Troy Rhodes, MD, PhD, FHRS, CCDS
A 63-year-old man with ischemic cardiomyopathy (Class IV, Stage D, LVEF 10%) was admitted with decompensated heart failure requiring vasopressor and mechanical (IABP) support. He underwent implantation of a HeartMate II left ventricular assist device (LVAD) as a bridge to transplantation. His postoperative course was uneventful except for paroxysmal atrial fibrillation (AF) for which he was started on amiodarone. Prior to discharge, he underwent implantation of a primary prevention implantable cardioverter-defibrillator (ICD). He presented several weeks later with multiple ICD shocks for sustained monomorphic ventricular tachycardia (SMVT) at 170 bpm that did not terminate with antitachycardia pacing (ATP). He was referred to for VT ablation with the assistance of anesthesia. He was accompanied to the EP lab by a LVAD-support nurse.
Right femoral venous and arterial accesses were obtained for vascular access and hemodynamic monitoring. Quadripolar catheters were placed in the right atrium and right ventricular apex, and a deflectable catheter was placed at the His bundle. Despite burst and programmed ventricular stimulation at baseline and with isoproterenol, his clinical VT was not inducible, and he underwent a substrate-based ablation.
Given severe aortic atheroma, a transseptal approach to the left ventricle was taken (Figure 23-1). He received a heparin bolus and infusion titrated to maintain an activated clotting time (ACT) between 300 and 350 seconds. Electroanatomic mapping was performed with a CARTO navigation system (Johnson & Johnson, New Brunswick, NJ; Biosense-Webster, Diamond Bar, CA) and radiofrequency (RF) ablation was performed with an irrigated, deflectable mapping-ablation catheter. Intracardiac ultrasound catheter was used for transseptal access, to identify catheter-tissue interface and anatomical landmarks such as the LVAD inflow cannula, and to monitor for pericardial effusion.
FIGURE 23-1 Left anterior oblique (LAO 35°) image during transseptal VT ablation.
Electroanatomical mapping showed endocardial scar (<0.5 mV) involving the mid to apical anteroseptum and the posterolateral walls with border zone surrounding the LVAD cannula. The endocardial scar seen was out of proportion to his cardiomyopathy. Linear ablation lines were extended from the LVAD cannula through both scar zones; the posterolateral line was extended to the mitral valve annulus while the anteroseptal line was limited to sites below the His-Purkinje system (Figure 23-2).
FIGURE 23-2 Electroanatomical CARTO bipolar voltage map (<0.5 mV and 1.5 mV color range). Orange dot shows most inferior His-Purkinje potential. Yellow dots depict apical LVAD cannula. Linear ablation lines extending from anteroseptal LVAD cannula to mid septum. The apical aspect of the posterior lateral ablation line is also seen.
Postablation, he had recurrent VT, and mexiletin was added to amiodarone. He initially did well on this regimen, but several months later he had recurrent slow VT 120 bpm below his detection limit (Figure 23-3) and was referred to the EP lab for repeat VT ablation. With programmed ventricular stimulation, his clinical VT (left bundle inferior axis CL 520 ms) was induced and hemodynamically tolerated. Activation and entrainment mapping was performed throughout the LV via a transseptal approach without sites of early activation being detected. Mapping of the right ventricle showed earliest activation with concealed entrainment (Figure 23-4) at 12 o’clock on the tricuspid annulus. During ablation, there was prolongation of the CL with termination of VT. Postablation, VT was no longer inducible.
FIGURE 23-3 Surface ECG showing left bundle inferior axis morphology VT 122 bpm. The artifact seen throughout the ECG is noise from the LVAD.
FIGURE 23-4 Concealed fusion during ventricular pacing during VT. The 12-lead ECG and intracardiac recordings from the proximal and distal electrodes of the ablation catheter are shown. Ventricular pacing stimuli (S) are delivered from the distal electrode of the ablation catheter at a cycle length of 400 ms showing concealed fusion. Ablation at this site (arrow) leads to slowing and then termination of the VT.
VENTRICULAR TACHYCARDIA DURING VAD SUPPORT
As seen with this patient, over one-third of patients will have ventricular tachyarrhythmia events (VTEs) within 30 days following LVAD implantation.1,2 While concomitant ICD implantation has increased survival in VAD supported patients, there is a 25% incidence of appropriate ICD therapies.3 The highest rates of VTEs are seen within the first 2 weeks following VAD support,1,4-7 and recurrent VTEs are common with an average of 5 events per patient during VAD support.8 Unfortunately, a lack of VTEs early following VAD support does not preclude late VTEs. While VTEs may be hemodynamically tolerated in the setting of VAD support,9,10 they are associated with increased hospitalization rates, need for antiarrhythmic drug therapy, and increased mortality.1,9,11-13
Several factors predict the likelihood of VTEs during VAD support. The most consistent risk factor for VTEs is a history of VTEs prior to VAD support which doubles the risk of VTEs during VAD support.13Early studies showed patients with ischemic heart disease had a greater risk for VTEs during VAD support,1,5 while a more recent study in patients with continuous support found that those with nonischemic heart disease had a 2.3-fold greater risk of VTEs.8
MECHANISMS OF VT
Inflow cannula effects, pathologic fibrosis of the failing heart, and electrical remodeling within the VAD-supported heart are mechanisms for ventricular arrhythmias in VAD patients. With continuous flow VADs, increased VAD speed, increased pulmonary venous return,14 and transient changes in venous return15 can cause negative pressure at the inflow cannula drawing the interventricular septum or left ventricular free wall toward the cannula causing arrhythmias due to mechanical stimulation (suction events). Antecedent myocardial fibrosis and localized myocardial injury and fibrosis at the cannula insertion site are proarrhythmic in VAD patients.
There are also molecular and cellular electrophysiologic adaptations that occur in the setting of VAD support. Changes in both QRS and QT interval are seen in the acute and chronic phase of VAD support and affect arrhythmic risk.13 In VAD patients who experienced VTEs, decreased expression of connexin-43 can lead to decreased electrical conduction velocity and increased risk of ventricular arrhythmias.16,17But no study has shown a correlation between QRS duration and VTEs.13 One study showed an early increase in QTc following initiation of VAD support correlated with the higher rate of VTEs early in VAD support.4 Altered myocyte calcium handling with upregulation of the sodium-calcium exchanger (NCX) can lead to delayed afterpotentials and VTEs in VAD patients.13 A recent study showed higher NCX gene expression in VAD patients with VTEs than those without VTEs.2
Typically, VT ablation reflects a second-line approach following failure of antiarrhythmic and heart failure therapies. The American College of Cardiology/American Heart Association/European Society of Cardiology guidelines recommend catheter ablation be considered for patients with drug refractory ventricular arrhythmias and recurrent ICD therapies.18 VT ablation has been shown to be safe and effective in VAD patients.19-23 Ventricular tachyarrhythmias are generally hemodynamically tolerated in VAD-supported patients,9,10 making VT ablation via activation and entrainment mapping more feasible. A large series of VT ablation in VAD patients showed scar-related VT in 75% of cases, 14% arising from the apical inflow, 2.7% due to focal or micro reentry, and 1.4% due to bundle branch reentry.22
There are several technical issues that require special consideration during VT ablation in VAD patients. Vascular access can be challenging due to the lack of pulsatile arterial flow and concurrent anticoagulation which may increase the risk of vascular-related complications (hematoma, pseudoaneurysm, retroperitoneal bleed). The use of ultrasound-guided vascular access may reduce this risk.22,23
Preprocedural evaluation of the aorta and aortic valve by transesophageal echocardiography (TEE) and/or intracardiac echocardiography (ICE) should be performed. If the aortic valve is immobile, thrombosed, oversewn, or greater-than-moderate aortic atheroma is present, then a transseptal approach to the LV should be taken; in other cases, a retrograde aortic approach is utilized. Transiently decreasing the LVAD flow to allow normal aortic valve opening may facilitate crossing the aortic valve. Inadvertent catheterization of the outflow cannula in the ascending aorta and the apical inflow cannula should be avoided.23
In some cases, LV unloading by the LVAD may lead to smaller LV volumes making catheter manipulation more challenging.23
Unfortunately, VAD patients may also have hemodynamically intolerant VTs likely due to RV dysfunction, leading to decreased LV preload and reduced cardiac output22,23 and requiring a substrate approach for ablation.
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23. Herweg B, Ilercil A, Kristof-Kuteyeva O, et al. Clinical observations and outcome of ventricular tachycardia ablation in patients with left ventricular assist devices. Pacing Clin Electrophysiol. 2012;35(11):1377-1383.