Key result
Ablation of the aortomitral continuity resolves post-TAVR sustained VT in a 94-year-old man.
Why the study?
New-onset ventricular arrhythmia following TAVR is rare, with limited reports of sustained ventricular tachycardia and unclear mechanisms.
Case Report (n=1)
Sustained ventricular tachycardia is a rare but potentially life-threatening complication following TAVR that can be successfully managed with electrophysiologic mapping and ablation.
Post-TAVR VT may respond to aortomitral continuity ablation; leaves open generalizability and safety in broader populations.
A 94-year-old man with prior coronary artery bypass surgery presented with symptomatic severe aortic stenosis with a normal ejection fraction. He underwent transfemoral transcatheter aortic valve replacement (TAVR) with a 29 mm Sapien-3 device without complication and had marked improvement in his symptoms. Six weeks later, during a routine echocardiogram he experienced acute dyspnoea with a heart rate of 220 beats per minute. Electrocardiography demonstrated wide complex tachycardia consistent with sustained ventricular tachycardia (VT) (rightward axis, positive concordance, QRS duration >160 ms) originating from the base of the left ventricle (positive V1 and no transition) (Panel 1A). Intravenous amiodarone successfully suppressed the VT. Coronary angiography demonstrated no obstructive lesions. Electrophysiologic anatomical and voltage mapping demonstrated a large electroanatomical scar in the region below the aortic valve and mitral perivalvular apparatus (Panel B). Spontaneous ventricular ectopy was detected and mapped to the aortomitral continuity, and ablation resulted in complete resolution of ventricular ectopy. After 6 months follow-up, the patient had no recurrences of VT and no ventricular ectopy recorded on his defibrillator. New-onset ventricular arrhythmia following TAVR is rare, with non-sustained VT found in 6% of pts, and only one prior report of sustained VT. The mechanism of VT in this patient was likely direct mechanical pressure of the valve stent against the myocardium and calcified mitral annulus. The subacute onset of the arrhythmia may have been due to delayed recovery from the acute injury of mechanical stress. Unexplained sudden cardiac death after TAVR may be attributable to VT. Panel A: Electrocardiogram demonstrating ventricular tachycardia arising from the left ventricular outflow tract, based on the right bundle branch morphology and vertical axis. The voltage ratio of lead II/III ratio of >1 and positive concordance V2–V5 makes the aortomitral continuity the most likely source of VT. Panel B: Electroanatomical voltage map of left ventricle. MV, mitral valve; Ao, aortic valve. Red area is scar (<0.5 mV). Red shaded dots are ablation points. Supplementary material is available at European Heart Journal online.
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Seto et al. (2017) conducted a case report in Severe aortic stenosis and sustained ventricular tachycardia (n=1). Transcatheter aortic valve replacement (TAVR) was evaluated on Sustained ventricular tachycardia. A 94-year-old man developed sustained ventricular tachycardia 6 weeks after TAVR, which was successfully treated with ablation of the aortomitral continuity with no recurrence at 6 months.
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