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Ann Thorac Surg 2008;86:996-998. doi:10.1016/j.athoracsur.2008.03.001
© 2008 The Society of Thoracic Surgeons
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Case Reports

Percutaneous Treatment of Periprosthetic Mitral Valve Leaks: Is it Just a Futile Exercise?

Tiziana Claudia Aranzulla, MDa,b,*, John Cosgrave, MDa, Giovanni La Canna, MDb, Francesco Maisano, MDc, Matteo Montorfano, MDb, Giuseppe Sangiorgi, MDa, Antonio Colombo, MDa,b

a Interventional Cardiology Unit, Emo Centro Cuore Columbus, San Raffaele Hospital, Milan, Italy
b Interventional Cardiology Unit, San Raffaele Hospital, Milan, Italy
c Department of Heart Surgery, San Raffaele Hospital, Milan, Italy

Accepted for publication March 3, 2008.

* Address correspondence to Dr Aranzulla, 48 Via Buonarroti, Milan, 20145, Italy (Email: aratizi{at}hotmail.com).


   Abstract
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Introduction
 Comment
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We report the percutaneous exclusion of a mitral peri-prosthetic valvular leak performed with the Amplatzer vascular plug. Device dislodgement occurred a few days later and surgical repair was ultimately required.


   Introduction
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 Introduction
Comment
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Percutaneous peri-prosthetic valvular leak (PVL) closure may represent an alternative treatment option for poor surgical candidates.

A 67-year-old man, former smoker, with hypertension, noninsulin dependent diabetes, obstructive pulmonary disease, and renal insufficiency underwent mitral valve replacement with a mechanical prosthesis for rheumatic regurgitation. Two years later, a spontaneous thigh hematoma with associated sciatic nerve paralysis occurred and the mechanical valve was replaced with a bioprosthetic one to avoid further anticoagulation. Two months later, due to prosthesis detachment, a second redo was performed with another bioprosthesis.

Four months later, he was admitted for acute pulmonary edema. His abnormal laboratory findings were: creatinine, 2.21 mg/dL; hemoglobin, 9.6 g/dL; lactic dehydrogenase, 518 units/L. Urinalysis (urobilinogen, 2 mg/dL) and peripheral blood smear (schistocytes and polychromasia) were consistent with hemolytic anemia. Serial blood cultures were negative. Transesophageal echocardiography (TEE) (Fig 1) showed an anterolateral PVL close to the left atrium appendage, with a 4-mm fibrotic neck and a winding crescent-shaped course (maximum diameter, 8 mm), associated with severe periprosthetic regurgitation and pulmonary hypertension (PAPs, 80 mm Hg).


Figure 1
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  		Fig 1. Procedural steps: Angiographic views showing transseptal catheterization with Mullins Sheath (Cook Inc, Bloomington, IN), peri-prosthetic valvular leak (PVL) crossing with Storq (Cordis Corp, Miami, FL) and Ironman guidewires (Abbott Vascular Devices, Redwood City, CA; Guidant, Santa Clara, CA), multipurpose catheter advanced into the left ventricle (LV) across the leak, wires captured from the LV to the right femoral artery with a (A) Gooseneck (ev3 Inc, Plymouth, MN) and (B) Amplatzer vascular plug (AGA Medical Corp, Golden Valley, MN; dotted oval outline) deployment.(C) Baseline transesophageal echocardiography (TEE) mitral-commissural view showing a crescent-shaped PVL close to the left atrium appendage (LAA) with a 4-mm fibrotic neck (arrow) and associated severe mitral regurgitation. (LA = left atrium.)

 
In view of his cardiac history and comorbidities, we did not believe the patient to be a suitable surgical candidate. After consultation with our surgical colleagues, and after obtaining written informed consent, we proceeded with the percutaneous exclusion of the PVL under general anesthesia. A heart surgeon was actively involved in the entire procedure.

Vascular accesses were the right femoral artery (6-French sheath) and vein (10-French sheath). Transseptal catheterization was followed by PVL crossing with 0.035-inch Storq (Cordis Corp, Miami, FL) and 0.014-inch Ironman (Abbott Vascular Devices, Redwood City, CA; Guidant, Santa Clara, CA) guidewires. A 6-French multi-purpose guide catheter was advanced over both wires into the left ventricle across the leak. These wires were snared in the left ventricle with a Gooseneck (ev3 Inc, Plymouth, MN) and pulled into the right femoral artery to provide extra support (Fig 1A). The Storq wire was removed and the 12-mm diameter, 8-mm length AVP (AGA Medical Corp, Golden Valley, MN) was advanced through the multipurpose catheter and deployed across the leak under TEE and fluoroscopic guidance (Fig 1B).

Transesophageal echocardiography color flow mapping soon after deployment showed persistence of severe peri-prosthetic regurgitation (Fig 2A); however, after a few minutes, nearly a complete leak exclusion with normalized pulmonary artery pressures was demonstrated (Fig 2B).


Figure 2
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  		Fig 2. Transesophageal echocardiography after Amplatzer vascular plug (AGA Medical Corp, Golden Valley, MN) deployment. (A) Persistence of severe periprosthetic regurgitation soon after device deployment, and (B) nearly complete leak exclusion a few minutes later. (C) The Amplatzer vascular plug (arrow). (LA = left atrium; LV = left ventricle.)

 
Pre-discharge TTE (5 days later) showed mild peri-prosthetic regurgitation, but TEE revealed it to be severe and likely related to AVP dehiscence (Figs 3A and 3B). In view of these findings and the risk of device embolization, the patient underwent his fourth open heart surgery.


Figure 3
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  		Fig 3. (A) Transesophageal echocardiography 5 days after the procedure. (B) Severe peri-prosthetic regurgitation recurrence due to (C) Amplatzer vascular plug (arrow; AGA Medical Corp, Golden Valley, MN) distortion. (LA = left atrium; LV = left ventricle.)

 
Left lung laceration occurred during the lysis of strong adhesions existing between the chest, heart, and lungs, and was repaired with a Teflon string. The AVP, which appeared properly positioned (Fig 3C), was removed, and the prosthetic ring was re-sutured with three interrupted stitches.

Prolonged weaning from ventilation, worsening of renal insufficiency, and severe anemia requiring blood transfusions complicated the postoperative course. The patient was discharged 1 month after admission. After 6 months, the patient is asymptomatic. No further hospitalizations occurred.


   Comment
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 Abstract
 Introduction
 Comment
References
 
The value of PVL percutaneous closure remains a subject of debate [1]. A dedicated device is not available [2], follow-up data are limited and many uncertainties exist about the mechanisms of failures. We chose the AVP, a self-expandable nitinol device that was approved by the Food and Drug Administration for peripheral vessels occlusion [3] in view of its conformability and low bulk. Incomplete device thrombosis could be one possible reason for failure. However, the regurgitation jets morphology at pre-discharge TEE was clearly different (Fig 3B) from that observed after AVP deployment, when regurgitation was all located intra-device (Fig 2B). Furthermore, as compared with the post-procedural TEE (Fig 2C), the AVP tip no longer appeared to be in the same plane as the prosthetic ring (Fig 3A). Therefore, AVP dislocation seemed the likely explanation.

Current criteria for sizing (the choice of an AVP, 30% to 50% larger than the target vascular district) were fully accomplished. Our surgeons reported a correct device position, as it happened in other reported failures [2, 4]. Nevertheless, correct sizing and positioning are not sufficient; the device should precisely fit the leak morphology to obtain its stable and complete exclusion. This is unlikely to be achieved within crescent-shaped defects. A practical strategy may be to oversize the device. However, the larger the pore size, the lower the likelihood of an occlusive thrombus forming. The use of additional coils either behind the AVP [3] or inserted inside it before deployment, may enhance device thrombogenicity. Furthermore, consideration about the cause of the leak (prior, recurrent infections) and the local tissue strength (ie, collagen disease) are relevant to decision making and anticipated outcomes.

Finally, we strongly recommend TEE. In a previous experience [5], device dislodgement was diagnosed after 2 months, but no mention is made if pre-discharge transthoracic echocardiography or TEE was performed. Therefore, we cannot exclude the possibility that device dislodgement had occurred earlier.

In conclusion, we advise restricting percutaneous PVL closure when contraindications to surgery exist. However, rather than concluding that "effort, expense, and expert maneuvering of a device in this situation are ... a futile exercise," [4] we aim to identify conditions enhancing the probability of a successful procedure.


   References
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 Abstract
 Introduction
 Comment
 References
 

  1. Hijazi ZM. Transcatheter management of paravalvular mitral leaks: far from ideal Catheter Cardiovasc Interv 2004;61:552-553.[Medline]
  2. Shapira Y, Hirsch R, Kornowski R, et al. Percutaneous closure of perivalvular leaks with Amplatzer occluders: feasibility, safety, and short-term results J Heart Valve Dis 2007;16:305-313.[Medline]
  3. Hill SL, Hijazi ZM, Hellenbrand WE, Cheatham JP. Evaluation of the Amplatzer vascular plug for embolization of peripheral vascular malformations associated with congenital heart disease Catheter Cardiovasc Interv 2006;67:113-119.[Medline]
  4. Hussain ST, Devagourou V, Sampath Kumar A. Management of mitral paravalvular leak: therapy or misadventure? J Thorac Cardiovasc Surg 2003;126:879-880.[Free Full Text]
  5. Ussia GP, Scandura S, Calafiore AM, et al. Late device dislodgement after percutaneous closure of mitral prosthesis paravalvular leak with Amplatzer muscular ventricular septal defect occluder Circulation 2007;115:e208-e210.[Free Full Text]



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