Ablation of ventricular tachycardia from the aortic root after transcatheter aortic valve replacement

Introduction

Key Teaching Points.

• •Iatrogenic ventricular tachycardia can occur after transcatheter aortic valve replacement.
• •The mechanism of this ventricular tachycardia likely is trigger or automaticity.
• •Ablation is safely possible between the valve strut and the sinus of Valsalva.

Transcatheter aortic valve replacement (TAVR) is an increasingly common procedure for treatment of patients with severe symptomatic aortic stenosis who are at intermediate to high risk for traditional surgical valve replacement. Although conduction disturbances and the need for pacemaker implantation postprocedure are well-recognized complications, ventricular arrhythmias (VAs) have not been widely reported. We present a case of focal outflow tract tachycardia occurring late post-TAVR accessible from the left coronary cusp (LCC)/noncoronary cusp junction adjacent to the valve strut, which was treated successfully with radiofrequency (RF) ablation.

Case report

A 78-year-old Caucasian man with diabetes, hypertension, and previous coronary artery bypass surgery presented with complaints of progressive dyspnea on exertion and was found to have severe aortic valve stenosis. Transthoracic echocardiography revealed preserved left ventricular (LV) ejection fraction, with an estimated valve area of 0.8 cm² and mean gradient of 40 mm Hg. Because of the high surgical risk associated with redo sternotomy, the patient underwent successful transfemoral TAVR with a 26-mm Edwards SAPIEN valve (Edwards Lifesciences Corp, Irvine, CA), which resulted in improved symptoms and function. However, 3 years later, he complained of fatigue and palpitations. Electrocardiography showed frequent premature ventricular contractions (PVCs), and 24-hour monitoring revealed high PVC burden (53% of total beats) and 368 runs of nonsustained ventricular tachycardia. The patient did not improve on medical therapy with beta-blocker. Repeat transthoracic echocardiography showed interval dilation of the LV and a reduction in LV ejection fraction from 65% to 55%. PVC morphology suggested left ventricular outflow tract (LVOT) origin (Figure 1A) based on QS pattern in leads aVR and aVL, rS in lead V₁, and inferior axis in leads II, III, and aVF. The patient was referred for ablation of symptomatic PVCs. A 3.5-mm NaviStar ThermoCool RMT catheter (Biosense Webster Inc, Diamond Bar, CA) was advanced in retrograde aortic fashion to the ascending aorta via femoral arterial access. Intracardiac echocardiography was used to monitor valve function and visualize the valve struts and the sinuses of Valsalva (Figure 1B). A stereotaxis magnetic navigational system was used to advance the catheter through the TAVR bioprosthesis and map the LV. Irregularity of coupling intervals between PVCs and the preceding QRS complexes was noted, suggesting a nonreentrant mechanism. Electrophysiologic study and mapping with the CARTO system (Biosense Webster) identified earliest activation of the PVCs in the LVOT at the site of a focal area of scar at the septal end of the LCC (Figures 1C and 2A, left). Using stereotaxis magnetic navigation, the catheter was positioned into the cusp junction between the valve strut and the sinus of Valsalva (Figure 2B). Pace-mapping performed at this location (2-ms pulse width and lowest captured output) revealed a 98% match to the clinical PVCs (Figure 2A, middle). After the safety of the location was confirmed by coronary angiography, focal ablation was initiated at 25 W and titrated up to 35 W for an average delivery of 33 W (Figure 2A, right, and 2B). PVCs were eliminated within 1.2 seconds, and ablation was delivered for a total 90 seconds. Postablation intracardiac echocardiographic imaging revealed no damage to the aortic valve apparatus, and PVCs could not be reinduced by pacing or isoprenaline administration. At 2-year follow-up, the patient has improved symptoms and no recurrence of PVCs.

Figure 1.

A: Baseline 12-lead electrocardiogram reveals frequent premature ventricular complexes of left bundle branch morphology. B, C: Images of the left ventricular outflow tract (LVOT). Cusps are labeled. B: Intracardiac echocardiography. Green lines represent valve cusps. Red arrow indicates the valve strut. Red ablation tags (white location tags) are seen at the septal end of LCC. C: CARTO sound image of the LVOT. White arrow and black arrow indicate LCC and NCC, respectively. The ablation catheter can be seen. LCC = left coronary cusp; NCC = noncoronary cusp; RCC = right coronary cusp.

Figure 2.

A: Activation mapping of the left ventricular outflow tract (LVOT). Left: Earliest activation spot on the intracardiac electrogram is seen at –116 ms. Middle: Pace-map. Right: Ablation spot. B: Fluoroscopic image of the LVOT in an anteroposterior view. Edwards SAPIEN 3 valve struts are seen. Ablation catheter is located between the struts and the left sinus of Valsalva.

Discussion

VAs occurring post-TAVR are not commonly reported despite the increasing prevalence of the procedure. The feasibility and safety of RF ablation in the coronary sinuses or LVOT after TAVR have not been reported. The previous case reported in the literature was also suspected to be of LVOT origin based on surface ECG morphology but was treated medically without further evaluation by invasive electrophysiologic study.¹ Here we report a successful case of RF ablation from the left coronary sinus of Valsalva, behind the TAVR valve strut, assisted by intracardiac echocardiography and a magnetic catheter navigation system.

VAs arising from the outflow tracts in structurally normal hearts are thought to be attributable to triggered activity; however, even in structural heart disease, nonreentrant mechanisms of outflow tract VA are not uncommon.2, 3 Conduction disturbances post-TAVR are well-recognized complications and speculated to be due to local tissue injury of the proximal His–Purkinje system in the intraventricular septum.⁴ In the patient reported here, the development of VA occurred several years after TAVR placement and therefore was not due to acute tissue injury. The origin of the PVC is inconsistent with the right coronary cusp based on rS in lead V₁ but is suggestive of an LCC origin based on the amplitude of leads II/III, although R in lead II is slightly taller in our case.⁵ We localized the PVC to the LCC on the septal end by activation mapping. The presence of a small focal scar was noted at the site of PVC localization, which may be consistent with remote injury. Early study of patients with aortic stenosis revealed a higher prevalence of PVCs, which was not lowered after surgical aortic valve replacement.⁶ Ventricular tachycardia after surgical aortic valve replacement has been shown to be due to reentry, bundle branch reentry, or triggered activity, and ablation has been successfully performed in these situations.7, 8, 9, 10 In our case, the varying coupling intervals and rapid success of point ablation are suggestive of triggered activity or abnormal automaticity as a possible mechanism.

Conclusion

We report the first case of successful RF ablation of frequent focal LVOT PVCs from the LCC adjacent to the TAVR valve. Placement of the ablation catheter into the sinuses of Valsalva adjacent to the valve struts in post-TAVR patients is feasible, without causing damage to percutaneously placed aortic valve prostheses.