Idiopathic ventricular arrhythmias typically arise in structurally normal hearts. They may present as frequent premature ventricular contractions (PVCs) or sustained ventricular tachycardia. They classically arise from the right ventricular outflow tract but may also originate from the aortic cusps, left ventricular outflow tract (LVOT), and intraventricular septum. Up to 14.5% of such arrhythmias may also originate from the left ventricular summit, a particularly difficult region of the heart to treat with ablation due to the risk of collateral damage and recurrence.1
The LV summit is defined as the highest point of the left ventricular myocardium. It is located superior to the interventricular sulcus and LV ostium (the LVOT just below the aortic valve annulus). It is a triangle-shaped region bordered by the bifurcation of the left anterior descending (LAD) and left circumflex (LCx) arteries and laterally by the great cardiac vein (GCV).2 Due to its relative inaccessibility and proximity to critical coronary vasculature, arrhythmias that originate from this region present a great challenge. In this article, we describe a method for mapping and ablating arrhythmias originating from the left ventricular (LV) summit when coronary anatomy precludes ablating in the coronary venous system.
A 51-year-old male with a history of hypertension, bladder cancer s/p cystectomy, pelvic node dissection, and chemotherapy presented to the hospital with palpitations and near syncope. CT pulmonary angiogram revealed moderate size lobar pulmonary emboli. He was started on anticoagulation and admitted to the hospital. Shortly after admission he developed PVCs, ventricular bigeminy, and eventually sustained ventricular tachycardia (VT) (Figure 1).
During the index hospitalization, his VT was managed medically due to significant PE burden and the associated risk of ablation. A coronary angiogram was performed, which revealed no angiographic disease. A transthoracic echo revealed a structurally normal heart with an LVEF of 60%. He was loaded with IV amiodarone over a period of two days, but continued to have sustained VT. IV lidocaine was later added with eventual control. These medications were converted to oral amiodarone and mexiletine, and he was eventually discharged home with a LifeVest Wearable Defibrillator (ZOLL Medical) programmed for detection and treatment of fast ventricular arrhythmias (cycle length 330 ms). He was noted to have mild tinnitus during the hospitalization, which improved with reduction of the dosage of his mexiletine.
At two-week follow-up, the patient had developed numbness of the plantar aspects of both feet with associated tingling. His mexiletine was discontinued with resolution of the symptoms. At two-month follow-up, he underwent CT pulmonary angiogram, which showed resolution of some of his pulmonary emboli with re-cannulation of the more peripheral thrombi. At three-month follow-up, given lack of alerts and therapy, his wearable defibrillator was discontinued. At five months, his amiodarone was discontinued and a monitor was utilized two weeks afterwards, which revealed the return of frequent PVCs and sustained ventricular tachycardia. He had mild symptoms of palpitations and fatigue. He was noted to have a dominant PVC that at times triggered ventricular tachycardia, although the VT was also noted to initiate spontaneously (Figures 2A and 2B). Following these results, another CT pulmonary angiogram was performed, which revealed resolution of lobar and central PEs with minimal residual subsegmental disease with re-cannulation. As the patient did not desire to take any further antiarrhythmics, ablation of his PVC and VT was planned. A cardiac MRI revealed a structurally normal heart with normal LV function with no late gadolinium enhancement.
EP Study and Ablation
The patient was brought to the electrophysiology laboratory in a fasting state. Prior to administering any sedation, he was noted to have frequent PVCs (Figure 3), which were captured on the recording (GE CardioLab) and mapping (CARTO 3, Biosense Webster, Inc., a Johnson & Johnson company) systems. The patient was then sedated with IV propofol (without other medications) for the remainder of the case to avoid any arrhythmia suppression. He continued to have arrhythmias while deeply sedated with propofol.
Venous and arterial access were obtained. Heparin was administered and an ACT of 300-350 seconds was targeted when prolonged left-sided ablation was performed. An intracardiac echo (ICE) catheter was advanced into the right ventricular outflow tract. ICE was used to confirm the absence of a baseline pericardial effusion and to draw contours of the ventricles, aortic valve, and the course of the left main and LAD coronary arteries, which were integrated with electroanatomic mapping. A quadripolar catheter was advanced into the right ventricular apex.
The ablation catheter (THERMOCOOL SMARTTOUCH D/F bidirectional catheter, Biosense Webster, Inc., a Johnson & Johnson company) was then advanced into the right ventricular septum and outflow tract. Baseline measurements of the patient’s conduction were taken, which were normal. Activation points in the right ventricle were late, suggesting that the PVCs were left sided. The left ventricle was then accessed via a retrograde aortic approach with the ablation catheter. Of note, when crossing the aortic valve, a left bundle branch block developed that persisted until the end of the case. Measurements at the left-sided bundle of His revealed slight delay below the His. This bundle branch resolved during follow-up.
Activation mapping was then performed at the mitral annulus. At the inferomedial mitral annulus, activation timing was very early (-30 ms pre QRS) (Figure 4) and accurate pace maps (98% match) were observed. Ablation was then performed in this region up to 50 W (gradual titrating up from 40W) for lesions up to one minute. This eliminated the PVC. Isoproterenol was then infused up to 2 mcg/min and one milligram of calcium chloride was administered intravenously. During programmed ventricular stimulation, sustained ventricular tachycardia (Figure 5) matching the clinical tachycardia seen on the monitor was reproduced. Given the slurred morphology and early precordial transition, the decision was made to initially map the coronary venous system.
The ablation catheter was advanced into the coronary sinus (CS) under guidance by ICE, intracardiac mapping, and fluoroscopy. The catheter was then advanced into the great cardiac vein and eventually into the anterior interventricular vein (AIV). Pace mapping was then performed, which revealed a good pace map (97% match) in the AIV. A coronary angiogram was performed to visualize the relationship between the coronary arteries and ablation. Despite multiple views, advancing and pulling back the ablation catheter, the catheter was too close to the coronary vasculature (<5 mm) to allow safe delivery of radiofrequency (RF) (Figures 6A and 6B).
Higher resolution mapping of the CS was then undertaken. The ablation catheter was removed, and a venous sheath was exchanged for a braided 80 cm 10 Fr Arrow sheath (Teleflex). The ablation catheter was advanced into the coronary venous system and AIV. The sheath was advanced over the ablation catheter into the great cardiac vein under fluoroscopy. The ablation catheter was then removed, and a 20-pole (2-5-5-2 spacing) Map-iT catheter (Access Point Technologies EP, Inc.) was advanced through the sheath and down the AIV. The arrow sheath was withdrawn into the proximal CS. The patient was having spontaneous PVCs from the site of VT at this point. Excellent bipolar and unipolar signals were noted (-30 ms pre-QRS) (Figure 7) at the most distal poles of the Map-iT catheter. This location was similar although slightly farther down the AIV than the point identified by the ablation catheter. The catheter position was then shadowed on the mapping system, and the catheter and sheath were removed from the coronary venous system.
The location of this likely site of origin was studied relative to other structures identified on the electroanatomic and ICE contour maps. The LVOT just below the left coronary cusp (LCC) was directly opposite this point in the AIV, and appeared to be a safe location to map and ablate. The ablation catheter was again advanced into the left ventricle via a retrograde aortic approach. Using the D-curve, a loop was maintained and the catheter was withdrawn into the LVOT with the tip in the LV ostium. The loop was released in the LV ostium with the tip just below the LCC with good contact force and stability. This position was approximately 8 mm from the earliest target site noted in the AIV with the Map-iT catheter. RF was delivered in this region up to 50 watts for up to one minute. During RF, automaticity matching the VT was observed that accelerated, slowed, and then terminated. Several lesions were delivered in this area (Figure 8).
The ablation catheter was then withdrawn. A 30-minute waiting period was undertaken, during which isoproterenol was infused up to 6 mcg/min and another one milligram of calcium chloride was administered. No arrhythmias were noted despite aggressive ventricular stimulation. After a final ICE survey, the procedure was terminated.
Ablation of arrhythmias originating from the LV summit will continue to pose a significant challenge to practicing electrophysiologists. The challenge of determining a safe ablation site with a low risk of collateral damage has fostered a number of unique ablative approaches. Operators should be prepared to explore multiple strategies, as anatomy in this region is highly variable and one approach does not fit all patients.
Sequential unipolar ablation from the endocardium of the outflow tracts, aortic cusps, coronary venous system, and left atrial appendage have all been reported as successful target sites and are a good first approach in idiopathic ventricular arrhythmias.3 Sequential unipolar ablation provides sufficient lesion depth for many cases and can be done safely.2 Care should be made to understand the coronary anatomy if ablation in the AIV, anterior RVOT, or close to the pulmonic valve is to be undertaken. As in our case, a coronary angiogram was performed to avoid rare yet potentially catastrophic coronary complications.
Our case highlights the value of high resolution activation and pace mapping in the coronary sinus to determine the best ablative sites in the coronary sinus and closely related structures. The small and flexible design of the Map-iT catheter permits mapping the distal CS and its branches at a lower risk of vessel perforation. In our procedure, the successful ablation site within the left ventricular ostium was of sufficient proximity to the AIV to eliminate the VT focus. If a site can support higher power RF for a reasonable duration, lesion delivery from adjacent structures to a putative site of origin can be quite effective. High power and long duration has the highest likelihood of success due to significantly larger lesion size.4
Epicardial ablation has been reported to be successful when endocardial approaches have failed. However, taking this approach is challenging given proximity to the coronary vessels and epicardial fat. This tactic should typically be reserved for redo cases with appropriate expectations.5
Alternative ablative techniques such as bipolar and lower ionic concentration irrigation have also shown promise for delivering deeper lesions in cases of intramural origins within the LV summit.6,7 These technologies are aimed at delivering lesions deeper into the tissue, which is commonly needed in the case of a deep focus. Promising results have also been described using endoscopic robotic surgery to directly visualize the LV summit and retract coronary arteries for ablation delivery.8 While these technologies show great potential, they are still investigative and are not employed broadly.
Ablation of arrhythmias arising from the left ventricular summit are quite challenging and require mapping of multiple adjacent structures. The coronary vasculature acts as the boundaries of the LV summit and must be visualized to avoid serious potential complications before delivering RF. High resolution mapping of the coronary venous system can be effective at determining successful ablation sites within the CS and at adjacent structures when coronary anatomy is not favorable. Further study and development of novel techniques is needed to improve the efficacy and durability of ablation of LV summit arrhythmias.
Disclosures: The authors have no conflicts of interest to report regarding the content herein.
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- Enriquez A, Malavassi F, Saenz LC, et al. How to map and ablate left ventricular summit arrhythmias. Heart Rhythm. 2017;14:141-148.
- Sosa E, Scanavacca M, d'Avila A. Catheter ablation of the left ventricular outflow tract tachycardia from the left atrium. J Interv Card Electrophysiol. 2002;7:61-65.
- Borne RT, Sauer WH, Zipse MM, Zheng L, Tzou W, Nguyen DT. Longer duration versus increasing power during radiofrequency ablation yields different ablation lesion characteristics. JACC Clin Electrophysiol. 2018;4:902-908.
- Santangeli P, Marchlinski FE, Zado ES, et al. Percutaneous epicardial ablation of ventricular arrhythmias arising from the left ventricular summit: outcomes and electrocardiogram correlates of success. Circ Arrhytm Electrophysiol. 2015;8:337-343.
- Futyma P, Sander J, Ciąpała K, et al. Bipolar radiofrequency ablation delivered from coronary veins and adjacent endocardium for treatment of refractory left ventricular summit arrhythmias. J Interv Card Electrophysiol. 2019 Aug 11.
- Nguyen DT, Olson M, Zheng L, Barham W, Moss JD, Sauer WH. Effect of irrigant characteristics on lesion formation after radiofrequency energy delivery using ablation catheters with actively cooled tips. J Cardiovasc Electrophysiol. 2015;26:792-798.
- Aziz Z, Moss JD, Jabbarzadeh M, Hellstrom J, Balkhy H, Tung R. Totally endoscopic robotic epicardial ablation of refractory left ventricular summit arrhythmia: first-in-man. Heart Rhythm. 2017;14:135-138.