Substrate Ablation by Multivein, Multiballoon Coronary Venous Ethanol for Refractory Ventricular Tachycardia in Structural Heart Disease

Abstract

Background: Ablation of ventricular tachycardia (VT) in the setting of structural heart disease often requires extensive substrate elimination that is not always achievable by endocardial radiofrequency ablation. Epicardial ablation is not always feasible. Case reports suggest that venous ethanol ablation (VEA) through a multiballoon, multivein approach can lead to effective substrate ablation, but large data sets are lacking.

Methods: VEA was performed in 44 consecutive patients with ablation-refractory VT (ischemic, n=21; sarcoid, n=3; Chagas, n=2; idiopathic, n=18). Targeted veins were selected by mapping coronary veins on the epicardial aspect of endocardial scar (identified by bipolar voltage <1.5 mV), using venography and signal recording with a 2F octapolar catheter or by guidewire unipolar signals. Epicardial mapping was performed in 15 patients. Vein segments in the epicardial aspect of VT substrates were treated with double-balloon VEA by blocking flow with 1 balloon while injecting ethanol through the lumen of the second balloon, forcing (and restricting) ethanol between balloons. Multiple balloon deployments and multiple veins were used as needed. In 22 patients, late gadolinium enhancement cardiac magnetic resonance imaged the VEA scar and its evolution.

Results: Median ethanol delivered was 8.75 (interquartile range, 4.5-13) mL. Injected veins included interventricular vein (6), diagonal (5), septal (12), lateral (16), posterolateral (7), and middle cardiac vein (8), covering the entire range of left ventricular locations. Multiple veins were targeted in 14 patients. Ablated areas were visualized intraprocedurally as increased echogenicity on intracardiac echocardiography and incorporated into 3-dimensional maps. After VEA, vein and epicardial ablation maps showed elimination of abnormal electrograms of the VT substrate. Intracardiac echocardiography demonstrated increased intramural echogenicity at the targeted region of the 3-dimensional maps. At 1 year of follow-up, median of 314 (interquartile range, 198-453) days of follow-up, VT recurrence occurred in 7 patients, for a success of 84.1%.

Conclusions: Multiballoon, multivein intramural ablation by VEA can provide effective substrate ablation in patients with ablation-refractory VT in the setting of structural heart disease over a broad range of left ventricular locations.

Keywords: ablation techniques; arrhythmias, cardiac; ethanol; heart ventricles; veins.

Figure 1.

Procedural approach and patient flow. A, schematic of the procedural approach. After delineating the scar -VT substrate- location, epicardial veins overlying the substrate are cannulated using the double-balloon approach. VEA aims to deliver ethanol to the substrate via its venous return. B, example in one patient showing the scar map with overlying vein, the venogram, and the double balloon approach. C, patient flow. LAD: left anterior descending. LCx: left circumflex. RCA: right coronary artery. Sarc: sarcoidosis.

Figure 2.

Triple-vein VEA in ischemic VT caused by apical infarct. A, 12-lead ECG of the VT. B, endocardial activation map showing reentry in the apex. C, endocardial voltage map showing epical scar and RFA lesions. D-E-F, 3D anatomy of the epicardial veins in relationship with the endocardial map and apical scar, showing the consecutive positioning of the octapolar catheter in the lateral, middle cardiac (MCV) and anterior interventricular (AIV) veins. G, epicardial voltage map. H-I-J, lateral vein venogram (H), octapolar cannulation (I) and balloon for VEA (J). K, VEA via balloon in MCV. L-M-N-O, AIV venogram, balloon cannulation and VEA in AIV. P-Q: localization of targeted veins and VEA relative to the apical scar. R, apical echogenicity increases after VEA. RAO, LAO, right and left anterior oblique projection, respectively.

Figure 3.

Multi-vein VEA in ischemic VT caused by a lateral (circumflex artery) infarct. A, 12-lead ECG of the VT. B, bipolar voltage map of the LV endocardium showing large scar with the location of lateral vein superimposed on it. C, after extensive endocardial ablation, activation map supports exit site at the lateral edge of the scar. D, Lateral vein activation supports epicardial activation preceding exit site. E-F, Lateral vein venogram and cannulation with octapolar catheter (signals in VT and paced rhythm in F insets). G-H-I, sequential double-balloon deployments for lateral vein VEA. J-K, second VT induced, with exit site mapped at the septal edge of the scar. L-M, octapolar catheter in a branch of the middle cardiac vein (MCV), and corresponding signals and entrainment suggesting location at exit site. N-O, balloon in posterior MCV branch for VEA. P-R, VEA in basal branch of lateral vein. S-T, schematics of multi-vein, multi-balloon VEA.

Figure 4.

Double-balloon VEA in a patient with VT from cardiac sarcoidosis and prior RFA failure. A, VT morphology. B, Endocardial, epicardial and anterior interventricular vein (AIV) voltage maps showing a large anterior scar. Activation maps (right) shows earliest activation at basal anterior wall, latest in the proximal AIV, and no apparent reentrant circuit. C-D, Venogram showing a large diagonal vein, cannulated with octapolar catheter. E, location of the octapolar catheter in diagonal vein relative to the endocardial and epicardial scar. F, mid-diastolic diagonal vein signals precede those in the AIV. G, Concealed entrainment from diagonal vein shows post-pacing interval and stimulus-QRS consistent with location within reentrant circuit. H, schematic of double-balloon VEA in diagonal vein. I-K, sequential double balloon VEA. L-M, increased echogenicity in targeted region after VEA.

Figure 5.

Double-balloon VEA in a lateral vein in idiopathic cardiomyopathy and prior RFA failure. A-B, venogram and octapolar vein cannulation of a large lateral vein. Epicardial mapping had been performed with PentaRay catheter. C-D, voltage maps of epicardial and endocardial surfaces showing disproportionately large epicardial scar, with location of octapolar catheter in lateral vein superimposed. E, epicardial (Penta) and vein signals from the scar, showing late potentials. Pacing from lateral vein leads to long latency and QRS morphology matching VT (F). G-J, sequential double-balloon VEA along lateral vein. K-L, and M-N, Pre- and post-VEA epicardial voltage maps showing marked voltage reduction (note scale of 0 to 1.5 mV). O-P, increased echogenicity in targeted region after VEA.

Figure 6.

Scar progression after VEA by LGE-CMR. In 1-day post-VEA scans, areas of hypoenhancement (red arrows) consistent with microvascular obstruction are seen. These are variably replaced by scar (yellow arrows) on long-term scans. A, ischemic VT substrate, B, nonsischemic VT substrate.

Figure 7.

Outcomes after VEA. A, Kaplan-Meier plot of freedom from VT. Recurrences after 1 year were truncated at 400 days. B, antiarrhythmic drug therapy distribution before and after VEA. C, VT episodes before and after VEA in all 44 patients. D, box plot of VT episodes before and after VE.