Transcoronary mapping and chemical ablation of ventricular tachycardia in no-entry left ventricle

Abstract

It is challenging to perform ablation of ventricular tachycardia (VT) from the left ventricle (LV) in patients without catheter access to the LV. A 50-year-old man was referred to our hospital for VT. He underwent mechanical aortic and mitral valve replacement for infective endocarditis and embolic myocardial infarction in the left ventricular inferior wall during a surgery. Anti-arrhythmia drugs (AADs) such as sotalol and bisoprolol were initiated and implantable cardioverter defibrillator was implanted. However, 2 months after discharge, he was admitted again for cardiac implantable electronic device (CIED) infection and underwent complete CIED system removal. During hospitalization, VT easily occurred despite the use of AADs. We decided to perform transcoronary chemical ablation to treat this drug-refractory VT. A 0.014-inch guide-wire and a micro-catheter were advanced into coronary arteries. Pace map was conducted using a guide-wire and the micro artery branch feeding the VT exit area was detected. Ethanol infusion to this branch and the slightly basal side of the area eliminated the VT. We successfully treated VT in the no-entry LV by wire-guided mapping and ethanol ablation via coronary arteries. VT has not recurred during the follow-up period of 12 months. <Learning objective: It is challenging to perform ventricular tachycardia (VT) ablation in patients with mechanical aortic and mitral valve replacement, because there is no catheter access to the left ventricle. Mapping via coronary arteries using guide-wires enables pace-mapping, finding VT exit sites, and identification of the appropriate branches for ethanol infusion. Therefore, transcoronary mapping and chemical ablation may be an alternative treatment for VT in a no entry left ventricle situation.>.

Keywords: Mechanical valve replacement; Transcoronary chemical ablation; Transcoronary mapping; Ventricular tachycardia.

Fig. 1

(A) Double stimuli from the right ventricular apex (600 ms-290 ms-260 ms) induces a ventricular tachycardia, which has a right bundle branch block morphology with a superior axis and deep S wave in V3-5. (B, C) Coronary angiography reveals two major posterior descending arteries (PDAs) from the left circumferential artery. (Red and yellow arrows). Panels B and C are the right anterior oblique and left anterior oblique views. (D, E) A 0.014-inch angioplasty guide-wire and micro-catheter are advanced to PDAs. Micro-arteries from PDAs are contrasted by the tip injection technique using the micro-catheter.

Fig. 2

Unipolar pacing via coronary arteries using a guide-wire is performed in several branches of posterior descending arteries (PDAs). The pace map from the middle portion of the PDA (A) is different from the clinical ventricular tachycardia morphology, while that from the distal portion of the PDA (B) resembles the clinical ventricular tachycardia morphology.

Fig. 3

(A, B) Further programed stimulation induces another ventricular tachycardia (VT) and mapping of this VT using a guide-wire is started again. A guide-wire is advanced to several micro-arteries near the earliest activation site recorded by the intracardiac multi-electrode catheters. Intracoronary electrocardiogram recorded by the guide-wire precedes the onset of the VT by 41 ms. (C, D) An over-the-wire balloon is deployed in the ostium of the target artery branches, and 100% ethanol is injected after wire removal and balloon inflation. Ethanol infusion to this branch directly terminates this VT.