricles with a 1:1 relationship.  He is now on the waiting list for an atrial tachycardia ablation. Upgrade to CRT-D remains an option should he develop symptoms of heart failure in the future. 

Interestingly given the patient’s presumed diagnosis of ARVC no low-voltage areas of scar were found in either RV, LV, or epicardium. This is not consistent with an ARVC phenotype (Garcia et al, Circulation, 2009). Even in NIDCM VT ablation, regions of scar would be expected. A healthy bipolar voltage map is the exception, as is well tolerated, slow VT (Deyell and Callans, JICRM, 2011). The tachycardia mechanism in this case was thought to be focal, with posterior and anterior exits explaining the two different morphologies of VT. It would have been useful to perform entrainment to elucidate the mechanism of the tachycardia, however given the previous spontaneous termination this was not done. Any further substrate ablation in this patient should include high-density LV and epicardial voltage maps, as areas of scar are often patchy rather than diffuse in this condition (Deyell and Callans, JIRCM, 2011) Certainly Lamin A/C mutation analysis may be helpful as a diagnostic tool for screening his family (Brodksy et al, Circulation, 2000).

Figures and Images

Figure 1 – VT-1
Figure 2 – VT-2
Figure 3 – Distal CS ablation signal, with sinus activity seen in atrium.
Figure 4 – Is this a diastolic potential?
Figure 5 – Pre-ablation diastolic signal
Figure 6 – VT termination to Atach + LBBB
Image 1 – Shows RV and LV maps with ablation sites in red (projection is PA, tilted down).
Image 2 – Shows RV, LV and Epicardial maps from a right lateral projection
Figure 7 – End procedure atrial activity + LBBB


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