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. 2026 Jul 8;108(3):991–994. doi: 10.1002/ccd.70743

The Hidden Burden of Iatrogenic Atrial Shunting in Severe Tricuspid Regurgitation: A Case Report

Clara Lopiano 1,2, Beatrice Pezzuto 1, Manuela Muratori 3, Carlo Vignati 1,✉
PMCID: PMC13532500  PMID: 42419354

ABSTRACT

Background

Iatrogenic atrial septal defects (iASDs) following transseptal puncture are usually benign. However, in the presence of severe tricuspid regurgitation (TR), even small defects may become hemodynamically significant, leading to hypoxemia and worsening right heart failure.

Aims

To describe the clinical and hemodynamic consequences of a persistent iASD after heterotopic caval valve implantation in a patient with severe TR and the outcome of percutaneous ASD closure.

Methods and Results

We present the case of an 82‐year‐old woman with severe TR and a persistent iASD following atrial fibrillation ablation, who developed progressive exertional desaturation evolving into resting hypoxemia. Because of prohibitive surgical and transcatheter risk for tricuspid valve repair or replacement, a heterotopic caval valve implantation was performed as a palliative strategy to reduce systemic congestion. Although the procedure was technically successful, hypoxemia worsened due to increased right‐to‐left shunting. Percutaneous ASD closure resulted in immediate normalization of systemic oxygenation and substantial improvement in symptoms and exercise capacity.

Conclusions

Heterotopic caval valve may increase right atrial pressure and unmask or exacerbate right‐to‐left shunting in patients with pre‐existing interatrial defects. Comprehensive hemodynamic evaluation and a tailored, stepwise management strategy are essential.

1. Introduction

Transcatheter ablation of atrial fibrillation (AF) can lead to rare yet clinically significant complications, such as the formation of iatrogenic atrial septal defects (ASDs) [1, 2]. In cases of severe tricuspid regurgitation (TR), the resulting interatrial shunt can become relevant from a hemodynamic perspective over time, leading to progressive right‐sided heart failure and hypoxemia [3, 4]. Thorough hemodynamic assessment and a personalized therapeutic approach are required for clinical management.

2. Case Presentation

An 82‐year‐old woman with a complex cardiovascular history was referred for evaluation after episodes of right‐sided heart failure and hypoxemia. Her medical history included three‐vessel percutaneous coronary intervention in 2015, implantation of a dual‐chamber pacemaker for bradycardia–tachycardia syndrome, surgical aortic valve replacement with concomitant left atrial appendage closure in 2018. She had paroxysmal AF and underwent transcatheter ablation in 2019, which was complicated by the development of an iatrogenic ASD (iASD). Post‐procedural echocardiography demonstrated a defect measuring 5 × 7 mm following a single transseptal puncture.

Initially, the shunt was predominantly left‐to‐right, with intermittent bidirectional flow in the context of moderate TR. Exertional oxygen desaturation, which resolved spontaneously, was observed only at peak exercise during cardiopulmonary exercise testing (CPET), beyond the anaerobic threshold (VT1), a level more representative of daily activities, particularly in frail patients.

Right heart catheterization performed in 2021 demonstrated a Qp/Qs ratio of 1.29:1, normal pulmonary vascular resistance (1.78 WU), and preserved right ventricular size and function (right atrial pressure 16 mmHg; pulmonary artery pressure 35/14/23 mmHg; pulmonary capillary wedge pressure 16 mmHg; cardiac index 2.08 L/min/m2). Although exertional desaturation was reproduced during CPET, closure of the iASD was not pursued based on an integrated clinical and hemodynamic assessment. The Qp/Qs ratio at rest was 1.29:1, consistent with a net left‐to‐right shunt; however, in the presence of bidirectional flow, this parameter reflects only the balance between opposing shunt components and may underestimate the overall hemodynamic impact of the defect. No significant right ventricular volume overload or dysfunction was observed. Importantly, the patient had heart failure with preserved ejection fraction (HFpEF) with mildly elevated left atrial pressure, suggesting that the interatrial communication may have contributed, at least in part, to left atrial decompression. In this context, closure of the defect carried a potential risk of increasing left‐sided filling pressures and worsening symptoms. Therefore, a conservative management strategy was considered appropriate. Over subsequent follow‐up, TR progressed from moderate to severe, with echocardiography revealing severe leaflet tethering and pacemaker lead interference with coaptation (Figure 1).

Figure 1.

Figure 1

Severe functional tricuspid regurgitation caused by right ventricular pacing lead interference with the septal leaflet. [Color figure can be viewed at wileyonlinelibrary.com]

In 2022, the patient was hospitalized for right‐sided heart failure. Following effective treatment, she remained stable at follow‐up until 2025, when she was hospitalized twice for right‐sided heart failure refractory to maximal medical therapy.

Comprehensive echocardiographic reassessment revealed a dilated and dysfunctional right ventricle (indexed end‐diastolic volume 94 mL/m2, TAPSE 8 mm, FAC 30%), massive TR, and a bidirectional interatrial shunt (ASD measured 10 × 15 mm) (Figures 2 and 3). The left ventricle remained normal in size with preserved systolic function (LVEF 60%). The mechanism of TR was due to impingement of the right ventricular pacing lead on the septal leaflet, resulting in restricted motion and lack of leaflet coaptation. The coaptation gap measured approximately 10 mm, hampering the feasibility of an edge‐to‐edge repair (Figure 4). She developed resting desaturation (SpO2 85%–90%), necessitating supplemental oxygen. Hemodynamic reassessment revealed a Qp/Qs of 1.22:1, pulmonary arterial pressures of 30/15/21 mmHg, pulmonary capillary wedge pressure of 13 mmHg, cardiac index of 2.05 L/min/m2, and pulmonary vascular resistance of 2.35 WU.

Figure 2.

Figure 2

Subcostal transthoracic echocardiography demonstrates color‐flow Doppler evidence of shunting across the iatrogenic atrial septal defect. [Color figure can be viewed at wileyonlinelibrary.com]

Figure 3.

Figure 3

Transesophageal echocardiography confirms a 15‐mm iatrogenic ASD with predominant right‐to‐left flow on color Doppler. [Color figure can be viewed at wileyonlinelibrary.com]

Figure 4.

Figure 4

Impingement of the pacing lead on the septal leaflet producing a 10 mm coaptation gap and precluding edge‐to‐edge repair. [Color figure can be viewed at wileyonlinelibrary.com]

Following a multidisciplinary evaluation, both surgical and transcatheter correction of the tricuspid valve disease were deemed unfeasible. Lead extraction or repositioning was not pursued due to the high procedural risk related to lead dwell time and patient frailty, and because TR was considered multifactorial. A less invasive approach was therefore adopted after Heart Team evaluation. Given that direct intervention on the tricuspid valve was not possible, a heterotopic approach was adopted, involving implantation of a caval valve prosthesis (TricValve system, 25–35 mm) as a safer, palliative strategy [5].

Despite procedural success, she developed worsening cyanosis and hypoxemia shortly after the procedure, consistent with increased right‐to‐left shunting. Cardiac catheterization demonstrated elevated right atrial pressure (21 mmHg), increased right ventricular systolic pressure (46 mmHg), mild pulmonary hypertension (mean pulmonary artery pressure 28 mmHg), and elevated left atrial pressure (pulmonary capillary wedge pressure 26 mmHg).

The hemodynamic changes observed after TricValve implantation likely reflect a complex interplay between right‐ and left‐sided cardiac physiology. In this patient with HFpEF, the increase in pulmonary capillary wedge pressure may be partly explained by restoration of effective right ventricular forward flow following elimination of caval reflux, resulting in increased pulmonary blood flow and left atrial filling in the setting of reduced diastolic compliance. In addition, interatrial coupling via the pre‐existing iASD may have contributed to transmission of elevated right atrial pressures to the left atrium, thereby contributing to the increase in left‐sided filling pressures, while also favoring right‐to‐left shunting and consequent systemic desaturation.

A balloon occlusion test of the iASD resulted in immediate normalization of systemic oxygen saturation (from 86% to 100%) without any increase in left ventricular filling pressures, confirming the safety and hemodynamic benefit of closure. Percutaneous closure of the iASD was therefore performed using a 27‐mm Cardioform ASD occluder (Figure 5).

Figure 5.

Figure 5

Fluoroscopic frame showing successful implantation of the TricValve system (SVC and IVC) and Cardioform ASD occluder positioned at the atrial septum.

Post‐procedural evaluation showed complete closure with no residual shunt and normalization of oxygen saturation (Figure 6). CPET confirmed the resolution of exertional desaturation and demonstrated improvement in ventilatory efficiency (VE/VCO2 slope from 77 to 48, end‐tidal pressure of CO2 at anaerobic threshold from 19 to 32 mmHg) and a reduction of dead space (VE/VCO2 at anaerobic threshold from 64 to 34 mmHg, VE/VO2 at anaerobic threshold from 60 to 32 mmHg) [6]. The patient experienced marked improvement in symptoms and overall clinical status.

Figure 6.

Figure 6

Color Doppler imaging confirms closure of the ASD and absence of residual shunt. [Color figure can be viewed at wileyonlinelibrary.com]

3. Discussion

Post‐ablation iatrogenic interatrial shunts are typically asymptomatic but may evolve into clinically significant lesions, particularly in the setting of right ventricular dysfunction and severe TR [7]. Heterotopic caval valve implantation (e.g., TricValve) may offer a non‐surgical strategy to reduce systemic congestion and improve symptoms associated to right‐sided heart failure [8]. While effective in alleviating congestion, the procedure can increase right atrial pressures and venous return, potentially worsening right‐to‐left shunting and hypoxemia in patients with pre‐existing interatrial defects. This case illustrates how an interatrial shunt can act as a double‐edged sword in HFpEF and right heart disease, serving both protective and potentially harmful roles depending on hemodynamic context. In selected patients, percutaneous closure of the interatrial septal defect can restore hemodynamic balance and resolve hypoxemia. This case highlights the importance of individualized, stepwise management strategies in complex valvular and shunt‐related pathophysiology.

Ethics Statement

The authors have nothing to report.

Conflicts of Interest

The authors declare no conflicts of interest.

Acknowledgments

The authors have nothing to report.

Data Availability Statement

The authors have nothing to report.

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Associated Data

This section collects any data citations, data availability statements, or supplementary materials included in this article.

Data Availability Statement

The authors have nothing to report.


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