Peripheral Embolization of Amplatzer Device to External Iliac Artery: Do Asymptomatic Patients Require Intervention? A Case Report and Literature Review

Introduction

The original Amplatzer Septal Occluder (ASO) was developed by interventional radiologist Kurt Amplatz in 1997 at the University of Minnesota for closure of atrial septal defects (ASD) [1]. The ASO is made of nitinol, a nickel and titanium alloy [2]. Since its initial production, the ASO prototype has been modified to suit other purposes. One of these adaptations is the Amplatzer Vascular Plug (AVP, AVP II, and AVP 4), a family of devices designed for arterial or venous embolization of the peripheral vasculature [3]. Only 2 devices have been specifically approved for transcatheter PVL closure (tPVLc): the Paravalvular Leak Device (PLD) (Occlutech GmbH, Jena, Germany) and the Amplatzer ParaValvular Plug 3 (AVP 3) (Abbott Medical, Plymouth, MN, USA) [4]. The advantages of the Amplatzer device include its low profile and its fine nitinol mesh construction allowing for deliverability through a variety of catheters. It is also the most cost-effective of the commonly available closure devices [5]. Notably, the nitinol mesh of these devices is stiffer and of larger caliber and is associated with a higher risk of hemolysis [6]. Notably, the Amplatzer PDA occluder has only 1 retention skirt, increasing its risk of embolization.

Most device embolization occurs during the placement procedure and is typically recognized at that time. Delayed embolization cases, however, are often discovered during routine follow-up in asymptomatic patients. Reported embolization sites include the left and right atria, the left and right ventricles [7], and the pulmonary artery [8]. Additionally, a few authors have reported distant embolization of the ASO devices to the iliac artery [9] and the aorta [10]. Peripheral embolization of the Amplatzer device is amenable to percutaneous or surgical intervention. While intervention may be considered to prevent complications such as distal vessel occlusion and ischemia, it inevitably exposes the patient to the risks associated with performing another invasive procedure and anesthesia. The rationale for early retrieval in asymptomatic patients is largely based on the theoretical risks of future embolization and symptomatic ischemia. However, there is a paucity of data regarding the natural history and outcomes of asymptomatic patients whose treatment was deferred until onset of symptoms. Moreover, it remains unclear whether a second embolization event in such patients usually leads to clinical symptoms, or if such risks are overestimated.

Unlike previous reports [9,11,12], where authors describe immediate intervention upon diagnosis of peripheral device embolization, we report a case of embolization of an Amplatzer device to the left external iliac artery after aortic PVL closure and the clinical course of a patient who declined immediate intervention. This patient has remained asymptomatic 1 year after diagnosis of the embolization.

Case Report

This report presents the case of a 73-year-old man with a past history of hypertension, dyslipidemia, melanoma, and atrial fibrillation on Eliquis, family history of premature CAD, prior surgical aortic valve replacement (a 25-mm Intuity bioprosthetic valve), coronary artery bypass x 4 (left internal mammary artery anastomosed to left anterior descending coronary artery, a reversed saphenous vein graft anastomosed to the posterior descending coronary artery, a reversed sequenced saphenous vein graft anastomosed to the first obtuse marginal and second obtuse marginal), and a Maze procedure with pulmonary vein isolation and left atrial appendage occlusion with a clip. This patient was found to have stable mild-to-moderate paravalvular aortic leak 5 months after surgical aortic valve replacement (sAVR). At that time, he had no cardiovascular concerns; his echocardiogram is shown in Table 1. He remained largely asymptomatic at his yearly clinical follow-up visits and his echocardiogram remained stable. However, 3.5 years after his initial operation, he started experiencing dyspnea on exertion, and a repeat TEE showed a well-seated bioprosthetic valve with evidence of early structural degeneration and moderate aortic valve stenosis. It also showed moderately severe (3+) perivalvular regurgitation and mild transvalvular regurgitation. See Table 1 for details.

At that point, a repeat aortic intervention, either a surgical approach or catheter-based approach, was discussed with the patient. The patient opted for the latter. He had an appropriate TAVR anatomy for valve-in-valve. His preoperative CT CTAVR parameters are shown in Table 2. His cardiac catheterization showed severe multivessel disease, patent grafts, and mildly elevated left-sided filling pressure.

He subsequently underwent TF TAVR 26 mm under general anesthesia exactly 49 months (about 4 years) after his initial sAVR with the intent to relieve the bioprosthetic aortic stenosis and ideally to reduce the PVL. A repeat echocardiogram after TAVR is shown in Table 3. After the TAVR procedure, he continued to report dyspnea on exertion and early fatigue with no change in symptoms before and after the TAVR. Due to persistent PVL with associated clinical symptoms, he underwent AVP closure of the PVL with a 4×7 mm VSD occluder 4 months after the TAVR procedure. One month after Amplatzer device placement, echocardiography showed no improvement in the PVL. Interestingly, despite this, he felt much better than before the procedure thus, no intervention was offered. A repeat echocardiogram 4 months later to allow for re-endothelialization of the occluder did not show any improvement. His symptoms returned 5 months after AVP placement. On physical examination, he had a 3 out of 6 systolic ejection murmur heard at the aortic position, with a minimal diastolic murmur that increased minimally with a handgrip maneuver. The lower extremities showed trace/1+ pitting edema.

He then underwent a redo sternotomy with the removal of the existing aortic valve prostheses and re-replacement with a 27-mm Inspiris bioprosthesis. The AVP device was not in place at the time of surgery. A subsequent abdominal radiograph showed the pelvic location of the device, and a CT angiogram showed that the device was lodged in the left external iliac artery (Figures 1–6).

The patient did not have any lower-extremity symptoms associated with the embolization of the device. His exercise tolerance had improved after surgical AVR. As the result of shared decision-making, he opted for watchful waiting with intervention if symptoms developed. In addition, he was advised to continue apixaban (which he was already taking for atrial fibrillation) along with aspirin. At his 6-month follow-up, aspirin was discontinued by his cardiologist to reduce bleeding risk. He was seen at 1 month following the discovery of the embolization, then every 6 months for the first year. He is now followed annually by his cardiologist. No further imaging is planned unless new symptoms develop.

Discussion

Few studies have reported the incidence of late embolization of Amplatzer Vascular Plugs (AVP) following paravalvular leak (PVL) closure, and these studies are largely limited to case reports and small case series. A combined study conducted in the UK and Ireland indicated a rate of late device embolization of 0.4% [13]. A meta-analysis by Heaton et al [14] found that device embolization of Amplatzer Vascular Plugs occurred in 0.4% to 3.5% of cases involving transcatheter PVL closure, reflecting embolization of the device, performed by experienced clinicians. These findings suggest that embolization rates may be higher when the procedure is performed by less experienced clinicians, particularly in the context of off-label use for PVL closure, as discussed in this case. When considering a percutaneous approach for treating PVL, it is essential to assess the size, location, and shape of the defect, as these factors influence the selection of the most suitable occluding device. Paravalvular leaks are highly variable and complex, but most are crescent-shaped. Consequently, oblong devices, such as the AVP 3 and the PLD, are generally better suited for this application than devices with circular cross-sections [13].

Three mechanisms have been proposed to explain device embolization following the closure of paravalvular leaks (PVLs): anatomic, procedural, and device-related [15]. Anatomic factors include using an undersized device, inadequate quality or size of rim, and attempting to close large leaks. Procedural factors include inadequate polar protrusion, excessive tug testing, stored cable tension, and removal of the safety wire after the device has been released. An example of a device-related factor is malfunction of the delivery cable. Some preventive strategies include comprehensive pre-procedural planning and consistent application of the recommended safety checks before device deployment and release (eg, performing an adequate tug test and removing the safety wire or rail before the final device release).

Device embolization can typically be identified during the procedure, whereas delayed embolization is often more challenging to detect, particularly peripheral embolization in asymptomatic cases. While device embolization that occurs during deployment can easily be retrieved by a percutaneous approach, delayed embolization may require surgical removal because of the possible dangerous complications, yet the incidence of these complications is largely unknown and may be overestimated. This case raises the question of whether all cases of peripheral embolization of Amplatzer devices need immediate intervention, or is delayed intervention/and watchful waiting an acceptable option. While this case does not definitively address the question, it suggests that delayed intervention may be a reasonable approach in carefully selected patients, such as those with significant comorbidities, high anesthesia risk, or those reluctant to undergo immediate surgical retrieval. The device–blood vessel size ratio needs to be considered, as a favorable ratio resulting in only partial occlusion may permit deferral of urgent intervention in patients with high procedural risk. In our case, the left iliofemoral vasculature had a minimum luminal diameter of 10.4 mm in the external iliac artery and 9.9 mm in the common femoral artery. In comparison, the Amplatzer 4×7 mm ventricular septal defect (VSD) occluder is designed with a waist diameter of 4 mm, which represents the portion of the device that occupies the defect, and disc diameters measuring approximately 7 mm on either side, serving as retention structures. Taken together, these dimensions indicate the potential for partial, but not complete, luminal obstruction.

We reviewed the literature and compared the profile of our patient with other cases of embolization after PVL closure. We found that PVLs occur more often in mitral valve replacements than in aortic valve replacements, unlike in our patient [16], and most of the cases had either percutaneous or surgical interventions [17–19]. The present case demonstrates that any use of AVP for PVL closure requires adequate equipment and training to remove it either percutaneously or surgically if it becomes displaced, and multidisciplinary collaboration is invaluable in achieving safe retrieval. Management of late device embolization depends on the embolization site. Devices lodged in critical areas require immediate removal, while devices that embolized to non-critical areas in patients with high procedural risk in the setting of partial vessel occlusion and favorable device–vessel size ratio may be observed. Nevertheless, these patients require surveillance and follow-up.

Conclusions

Embolization of Amplatzer devices to peripheral arteries, including the iliac vessels, is a rare but clinically significant complication. This case highlights the need for individualized strategies to manage cases of device embolization. While endovascular or surgical intervention remains the standard approach, watchful waiting may be appropriate in selected non-acute asymptomatic patients with peripheral device embolization. Longitudinal studies are needed to evaluate whether embolized devices in asymptomatic patients lead to long-term sequelae. Such investigations could help in risk stratification and with development of surveillance protocols in conservatively managed patients.