Catheter ablation for idiopathic premature ventricular complexes: a single-centre experience

The most common site of origin of idiopathic premature ventricular complexes (PVCs) is the right ventricular outflow tract (RVOT). This study reports a single-centre UK National Health Service (NHS)-based experience of catheter ablation (CA) for idiopathic PVCs.

We conducted a retrospective review of the electronic patient record, searching for all patients undergoing idiopathic PVC ablation at Guy’s and St Thomas’ NHS Foundation Trust (GSTT) between January 2016 and June 2023. There were 147 procedures performed in 118 patients: 21 patients underwent repeat ablations. There were 75% originating in the RVOT and 11% from the left ventricular outflow tract (LVOT). Acute suppression of PVCs was achieved in 121 procedures (82%). Following acutely successful ablations, PVC burden reduction was greater in RVOT (85% decrease) than LVOT PVCs (44% decrease) at follow-up (p=0.03). There were 12 patients with PVC-induced cardiomyopathy identified. Following successful ablation (n=9), left ventricular ejection fraction (LVEF) increased from 38% to 49%. Symptomatic improvement after ablation was reported by 80%, with 64% having complete symptomatic resolution. Patients experiencing complete symptom resolution had a 92% decrease in PVC burden, whereas patients with residual symptoms had a 76.2% decrease (p=0.03).

Procedural complications occurred in 10 procedures (6.8%): five were classified as major, including four pericardial effusions requiring pericardiocentesis, and one cardioversion for pulseless ventricular tachycardia.

In conclusion, CA is an effective and safe strategy for PVC suppression in idiopathic PVCs, and may result in a significant symptomatic improvement even without complete PVC suppression. Among those with PVC-induced cardiomyopathy, CA results in improved LVEF.

Introduction

Premature ventricular complexes (PVCs) are a common arrhythmia, defined as a propagating impulse arising from an ectopic ventricular focus.¹ When PVCs arise from a single focus, they typically give rise to a monomorphic QRS complex on the surface electrocardiogram (ECG). While most PVCs are benign, in some cases, a high burden of PVCs may be complicated by PVC-induced cardiomyopathy,² and a small proportion of PVCs are implicated in triggering malignant ventricular arrhythmias.³ PVCs arising from the distal Purkinje system have been observed to induce ventricular fibrillation (VF) more commonly than PVCs arising from other sites.⁴ PVCs/ventricular tachycardia (VT) in patients without structural heart disease may be defined as idiopathic PVCs/VT.⁵

Catheter ablation (CA) may be more effective than pharmacologic management of PVCs, and treatment is indicated when patients are symptomatic or when there is a decline in left ventricular (LV) systolic function.⁵ There is a relatively limited amount of data on outcomes of CA for idiopathic PVCs. We report our experience of procedural outcomes and follow-up after CA of idiopathic PVCs in a single National Health Service (NHS) centre.

Materials and method

Data acquisition

We conducted a retrospective analysis of the electronic patient record (EPR) for patients undergoing CA for PVCs at Guy’s and St Thomas’ NHS Foundation Trust (GSTT) between January 2016 and June 2023. We collected information on patient demographics, pre- and post-ablation investigations and anti-arrhythmic medication, procedural characteristics, complication rates, and clinical outcomes.

Pre-procedural data reviewed included 12-lead ECGs, ambulatory ECG monitoring, and cardiac imaging. Cardiac chamber measurements and ventricular function were derived from cardiovascular magnetic resonance (CMR) imaging, and echocardiographic results for those without CMR.

PVC-induced cardiomyopathy was defined in patients with a LV ejection fraction (LVEF) <50% in cases when the LV dysfunction had been attributed to the high PVC burden. Site of origin (SOO) was categorised as right ventricular outflow tract (RVOT), left ventricular outflow tract (LVOT), other right ventricular (RV) locations, and other LV locations. RVOT PVCs were divided into anterior and posterior RVOT SOO. Complications were classified as major and minor, in which major complications required an intervention or resulted in a prolonged hospital visit.

All patients provided written and informed consent for their clinical procedure. Procedures were carried out per the institutional standard of care. The procedures were carried out under conscious sedation or general anaesthesia. Vascular access (venous ± arterial) was acquired using the Seldinger technique under ultrasound guidance. An electrophysiology recording system (Bard – Bard Electrophysiology, Lowell, MA, USA or Sensis – Axiom Sensis EP System, Siemens) was used in combination with an electro-anatomic mapping system (EAMS) and fluoroscopy. A combination of pace and activation mapping was used to localise the SOO of the PVC. For procedures involving access to the LV, unfractionated heparin was given as a series of boluses with regular activated clotting time (ACT) measurements aiming for an ACT >300 s. Power-controlled, temperature-limited radiofrequency (RF) energy was delivered at the identified PVC SOO according to the discretion of the operator. Following treatment, pharmacological provocation was repeated at the discretion of the operator.

Acute procedural success was defined as the complete suppression of targeted PVCs at the end of the clinical procedure. Follow-up ambulatory ECG monitoring was acquired during follow-up at the discretion of the responsible clinician. Pre- and post-ablation PVC burden were determined by 24- or 48-hour Holter monitoring.

Symptoms were assessed at routine clinical follow-up post-ablation. Symptomatic response was classified into complete resolution of symptoms, improvement in symptoms but with residual arrhythmia-related symptoms, or no symptomatic improvement. These data were recorded at first follow-up post-procedure and at most recent follow-up. Further data, including post-procedure implantable cardiac device insertion and malignant outcomes, were recorded.

Statistical analysis

Data were analysed using Statistical Package for Social Sciences software (version 29.0; IBM, Armonk, New York, USA). Continuous, normally distributed, variables are expressed as mean ± standard deviation (SD). Comparison of means for discrete and non-normally distributed variables were done using chi-squared tests, and for continuous variables, independent student t-tests were performed. The null hypothesis was rejected with a p value <0.05.

Results

Baseline/patient characteristics

There were 163 CA planned at GSTT, of which 147 procedures were completed on the day. The 16 ablations not conducted were most commonly due to the absence of PVCs on the day (n=8, 5%), despite isoproterenol provocation in each of these cases. Other reasons for abandoning the procedure included an assessment that the QRS morphology represented an unsuitable target (which was due to perceived proximity to the His bundle in two cases). Two patients presented with multi-focal PVCs on the day, and a decision was made that CA would, therefore, unlikely be effective.

Of the completed procedures, these were undertaken in 118 patients, with repeat procedures in 21 patients. The mean age was 56 ± 16 years (table 1). The mean pre-ablation PVC burden was 20.5 ± 13.1% and the mean LVEF was 51.5 ± 12.7% (table 1). There were 37 patients (31%) with a pre-ablation LVEF <50%. Most patients (90.4%) presented with symptomatic PVCs.

Procedural duration

The mean procedure duration for all acutely successful cases was 157 ± 60 minutes. For acutely successful CA, the mean procedure time was shorter for RVOT ablation when compared with LVOT ablations (p<0.04), and all other locations (p<0.001). The procedure duration was longer in unsuccessful cases (199 ± 54 minutes, p<0.002). There were three cases that were done without fluoroscopy.

Procedural details

Overall, 72.8% of procedures were carried out under conscious sedation and 27.2% under general anaesthesia. Intra-cardiac echocardiography was not used in any cases. The procedures were conducted with the Carto3 (CARTO, Biosense Webster Inc., Diamond Bar, CA, USA), EnSite NavX (Abbott, St. Jude Medical, Saint Paul, MN, USA), or Rhythmia HDx (Boston Scientific, Marlborough, MA, USA) EAMS. Activation mapping was undertaken in 55% of cases and pace mapping in 70% of cases; in 28%, a combination of activation and pace mapping strategies was used. The number of RF applications in each procedure was available in only 32 cases, and in these the average number of RF applications was 12.8 (range 1 to 41). Average radiofrequency duration was 7:00 ± 4:39 minutes (n=41).

Acute success was achieved in 121 (82.3%) of cases (figures 1 and 2). Among acutely successful cases, the most common SOO was the RVOT (n=108, 73.5%). Of the 108 RVOT cases, 41% were mapped to the anterior RVOT and 59% to the posterior RVOT. Acute success according to SOO is shown in table 2. The other LV locations included: lateral LV wall, anteroseptal LV (n=3), basolateral LV, aortomitral continuity, LV summit (n=2), posteromedial papillary muscle, anterobasal LV, anterior mitral valve annulus (n=2), ascending aorta, right coronary cusp. Other RV locations included: RV septum (n=2), posterior papillary muscle, inferolateral basal RV, RV anterior wall, RV inferior free wall, anterolateral papillary muscle, RV annulus.

Outflow tract ablation outcomes

Outcomes are reported for acutely successful outflow tract ablation cases, defined as whether there was good evidence the correct site was targeted. All patients undergoing ablation of idiopathic PVCs arising from the RVOT were younger than patients undergoing ablation of PVCs arising from the LVOT. The procedures targeting LVOT PVCs were numerically longer (although not reaching statistical significance) and associated with a lower acute success rate and a higher PVC burden on repeat ambulatory ECG monitoring, despite acute success (table 2).

Repeat ablations

Overall, 21 patients (14.3%) underwent repeat ablation procedures: 16 patients had a total of two ablations, two patients had a total of three ablations, and three had a total of four ablations. The acute success rate for the first ablation procedures was 66.7%. This increased to 81.0% for final ablation procedures. The targeted SOO changed in 57% of cases.

Symptomatic improvement

On average, first clinical follow-up occurred 5.7 ± 0.7 months after ablation. Post-ablation symptom data were collected from clinic notes, which were available after 124 cases. In acutely successful ablations with PVC-related symptoms, 79.7% experienced symptomatic improvement after ablation. Of those with symptomatic improvement, 63.6% experienced a complete resolution to their symptoms.

Patients experiencing complete symptom resolution had a 92.1% decrease in PVC burden (pre-CA 19.8%, post-CA 1.6%), whereas patients with residual symptoms had a 76.2% decrease (pre-CA 13.3%, post-CA 3.2%) (p=0.03).

In total, 10 patients had a modified European Heart Rhythm Association (EHRA) score of 1, i.e. asymptomatic at baseline, which increased to 54 at first follow-up; 57 patients had an EHRA score of 2, i.e. mildly symptomatic, which decreased to 34 at first follow-up; 16 patients had an EHRA score of 3, i.e. severely symptomatic, which decreased to 8 at first follow-up. All eight patients with severe symptoms after ablation had no symptomatic improvement following CA.

PVC-induced cardiomyopathy

There were 12 patients (10.2%) identified with PVC-induced cardiomyopathy. Following ablation, the mean PVC burden decreased from 21.6% to 9.3%, and LVEF improved from 37.9% to 48.6%, representing a 56.9% absolute decrease in PVC burden and a 28.2% absolute increase in LVEF. Two patients had biventricular pacing after CA.

Procedural complications

There were procedural complications in 10/147 procedures (6.8%): five cases (3.4%) were classified as major and five cases (3.4%) as minor. The most common major complication was pericardial effusion requiring pericardiocentesis (n=4); one patient developed pulseless VT requiring direct-current cardioversion. Minor complications included haemodynamically non-significant pericardial effusions managed conservatively (n=4). The final minor complication was a bleeding complication at the vascular access site in the groin.

Anti-arrhythmic medication

The most prescribed drug class was beta blockers, including bisoprolol, metoprolol, carvedilol, and sotalol. Prescribed calcium-channel blockers were verapamil and diltiazem. Anti-arrhythmic drugs were prescribed pre-ablation in 89% of patients, this decreased to 54% post-ablation: 6.9% (n=10) were taking two anti-arrhythmic drugs pre-ablation and 5.5% (n=8) post-ablation.

Discussion

Main findings

We report a single-centre experience of idiopathic PVC ablation within the NHS. In this contemporary cohort, CA has been shown to be an effective strategy for PVC suppression in the context of idiopathic PVCs, and can result in significant symptomatic improvement, even without complete eradication of PVCs. The overall acute ablation success rate of this cohort was 82.3%, with a low rate of serious complications (3.4%). In the PVC-induced cardiomyopathy cohort, successful PVC ablation resulted in improved LV function and reduced PVC burden.

Ablation outcomes

CA for idiopathic PVCs is often effective in reducing symptomatic burden from PVCs, while treating PVC-induced cardiomyopathy. PVCs originating from the RVOT had greater acute success than LVOT, which is consistent with previously published studies. A US multi-centre study,⁷ looking at 1,185 patients across eight centres who underwent CA for idiopathic PVCs from 2004 to 2013, found the significant predictors of acute success were PVC location (odds ratio [OR] 3.78, confidence interval [CI] 1.87 to 7.60) with the highest success achieved in the RVOT. Factors associated with reduced acute success included an epicardial SOO of PVCs (OR 0.49, CI 0.27 to 0.91) and multi-focal PVC configurations (OR 0.89, CI 0.82 to 0.98). RVOT SOO location was the only significant predictor of continued success at follow-up. This is consistent with the current cohort, in which a greater decrease in PVC burden at follow-up was seen in the RVOT group when compared with the LVOT group (85.1% vs. 44.2%, respectively).

CA is usually considered the most effective means for durably suppressing monomorphic PVCs. A prior study looking at the relative efficacy of CA, as compared with anti-arrhythmic drugs (AAD), in treating PVCs suggested CA resulted in better overall outcomes than AADs.⁸ Notably, a 61.6% decrease in PVC burden was observed in follow-up Holter monitoring in patients who underwent CA, as compared with those on AADs. This was taken at 6.3 ± 2.4 months after therapy, a similar interval to this cohort. Of note, in the prior study, the relative efficacy of CA compared with AAD was dependent on the SOO of the PVC. Specifically, CA was more effective than AAD in reducing PVC frequency in all PVC origins except for the RV non-outflow tract PVCs. While this study did not specifically compare the efficacy of CA with AAD, the procedural outcomes following CA are consistent with these prior data, and indicate that good outcomes may be seen following CA of idiopathic PVCs.

The US multi-centre study conducted by Latchamsetty et al.⁷ achieved acute success (by the same definition) in 84% of cases, which is comparable with the results in this report (82.3%). One difference in our cohort was the use of intracardiac echocardiography (ICE); some sites included in the US study used ICE for CA.⁷

Left versus right SOO

The older age group of those treated for LV PVCs indicates the possibility that the emergence of LV PVCs may, at least in part, reflect age-related structural remodelling, specifically the development of fibrosis, as a more significant contributory mechanistic factor. Our data indicate less successful outcomes following ablation of LV PVCs. This finding is consistent with previous reports as well.⁹ We hypothesise that the outcomes in this group reflect this underlying pathophysiologic process, as well as procedural aspects that may make LV PVC ablation more difficult. Sub-clinical age-related myocardial fibrosis would be expected to result in a more diffuse anatomic substrate. This adds to the technical aspects of treating LV PVCs, which include anatomic factors, such as thicker tissue, proximity to the coronary arteries and aortic valve cusps, which represent important considerations during attempted ablation in the LV.

PVC-induced cardiomyopathy

There a number of proposed mechanisms by which PVCs can result in cardiomyopathy. One proposed mechanism for PVC-induced cardiomyopathy is ventricular dyssynchrony induced by frequent PVCs.^10,15 Following a PVC, there is disruption of the normal sequence of ventricular contraction, leading to asynchronous myocardium activation. The adverse effects of dyssynchrony, especially when PVC burden is high, are similar to those seen in left-bundle branch block or chronic right ventricular pacing. This abnormal contraction pattern increases myocardial workload (inducing asymmetrical myocardial hypertrophy), alters myocardial blood flow and reduces contractile efficiency, which may contribute to the development of chronic LV dysfunction.

Another potential contributory mechanism is neurohormonal activation due to the PVCs increasing sympathetic drive and contributing to maladaptive structural remodelling. Indeed, cyclic adenosine monophosphate (cAMP)-mediated activity has been postulated as a potential mechanism in selected patients, with long-term exposure to PVCs leading to transient alterations in ionic currents, and myocardial and peripheral vascular autonomic stimulation/inhibition. PVC-induced cardiomyopathy only develops in a subset of individuals with a high burden of PVCs, and it is likely that genetic factors represent a critical risk factor, resulting in a vulnerable myocardial substrate for the development of PVC-induced cardiomyopathy. The specific genetic factors that predispose to the development of PVC-induced cardiomyopathy are yet to be fully characterised, but include those with a genetically mediated dilated cardiomyopathy (DCM), which is exacerbated by PVC emergence, and to which the genetic abnormality is also likely a contributory factor to the emergence of the PVCs themselves.¹¹

Additionally, the duration and the absence of symptoms are risk factors for the development of PVC-induced cardiomyopathy.¹² However, there remains uncertainty about the optimal timing of intervention. For instance, in most cases, intervention is considered when there is LV dysfunction and a PVC burden greater than 10%. Similarly, European Society of Cardiology (ESC) guidelines suggest consideration of catheter-based intervention if the PVC burden is greater than 20%, even if LV function is preserved.¹³ This is guided by the principle that the development of PVC-induced cardiomyopathy is positively correlated with PVC burden. It is important to note other relevant factors, including PVC-QRS duration and SOO, may determine the degree of dyssynchrony induced by PVCs.¹⁴

Relationship between symptoms and PVC burden

There was a clinically significant correlation between suppression of PVCs and symptomatic benefit, with patients reporting a greater degree of symptom control with a greater suppression of PVCs at follow-up. Despite this, it is important to note that some patients derived a symptomatic benefit despite incomplete suppression of PVCs. Indeed, in general, despite the varying degrees of symptomatic burden our patient cohort reported, ablation resulted in a statistically significant reduction in PVC burden across all groups.

Study limitations

The cohort size in this study is small, which might limit the generalisability of our findings. Another key limitation is the lack of long-term follow-up data. Given the progressive nature of PVC-induced cardiomyopathy and the potential for arrhythmia recurrence, the absence of extended outcome data may affect the ability to comprehensively assess the durability of ablation success and the long-term impact on LV function. Furthermore, the data collection period was influenced by various external factors, notably the COVID-19 pandemic. The widespread disruptions to routine healthcare services during this period led to delays in planned procedures, interruptions in structured follow-up, and potential inconsistencies in data acquisition. These challenges may have introduced bias or gaps in our dataset, potentially affecting the robustness of some findings.

Despite these limitations, our study provides valuable insights into post-ablative outcomes for PVCs and underscores the need for further multi-centre research with larger cohorts and comprehensive long-term follow-up.

Conclusion

In this single-centre NHS Trust experience, CA for PVCs proved to be a safe and effective procedure with favourable outcomes. Our findings also highlight the important role of PVC ablation in patients with PVC-induced cardiomyopathy, where reducing PVC burden can significantly contribute to symptomatic and functional improvement. RVOT PVCs were more successfully suppressed with ablation, and demonstrated greater long-term suppression, compared with non-RVOT PVCs. These results reinforce the value of PVC ablation in appropriately selected patients, and underscore the need for further research to optimise patient selection and long-term management strategies.

Key messages

• Catheter ablation outcomes for idiopathic premature ventricular complexes (PVC) have been reported from centres in the US and within Europe, however, to our knowledge, there are no reports of outcomes from a UK National Health Service (NHS) centre
• In a UK healthcare setting within the NHS, outcomes following PVC ablation are consistent with prior reports
• We have demonstrated that outcomes for right ventricular outflow tract PVCs are more favourable when compared with the left ventricular outflow tract
• Complication rates within a NHS cohort are comparable with other centres in Europe and the US

Conflicts of interest

None declared.

Funding

None.

Study approval

All patients provided informed consent for the procedure. The retrospective study and data use was conducted in accordance with the Declaration of Helsinki following a favourable opinion from Haydock Research Ethics Committee (REC reference 22/NW/0298, IRA project ID 306914).

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