Case 1

A 77-year-old woman with an electrical storm was referred for epicardial ablation after failed endocardial ablation for monomorphic ventricular tachycardia (VT). She underwent emergency cardiac catheterization at a different center, which revealed no coronary stenosis. However, echocardiography identified a suspicious left ventricular (LV) aneurysm at the postero-basal area without LV dysfunction (see Video 1). Her ECG showed monomorphic ventricular tachycardia (MMVT) with right bundle branch block (RBBB) morphology and a superior axis, suggesting the origin of the inferoseptal papillary muscle (see Figure 1A). LV endocardial mapping using a three-dimensional electroanatomical (3D-EAM) system (CARTO 3 System; Biosense Webster) was performed but did not reveal any diastolic pathway or early focal activity.

Since the patient's VT morphology displayed pleomorphism, indicating multiple exits and focal trigger activity (see Figure 2), we decided to map the middle cardiac vein (MCV) via the coronary sinus (CS). After gaining venous access, we utilized a long sheath (Agilis®, Saint Jude Medical™) to facilitate catheter manipulation within the coronary venous system (CVS). However, we could not detect early focal activity or diastolic pathway electrograms within the MCV. Subsequently, we opted to perform CS venous angiography, which revealed the MCV and posterolateral (PL) branches (see Figure 3 and Video 2). During the mapping of the PL branch, we detected very long fragmented signals (see Figure 4 and Video 3). Irrigated radiofrequency ablation (RFA) from the PL branch completely suppressed the VT (see Videos 4 and 5), resulting in transient RBBB development (Figure 5 and Video 5).

The patient was discharged three days later with an implantable defibrillator for secondary prophylaxis. No arrhythmic events recurred during the three-month follow-up.

Case 2

A 19-year-old man had been experiencing palpitations since adolescence. A cardiac ultrasonographic study revealed a left ventricular ejection fraction (LVEF) of 34% and moderately severe mitral regurgitation with apical hypertrabeculation. Extensive investigation for other causes of cardiomyopathy yielded no results. Previous endocardial ventricular tachycardia (VT) ablation attempts for monomorphic VT (MMVT) had failed.

On MRI, no late gadolinium enhancement was observed. Given the patient's frequent ventricular premature complexes (VPD) and VT with a QRS morphology featuring right bundle branch block (RBBB) and an inferior axis (see Figure 6A), we initially attempted endocardial mapping once more. However, all endocardial radiofrequency ablation (RFA) attempts, conducted through both trans-septal and retro-aortic approaches, only temporarily suppressed the VT at the earliest ventricular activation point (EVAP) in the mid-left ventricle (LV) cavity (see Figure 6B and Video 6).

Subsequently, we accessed that area through the lateral branch of the coronary sinus (CS) (Figure 7B and Videos 7 and 8). Despite successful pace-mapping (see Video 7), RFA at the EVAP within the lateral branch of the CS also only temporarily suppressed the VT (see Figure 7B and Video 8). Finally, epicardial RFA at the EVAP eliminated all ventricular arrhythmias (see Figure 7C and Figure 1B and Video 9).

Three layers of myocardial mapping, facilitated by the transparency mode on the CARTO software, confirmed the close relationship (see Figure 8). Three months later, the LVEF had improved to 44%, leading to the cancellation of the implantable defibrillator decision.

Case 3

A 56-year-old man with nonischemic cardiomyopathy and an implanted cardioverter-defibrillator (ICD) was admitted to the electrophysiology laboratory due to incessant monomorphic ventricular tachycardia (MMVT) with left bundle branch block (LBBB) morphology and late precordial transition (see Video 10).

The 3D electroanatomical mapping (3D EAM) of the left ventricle (LV) revealed a basal-to-apical anteroseptal low-voltage area, suggesting a previous extensive myocardial infarction. However, coronary angiography revealed no coronary stenosis or occlusion.

Since some patients may also have an overlap of ischemic and non-ischemic etiologies of scar,¹ we performed activation mapping of the tachycardia and detected the earliest ventricular activation point (EVAP) at the anteroseptal portion of the right ventricular outflow tract (RVOT) (see Video 11). The post-pacing interval (PPI) indicated that the circuit was outside this area.

We then mapped the left ventricular outflow tract (LVOT) (see Video 12), and since the neighboring LV area (see Video 12) was also outside the circuit according to PPI evaluation, we mapped the septal branches of the anterior interventricular vein (AIV) using VisionWire (Biotronik SE & Co KG, Berlin, Germany) to rule out intra-septal reentry (see Video 13). Unfortunately, we could not evaluate the local electrograms due to noisy artifacts. We applied cold saline applications to these septal branches at this stage,² but no effect on the tachycardia was observed. Next, we proceeded to map the anterior interventricular vein (AIV) using a CS catheter (Webster®; Biosense Webster, Irvine, CA) (see Videos 14 and 15). We observed a positive PPI response, but our attempts to ablate the AIV were limited due to its proximity to the left anterior descending artery, and we were unable to terminate the ongoing VT (Videos 16 and 17). As a last resort, we decided to perform epicardial mapping, which revealed a figure-of-eight activation pattern on the epicardium, despite encountering a catheter out-of-mapping-range error (Video 18). Remarkably, we successfully terminated the tachycardia with just one ablation point (Video 19). Following additional consolidating ablations, the patient was discharged three days later without complications.

Epicardial ablation via the arterial and venous systems provides an excellent opportunity to map and intervene in complex arrhythmias of epicardial origin, areas inaccessible through a standard epicardial approach, and arrhythmias of intramural origin.² However, having accurate knowledge of coronary venous anatomy is essential for electrophysiologists performing LV pacing procedures or radiofrequency ablation.³⁴⁵ The coronary venous system (CVS) offers access to the basal LV epicardium through the great cardiac vein (GCV) and to the septal aspects of the anterior and posterior epicardium through the anterior interventricular vein (AIV) and middle cardiac vein (MCV), respectively.⁶⁷ In addition to the epicardial CVS branches, intramuscular venous branches allow for wire mapping techniques and targeted delivery of ablative ethanol.⁸ In this report, we present three cases of VT in which epicardial and CVS mapping was conducted using the MCV, PL, lateral, and AIV branches of the coronary sinus (CS). It is worth noting that presumed epicardial arrhythmias typically require comprehensive mapping on both the epicardial and endocardial surfaces to formulate appropriate therapeutic strategies. In general, percutaneous epicardial ablation is pursued when an endocardial approach has failed. Since the CVS is partly an epicardial structure but also extends into the myocardium through perforator veins, intracoronary arterial and CVS mapping or intervention can be highly valuable for intramyocardial or epicardial sites of origin without requiring access to the epicardial space.8 The CVS offers a more effective access route for ablation along the basal epicardial left ventricle (LV) than direct percutaneous epicardial access due to the presence of epicardial fat along the atrioventricular and interventricular grooves, which can make ablation of an underlying epicardial substrate challenging.⁶ In these cases, mapping of the large coronary venous branches (the middle cardiac vein [MCV], posterolateral [PL] and lateral ventricular branches, great cardiac vein [GCV], and anterior interventricular vein [AIV]), along with smaller septal branches, can be very helpful in identifying a critical arrhythmic substrate.8 However, the very thin lumen of these vessels often limits detailed mapping and ablation in this region. Furthermore, limitations in delivering sufficient radiofrequency energy due to anatomical constraints, high impedance, and inadequate irrigation flow may reduce the efficacy of ablation.⁹¹⁰

For these reasons, lower power settings are often used during CVS ablation, starting as low as 5 W to 10 W and gradually titrating the power to achieve a 10-ohm impedance drop.⁶ Moreover, potential anatomical factors such as the presence of venous valves (Thebesian valve and Vieussens valve), deflections of the GCV, and the acute angle between the distal GCV and AIV can hinder catheter ablation of distal CVS vessels.¹¹ As with any intravascular procedure, there is a risk of dissection and perforation when injecting contrast, advancing wires, or accessing the vessel using guide sheaths.²¹² Therefore, coronary angiography should always be performed before ablation to assess the distance between the optimal site and the coronary arteries, and aggressive movements should be avoided.¹³ Operators must possess a clear understanding of the nearby anatomical structures to prevent potential complications when ablating ventricular arrhythmias (VAs) from within the CVS.⁶¹¹¹⁴

The CVS approach is also valuable when access to the left ventricular endocardium is contraindicated or deemed risky (due to factors such as left ventricular thrombus, mechanical aortic and mitral prostheses, vascular issues, etc.), as well as in patients with challenging percutaneous pericardial access (due to factors such as pericardial adhesions, previous cardiac surgery, liver interposition, etc.).¹³

In conclusion, endocardial mapping is typically considered the first step in VT ablation procedures. This report emphasizes that a stepwise approach involving mapping and ablation in the endocardium, followed by ablation within the CVS, can reduce the necessity for subxiphoid epicardial access in certain patients with idiopathic or scar-related ventricular arrhythmias.¹⁵