Electrical isolation of the right ventricular outflow tract in idiopathic ventricular tachycardia: a case report

Abstract

Background

Ventricular tachycardia (VT) originating in the right ventricular outflow tract (RVOT) is the most common form of idiopathic VT. Catheter ablation of right ventricular outflow tract tachycardia (RVOT-VT) is associated with high success rates. However, non-inducibility of VT on electrophysiological (EP) study can severely impact ablation outcome. We describe a novel catheter ablation strategy which proved feasible and safe in a case of highly symptomatic, non-inducible RVOT-VT.

Case summary

A 51-year-old male with a history of non-sustained VT (NSVT) was referred to our hospital after two syncopal episodes resulting in collapse. Upon admission, a cluster of monomorphic NSVT (250–270 b.p.m.) resulted in haemodynamic instability and required transfer to the intensive care unit. On twelve-lead electrocardiogram, NSVT showed inferior axis and left bundle branch block, suggestive of RVOT-VT. Diagnostic workup including echocardiography, coronary angiography, and late enhancement computed tomography (CT) revealed no evidence of structural heart disease. On two EP studies, non-inducibility of clinical VT despite repeated ventricular pacing and isoproterenol infusion rendered precise mapping of triggered activity unfeasible. Therefore, a bailout ablation strategy was developed by performing a circumferential electrical RVOT isolation using a 3.5 mm irrigated-tip ablation catheter under the guidance of high-density electroanatomic mapping (CARTO® 3) and CT reconstruction of cardiac anatomy. No procedural complications occurred, and the patient remained arrhythmia-free during a 6-month follow-up period.

Discussion

Catheter ablation is a first-line therapy for symptomatic and drug-refractory idiopathic RVOT-VT. Non-inducibility of RVOT-VT represents a relevant limitation for successful ablation which might be overcome by electrical RVOT isolation as a bailout ablation strategy.

Learning Points.

• Catheter ablation represents a first-line therapy for symptomatic or drug-refractory idiopathic right ventricular outflow tract tachycardia (RVOT-VT) and relies on the precise identification of triggered activity in the right ventricular outflow tract (RVOT) region using mapping strategies.

• Non-inducibility of idiopathic RVOT-VT on electrophysiological study represents a relevant limitation for successful ablation, which might be overcome by electrical RVOT isolation as a novel bailout ablation strategy.

Introduction

Idiopathic ventricular tachycardias (VT) account for 10% of VT diagnoses and occur in patients with no apparent structural heart disease.^1–3 The right ventricular outflow tract (RVOT) is the most common site of origin for idiopathic VT.⁴ Catheter ablation represents the treatment of choice for symptomatic or drug-refractory right ventricular outflow tract tachycardia (RVOT-VT) and is characterized by high success rates.^3–5 However, non-inducibility during the electrophysiological (EP) study may severely impact ablation outcomes.⁶ We describe a novel ablation strategy for non-inducible RVOT-VT which proved feasible and safe.

Timeline

Age 48 y	Initial presentation with dizziness Electrocardiogram (ECG): First diagnosis of monomorphic premature ventricular complex (PVC) and non-sustained ventricular tachycardia (NSVT) on Holter monitoring Transthoracic echocardiography (TTE): No evidence of structural heart disease Coronary angiography: Exclusion of coronary artery disease Diagnostic EP study: Non-inducibility of clinical PVC/VT Therapy: Initiation of pharmacologic therapy with metoprolol 47.5 mg twice daily
3-year interval	Recurrent dizziness and palpitations: Symptom frequency (1–2×/month) and duration (few seconds) were significantly reduced under beta-blocker therapy and therefore not further bothersome to the patient.
Age 51 y	Presentation after two syncopal episodes at rest. Symptom frequency (up to 2–3×/day) and severity (pre-syncope) had gradually increased in the prior 3 months, prompting the patient to seek medical advice. ECG: Recurrent monomorphic NSVT (250–270 b.p.m.) with haemodynamic instability requiring amiodarone infusion and ICU admission Laboratory results: Normal range TTE: Preserved RV and LV function, no evidence of structural heart disease Late enhancement CT: No evidence of CAD, no pathologic late enhancement Diagnosis: Idiopathic RVOT-VT EP study: Non-inducibility of clinical PVC/VT, rendering activation mapping and pace mapping unfeasible Therapy: Circumferential electrical RVOT isolation as bailout ablation strategy Implantation of an implantable cardioverter–defibrillator (ICD) for secondary prevention of sudden cardiac death (SCD)
6-month follow-up off antiarrhythmic drugs	Freedom of any symptoms and of any VT on ICD interrogation. TTE: Preserved LV and RV function (TAPSE 26 mm), no evidence of RVOT obstruction

Case presentation

A 51-year-old male was referred to our hospital after two syncopal episodes at rest resulting in collapse and minor face injury. The patient had a history of arterial hypertension and non-sustained VT (NSVT) which had been diagnosed on Holter 3 years before due to recurrent dizziness. Prior diagnostic workup with echocardiography and coronary angiography had revealed no evidence of structural heart disease and ruled out coronary artery disease (CAD). After a diagnostic EP study had failed to induce clinical VT 3 years before, pharmacological therapy with metoprolol (47.5 mg twice daily) was initiated, which resulted in significant symptom relief. The patient had no family history of SCD and no further comorbidities.

On admission, the patient was in a stable cardiopulmonary condition (pulse 79 b.p.m., blood pressure 150/90 mmHg, SpO₂ 97%) and showed no neurological deficit. Physical examination did not reveal any pathology besides minor face haematoma. The patient reported that symptom frequency and severity had been increasing in the prior 3 months despite continued beta-blocker treatment, culminating in recurrent pre-syncope and two syncopal episodes. Resting ECG showed sinus rhythm without evidence of conduction disturbances or depolarization/repolarization abnormalities (Figure 1). Laboratory results, including electrolytes, creatinine, high-sensitive troponin T, and thyroid-stimulating hormone (TSH), were within normal range. Neurologic workup including cranial computed tomography (CT) and electroencephalography delivered normal results. Echocardiography revealed preserved RV and LV function (TAPSE 25 mm, LV-EF 60%) and no evidence of structural heart disease.

Figure 1.

Twelve-lead resting electrocardiogram on admission shows sinus rhythm (84/min), normal heart axis, normal conduction intervals (PQ 164 ms, QRS 100 ms, QT 368 ms, QTc 435 ms), normal R progression in precordial leads, and no depolarization or repolarization abnormalities.

Within hours after admission, a cluster of symptomatic NSVT (250–270 b.p.m., duration up to 20 s) was noted on telemetry and correlated with clinical signs of hypotension and pre-syncope. Twelve-lead Holter ECG recordings revealed monomorphic NSVT with inferior axis and left bundle branch block (LBBB) morphology, suggestive of RVOT-VT (Figure 2). Premature ventricular complex (PVC) burden was <1% and did not trigger NSVT. The patient was transferred to the intensive care unit, where rhythm stability was achieved with continuous amiodarone and magnesium infusion. Late enhancement cardiac CT showed no evidence of CAD or myocardial scar. While discussing treatment options, the patient expressed his preference for a definitive interventional therapy over a long-term antiarrhythmic drug (AAD) treatment.

Figure 2.

Twelve-lead Holter electrocardiogram (ECG) recordings on the day of admission. (A) Overall diagram illustrating the heart rate trend during the 24 h monitoring period. Note the upstrokes showing abrupt increase in heart rate (>200 b.p.m.), which correspond to ventricular couplets or non-sustained ventricular tachycardia (NSVT) (black bars below). A total of 147 NSVT occurred during this Holter monitoring. (B) Representative rhythm strip (8 mm/s) showing clustering of monomorphic NSVT. Isolated premature ventricular complexes (PVC) were rarely observed (PVC burden <1%) and did not precede NSVT. (C) Twelve-lead ECG tracings (25 mm/s) showing monomorphic NSVT with inferior axis and left bundle branch block (LBBB) morphology with delayed R-wave transition in precordial leads. R-wave transition of ventricular complexes occurred later than in sinus rhythm. V2 transition ratio was 0.4. NSVT occurred with variable coupling intervals (420 ms, left panel, and 280 ms, right panel).

Antiarrhythmic drug therapy was subsequently discontinued 72 h prior to a second EP study that was performed in the conscious patient. High-density electroanatomic mapping of the RV and RVOT region using the CARTO® 3 system and Pentaray™ multipolar mapping catheter (Biosense Webster, Irvine, California) revealed ubiquitous normal voltage and no abnormal potentials (Figure 3A–C). An accessory pathway was ruled out by atrial and ventricular pacing. Despite repeated ventricular rapid burst pacing, programmed ventricular stimulation with up to four extrastimuli, isoproterenol infusion, and the lack of sedation, no clinical PVC or VT was inducible. The RVOT was confirmed as site of origin of the clinical VT using pace mapping. However, precise identification of triggered activity was not possible in the absence of any spontaneous PVC. It was therefore decided to perform an electrical RVOT isolation using radiofrequency (RF) energy. The RVOT was encircled using point-by-point lesions (38 Watt) with a 3.5 mm irrigated-tip ThermoCool SmartTouch® SF ablation catheter (Biosense Webster) under the guidance of electroanatomic mapping and 3D reconstruction of cardiac anatomy on CT using the inHEART software (Figure 3D–I). The His potential was marked by 3D points, and a safety margin to the His bundle was maintained (Figure 3F). Circumferential electrical RVOT isolation was achieved after 26 min RF time and demonstrated by entrance and exit block (Figure 4). No complications occurred, and pericardial effusion was excluded by echocardiography. Post-procedural twelve-lead resting and Holter ECG showed no significant changes. An ICD was placed for secondary prevention of SCD following the ablation procedure. During a 6-month follow-up period off AAD, the patient remained free of symptoms, while freedom of any VT was confirmed on ICD interrogation.

Figure 3.

High-density electroanatomic voltage map (0.5 mV–1.5 mV) of the RV and RVOT is presented in AP, LAO cranial, and PA views before (A–C) and after (D–F) electrical RVOT isolation. Ablation lesions are presented as 3D points encircling the RVOT. Entrance block is demonstrated by the voltage map performed after ablation (D–F). Fast anatomical map of the tricuspid annulus and RA region is presented in light green. Note the marked His potential (indicated by the yellow arrow in C and F), the pulmonary valve level (white dashed line in C and F), and CS catheter (green arrows in B and E). Overlay of electroanatomic map and CT segmentation of adjacent anatomical structures (G–I) shows the aorta and coronary arteries (pink), RV (transparent), LV (dark green), and RVOT with pulmonary artery region (blue). The LV is faded out in (I) to allow a better view on the posterior RVOT region. CS, coronary sinus; RA, right atrium; RV, right ventricle; RVOT, right ventricular outflow tract.

Figure 4.

Voltage map (A–B), intracardiac signals (C), and surface ECG (D) after circumferential RVOT isolation demonstrating exit block. Pacing with the ablation catheter (cycle length 600 ms, output 10 mA; black arrows in D) in the electrically isolated RVOT did not generate RV capture (A–D).

Discussion

This is to the best of our knowledge the first description of a novel catheter ablation strategy for highly symptomatic, non-inducible idiopathic RVOT-VT using electrical RVOT isolation.

Idiopathic ventricular arrhythmia (VA) manifests at an average age of 52.1 ± 17.2 years¹ and is defined by occurrence in patients without apparent structural heart disease and without evidence of a genetic arrhythmia syndrome.^3,5 RVOT-VT is the most common type of idiopathic VT, accounts for 70–80% of cases,^3,5 and frequently occurs as repetitive NSVT at rest.^5,7,8 Other sites of origin for idiopathic VT include the LVOT (16%), fascicular system (10–15%), papillary muscle (2.4–5.2%), moderator band (2.5%), tricuspid annulus (8%), mitral annulus (5%), and epicardium (1.8–9.2%).³ RVOT-VT can be accurately diagnosed and differentiated from LVOT-VT based on the typical twelve-lead ECG pattern presenting an inferior axis and a LBBB with precordial delayed R-wave transition at or after V3. All ECG criteria for RVOT-VT were met in the present case, including a V2 ratio <0.6 and R/S transition later than in sinus rhythm, which is reported to exclude an LVOT origin with 100% accuracy.⁹ Both NSVT with long and short coupling intervals (Figure 2C) were observed in our patient. A previous case series suggested a potential increased risk of syncope or cardiac arrest for the short-coupled variant of RVOT-VT.¹⁰ However, its prognostic significance remains to be determined.

Potential differential diagnoses such as arrhythmogenic right ventricular cardiomyopathy, long QT syndrome, AVRT associated with Mahaim fibres, and transient causes such as electrolyte imbalance were rendered unlikely by above-mentioned findings on ECG, laboratory testing, cardiac imaging, and EP study. The idiopathic nature of the RVOT-VT was further demonstrated by normal echocardiographic and CT findings and confirmed by the lack of substrate on electroanatomic mapping.

According to current European Society of Cardiology (ESC) guidelines and the Heart Rhythm Society (HRS)/European Heart Rhythm Association (EHRA)/Asia Pacific Heart Rhythm Society (APHRS)/Latin American Heart Rhythm Society (LAHRS) expert consensus, catheter ablation is recommended as a first-line therapy in symptomatic and drug-refractory idiopathic RVOT-VT, being a safe procedure with excellent long-term success rates (80–95%).^4,5 Catheter ablation strategies for RVOT-VT are based on the precise identification of triggered activity in the outflow tract region, which is considered the underlying pathophysiological mechanism.^3,4 Activation mapping is the preferred mapping strategy, while pace mapping is a less accurate alternative in case of infrequent ventricular ectopy.^11,12 Therefore, intraprocedural inducibility of PVC/VT is a critical prerequisite for ablation success in idiopathic RVOT-VT.³ Indeed, paucity of PVC during EP study is independently associated with a significantly reduced ablation success rate as compared with frequent intraprocedural PVC (56% vs. 85%) in patients with idiopathic ventricular ectopy.⁶ In the present case, the occurrence of a single clinical PVC would have allowed ablation guided by pace mapping; however, this condition was not fulfilled. A potential residual anti-arrhythmic effect of the amiodarone infusion which had been discontinued 72 h prior to the EP study could have impacted arrhythmia inducibility, considering the serum half-life of 14 days of intravenous amiodarone.¹³ Nevertheless, complete elimination of AAD treatment prior to ablation is often not feasible in unstable patients requiring emergency ablation.

RVOT-VT manifested as haemodynamically relevant NSVT leading to dizziness and syncope and was refractory to beta-blocker therapy. Considering non-inducibility of clinical VT and PVCs on two EP studies, the absence of substrate on electroanatomic mapping, and the patient’s preference for a definitive interventional therapy, a bailout ablation strategy was developed by isolating the RVOT from the rest of the RV myocardium. To the best of our knowledge, there are no alternative ablative strategies available at the present moment for non-inducible idiopathic VA.

This case illustrates that circumferential RVOT isolation is feasible and can be safely performed under the guidance of electroanatomic mapping and CT reconstruction of cardiac anatomy. The procedural endpoint is the documentation of entrance and exit block in the RVOT. Tagging the His bundle is imperative before performing RVOT isolation in order to avoid accidental damage to the conduction system and atrioventricular block. Other potential complications include cardiac tamponade and RVOT obstruction. Therefore, this technique may be considered in experienced EP centres until further validation, while long-term success rates and safety profile have to be assessed in future studies.

Idiopathic RVOT-VT is associated with a good prognosis and with a low risk of SCD.³ However, rare cases of ‘malignant’ RVOT-VT resulting in haemodynamic compromise and syncope are described.^5,10 Considering the two syncopal events, the novel ablation technique applied, and the absence of a validated endpoint for ablation success in our patient, an ICD was implanted for secondary prevention of SCD following the ablation procedure.

In conclusion, non-inducibility of idiopathic RVOT-VT on EP study can represent a relevant limitation for successful ablation which might be overcome by electrical RVOT isolation as a bailout ablation strategy in selected cases.

Lead author biography

Miruna A. Popa obtained her MD degree from Heidelberg University, Germany, in 2017. She currently works in the Department of Electrophysiology at the German Heart Center in Munich and takes research interest in ablation strategies of cardiac arrhythmias.

Supplementary material

Supplementary material is available at European Heart Journal – Case Reports.

 

Funding: None declared.