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Incessant ventricular tachycardia (VT) has presented a therapeutic challenge over the years. After animal studies demonstrating successful termination of VT by intracoronary injection of phenol or ethanol by Inoue and colleagues,1 interruption of coronary flow to arrhythmogenic substrates by balloon occlusion and the infusion of antiarrhythmic drugs or obliterative agents like ethanol^2–4 were developed as treatment options for VT uncontrolled by antiarrhythmic or device therapy.

Interest in transcoronary ethanol ablation (TCEA) decreased as endocardial RF catheter ablation matured into a successful treatment option for drug-resistant VT. However, many VT circuits are intramural or epicardial. Intramural circuits are potentially difficult to damage endocardially even with the use of irrigated catheters for increased depth of energy delivery. While epicardial access can be attained by percutaneous pericardial puncture with relative ease by a subxiphoid approach, this approach may be precluded by adhesions from previous cardiac surgery or pericardial fat, preventing adequate energy delivery to the myocardium. In addition, an epicardial approach does not allow access to circuits deep in the septum. For these patients, one option is ablation through chemically induced necrosis of the involved myocardium by the instillation of corrosive agents through the associated vasculature. Hence there has been renewed interest in and use of TCEA.

An understanding of how instillation of ethanol into coronary arteries results in permanent damage to tachycardia substrates through myocardial necrosis and scarring comes largely from animal studies, with limited confirmatory evidence in human pathological specimens.⁵ Ethanol results in a coagulative necrosis of the myocardium that can be seen as early as 5 minutes after instillation in canine coronary arteries.⁶ Necrotic tissue is eventually replaced by scar late after ablation.⁵ Ethanol also has a direct cytotoxic sclerosant effect on arteries and a denaturing effect on blood components, resulting in fixation of blood and development of acute vascular occlusion by intraluminal necrotic debris, even in the absence of intimal injury.¹ This intraluminal occlusion causes an ischemic infarction distally, which contributes further to coagulative necrosis of the subtended myocardium. While one would expect the extent of infarcted tissue to be predicted by the perfusion bed of the targeted artery, this correlation is not perfect. Pathological examination has demonstrated areas of resultant necrosis to be variably focal, confluent, and nonconfluent. Studies in pigs have demonstrated ablated tissues to be smaller than the areas perfused. This may be a result of collateral blood supply at the watershed of the perfusion bed of the selected artery.⁷ Reflux of ethanol into nontargeted vascular beds also contributes to the potential imprecision of the created infarct. The concentration of ethanol used can also influence the size of the ablative lesion.⁸ The purpose of this review is to detail the practical aspects of performing the procedure of TCEA for VT.

Suitable patients are those with a monomorphic VT or premature ventricular complexes, with likely scar-based substrates. The majority of patients with scar-based VT will have an underlying pathology of CAD. The VT circuit(s) in these patients are most often located subendocardially, given the typical location of coronary arterial watershed areas, and therefore, these substrates are typically amenable to endocardial ablation. Nonischemic pathologies underlying scar-based VT, on the other hand, have no particular predilection for the endocardial portion of the ventricular myocardium, and therefore are often considered for TCEA. One exception is CAD-associated scar involving the septal myocardium, particularly in the basal portion of the septum, which is relatively thick. Nonischemic pathologies considered for TCEA have included idiopathic dilated cardiomyopathy, ARVC, and infiltrative cardiomyopathies.9

The most common treatment algorithm that leads to TCEA is as follows:

1. Patients undergo endocardial mapping and attempted ablation.

2. After endocardial ablation fails, a determination is made that the likely substrate location is intramural or epicardial, most commonly based on mapping information obtained during the initial ablation attempt.

3. An epicardial approach to mapping and ablation is attempted if the substrate is thought to be potentially accessible through such an approach.

4. If an epicardial attempt is unsuccessful because the substrate is thought to be intramural rather than epicardial, or if the substrate is thought to be septal and intramural after the initial ablation attempt, TCEA is then considered as a therapeutic strategy.

Additional patient groups in whom TCEA is considered earlier are those in whom epicardial access is difficult, most commonly due to a prior sternotomy and resultant adhesions, and/or patients in whom endocardial access is precluded due to the presence of mechanical aortic and/or mitral valves.

Review of ECG Morphology

ECGs of suitable VTs typically appear to have a septal origin, or if nonseptal, intramural or epicardial. ECG characteristics of a septal origin VT include a left or right bundle branch morphology and possibly a narrow QRS from early engagement of the HPS. The frontal plane axis, as well as the precordial transition, may vary, depending on the site of exit along the septum. The ECG morphology of VT substrates outside of the septum considered for TCEA will often demonstrate a relatively slow intrinsic deflection.¹⁰

Discontinuation of Antiarrhythmic Drugs

As with all arrhythmias, inducibility and sustainability are necessary for optimal mapping of VTs. This is particularly important in TCEA, as mapping for the involved coronary artery typically relies on termination of sustained VT with test infusions. Hence, as much as can be tolerated, antiarrhythmic drugs should be discontinued for at least 5 half-lives prior to the procedure. If necessary, the patient can be admitted to hospital for this drug washout.

Preprocedural Imaging

Cardiac imaging should be undertaken and/or reviewed if previously performed for several reasons. First, VT circuits are often located within or adjacent to scarred myocardium that manifests as areas of decreased contractility, decreased enhancement, and decreased perfusion on echocardiography, MRI, and nuclear imaging. Hence, all preprocedural imaging should be reviewed carefully to predict the likely target of ablation. Secondly, the risk of complications can be minimized by assessing left ventricular function, identifying the presence of thrombus, and localizing areas of excessively thinned myocardium.

Review of Previous Endocardial and/or Epicardial VT Mapping

Data from all prior endocardial and epicardial ablation attempts should be reviewed carefully. Electroanatomical data should be reviewed to identify low-voltage areas and electrically unexcitable scar. Pace mapping and entrainment mapping from previous studies should be reviewed to identify the likely exit and possible isthmi of the VT circuits.

Intraoperative Requirements

An electrophysiologist experienced in the mapping and ablation of scar-based VT is required. In addition, an experienced interventional cardiologist facile in the technique of TCEA, most commonly applied to hypertrophic cardiomyopathy septal ablation, needs to be involved.11

Vascular Access

Femoral venous access is typically obtained for placement of diagnostic catheters. Catheters required are typically a quadripolar catheter that can be manipulated to the RVA and RVOT for programmed stimulation for induction of VT, and a His catheter for marking the location of the HB and septum, in part to allow for closer monitoring of AV conduction. Femoral arterial access is necessary both for arterial blood pressure monitoring and for placement of the coronary angiography catheters (6- to 7-Fr) through which TCEA is performed.

Procedure

The initial mapping depends on whether the VT is stable and tolerated. Nonetheless, voltage mapping in sinus rhythm is typically undertaken first to delineate the likely scar substrate for the VT, if not previously performed. This will usually have been undertaken during a prior endocardial and epicardial attempt and can be used to guide higher-resolution mapping in the area of interest during the TCEA procedure. If the VT is hemodynamically stable and sustained, termination mapping and more classical mapping methods can be employed for localization of the target vessel. VT originating from an automatic focus may be activation-mapped as well.

VT Induction

VT induction should be attempted with programmed electrical stimulation from multiple ventricular sites, at different pacing cycle lengths, with multiple extrastimuli. The ease of inducibility is also important for determining the endpoint of the procedure on postablation testing.

IV Heparin

Similar to the requirement for percutaneous coronary intervention, intravenous heparin at a dose of 60 to 100 IU/kg should be administered once the coronary arteries are cannulated. The ACT should be maintained at > 250 seconds.¹²

Selective Coronary Angiography

Using in part the VT morphology to predict the location of scar and VT substrate, the relevant coronary artery should be selected using an 0.014” angioplasty guidewire. An over-the-wire balloon catheter that has been sized to be larger than the angiographic diameter of the target vessel to allow occlusion of its ostium when deployed is passed over the wire using standard percutaneous techniques.¹³

Contrast Sonography

To confirm that the target myocardium is supplied by the suspected vessel, echocardiography may be performed and sonographic contrast agent injected through the over-the-wire infusion catheter to confirm the territory supplied by the target vessel.

Mapping

After a candidate target vessel is selected, the VT still needs to be mapped to the corresponding coronary vessel before any ethanol is instilled to perform the ablation. More commonly, mapping by termination of the tachycardia is undertaken; however, there are ways to undertake more classical EP mapping through the target vessel.

Mapping by Termination

After having intubated the suspect vessel, the VT is reinduced. The balloon of the infusion catheter is fully inflated to occlude the ostium of the artery and prevent retrograde flow of infusate. Two to 3 mL of ice-cold sterile saline is then injected through the central lumen. If the VT terminates (Figure 46.1) with the injection and without evidence of potential associated complications such as PR prolongation or AV block, that artery is suitable for ethanol injection. Termination may also be assessed with injection of contrast media¹⁴ or lidocaine in place of saline.¹⁵ These methods result in transient termination of blood flow to the potential target tissue, which should result in transient conduction block and termination of arrhythmia as a result. The arrhythmia may or may not spontaneously reinitiate. If the clinical VT is not inducible during EP study, or if it is unstable, precise localization of the ideal target coronary vessel will be difficult. In fact, strong consideration should be made whether or not to proceed further with ablation, as targeting the incorrect vessel will not only fail to terminate the clinical VT, but given the relatively large area of myocardial damage induced, a significant unwanted myocardial infarct may result.

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