Periaortic scar-related ventricular tachycardia in patients with aortic valve replacement: transcatheter ablation is feasible and decisive

Abstract Funding Acknowledgements Type of funding sources: None. Background Aortic valve replacement (AVR) is a common procedure. While conduction disturbances are well-recognized complications, ventricular tachycardias (VTs) have not been widely reported neither described mainly because prosthetic valves represent a potential practical problem in the access to the ventricles, and this may limit the use of radiofrequency ablation (RF). Purpose and Methods We report three cases of periaortic scar-related VT in patients with AVR. Results The first case was a 85 years old (yo) man, with both aortic and mitral biological valve replacement. The left ventricular ejection fraction (LVEF) was normal and the clinical VT (left bundle branch block (BBB) and inferior axis, cycle length (CL) = 305 ms) was induced. Left ventricle (LV) was mapped with a retrograde transaortic approach: to cross safely the prosthesis, a 6-French (F) pigtail catheter was first placed in the ventricle; a 8.5-F Braided Guiding Introducer (SL1) was placed across the valve over a guidewire. The 8.5-F ablation catheter allowed to locate the VT origin underneath the septal portion of prosthetic aortic valve (PAV). The second case was a 85 yo man, with bioprosthetic AVR and replacement of the ascending aorta. LVEF was 40% with mild PAV degeneration. The clinical VT had left BBB morphology and inferior axis (CL = 352 ms). Transaortic approach was hampered by an unfavorable entry angle and by valve degeneration. Then we opted for the technique commonly used during transcatheter AVR: the access to the LV was obtained using a 6-F coronary catheter (AL1) and a stright tip 0.034" angiographic guidewire; subsequently a 8.5-F, 81 cm long, introducer sheath (SL0) was positioned across the PAV. The reentry circuit was mapped in the high anterior region, just below the PAV insertion. The third case was a 65 yo man, with mechanical PAV. LVEF was normal and the clinical VT had right BBB and left inferior axis (CL = 290 ms). After transseptal puncture, a steerable introducer was placed in left atrium. The mapping catheter allowed to identify early and fractional potentials in the anterior portion of PAV. In all cases, RF applications was delivered at the earliest ventricular activation site with termination of the VTs. Thereafter, no VTs could be induced. At 12 months follow-up, the patients are free of any VT relapses. Conclusions The most common origin of sustained monomorphic VT occurring after PAV is the surgical scar and catheter ablation is a feasible option. In case of mechanical PAV, the only practicable access is the transeptal one; on the contrary, with biological PAV the transaortic approach can also be used. In difficult cases, the access to the LV can be obtained with the technique routinely performed during transcatheter AVR.