Percutaneous Transfemoral Closure of a Pseudoaneurysm at the Left Ventricular Apical Access Site for Transcatheter Aortic Valve Implantation

Abstract: This case report illustrates a left ventricular pseudoaneurysm that developed at the transapical access site for transcatheter aortic valve implantation and was successfully excluded percutaneously through a femoral approach using an Amplatzer muscular VSD occluder (St. Jude Medical). We also discuss various currently available devices and technical pearls for percutaneous closure of left ventricular pseudoaneurysms.

J INVASIVE CARDIOL 2015;27(2):E27-E29

Key words: transcatheter aortic valve implantation, new devices, complications

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Left ventricular (LV) pseudoaneurysm is known to occur as a complication of myocardial infarction, trauma, infection, or cardiac surgery. It is also reported following LV apical venting, which is used during cardiac surgery to decompress and de-air the heart.¹ Transapical aortic valve implantation (TA-AVI) can similarly lead to pseudoaneurysm formation. LV pseudoaneurysms carry a 30%-45% risk of free rupture and are traditionally repaired surgically;² however, patients who undergo transcatheter aortic valve implantation (TAVI) are elderly, frail, high operative-risk patients with multiple comorbidities, and the risk of surgical repair is significant. Our patient underwent successful percutaneous closure of his LV pseudoaneurysm through a femoral approach by using an Amplatzer muscular VSD occluder (St. Jude Medical).

Case Report

The patient is an 86-year-old Caucasian male with past medical history of coronary artery disease requiring four-vessel coronary artery bypass surgery, hypertension, hyperlipidemia, diabetes, peripheral arterial disease, spine surgery, and medullary thyroid cancer in remission. He was admitted to an outside hospital for presyncope; transthoracic echocardiogram (TTE) revealed severe aortic valve stenosis with peak gradient of 88 mm Hg, mean gradient of 55 mm Hg, calculated aortic valve area (AVA) of 0.8 cm², and preserved LV function. He was subsequently referred to our multidisciplinary valve clinic for management. He was frail in appearance and reported New York Heart Association class II heart failure symptoms. His calculated STS risk score for an open aortic valve surgery was 7.1%; therefore, TAVI was recommended. Left heart catheterization showed significant stenoses in two of the previously placed vein grafts requiring percutaneous coronary intervention. Computed tomographic (CT) angiography demonstrated severely calcified iliac arteries of 7 mm diameter and a right common iliac artery dissection into the distal aorta; therefore, a transapical approach was preferred. Three dimensional reconstruction of the CT images with M2S software (M2S, Inc) showed an aortic valve annular area of 535.3 mm². He underwent TA-AVI with a 26 mm Edwards Sapien valve (annular valve area 531 mm², 0.8% undersized) using the Ascendra 1 delivery system (Edwards Lifesciences). Postimplantation TEE showed trace amount of paravalvular leak (PVL). At the conclusion of the procedure, the apical access site was secured with two perpendicular 3-0 prolene horizontal mattress sutures (Ethicon, Inc) that were buttressed with large felt pledgets. The patient recovered from the procedure well and was discharged home. He was admitted 2 months later for congestive heart failure exacerbation. Repeat TTE showed progression of the PVL to moderate, involving approximately 25% of the circumference of the implanted valve. He responded well to medical therapy and was discharged after a brief hospitalization. At 3-month follow-up, he was noted to have a dynamic LV apical impulse with visible pulsations through the skin at the site of the anterolateral minithoracotomy incision (Video 1). TTE demonstrated a 1.5 x 1.4 cm apical pseudoaneurysm (Figure 1A, Video 2) and persistent moderate PVL. The pseudoaneurysm was confirmed with chest CT scan (Figures 1B and 1C). After discussion with the patient and his family the decision was made to proceed with percutaneous closure, of the pseudoaneurysm, as well as balloon postdilation of the valve to address the PVL. The procedure was performed in the catheterization laboratory under general anesthesia using both fluoroscopic and TEE guidance with cardiopulmonary bypass and a cardiac surgeon on standby. Vascular access was obtained using standard Seldinger technique and included a 6 Fr sheath in the left femoral artery (LFA), a 4 Fr sheath in the right femoral artery, and a 7 Fr sheath in the right femoral vein. Right and left heart hemodynamics were obtained.  The LFA access site was pre-closed using a Perclose device (Abbott Vascular Devices). The LFA access site was serially dilated to 12 Fr, and a 12 Fr x 30 cm sheath was placed in the LFA. A balloon-tipped pacing catheter was positioned in the right ventricular apex and the pacing threshold was tested for planned right ventricular pacing during balloon postdilation of the valve. LV angiography was then performed using a pigtail catheter and demonstrated the apical pseudoaneurysm (Figure 1D, Video 3). The width of the neck of the pseudoaneurysm was measured at approximately 4 mm, which was consistent with the echocardiographic and CT scan measurements. A modified 9 Fr JR guide catheter was advanced retrograde into the LV and a 0.035˝ Wholey wire was then used to enter the pseudoaneurysm. A 4 mm Amplatzer muscular VSD occluder (St. Jude Medical) was successfully delivered; however, ventriculography prior to device release demonstrated contrast flow through and around the device into the pseudoaneurysm (Video 4), and the device was removed prior to release. Repeat measurements of the pseudoaneurysm neck demonstrated a diameter of approximately 6-7 mm, which was significantly larger than our initial measurements. As a result, a 10 mm Amplatzer muscular VSD occluder was deployed within the neck of the pseudoaneurysm. Postdeployment ventriculography demonstrated good device positioning with trivial flow through the device into the pseudoaneurysm; therefore, the device was released (Video 5). We then turned our attention to post-balloon dilation of the valve. Dilation of the valve was performed using a 26 x 4 mm Z-Med balloon (NuMED, Inc); however, the moderate PVL persisted. No further dilation was performed. Upon completion of the procedure, hemostasis was obtained using manual pressure to the right femoral access sites and suture closure of the LFA access site using the previously placed Perclose device. The patient had a smooth postoperative recovery and repeat TTE 2 months later showed complete resolution of the pseudoaneurysm (Video 6).

Discussion

The reported incidence of LV apical access-site pseudoaneurysm is 1%-6.6% after TA-AVI.^3-5 Reinforcing the apical puncture site is paramount to prevent pseudoaneurysm formation and two surgical techniques are noted to provide adequate reinforcement. One technique is two concentric purse-string sutures with multiple pledgets and the other technique is two perpendicular horizontal mattress pledgeted sutures, as used in this case report.^5,6 Other than surgical technique, postoperative dual-antiplatelet therapy, poor hypertensive control, and deep wound infection also play a role in pseudoaneurysm formation at the access site.⁵ 

LV pseudoaneurysms may present with chest discomfort and visible pulsation at the site of surgical incision (as in our case), and if large enough can lead to heart failure symptoms. Sometimes, they are asymptomatic and are detected by follow-up echocardiography performed to assess the valve⁷ or are incidentally detected on a chest CT scan performed for a non-cardiac indication.⁸ The natural history of LV pseudoaneurysms is largely unknown and hard to study. Data from studying post-myocardial infarction LV pseudoaneurysms, which certainly have a different pathophysiology, have shown a 30%-45% risk of rupture;² therefore, LV pseudoaneurysms are traditionally repaired surgically; nonetheless, several studies have suggested that the risk of rupture may be overstated. For example, Moreno et al reported no incidence of rupture in 10 post-infarction LV pseudoaneurysms that were conservatively followed over a mean period of 3.8 years.⁹ In our review of the literature, we found three therapeutic approaches toward transapical access-site pseudoaneurysm after TA-AVI. In the majority of cases, the patients underwent open surgical repair either on cardiopulmonary bypass^3,10 or off-pump.⁴ In some cases, the pseudoaneurysm was watched conservatively.^3,5,7,11 We found 2 cases of documented spontaneous pseudoaneurysm closure in follow-up imaging: in 1 case, a 30 x 50 mm pseudoaneurysm thrombosed 6 months after discovery¹¹ and in the other case the authors did not elaborate on the size of the pseudoaneurysm or timing of spontaneous closure.⁵ The third therapeutic approach was percutaneous closure of the pseudoaneurysm. There are case reports of successful off-label closure of LV pseudoaneurysms using a variety of different devices and techniques.^12-15 We found only 1 case report of percutaneous closure of a LV pseudoaneurysm post TA-AVI with an Amplatzer muscular VSD occluder.⁸

 We recommend that the percutaneous approach for LV apical pseudoaneurysm closure be performed in a hybrid suite with cardiopulmonary bypass and a cardiac surgeon on standby, since there is a risk of iatrogenic rupture from engaging the pseudoaneurysm with catheters or guidewires. Coils may be best suited for pseudoaneurysms with a narrow neck and care must be taken to avoid extension of the coils into the LV cavity, which could lead to coil embolization. In general, we favor the use of Amplatzer occluders over vascular plugs and coils, given that they can be anchored securely in the pseudoaneurysm neck, thereby providing closure of the neck of the pseudoaneurysm and reducing the risk of device embolization. The width of the neck of the pseudoaneurysm should be measured using multiple modalities, such as echocardiogram, CT scan, and angiography. We recommend that the device waist be oversized at least 2 mm larger than the pseudoaneurysm neck diameter in order to provide adequate closure of the neck. It is also important to consider the length of the pseudoaneurysm neck, as this may affect the choice of device used for closure. Since the myocardium is hypertrophied in patients with preexisting aortic stenosis, the Amplatzer septal occluder, which is designed for atrial septal defect closure and has a waist length of 3-4 mm, may not be long enough to span the neck of the pseudoaneurysm and maintain its original configuration; however, the Amplatzer muscular VSD occluder (waist length, 7 mm) or ductal occluder (device length, up to 8 mm) have longer waist lengths, which may allow better device positioning within the neck and more optimal device configuration leading to occlusion; nonetheless, these devices may still not be long enough to span the length of the pseudoaneurysm neck, leading to incomplete expansion of the terminal disk. In this situation, as shown in our case and reported by others,¹³ if the post-implantation angiogram demonstrates no or minimal flow into the pseudoaneurysm sac through the device, the result is adequate and leads to exclusion of the pseudoaneurysm in follow-up. Reported complications of percutaneous closure are stroke¹³ and occluder device migration¹² into the pseudoaneurysm without sequel. We did not find any report of pseudoaneurysm rupture. 

Conclusion

The natural history of LV transapical access-site pseudoaneurysm after TA-AVI is unknown. Surgical repair is the most commonly reported treatment, but is associated with high operative mortality and morbidity in the TAVI population. Percutaneous closure is a viable alternative in select patients with appropriate anatomy; however, there are also case reports of spontaneous closure of these pseudoaneurysms with conservative medical management and the treatment approach should be decided after discussion with the patient about the risks and benefits of each approach.

References

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From the ¹Department of Medicine; ²Division of Thoracic and Cardiovascular Surgery, Department of Surgery; and ³UF Health Congenital Heart Center, Division of Pediatric Cardiology, University of Florida, Gainesville, Florida. 

Disclosure: The authors have completed and returned the ICMJE Form for Disclosure of Potential Conflicts of Interest. The authors report no conflicts of interest regarding the content herein.

Manuscript submitted May 24, 2014, final acceptance given June 9, 2014.

Address for correspondence: James C. Fudge, Jr, MD, MHS, UF Health Congenital Heart Center, Division of Pediatric Cardiology, University of Florida, 1600 SW Archer Road, HD-303, Gainesville, FL 32610. Email: jcfudge@ufl.edu