Alcohol Ablation of Premature Ventricular Complexes Originating from Left Ventricular Summit

Authors:Makoto Nagahama, MD, Kutaiba Nazif, MD, Jeffrey P. Gordon, MD,BabakBozorgnia, MD, andTalha F. Nazir, MD

A 42-year-old male with no significant past medical history presented with shortness of breath for a few months. EKG and telemetry showed frequent premature ventricular complexes (PVCs).Echocardiogram revealed severely reduced left ventricular ejection fraction (LVEF) <20%.Coronary angiogram did not show obstructive CAD. Cardiac MRI showed severely dilated left ventricle and global hypokinesis without evidence of late gadolinium enhancement. PVC morphology was consistent with LVOT/LV summit origin (Panel A).

PVC activation was acquired endocardially in the great cardiac vein(GCV), anterior interventricular vein(AIV),coronary cusps, and LVOT as well as RVOT. The site of earliest activation was proximal AIV where local EGM preceded surface QRS onset by 30 msec. This was followed by later activations in the LVOT endocardially and even later in the RVOT. A coronary sinus venogram showed stenosis in the GCV, precluding safe advancement of ablation catheter to AIV. Radiofrequency (RF) energy using power of 35 W to 40 W, was delivered at sites of early endocardial breakout in the LVOT and opposite to the earliest epicardial activation. However, the PVC could not be eliminated. Additional RF ablation was attempted from RVOT but failed to affect the PVC (Panel B). Patient was discharged on amiodarone and life vest.

Holter 3 weeks later showed 38%PVCs burden and the following week, patient presented after receiving appropriate shock for PVC induced ventricular  fibrillation.

The patient underwent repeat PVC ablation using transvenous alcohol ablation. Left axillary vein approach was used and the CS was cannulated using Medtronic Attain catheter. Balloon occlusive venograms were performed to delineate AIV branches. Proximal AIV branches were sequentially cannulated using Run through wire and OTW balloon. Activation as well a space mapping was performed (in a unipolar fashion) from each of the branches. The earliest activation was 35 ms pre-QRS from the proximal septal perforator where pace map match was over 90%. A2 x 10 mm OTW balloon was inflated to nominal pressure and contrast was injected. It did not show any collaterals and no contrast leaks around the balloon. Four milliliters of ethyl alcohol was slowly injected while balloon remained inflated for 5 minutes.  Myocardial staining was seen (Panel C).The PVCs were abolished immediately after alcohol injection and were not seen during the waiting period. Holter 6 weeks afterwards showed 0.2% PVC burden. Echocardiogram 2 months post ablation showed improvement in LVEF to 45%.

High burden of PVCs is a well-recognized cause of cardiomyopathy (1,2). Effective treatment of PVC scan restore LV function. RFA of ventricular arrythmias originating from the LV summit is particularly challenging because of proximity to major coronary vessels, limitations of ablation from CS venous system as well as epicardium and sometimes deeper intramural origin.

This case illustrates that detailed mapping of PVCs from the coronary venous system and methodical delivery of alcohol was feasible and effective in eliminating the PVCs. Alcohol ablation is an effective bail out option for failed RF ablation.

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