Therapeutic Effects on Ectopic Burden and LV Ejection Fraction in a Patient With Aortic Stenosis Undergoing TAVR

Abstract

Background

The etiology of reduced left ventricular ejection fraction (LVEF) is often multifactorial, making it difficult to isolate a primary cause.

Case Summary

A patient presented with symptomatic heart failure, severe aortic stenosis, reduced LVEF (35%), and frequent premature ventricular contractions (PVCs). Transcatheter aortic valve replacement led to modest improvement. Syncope later revealed high-degree trifascicular atrioventricular block, prompting cardiac resynchronization therapy (CRT). Despite CRT and optimized medical therapy, LVEF declined, and PVC burden increased. PVC ablation at the left ventricular outflow tract reduced PVC burden to <1%, restoring LVEF to 55%.

Discussion

This case highlights the complex interaction between aortic stenosis, conduction disease, and ventricular ectopy. Although transcatheter aortic valve replacement and CRT offered partial benefit, significant improvement occurred only after PVC ablation, supporting the concept of ectopy-induced cardiomyopathy and its reversibility after rhythm control.

Take-Home Message

In persistent cardiomyopathy, PVCs should be considered a reversible cause, warranting stepwise and multimodal management.

Visual Summary

The etiology of reduced left ventricular ejection fraction (LVEF) often presents a complex interplay of various factors, making it challenging to pinpoint the primary driver of compromised ejection fraction. The intricate relationship between physiological and anatomical changes in aortic stenosis (AS), along with alterations in electrophysiological properties, further add to the complexity of understanding the causative mechanisms. In this case study, we delve into the details of a man in his seventies with AS who initially exhibited symptoms of heart failure. His journey toward recovery involved a transcatheter aortic valve replacement (TAVR) procedure to address severe AS, cardiac resynchronization therapy (CRT) for trifascicular block, right bundle branch block (RBBB) with right-axis deviation and prolonged PR interval and syncope, and ablation for premature ventricular contractions (PVCs). The fundamental premise lies in the expectation that addressing underlying causes such as AS or bundle branch block should ideally result in improvement, if not full recovery, of the LVEF. The absence of such reversibility suggests different plausible scenarios: enduring cardiac tissue damage, remodeling from the initial etiologies, presence of an additional causative factor, or the interaction among the various causative factors. Our objective is to describe the interplay among the mentioned etiologies, ejection fraction dynamics, and ectopic burden, ultimately raising the pivotal question of whether earlier intervention to mitigate ectopic burden could potentially expedite the restoration of the heart to physiological norms.

Case Presentation

A man in his 70s sought medical attention owing to shortness of breath. The initial assessment revealed a reduced ejection fraction at 30% and a ventricular ectopic burden of 30% (Figure 1), showing transition in lead V3, inferior axis, suggesting outflow tract ectopics. He also had RBBB and prolonged PR interval. The journey he subsequently underwent to ameliorate this and other symptoms, and their impact on his ejection fraction and PVC burden are summarized in Figure 2.

Figure 1.

Electrocardiogram Showing Transition in Lead V₃, Inferior Axis, Suggesting Outflow Tract Ectopics

Figure 2.

The Patient Journey From Initial Presentation Through TAVR and Ablation to the Final Outcome

AS = aortic stenosis; AV = atrioventricular; CRT = cardiac resynchronization therapy; DOAC = direct oral anticoagulant; EF = ejection fraction; LV = left ventricle; LVEF = left ventricular ejection fraction; LVF = left ventricular function; LVOT = left ventricular outflow tract; PVC = premature ventricular contraction; TAVI/TAVR = transcatheter aortic valve implantation/reconstruction; TIA = transient ischemic attack.

Severe AS, accompanied by moderate to severe left ventricular (LV) systolic dysfunction, was identified on echocardiography. In response to the severe AS, a TAVR procedure was performed using a 26-mm Edwards Sapien 3.

Follow-up echocardiography post-TAVR showed successful valve placement without leaks and a slight immediate improvement in ejection fraction by 5%. Heart failure medications were commenced. A Holter monitor 3 weeks later revealed a reduced ectopic burden of 22%, accompanied by a first-degree atrioventricular (AV) block and right bundle branch pattern (present before the procedure). However, 2 months later the ectopic burden decreased to 5.5%. The patient had an episode of syncope with evidence of intermittent high-degree AV block. The following month, a CRT pacemaker (left bundle area pacing) was implanted to address the AV block and presyncope with RBBB and impaired LV function.

Concerns persisted as the patient's LV function remained impaired at 35% and even deteriorated back to 30%. Over the subsequent 4 months, medication optimization ensued. Notable considerations included lisinopril to Entresto (sacubitril/valsartan), and the addition of dapagliflozin. He was already taking bisoprolol and spironolactone. Because of a recent episode of paroxysmal atrial fibrillation, the direct oral anticoagulant apixaban was initiated.

In the same month, the patient experienced left amaurosis fugax and hence a transient ischemic attack, leading to the discovery of a 95% stenosis in the left internal carotid artery. Left endarterectomy was performed. Subsequent Holter monitoring indicated persistent PVC at 22% (Figure 3), severely impaired LV function (estimated at 30%), and increase in LV size. Cardiac magnetic resonance imaging confirmed severe LV dysfunction and showed only minimal subendocardial scar inferiorly.

Figure 3.

Trends in Ejection Fraction and Ectopic Burden Over Time, With Significant Event Points Highlighted: TAVR, CRT, and Ablation

CRT = cardiac resynchronization therapy; EF = ejection fraction; PVC = premature ventricular contraction; TAVI/TAVR = transcatheter aortic valve implantation/reconstruction.

Ablation for ventricular ectopics was carried out. The ventricular ectopics had an origin from the LV, just below the TAVR valve, and ventricular ectopic ablation was performed via the transseptal approach, as the TAVR valve precluded the retrograde approach via the aortic valve (Figure 4). Echocardiography in the next month showed an increase in ejection fraction to 40%, with minimal PVC burden of ≤1%.

Figure 4.

Radiographic Imaging of the Heart During Ablation Procedure

The ablation site is indicated, with the origin of the ectopics from the left ventricle, just below the TAVR valve (yellow arrow), which precluded the retrograde approach via the aortic valve and hence required a transseptal approach. The conduction lead is shown also. TAVI/TAVR = transcatheter aortic valve implantation/reconstruction.

Outcome and Follow-Up

The patient continued to improve, with improved exercise tolerance and well-being, and a subsequent echocardiography 12 months later revealed an improved LVEF of 55% to 60%, normal LV size, and only mild LV diastolic dysfunction (Figure 3). A follow-up 18 months later confirmed sustained improvement in ectopic burden (<1%), LVEF, and symptoms.

Discussion

Degenerative AS affects 2% to 4% of people older than 65 years, with one-third experiencing concomitant LV dysfunction.¹ The exhaustion of initial adaptation capacities is attributed to myocyte apoptosis and myocardial fibrosis, leading to LV hypertrophy.² Reversibility of cardiac fibrosis and muscle damage depends on disease extent and matrix cross-linking, determining LV geometry. Although aortic valve replacement improves LV function, about one-third of patients show no significant improvement, associated with a 3-fold increase in 1-year mortality after TAVR.³ This suggests either permanent muscle damage or other factors such as conduction system disorders or ventricular arrhythmias. A high prevalence of arrhythmias and AV conduction disturbances is common with AS,⁴ which may influence the long-term LV function in these patients.

In our patient, who presented with severe high-gradient AS with symptomatic heart failure and impaired LV function, TAVR was necessary given the urgent clinical scenario. Complex PVCs are prevalent in AS patients, and they significantly improve post-TAVR.⁵ Our patient initially improved, with some recovery of LV function and reduction of PVC, but he subsequently experienced PVC burden increase, likely from TAVR-induced tissue injury. TAVR can trigger ventricular arrhythmias owing to automaticity activity or bundle branch re-entry ventricular tachycardia.⁶ While bundle brunch block on the left is the most common TAVR complication, our patient had pre-existing RBBB, predicting significant AV block post-TAVR owing to structural changes, trauma, or infiltrative processes, possibly linked to AS-associated cardiac remodeling.⁶

Bundle branch block can negatively affect LV function by lacking synchrony in LV contraction and causing diastolic dysfunction.⁷ A permanent pacemaker was required post-TAVR in our patient, as he had RBBB and episodes of high-degree AV block. Conduction system pacing was performed for physiological pacing, more effective than epicardial LV lead in LV dysfunction and RBBB patients,⁸ also preventing pacing-induced cardiomyopathy in high-burden RV pacing.

Despite CRT implantation and introduction of heart failure medication, our patient's PVC burden increased, and his ejection fraction subsequently dropped, a strong predictor of mortality in CRT patients.⁹ With the high PVC burden, adequate cardiac resynchronization could not be achieved and may have affected LV function recovery. Alternatively, high PVC burden can independently cause PVC-induced cardiomyopathy, and reducing PVCs can restore LV function. Significant LV function improvement with normalization of LV function was observed in our patient.

The 2019 expert consensus of the Heart Rhythm Society/European Heart Rhythm Association/Asia Pacific Heart Rhythm Society/ Latin American Heart Rhythm Society identifies several key indications for PVC ablation:

• •In patients with structural heart disease, including valvular conditions such as AS, frequent PVCs can exacerbate LV dysfunction. Ablation in such cases may improve cardiac function, even when structural heart disease is the primary pathology (Class IIa, Level of Evidence: B-NR).
• •In clinical nonresponders to CRT, where frequent PVCs reduce the effectiveness of biventricular pacing, ablation can lead to symptomatic improvement and modest increases in LVEF (Class IIa, Level of Evidence: B-NR).
• •When alternative causes of cardiomyopathy have been excluded and PVC burden is believed to be the primary driver, ablation is recommended to reverse LV dysfunction (Class I, Level of Evidence: B-NR).¹⁰

In our patient, ablation was performed in accordance with a Class I indication. However, the timeline of his clinical deterioration raises the question of whether earlier intervention could have mitigated progression and improved outcomes.

Conclusions

This case highlights the physiological impact of AS on LV function, conduction pathways, and ventricular arrhythmias, as well as the effects of TAVR and CRT on ectopic burden and systolic performance. Although each intervention provided incremental benefit, significant and sustained improvement in LVEF (from 35%-55%) occurred only after PVC ablation, supporting a role for ectopy-induced cardiomyopathy. This underscores how cumulative cellular remodeling and ectopic rhythms can disrupt LV function.

Although TAVR may improve LVEF, this case emphasizes the importance of understanding the long-term impact of AS. Persistent post-TAVR dysfunction may reflect underlying arrhythmic contributors requiring additional therapies. Continued research is needed to refine patient selection and improve long-term outcomes. A patient-centered approach and continuous research commitment are crucial for refining strategies and advancing transcatheter interventions in severe AS and LV dysfunction contexts.

Visual Summary.

Impact of Interventions on Cardiac Function

AF = atrial fibrillation; AV = atrioventricular; CRT = cardiac resynchronization therapy; EF = ejection fraction; LV = left ventricle; PVC = premature ventricular contraction; RBBB = right bundle branch block; TAVI = transcatheter aortic valve implantation; TIA = transient ischemic attack.

Funding Support and Author Disclosures

The authors have reported that they have no relationships relevant to the contents of this paper to disclose.

Take-Home Messages

• •This case demonstrates the value of a stepwise, multimodal strategy for managing complex heart failure—adhering to guidelines and escalating care to PVC ablation when clinically warranted.
• •After intervention, continuous monitoring of LVEF and PVC burden is crucial, as ectopy-induced cardiac dysfunction may only become evident once remodeling stabilizes.
• •Persistent cardiomyopathy despite optimization should prompt consideration of PVCs as a reversible factor.