Percutaneous closure of an iatrogenic left atrial-aortic perforation complicated by cardiac tamponade and coronary vasospasm during transseptal puncture: a case report

Abstract

Background

Iatrogenic atrial-aortic perforation during transseptal puncture is a rare but potentially life-threatening complication. Percutaneous closure using dedicated occluder devices has emerged as a less invasive alternative to surgical repair in selected patients.

Case presentation

A 68-year-old woman with hypertension and long-standing persistent atrial fibrillation (≥ 12 years) underwent catheter ablation. Pre-procedural imaging showed a markedly elevated left atrial (LA) volume (171 mL) with predominantly lateral enlargement. During a second transseptal puncture attempt, the sheath-dilator system inadvertently advanced through the LA wall and perforated the sinotubular junction of the aorta, confirmed by aortography. Although the sheath initially tamponaded the perforation, subsequent migration led to rapid hemopericardium requiring cardiopulmonary resuscitation (CPR) and emergent pericardiocentesis. With the access tract preserved, a 12/10 mm Amplatzer Duct Occluder was delivered percutaneously, achieving successful closure. Following device deployment, sudden cardiac arrest occurred due to diffuse coronary vasospasm, which resolved rapidly with intracoronary nitroglycerin. The patient was discharged in stable condition on an oral anticoagulant, a calcium channel blocker, and long-term nitrates.

Conclusions

This case describes the successful percutaneous management of an iatrogenic LA-to-ascending aorta perforation during transseptal catheterization, complicated by cardiac tamponade and coronary vasospasm. This case suggests that careful attention is warranted not only during the septal puncture itself, but also during subsequent sheath advancement, even after successful entry into the LA has been confirmed.

Supplementary Information

The online version contains supplementary material available at https://doi.org/10.1186/s12872-026-06334-2.

Background

Transseptal puncture (TSP) is an essential and routine step in catheter ablation for atrial fibrillation (AF). Although contemporary TSP has an overall complication rate of less than 1% to 2% in experienced centers, inadvertent perforation of the aortic root remains a rare but potentially fatal complication. Iatrogenic atrial-aortic communication can result in hemopericardium, cardiac tamponade, and cardiovascular collapse if not promptly recognized and treated.

Historically, surgical repair has been considered the definitive treatment for iatrogenic atrial-aortic perforations. However, percutaneous closure using dedicated occluder devices may serve as a less invasive alternative in selected patients. We report a patient undergoing TSP with an iatrogenic left atrial-aortic (LA-Ao) perforation during AF ablation, further complicated by acute cardiac tamponade necessitating cardiopulmonary resuscitation (CPR) and subsequent coronary vasospasm, which was successfully managed with percutaneous closure using an Amplatzer Duct Occluder (ADO) 12/10 mm device.

Case presentation

A 68-year-old woman with a history of hypertension and persistent AF for at least 12 years presented for catheter ablation. Preprocedural transthoracic echocardiography demonstrated an left atrial (LA) anteroposterior diameter of 46 mm, which was not markedly enlarged; however, the LA volume measured using the biplane disc method was substantially elevated at 171 mL, indicating marked volumetric remodeling. Cardiac computed tomography (CT) confirmed predominantly lateral, rather than anteroposterior, LA enlargement (Fig. 1). There was no imaging evidence of an interatrial septal aneurysm.

Fig. 1.

Pre-procedural cardiac computed tomography demonstrating left atrial anatomical remodeling

Access was established through the right femoral vein. The initial TSP was performed under intracardiac echocardiography (ICE) guidance using a Brockenbrough needle and a Swartz braided transseptal guiding introducer (SL1, Abbott Medical, 8.5Fr), allowing successful placement of the first ablation catheter into the LA. Subsequently, additional transseptal access was required. Under ICE guidance, a second puncture was attempted using a new 8.5Fr SL1 sheath. Successful entry into the LA was confirmed by ICE, evidenced by loss of septal tenting and visualization of agitated saline microbubbles within the LA chamber. However, during subsequent sheath advancement under left anterior oblique (LAO) fluoroscopic guidance, the pressure waveform at the sheath tip showed a clear arterial pattern rather than the expected LA pressure tracing. Contrast injection through the sheath under fluoroscopic guidance revealed opacification of the left coronary artery, confirming inadvertent aortic entry (Fig. 2A). Further heparin administration was discontinued immediately upon recognition of the perforation. The sheath itself appeared to tamponade the perforation, and the patient remained hemodynamically stable (Fig. 3A). However, the second SL1 sheath migrated out of position, and ICE demonstrated rapidly accumulating pericardial effusion, consistent with hemopericardium through the unoccluded perforation site. CPR was initiated on multiple occasions, with intravenous epinephrine administered as hemodynamic support. Emergent pericardiocentesis was performed via the subxiphoid approach which yielded hemorrhagic pericardial fluid and subsequent hemodynamic stabilization; approximately several hundred milliliters were evacuated in total, with drainage decreasing substantially once the sheath re-established tamponade of the perforation site. Autotransfusion was not performed.

Fig. 2.

Fluoroscopic images during the procedure. A Contrast injection through the SL1 transseptal sheath revealed opacification of the left coronary artery, confirming an inadvertent aorta entry. B Aortography via a pigtail catheter, confirming the position of the SL1 sheath within the aortic root. C Simultaneous aortography and right atrial angiography delineating the precise location of the LA-Ao perforation site. D Fluoroscopic image showing the retention disc of the ADO 12/10 mm device deployed within the Ao lumen before full device release. E Final aortography confirming the successful percutaneous closure of the LA-Ao defect with the ADO in a stable position, with no residual contrast extravasation. Abbreviations: ADO, Amplatzer duct occluder. Ao, aorta; LA, left atrium

Fig. 3.

Intracardiac echocardiography images. A ICE images demonstrate the SL1 sheath (arrowheads) traversing the interatrial septum into the aortic root, confirming the LA-Ao communication. B ICE showing the deployed ADO (arrow) at the LA-Ao defect. Abbreviations: ADO, Amplatzer duct occluder. Ao, aorta; ICE, intracardiac echocardiography; LA, left atrium

Following hemodynamic stabilization, right femoral arterial access was obtained, and a pigtail catheter was advanced to the aortic root for aortography (Fig. 2B). Aortographic imaging confirmed the perforation site at the LA-Ao junction and guided the device sizing (Fig. 2C). Because the transseptal guidewire remained in place across the original tract, no new septal puncture was required to regain access. The existing SL1 sheath was carefully advanced further across the LA-Ao communication under combined fluoroscopic and aortographic guidance to reestablish stable access for device delivery. The device selection was guided by the estimated defect size. Given that the SL1 sheath has an outer diameter of 8.5 Fr (~ 2.8 mm) and acknowledging that an oblique angle of entry would result in an effective tissue defect larger than the nominal sheath diameter, a percutaneous closure device (12/10 mm ADO, Abbott Medical) was selected to ensure adequate coverage. An ADO was preferred over alternative occluders, such as vascular plugs or muscular ventricular septal defect occluders, based on prior reports describing successful percutaneous closure of iatrogenic aortic perforations using this device. The device was delivered via an indwelling SL1 sheath, using an antegrade approach (Fig. 2D, E). Under fluoroscopic and ICE guidance, the retention disc was deployed within the aortic lumen, and the device body was positioned across the LA-Ao defect (Fig. 3B). Following confirmation of stable positioning, coaxial alignment, and the absence of impingement of the aortic valve or coronary ostia, the device was released. Immediate post-deployment aortography demonstrated no contrast extravasation or residual shunting, confirming successful closure.

Following successful device deployment, the patient was being prepared for transfer to the intensive care unit when sudden cardiac arrest occurred. Urgent coronary angiography revealed diffuse severe coronary vasospasm affecting multiple vessels without evidence of obstructive disease or thrombus, consistent with variant angina. Intracoronary nitroglycerin was administered, resulting in rapid resolution of vasospasm and prompt hemodynamic recovery (Fig. 4A-D). The patient was subsequently stabilized and transferred to the intensive care unit for close monitoring. Non-enhanced chest CT performed the following day confirmed that the percutaneous closure device was well-seated across the LA-Ao defect, with no evidence of device migration or residual communication (Fig. 5A, B). The patient was discharged in stable condition on an oral anticoagulant, a calcium channel blocker, and long-term nitrate therapy for secondary prevention of coronary vasospasm, without additional complications.

Fig. 4.

Coronary angiography demonstrating vasospasm. A, B Coronary angiography showing diffuse severe vasospasm of the left and right coronary artery. C, D Repeat coronary angiography following intracoronary nitroglycerin administration, showing near-complete resolution of coronary vasospasm

Fig. 5.

Post-procedural computed tomography imaging. A Axial CT image obtained the day following the procedure, demonstrating that the ADO device was well seated at the LA-Ao interface. B Coronal CT image confirming a stable device position bridging the Ao and LA walls. Abbreviations: ADO, Amplatzer duct occluder. Ao, aorta; CT, computed tomography; ICE, intracardiac echocardiography; LA, left atrium

Discussion and conclusions

Iatrogenic perforation of the aorta during transseptal puncture is a rare but potentially life-threatening complication, with a reported incidence of approximately 0.05% to 0.07% of transseptal procedures [1, 2]. These perforations typically originate from the right atrium and can be anatomically classified into three subtypes according to the site of aortic entry [2]. Clinical management depends critically on which instrument has traversed the defect; when only a needle has entered the aorta, conservative management with close hemodynamic monitoring is generally sufficient [3, 4]. However, if the sheath or dilator has been advanced, access should be deliberately maintained rather than withdrawn, as preserving the tract is essential to enable percutaneous closure [2]. Percutaneous closure can be achieved using various occluder devices, including ADO, muscular ventricular septal defect occluder, and Amplatzer Vascular Plug, as reported in prior studies [5–9]. Nevertheless, surgical repair remains necessary in most cases complicated by cardiac tamponade, as well as when percutaneous closure attempts are unsuccessful [4]. Additionally, one prior case of LA-Ao perforation has been reported, occurring during left atrial appendage closure in which the sheath inadvertently penetrated the LA wall and mediastinal tissues, resulting in perforation of the descending aorta; successful repair was achieved by simultaneously deploying two ductus arteriosus occluders through the original access tract [7].

For our patient, following successful TSP from the right atrium into the LA, the sheath-dilator system inadvertently advanced through the LA wall and penetrated the sinotubular junction of the aorta, immediately superior to the noncoronary cusp, resulting in communication between the LA and the ascending aorta. Notably, successful entry into the LA had already been confirmed by ICE, evidenced by loss of septal tenting and visualization of agitated saline microbubbles within the LA chamber, and there was no echocardiographic evidence of an interatrial septal aneurysm that might otherwise account for an anteriorly displaced puncture site. The perforation therefore did not arise from an initially misdirected puncture, but rather occurred during subsequent sheath advancement under LAO fluoroscopic guidance, when anterior deflection of the sheath-dilator system redirected its trajectory toward the aortic root.

Although such a perforation is anatomically improbable in a normal heart, severe LA remodeling, as seen in our patient with a markedly elevated LA volume and predominantly lateral enlargement, may distort the spatial relationship between the interatrial septum and the adjacent aortic root, thereby increasing susceptibility to such deflection. In this setting, subtle changes in the sheath torque during advancement following an otherwise successful transseptal puncture may redirect the trajectory toward the aortic wall, resulting in inadvertent perforation.

Given the hemodynamic instability associated with cardiac tamponade, emergency surgical repair was considered and discussed with the cardiac surgery team; because of the anticipated delay of approximately two hours to initiate surgery and the patient’s tenuous hemodynamic status, a joint decision was made with the surgical team to first attempt percutaneous closure via the already-established access tract, with surgical backup remaining available if needed. Despite cardiac tamponade necessitating CPR, percutaneous closure was ultimately achieved without surgical intervention. Successful device deployment requires particular attention to sizing. The oblique angle of sheath entry creates an effective tissue defect larger than the nominal sheath outer diameter, and accordingly, an 8.5Fr SL1 sheath necessitated a 12/10 mm ADO to achieve reliable occlusion. Furthermore, coronary vasospasm should be recognized as a potential late complication in this setting. While repeated epinephrine administration during resuscitation may have contributed via catecholamine-induced vasoreactivity, other factors—including profound hemodynamic stress, transient endothelial dysfunction, an underlying vasoreactive predisposition, and direct catheter-related mechanical irritation of the coronary ostia—may also have played a contributory role, and the precise mechanism could not be definitively established. Prompt identification and treatment with intracoronary nitroglycerin are essential to prevent further hemodynamic deterioration.

This case highlights several practical points. Once appropriate LA pressure tracing and ICE confirmation of septal crossing are obtained, careful fluoroscopic monitoring in biplane views during subsequent sheath-dilator advancement may help detect early deflection and reduce the risk of inadvertent perforation. EP laboratories should also maintain ready access to rescue equipment and prompt availability of a structural heart specialist, given that such complications, although rare, require immediate intervention. Continuation of the patient’s rhythm control strategy, including possible repeat ablation, remains to be determined and will be discussed at outpatient follow-up.

Abbreviations

Ao

Aorta

ADO

Amplatzer Duct Occluder

AF

Atrial fibrillation

CPR

Cardiopulmonary resuscitation

CT

Computed tomography

ICE

Intracardiac echocardiography

LA

Left atrium

LAO

Left anterior oblique

Authors’ contributions

J.L. drafted the manuscript and contributed to data acquisition. Y.S.L. conceptualized the case and revised the manuscript. Both authors read and approved the final manuscript.

Funding

None.

Data availability

No datasets were generated or analysed during the current study.

Declarations

Ethics approval and consent to participate

Ethics approval was waived as this is a single case report. Written informed consent was obtained from the patient.

Consent for publication

Written informed consent was obtained from the patient for publication of this case report and any accompanying images.

Competing interests

The authors declare no competing interests.