Importance of great cardiac vein signal in the differentiation of premature ventricular contraction origins in right and left ventricular outflow tracts

Amir-Farjam Fazelifar; Behzad Amanpour; Mona Heidarali; Abbas Bakhti Arani

doi:10.4103/rcm.rcm_23_20

ORIGINAL ARTICLE

Year : 2020 | Volume : 9 | Issue : 3 | Page : 61-64

Importance of great cardiac vein signal in the differentiation of premature ventricular contraction origins in right and left ventricular outflow tracts

Amir-Farjam Fazelifar¹, Behzad Amanpour², Mona Heidarali², Abbas Bakhti Arani³
¹ Cardiac Electrophysiology Research Center, Rajaie Cardiovascular Medical and Research Center, Iran University of Medical Sciences, Tehran, Iran
² Rajaie Cardiovascular Medical and Research Center, Iran University of Medical Sciences, Tehran, Iran
³ Imam Hossein Hospital, shahid Beheshti University of Medical Sciences, Tehran, Iran

Date of Submission	06-Jul-2020
Date of Decision	18-Aug-2020
Date of Acceptance	27-Aug-2020
Date of Web Publication	26-Oct-2020

Correspondence Address:
Dr. Abbas Bakhti Arani
Cardiac Electrophysiology Research Center, Rajaie Cardiovascular Medical and Research Center, Iran University of Medical Sciences, Niayesh Highway, Valisasr Street, Tehran
Iran

Source of Support: None, Conflict of Interest: None

DOI: 10.4103/rcm.rcm_23_20

Abstract

Background and Aim: “Idiopathic” ventricular arrhythmias most often arise from the right ventricular outflow tract (RVOT), although arrhythmias from the left ventricular outflow tract (LVOT) have also been observed. The aim of the study was to investigate the importance of signal of great cardiac vein (GCV) to distinguish premature ventricular contraction (PVC) originated from LVOT and PVC originated from RVOT. Materials and Methods: A coronary sinus catheter was placed in the GCV under fluoroscopy to measure the distance of GCV signal to the onset of QRS on surface electrocardiogram (ECG). Catheter ablation was performed utilizing radiofrequency energy in 31 patients. A 12-lead ECG was recorded during PVC. Successful ablation was defined as the complete disappearance of target PVC with no recurrence during the follow-up. Results: Thirty-one consecutive patients (16 male [51.6%]) were enrolled. Overall, 67.7% of the cases had PVC originated from the LVOT and 32.3% from the RVOT. Out of 48.4% of the females, 33.3% had PVC originated from the RVOT and 66.7% from the LVOT (P = 1). The mean ejection fraction regarding PVC originated from the LVOT and RVOT was 47.50 ± 8.95 and 45.50 ± 8.51, respectively (P = 0.7). The distance of GCV signal to the onset of QRS on surface ECG for LVOT- and RVOT-originated PVC was 15.38 ± 25.28 and −29.70 ± 25.66, respectively (P < 0.01). Conclusions: The differentiation between PVC originated from LVOT and RVOT is not entirely utilized through ECG criteria, thus the origin of PVC arising from RVOT/LVOT can be localized using the GCV signals.

Keywords: Catheter ablation, electrophysiology study, left ventricular outflow tract, premature ventricular contraction, right ventricular outflow tract

How to cite this article:
Fazelifar AF, Amanpour B, Heidarali M, Arani AB. Importance of great cardiac vein signal in the differentiation of premature ventricular contraction origins in right and left ventricular outflow tracts. Res Cardiovasc Med 2020;9:61-4

How to cite this URL:
Fazelifar AF, Amanpour B, Heidarali M, Arani AB. Importance of great cardiac vein signal in the differentiation of premature ventricular contraction origins in right and left ventricular outflow tracts. Res Cardiovasc Med [serial online] 2020 [cited 2022 May 22];9:61-4. Available from: https://www.rcvmonline.com/text.asp?2020/9/3/61/298988

Introduction

Outflow tract-ventricular tachycardia (OT-VT) is characterized by the most common subgroup of idiopathic VT and is usually seen in healthy young- to middle-aged patients with no structural heart disease. It might be aggravated by emotional stress, exercise, or dietary stimulants.^[1] OT-VT is heterogeneous, ranging from isolated premature ventricular contractions (PVCs) to recurring nonsustained VT and to sustained VT, which can be effectively treated by drugs or radiofrequency (RF) catheter ablation, though this diagnosis can be malignant.^{[2],[3],[4],[5]} Catheter ablation has been accepted as a curative treatment for patients with refractory tachyarrhythmias. The complete success is not usually obtainable in VT compared with supraventricular tachycardia because there is difficulty in localizing the origin of the VT.^[1],[2],[3] Comprehensive intracardiac electrical mapping has confirmed that a large number of OT-VTs derive from the anterior and superior septal portions of the right ventricular outflow tract (RVOT), immediately inferior to the pulmonic valve.^[6],[7] The site of origin can be localized to the right ventricular (RV) infundibulum, RV free wall, and posterior aspect of the interventricular septum, less common than the other sites. The arrhythmia originates from the left ventricular outflow tract (LVOT) and can be mapped to the aortic cusps in 10%–15% of the cases.^{[1],[8],[9],[10]} In rare occasions, OT-VT ablation site could be within the anterior interventricular vein, aortomitral connection, or the root of the pulmonary artery. OT-VT deriving in the RV is usually apparent at the inferior axis in the frontal view, and left bundle branch block (LBBB) mostly outlines the precordial R/S-wave transition at or after lead V3.^{[11],[12],[13]} On comparison, LVOT-VT usually clears both a right bundle branch block (RBBB)/inferior axis and LBBB/inferior axis with a precordial R/S-wave transition or before lead V3.^[1],[14] The electrocardiographic (ECG) distinctiveness of idiopathic VT foci originating from the aortomitral continuity, anterior interventricular vein, and the left coronary cusp–right coronary cusp junction has been described in some studies.^{[6],[10],[11],[13],[14],[15]} A considerable number of OT-VTs revealed lead V3 transition, and the requirement for left-sided ablation appreciably amends patient therapy regarding procedural time and risk.^[16] We investigated methods to estimate the origin or the optimum ablation site of PVC from the RVOT and LVOT using great cardiac vein (GCV) signal.

Materials and Methods

Study population

A total of 31 patients (16 males) with different PVC origins in RVOT and LVOT were referred to our tertiary care center.

Methods

Catheter ablation

A coronary sinus (CS) catheter was placed within the GCV under fluoroscopy to record the signal of PVC in order to measure the GCV signal distance to the onset of QRS on surface ECG. Successful ablation was defined as the complete disappearance of target PVC and no recurrence during the follow-up period. Catheter ablation was performed using RF energy, and all patients gave the written informed consent. All drugs were discontinued 72 h before electrophysiology study (EPS). Initially, PVC foci were labeled based on ECG. During the procedure, the location of the PVC was exactly determined by activation and pace mapping; the locations were burned, and subsequently, all the PVC foci disappeared. During the procedure, the catheter CS was introduced in the GCV, and electrical signals were recorded through PVC occurrence. The interval of GCV signals to the onset of QRS complex on surface ECG was measured. The origin of PVC was defined as the ablation site where the best pace mapping score was obtained and the targeted PVC disappeared by a single-energy delivery. Bipolar cathodal stimulation at an output which was larger than the diastolic threshold was utilized for pace mapping during sinus rhythm. A rate of 120–140 per min was utilized for the ventricle pacing. The location was considered the origin of PVC, if the QRS morphology and amplitude of 12-lead ECGs of the paced beat was perfectly similar to that of PVC. Successful ablation was distinct as the complete disappearance of target PVC, which was not induced without and with Isuprel during procedure and no recurrence during the follow-up period. The catheter ablation signal distance during the procedure to the onset of the QRS on surface ECG was used as an activation mapping (the earliest signal was defined as the best signal).

12-lead electrocardiogram

A 12-lead ECG was recorded during PVC. We used ECG to estimate the origin of PVC through the LBBB and RBBB pattern in lead V1, early or late transition in the precordial lead, broad R-wave in lead V1, and delta wave in PVC morphology.

Statistical analysis

Parametric data were expressed as mean ± standard deviation; the numeric variables in different groups were compared by Student's paired t-test. The mean value and percentages were compared by Pearson's Chi-square test or Fisher's exact test, depending on the variables. SPSS software version 15.0 (Chicago, IL, USA) was used for all statistical analyses. P < 0.05 was considered the level of statistical significance. The informed consent was obtained from all the patients, and the content of the study was accepted by the Ethics Committee of Iran University of Medical Sciences.

Results

Thirty-one patients (16 males [51.6%]) were enrolled. Totally, 21 (67.7%) cases had PVC origins in the LVOT and 10 (32.3%) cases had PVC origins in the RVOT. Out of 15 females (48.4%), five cases (33.3%) had PVC origins in the RVOT and ten cases (66.7%) had PVC origins in the LVOT (P = 1). Out of the 16 males, five cases (31.3%) had PVC origins in the RVOT and 11 cases (68.7%) had PVC origins in the LVOT (P = 1). Ejection fraction mean in LVOT- and RVOT-originated PVC was 47.50 ± 8.95 and 45.50 ± 8.51, respectively (P = 0.7). The GCV signal distance to the onset of QRS on surface ECG in LVOT-originated PVC and RVOT-originated PVC was 15.38 ± 25.28 and − 29.70 ± 25.66, respectively. A statistically significant relationship was found between the GCV signal distance and PVC origin in LVOT and RVOT (P < 0.01). The demographic and clinical characteristics of the patients with PVC origins in LVOT and RVOT are demonstrated in [Table 1].

Table 1: Baseline demographic data and clinical characteristics

Click here to view

Discussion

In the present study, the diagnostic accuracy of the origins of PVC with ECG is discussed. Sometimes, it is difficult to find the origin according to the surface ECG; hence, we try to find a method with more sensitivity and specificity other than ECG. These data provide a practical guide for the evaluation of PVC origins in the condition of any complicatedness during the EPS procedure. OT-VTs are usually hemodynamically stable and focal in derivation, and the ablation of OT-VT has been extremely successful. Accurate localization of OT-VT focus is an important contributing factor in successful RF ablation, nevertheless the site of origin of OT-VTs is not always easy to identify.^[17] Outflow tract tachycardias comprise a subgroup of VTs that are predominantly localized in and around the RVOT and LVOT. The mechanism underlying this group of arrhythmias appears to be a triggered activity due to delayed afterdepolarization.^[18],[19] In general, OT-VTs are apparent at a relatively early age and an equal distribution of the tachycardia between males and females is found.^[20] VT originating in the RVOT shows a predilection for females (69.6%), whereas LVOT is predominantly seen in males.^{[1],[20],[21]} We showed that LVOT and RVOT also have an equal distribution between both sexes (16 males [51.6%] and 15 females [48.4%]). In general, it is established that a precordial transition during the PVC/VT that comes about later than the V3 excludes an LVOT origin with 100% accuracy. Pace mapping has been reported as a reliable method for localizing the source of VT.^[2] Besides, activation and pace mapping had been shown as a practical and an ordinary method for PVC localization.

We showed that the GCV signal distance to the onset of QRS on surface ECG in PVC originating from the LVOT is significantly more and earlier than that of the other groups (15.38 ± 25.28 in PVC origins in LVOT and − 29.70 ± 25.66 in PVC origin in RVOT [P < 0.01]). Our findings could be used as a practical guide; meanwhile, the apparent positive value on GCV site suggests the mapping on left outflow (aortic valve cusps, aortomitral continuity, septal parahisian, superior and superolateral, and lateral mitral annulus) and the negative one suggests the mapping on right-sided outflow. Hence we should insert the catheter into the appropriate location to find the best PVC origin. To the best of our knowledge, this is probably the first report on the potential application of intra-CS mapping for differentiation of right versus left OT-VT designed for PVC origins.

Conclusions

Demarcation of PVC arising from LVOT from PVC origins in RVOT is not perfectly determined according to ECG criteria; thus, the origin of PVC arising from RVOT/LVOT can be localized using the GCV signal distance. CS catheter insertion into GCV to apply the signal for estimating the best origin of the PVC has been suggested in order to have the less procedural time and more successful process provided that the ECG findings were not completely distinctive.

Study limitation

The most significant complexity in our study was to insert the CS catheter into GCV; with taking time limitation into consideration, we performed a variety of catheter insertions in our procedure.

Acknowledgments

Through this, it is intended to thank Dr. Homan Bakhshandeh for assisting with the data analysis and methodology consultation.

Financial support and sponsorship

This study was financially supported by the funds of Iran University of Medical Sciences.

Conflicts of interest

There are no conflicts of interest.

References

1.	Callans DJ, Menz V, Schwartzman D, Gottlieb CD, Marchlinski FE. Repetitive monomorphic tachycardia from the left ventricular outflow tract: Electrocardiographic patterns consistent with a left ventricular site of origin. J Am Coll Cardiol 1997;29:1023-7.
2.	Shimizu W. Arrhythmias originating from the right ventricular outflow tract: How to distinguish “malignant” from “benign”? Heart Rhythm 2009;6:1507-11.
3.	Stevenson WG, Soejima K. Catheter ablation for ventricular tachycardia. Circulation 2007;115:2750-60.
4.	Samore NA, Imran Majeed SM, Kayani AM, Bhalli MA, Shabbir M. Outcome of radiofrequency catheter ablation as a nonpharmacological therapy for idiopathic ventricular tachycardia. J Coll Physicians Surg Pak 2009;19:548-52.
5.	Yamashina Y, Yagi T, Namekawa A, Ishida A, Sato H, Nakagawa T, et al. Distribution of successful ablation sites of idiopathic right ventricular outflow tract tachycardia. Pacing Clin Electrophysiol 2009;32:727-33.
6.	Latif S, Dixit S, Callans DJ. Ventricular arrhythmias in normal hearts. Cardiol Clin 2008;26:367-80.
7.	Movsowitz C, Schwartzman D, Callans DJ, Preminger M, Zado E, Gottlieb CD, et al. Idiopathic right ventricular outflow tract tachycardia: Narrowing the anatomic location for successful ablation. Am Heart J 1996;131:930-6.
8.	Alasady M, Singleton CB, McGavigan AD. Left ventricular outflow tract ventricular tachycardia originating from the noncoronary cusp: Electrocardiographic and electrophysiological characterization and radiofrequency ablation. J Cardiovasc Electrophysiol 2009;20:1287-90.
9.	Yamada T, Yoshida N, Murakami Y, Okada T, Muto M, Murohara T, 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;5:184-92.
10.	Bala R, Garcia FC, Hutchinson MD, Gerstenfeld EP, Dhruvakumar S, Dixit S, et al. Electrocardiographic and electrophysiologic features of ventricular arrhythmias originating from the right/left coronary cusp commissure. Heart Rhythm 2010;7:312-22.
11.	Lin D, Ilkhanoff L, Gerstenfeld E, Dixit S, Beldner S, Bala R, et al. Twelve-lead electrocardiographic characteristics of the aortic cusp region guided by intracardiac echocardiography and electroanatomic mapping. Heart Rhythm 2008;5:663-9.
12.	Dixit S, Gerstenfeld EP, Callans DJ, Marchlinski FE. Electrocardiographic patterns of superior right ventricular outflow tract tachycardias: Distinguishing septal and free-wall sites of origin. J Cardiovasc Electrophysiol 2003;14:1-7.
13.	Ouyang F, Fotuhi P, Ho SY, Hebe J, Volkmer M, Goya M, et al. Repetitive monomorphic ventricular tachycardia originating from the aortic sinus cusp: Electrocardiographic characterization for guiding catheter ablation. J Am Coll Cardiol 2002;39:500-8.
14.	Hachiya H, Aonuma K, Yamauchi Y, Harada T, Igawa M, Nogami A, et al. Electrocardiographic characteristics of left ventricular outflow tract tachycardia. Pacing Clin Electrophysiol 2000;23:1930-4.
15.	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;13:551-6.
16.	Tanner H, Hindricks G, Schirdewahn P, Kobza R, Dorszewski A, Piorkowski C, et al. Outflow tract tachycardia with R/S transition in lead V3: Six different anatomic approaches for successful ablation. J Am Coll Cardiol 2005;45:418-23.
17.	Miles WM. Idiopathic ventricular outflow tract tachycardia: Where does it originate? J Cardiovasc Electrophysiol 2001;12:536-7.
18.	Shimoike E, Ohba Y, Yanagi N, Hiramatsu SI, Ueda N, Maruyama T, et al. Radiofrequency catheter ablation of left ventricular outflow tract tachycardia: Report of two cases. J Cardiovasc Electrophysiol 1998;9:196-202.
19.	Gallagher JJ, Selle JG, Svenson RH, Fedor JM, Zimmern SH, Sealy WC, et al. Surgical treatment of arrhythmias. Am J Cardiol 1988;61:27A-44A.
20.	Thakur RK, Klein GJ, Sivaram CA, Zardini M, Schleinkofer DE, Nakagawa H, et al. Anatomic substrate for idiopathic left ventricular tachycardia. Circulation 1996;93:497-501.
21.	Suwa M, Yoneda Y, Nagao H, Sakai Y, Nakayama Y, Hirota Y, et al. Surgical correction of idiopathic paroxysmal ventricular tachycardia possibly related to left ventricular false tendon. Am J Cardiol 1989;64:1217-20.