Ablation of Ventricular Arrhythmias Originating from the Right Coronary Cusp–Left Coronary Cusp Commissure

DOI: 10.19102/icrm.2011.020105

RUPA BALA, MD

Cardiovascular Division, Department of Medicine, University of Pennsylvania School of Medicine, Philadelphia, PA

Download PDF

Follow Us >> Tweet

KEYWORDS. catheter ablation, ventricular tachycardia, electrophysiology, intracardiac echocardiography.

The author reports no conflicts of interest for the published content.
Manuscript received December 6, 2010, final version accepted December 17, 2010.

Address correspondence to: Rupa Bala, MD, Assistant Professor of Medicine, Department of Cardiology / Division of Electrophysiology, Hospital of the University of Pennsylvania, 3400 Spruce Street, 9 Founders Pavilion, Philadelphia, PA 19104. E-mail: balar@uphs.upenn.edu

Introduction

Ventricular tachycardia (VT) and ventricular premature depolarizations (VPDs) are known to originate from the aortic sinus of Valsalva (ASOV) and are typically described as originating from the individual right coronary cusp (RCC) or left coronary cusp (LCC) sinuses.^1–5 Several recent publications have noted ventricular arrhythmias (VAs) originating from the RCC–LCC commissure.^6–7 These VAs have distinct electrocardiographic and electrophysiologic features. This case report describes an example of a VPD originating from the RCC–LCC commissure, highlighting the important features and the mapping strategy utilized in ablation of aortic cusp VAs in this location.

Case presentation

A 73-year-old man presented to his primary physician with palpitations and dyspnea on exertion. His electrocardiogram (ECG) revealed frequent VPDs in a pattern of bigeminy. His cardiac work-up included the following: an echocardiogram revealed an ejection fraction (EF) of 30% with a left ventricular (LV) end-diastolic diameter of 5.6 cm; a 24-h Holter revealed 39% ventricular ectopy; and a cardiac catheterization was not significant for obstructive coronary artery disease. The patient was started on verapamil and experienced fatigue. He underwent an electrophysiology (EP) study/ablation at an outside hospital, and the clinical VPD was mapped to the right ventricular outflow tract (RVOT). Ablation at this site suppressed the VPD but did not eliminate it. His follow-up cardiac studies revealed no improvement in his EF and a high VPD burden on verapamil. He was subsequently referred for repeat EP study/ablation.

The clinical VPD had a left bundle morphology with a precordial transition at lead V3 and a characteristic QS morphology with notching on the downward deflection in lead V1 (Figure 1). VPDs that have a precordial transition at lead V3 can originate from either the RVOT or the LV outflow tract (LVOT).^7–8 The first step was to perform detailed activation mapping in the RVOT. A three-dimensional (3D) electroanatomical map (CARTO, Biosense Webster, Diamond Bar, CA) was constructed with a 7-Fr, 4-mm tip Navistar catheter (Biosense Webster). The site of earliest activation (30–35 ms pre-VPD) was the midseptal RVOT (Figure 2). Pacemapping at this site was not a good match, with a later precordial transition (V4) than the clinical VPD. Thus, the next step was to map the LVOT, specifically the aortic cusp region.

Prior to mapping the aortic cusp region, an 8-Fr intracardiac echocardiography (ICE) probe (Acuson AcuNav catheter, Siemens, New York, NY) was placed in the left femoral vein and advanced across the tricuspid annulus into the RV with the transducer placed at the base of the RVOT to obtain short-axis echocardiographic views of the aortic cusp region. Each cusp was identified and its relation to the coronary vasculature was noted. ICE imaging was used to accurately identify catheter tip location, to characterize the anatomy of the ASOV region, to assess the distance from the coronary vasculature, to monitor radiofrequency (RF) lesion formation, and to assess for complications.

A detailed activation map of the clinical VPD was created in the aortic cusp region. This electroanatomical map, created in conjunction with ICE imaging to confirm precise anatomy and catheter location, was merged with a preprocedure computed tomography (CT) angiogram of the ASOV and LV. Three cusp points, confirmed by catheter location on ICE, were tagged and used to register the CT scan to the electroanatomical map. The area of earliest activation was marked on the electroanatomical map and confirmed on ICE. The site of earliest activation (80 ms pre-VPD) was the RCC–LCC commissure. At this site, bipolar electrograms recorded in sinus rhythm revealed distinct late potentials (Figure 3). ICE imaging confirmed the site of origin at the RCC–LCC commissure and was used to confirm that the catheter tip was a safe distance from the coronary vasculature prior to RF ablation (RFA) at the RCC–LCC margin (Figure 4). The first RF lesion terminated the clinical VPD and it was no longer seen. A second VPD (VPD 2) was seen, but it was infrequent. VPD 2 was mapped anterior to the aortic valve. The patient subsequently had a sustained VT that was identical to VPD 2. The site of earliest activation of this VT was also anterior to the aortic valve, close to the site of successful ablation of the clinical VPD (Figure 5). During activation mapping, the sustained VT terminated with exit block (Figure 6). A perfect pacemap was obtained at this site for the VT. This pacemap had a long stimulus to QRS interval and was obtained at threshold pacing (Figure 7). RFA at this site terminated VPD 2 and the sustained VT. Burst pacing and isoproterenol failed to elicit any further VAs.

The patient was seen in follow-up in the outpatient EP clinic. A 6-month transthoracic echocardiogram (TTE) revealed an EF of 45–50%, and a 24-h Holter revealed 1.4% VPDs.

Discussion

This case highlights the important electrocardiographic and electrophysiologic features of VAs originating from the RCC–LCC commissure. In this case, the site of origin of the clinical VPD was the RCC–LCC commissure. The ECG morphology of the clinical VPD was consistent with the predominant ECG pattern of VAs originating from the RCC–LCC commissure: a QS morphology in lead V1 with notching on the downward deflection and precordial transition at lead V3. Mapping at the RCC–LCC commissure revealed distinct late potentials in sinus rhythm.

Initial activation mapping in the RVOT revealed electrograms that were 30–35 ms pre-VPD in the midseptal region. RFA was not performed at this site. Activation mapping in the RCC–LCC commissure, opposite to the midseptal RVOT, revealed presystolic activity that was 80 ms pre-VPD. The distance between the site of earliest activation in the RVOT and RCC–LCC commissure was small, emphasizing the importance of detailed mapping prior to performing ablation. The second VPD that was seen after ablation of the clinical VPD had a “w” morphology in lead V1 and a precordial transition at lead V2. This VPD and an identical sustained VT were mapped anterior to the aortic valve. VPDs with a “w” morphology in lead V1 can originate from the RCC–LCC commissure or the LCC.

Yamada et al⁶ published a paper on five patients with VAs originating from the junction of the left and right coronary sinus of Valsalva. The authors described a QRS pattern in leads V1–V3 from VAs originating from the RCC–LCC junction. They used aortic angiography, electroanatomic mapping, and limited echocardiography in their study. Our group recently published a study identifying the electrocardiographic and electrophysiologic characteristics of VAs originating from the RCC–LCC commissure.⁷ We reported on 19 patients with VAs originating from the RCC–LCC commissure. In 15 of 19 VAs, the ECG revealed a QS morphology in lead V1 with notching on the downward deflection, and in 4 of 19 VAs, the ECG revealed a “w” pattern in lead V1. At the site of earliest activation, 13 of 19 patients in our series manifested late potentials during sinus rhythm with reversal of activation during the clinical VPD/VT.

The origin of the RCC–LCC VAs is not fully understood. The apical junction of the RCC–LCC commissure is contiguous with the interleaflet triangle and is traditionally composed of fibrous tissue. The basal junction of the RCC–LCC margin is coincident with the distal parts of the left ventricle.^9–11 A recent review by Yamada et al¹² emphasizes the LV ostium as the origin of these VAs. Hasdemir et al¹³ published a study demonstrating ventricular myocardial extensions into the pulmonary artery and aorta beyond the ventriculoarterial junction. The late potentials in sinus rhythm may represent a tract of slow conducting fibers that are activated after the ventricles and may correlate to the depolarization of ventricular myocardial extensions seen in previous studies.

It is possible that the LV ostium served as the origin of the clinical VPD that was ablated at the RCC–LCC commissure. Given that the site of origin of VPD 2 and the sustained VT were anterior to the aortic valve, it is possible that ablation of the clinical VPD altered the exit of the focus, resulting in VPD 2 and the sustained VT.

In this case, a combination of electroanatomical mapping and ICE imaging was used to confirm anatomic location, catheter tip position and contact, distance to coronary vasculature, and to monitor RF delivery. ICE was used to assess the distance to coronary vasculature in place of coronary arteriography. Operators less experienced with ICE should utilize coronary arteriography prior to RFA in the aortic cusp region to ensure a safe distance from the coronary vasculature.

References

1. Shimoike E, Ohnishi Y, Ueda N, Maruyama T, Kaji Y. Radiofrequency catheter ablation of left ventricular outflow tract tachycardia from the coronary cusp: a new approach to the tachycardia focus. J Cardiovasc Electrophysiol 1999; 10:1005–1009. [CrossRef] [PubMed]
2. Sadanaga T, Saeki K, Yoshimoto T, Funatsu Y, Miyazaki T. Repetitive monomorphic ventricular tachycardia of left coronary cusp origin. Pacing Clin Electrophysiol 1999; 22:1553–1556. [CrossRef] [PubMed]
3. Kanagaratnam L, Tomassoni G, Schweikert R, et al. Ventricular tachycardias arising from the aortic sinus of Valsalva: an under-recognized variant of left outflow tract ventricular tachycardia. J Am Coll Cardiol 2001; 37:1408–1414. [CrossRef] [PubMed]
4. Ouyang F, Fotuhi P, Ho SY, et al. Repetitive monomorphic ventricular tachycardia originating from the aortic sinus cusp: electrocardiographic characterization for guiding catheter ablation. J Am Coll Cardiol 2002; 39:500–508. [CrossRef] [PubMed]
5. Hachiya H, Aonuma K, Yamauchi Y, Igawa M, Nogami A, Iesaka Y. How to diagnose, locate, and ablate coronary cusp ventricular tachycardia. J Cardiovasc Electrophysiol 2002; 13:551–556. [CrossRef] [PubMed]
6. Yamada T, Yoshida N, Murakami Y, et al. Electrocardiographic characteristics of ventricular arrhythmias originating from the junction of the left and right coronary sinuses of Valsalva in the aorta: the activation pattern as a rationale for the electrocardiographic characteristics. Heart Rhythm 2008; 5:184–192. [CrossRef] [PubMed]
7. Bala R, Garcia FC, Hutchinson MD, et al. Electrocardiographic and electrophysiologic features of ventricular arrhythmias originating from the right/left coronary cusp commissure. Heart Rhythm 2010; 7:312–322. [CrossRef] [PubMed]
8. Tanner H, Hindrick G, Schirdewahn P, et al. Outflow tract tachycardia with R/S transition in V3: six different anatomic approaches for successful ablation. J Am Coll Cardiol 2005; 45:418–423. [CrossRef] [PubMed]
9. Anderson RH. Clinical anatomy of the aortic root. Heart 2000; 84:670–673. [CrossRef] [PubMed]
10. Sutton JP III, Ho SY, Anderson RH. The forgotten interleaflet triangles: a review of the surgical anatomy of the aortic valve. Ann Thorac Surg 1995; 59:419–427. [CrossRef] [PubMed]
11. Anderson RH. The surgical anatomy of the aortic root. Multimed Man Cardiothorac Surg 2007; doi:10.1510/mmcts.2006.002527. [CrossRef] [PubMed]
12. Yamada T, Litovsky SH, Kay N. The left ventricular ostium: an anatomic concept relevant to idiopathic ventricular arrhythmias. Circ Arrhythmia Electrophysiol 2008; 1: 396–404. [CrossRef] [PubMed]
13. Hasdemir C, Aktas S, Govsa F, et al. Demonstration of ventricular myocardial extensions into the pulmonary artery and aorta beyond the ventriculo-arterial junction. Pacing Clin Electrophysiol 2007; 30:534–539. [CrossRef] [PubMed]