Iatrogenic ventricular septal defect following papillary muscle premature ventricular contraction ablation: a case report

Abstract

Background

Catheter ablation of monomorphic premature ventricular contractions (PVCs) in symptomatic or haemodynamically compromised patients has a Class I recommendation in cardiomyopathy and a Class IIa recommendation in patients comprising non-outflow tract PVC morphology and a physiologic anatomy according to current ESC guidelines. It is therefore widely performed and generally considered safe. Rare but clinically significant complications can occur and may present considerable diagnostic and therapeutic challenges.

Case summary

A 77-year-old woman underwent radiofrequency (RF) catheter ablation for symptomatic PVCs originating from the posteromedial papillary muscle. The acute procedural course was uneventful. Two months later, she presented with progressive dyspnoea. Transthoracic echocardiography revealed a newly developed haemodynamically significant ventricular septal defect (VSD) with left-to-right shunting. Retrospective analysis demonstrated anatomical concordance between the ablation site and the septal defect, suggesting an ablation-related iatrogenic VSD. Transoesophageal echocardiography confirmed an 8 mm defect. Cardiovascular magnetic resonance imaging demonstrated a significant shunt volume (Q_p:Q_s 1.7:1) and corresponding mild-to-moderate aortic, mitral, and tricuspid valve regurgitation secondary to volume overload. Right heart catheterization corroborated haemodynamic relevance. Following multidisciplinary heart team discussion, percutaneous closure was performed using a 12 mm muscular VSD occluder. Post-procedural imaging confirmed stable device position with minimal residual shunting and clinical improvement.

Discussion

Iatrogenic VSD represents a rare but potentially serious delayed complication of RF catheter ablation for PVCs. Given the possibility of insidious onset, new heart failure symptoms or murmurs after ablation should prompt timely multimodality imaging. Structured follow-up may facilitate early detection and appropriate management of this uncommon but clinically relevant complication.

Learning points.

• Ventricular septal defect is a rare but serious, sometimes delayed complication of ventricular catheter ablation. New-onset dyspnoea or haemodynamic instability should prompt urgent evaluation for this complication.

• Diagnosis and management rely on invasive haemodynamic assessment and multimodality imaging to guide interdisciplinary decision-making regarding defect closure.

• In cases with haemodynamic relevance following premature ventricular contraction ablation, percutaneous closure with an occluder should be considered when performed in carefully selected patients by experienced operators.

Introduction

Catheter ablation is an established and effective treatment for symptomatic premature ventricular contractions (PVCs), particularly in patients with a high PVC burden or intolerance to antiarrhythmic therapy.^1,2 Advances in electroanatomical mapping and catheter technology have substantially improved procedural efficacy and safety.³ However, ablation of PVCs originating from left ventricular (LV) papillary muscles remains technically demanding due to complex anatomy, pronounced mobility, and proximity to valvular and septal structures.⁴

Structural complications following ventricular ablation are rare but may include papillary muscle dysfunction, valvular regurgitation, myocardial perforation, and, exceptionally, ventricular septal defect (VSD).⁵ Iatrogenic VSD can present acutely or in a delayed manner and may initially manifest with non-specific symptoms.⁶

Here, we report a case of delayed, haemodynamically relevant iatrogenic VSD following radiofrequency (RF) ablation of PVC originating from the posteromedial papillary muscle and discuss diagnostic and therapeutic considerations.

Summary figure

Timeline of clinical events from premature ventricular contraction ablation to delayed diagnosis and percutaneous closure of the ventricular septal defect.

Case presentation

A 77-year-old Caucasian woman was referred to a tertiary electrophysiology centre for symptomatic PVCs, presenting with palpitations, exertional dyspnoea, and reduced exercise tolerance. Her medical history included hypertension and limited cutaneous systemic sclerosis without known structural heart disease. Twelve-lead electrocardiogram (ECG) showed sinus rhythm with monomorphic bigeminal PVCs displaying a superior axis, positive concordance in leads I and V1–V5, biphasic morphology in V6, and a coupling interval of 540 ms (Figure 1). Transthoracic echocardiography demonstrated preserved LV systolic function without relevant valvular disease. Ambulatory monitoring revealed a PVC burden of 20%.

Figure 1.

Twelve-lead electrocardiogram demonstrating the clinical premature ventricular contraction with superior axis and positive concordance in leads I and V1–V5, positivity in leads I and V1–V5, biphasic morphology in V6, and a coupling interval of 540 ms. PVC, premature ventricular contractions.

Owing to intolerance to beta-blocker therapy, catheter ablation was performed after shared decision-making. At the start of the electrophysiological study, the patient was in sinus rhythm with first-degree atrioventricular block and frequent spontaneous monomorphic PVCs. Ultrasound-guided femoral access was obtained [venous 8-French (F) and 8.5-F; arterial 8.5-F]. Both antegrade transseptal and retrograde aortic access to the LV (Vizigo 8.5 F sheath, mapping catheter SJA 6F 110 cm L-type) were established. Electroanatomical mapping demonstrated a normal LV voltage with a chamber volume of 71 mL. Due to PVC suppression under sedation, mapping and ablation were predominantly guided by pace-mapping, identifying the posteromedial papillary muscle as the site with highest concordance to the clinical PVC morphology (Figure 2A, blue visitags). A total of 30 RF applications [ThermoCool Smart Touch 8F 115 cm D-curve, ablation index (AI) guided RF delivery, median application duration 3948 s] were delivered to the posteromedial papillary muscle (Figure 2A). During one prolonged application, a steam pop with a 25 Ω impedance drop occurred (duration 65 s, maximum power 52 W, temperature 43°C, contact force 14 g). Retrospective review suggested continued RF delivery at this site, resulting in cumulative lesion metrics (AI 629 and AI 416 at the adjacent site). The procedure was otherwise uneventful, with near-complete PVC suppression, stable haemodynamics, and no immediate structural abnormality on echocardiography.

Figure 2.

Electroanatomical left ventricular map demonstrating normal voltage distribution and ablation sites at the posteromedial papillary muscle (red tags) (A). Subsequent transthoracic and transoesophageal echocardiography demonstrated spatial concordance between the ablation region and the ventricular septal defect location (B–E), supporting an iatrogenic origin. PVC, premature ventricular contractions; RF, radiofrequency; VSD, ventricular septal defect.

Two months later, the patient presented with progressive dyspnoea and a new holosystolic murmur. Echocardiography revealed a new VSD with left-to-right shunting, and moderate tricuspid regurgitation. N-terminal prohormone of brain natriuretic peptide levels were elevated. Retrospective review of the electroanatomical map demonstrated spatial concordance between the ablation site and the location of the VSD, suggesting an iatrogenic defect (Figure 2B–E). Transoesophageal echocardiography (TOE) confirmed an 8-mm VSD with significant left-to-right shunt. Cardiac magnetic resonance (CMR) imaging demonstrated a Q_p (pulmonary flow) to Q_s (systemic flow) ratio of 1.7, confirming haemodynamic relevance (Figure 3A–C), and moderate multivalvular regurgitation likely secondary to shunt-related volume overload (Figure 3D). Right heart catheterization confirmed a post-capillary pulmonary wedge pressure of 16 mmHg, mean pulmonary artery pressure of 27 mmHg, pulmonary vascular resistance of 2.0 Wood units, and Q_p:Q_s of 1.5.

Figure 3.

Cardiac magnetic resonance imaging confirming a haemodynamically significant ventricular septal defect with left-to-right shunt (Q_p:Q_s 1.7) (A–C). Three-chamber view demonstrating associated aortic regurgitation and a narrow membranous rim on the right ventricular aspect of the defect (D). CMR, cardiac magnetic resonance imaging; Q_p, pulmonary flow; Q_s, systemic flow; VSD, ventricular septal defect.

Following interdisciplinary heart team discussion, percutaneous VSD closure was performed. Owing to a narrow membranous rim on the right ventricular side (Figure 3D), a transseptal approach was chosen. After transseptal puncture and mitral valve crossing, the defect was wired (6F internal mammary artery catheter in 12-F steerable sheath; Oscor™, Integer Holdings®; Supplementary material online, Video S1). As initial wire back-up was insufficient to advance the delivery sheath, contralateral femoral access was obtained, and an arteriovenous rail was established using a snare (see Supplementary material online, Video S2). An 8-F Amplatzer™ delivery sheath was advanced from right to left across the defect (see Supplementary material online, Video S3). Repeated measurements confirmed a VSD diameter of 8.3–8.5 mm (Figure 4A). Finally, a 12-mm Amplatzer™ muscular VSD occluder was successfully deployed with immediate reduction of shunting (Figure 4B–D, Supplementary material online, Videos S4 and S5).

Figure 4.

Transoesophageal echocardiography and transthoracic echocardiographic imaging before and after implantation of a 12-mm Amplatzer™ muscular ventricular septal defect occluder. Pre-procedural transoesophageal echocardiography confirmed an 8-mm defect with significant left-to-right shunt (A). Post-deployment imaging demonstrated correct device positioning with immediate reduction of shunting (B–D). Follow-up transthoracic echocardiographic confirmed stable device position with minimal residual shunt (E–G). TOE, transoesophageal echocardiography; TTE, transthoracic echocardiography; VSD, ventricular septal defect.

The post-procedural course was uneventful. Follow-up echocardiography demonstrated stable device position with a minimal residual shunt (Figure 4E–G), while repeat ECG monitoring at 2 weeks showed negligible PVC burden and marked symptomatic improvement.

Discussion

This case illustrates a rare but clinically relevant delayed structural complication following LV catheter ablation. Papillary muscle ventricular arrhythmias (VAs) pose specific technical challenges due to catheter instability, myocardial thickness, and proximity to valvular and septal structures.^7–9 Achieving durable lesion formation often requires repeated or high-energy RF applications, increasing the risk of deep thermal injury. Consequently, ablation outcomes for papillary muscle VAs are often less favourable than for VAs originating at other LV sites.^4,9

Myocardial perforation is an uncommon, but recognized complication of VA ablation.^8,9 Steam pops represent a well-described mechanism associated with acute tissue disruption and may indicate excessive myocardial heating.⁹ In the present case, the documented steam pop during RF delivery likely constituted the initiating event leading to delayed septal tissue necrosis and subsequent VSD formation. The absence of immediate structural abnormalities suggests a progressive process rather than acute perforation. Importantly, post-procedural clinical assessment and transthoracic echocardiography may initially remain unremarkable despite evolving tissue injury. Adjunctive intracardiac echocardiography may improve procedural guidance and facilitate early detection of impending overheating,¹⁰ although its ability to fully prevent steam pops remains uncertain.

Emerging technologies such as pulsed-field ablation may offer a promising alternative, with early data demonstrating safe, effective lesion formation, including in challenging substrates, and potential advantages over conventional thermal ablation.^11,12 First-in-human results demonstrate high acute success and substantial reduction in ventricular tachycardia burden in scar-related disease.¹³ Further studies are required to establish long-term safety and efficacy.

Delayed presentation may complicate diagnosis. Symptoms are often non-specific and may include dyspnoea, fatigue, palpitations, or signs of heart failure. The detection of a new holosystolic murmur, rising natriuretic peptide levels, or unexplained clinical deterioration following ventricular ablation should prompt immediate echocardiographic assessment.⁶ Transthoracic echocardiography remains the cornerstone of diagnosis,¹⁴ while multimodality imaging, including TOE, CMR imaging, and invasive haemodynamic assessment, may be required to determine shunt severity and guide management.

Management strategies are guided by defect size, haemodynamic impact, and clinical status. Haemodynamically significant VSDs typically require intervention, either percutaneously or surgically, with treatment decisions best determined within a multidisciplinary heart team.¹⁵ In this case, percutaneous device closure provided effective haemodynamic correction with raid symptomatic improvement.

In conclusion, clinicians should maintain suspicion for structural complications following papillary muscle ablation, particularly when new murmurs or heart failure symptoms occur. Judicious energy delivery, awareness of steam pop risk, and early echocardiographic assessment may facilitate timely diagnosis and management of this rare but potentially serious complications. Structured follow-up 4–6 weeks after ablation may facilitate early detection of delayed complications, particularly following complex procedures.

Lead author biography

Maria Luisa Benesch Vidal is a junior cardiologist currently in training at the University Heart and Vascular Centre in Hamburg, Germany. She completed her medical studies at the University of Münster, Germany, where she also completed her doctoral thesis on the use of artificial intelligence in the diagnosis and prognostic assessment of PAH. Her investigatory fields of interest comprise clinical research in heart failure, arrhythmias and congenital heart disease.

Supplementary material

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

Author contributions

Maria Luisa Benesch Vidal (Conceptualization, Data curation, Investigation, Writing—original draft [lead], Formal analysis, Methodology, Project administration, Resources, Software, Supervision, Validation, Visualization, Writing—review & editing [equal]), Niklas Schenker (Conceptualization, Validation, Writing—review & editing [equal], Data curation, Resources, Software [supporting]), Katharina Alina Riedl (Data curation [supporting], Resources, Visualization, Writing—review & editing [equal]), Daniel Kalbacher (Conceptualization, Resources, Writing—review & editing [equal], Data curation, Formal analysis, Software, Supervision, Validation, Visualization [supporting]), and Andreas Rillig (Conceptualization, Project administration, Supervision, Validation, Writing—review & editing [lead], Data curation, Investigation, Methodology, Software, Visualization [equal])

Consent: Written informed consent was obtained from the patient for publication of this case report. The report was prepared in accordance with the ethical standards and best practice guidelines of the Committee on Publication Ethics (COPE).

Funding

N.S. has received educational grants from Boston Scientific, Johnson & Johnson and travel grants from the German Society of Cardiology and serves as an Associate Editor of this journal. In accordance with the journal’s policies on editorial independence and conflicts of interest, he had no involvement in the peer review process, the evaluation of the manuscript, or the editorial decision-making pertaining to this article. D.K. has received personal fees from Abbott Medical, Edwards Lifesciences, Medtronic Inc. and Pi-Cardia Ltd. A.R. served as a consultant for Medtronic, KODEX-EPD, Biosense Webster, Boston Scientific, and received travel grants and lecture fees from Medtronic, Cardiofocus, Biosense Webster, Abbott, Boehringer Ingelheim, Philips KODEX-EPD, Ablamap, Bayer, Novartis, Lifetech, Boston Scientific. All of these outside the submitted work.

Data availability

The data underlying this article will be shared on reasonable request to the corresponding author. Further details regarding the patient’s medical history beyond those presented in this case report cannot be shared without explicit patient consent.

Ethics statement

The authors are accountable for all aspects of the work in ensuring that questions related to the accuracy or integrity of any part of the work are appropriately investigated and resolved.