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Ann Thorac Surg 2009;88:989-992. doi:10.1016/j.athoracsur.2009.01.034
© 2009 The Society of Thoracic Surgeons

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Case Reports

Acute Fibrin Deposition Causing Acute Failure of Two Tissue Pericardial Valves

Amal K. Bose, MDa,*, Jimmy Kim Fatt Hon, FRCS(CTh)b, Binayak Chanda, MRCSa, Rakesh Uppal, FRCS(CTh)b, Simon Kendall, FRCS(CTh)a

a The James Cook University Hospital, Middlesbrough, United Kingdom
b The London Chest Hospital, London, United Kingdom

Accepted for publication January 13, 2009.

* Address for correspondence to Dr Bose, Department of Cardiothoracic Surgery, The James Cook University Hospital, Marton Rd, Middlesbrough, TS4 3BW, United Kingdom (Email: amal{at}doctors.net.uk).


    Abstract
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 Abstract
 Introduction
 Case Reports
 Comment
 References
 
We report the early failure of two tissue valves within hours of surgery due to the accumulation of cellular debris in two different institutions in the United Kingdom. The valves were both found at explant to be covered in a cellular material — possibly fibrin. From clinical experience and careful review of the literature we have found no other reports of such early valve failure due to the build up of material on the structure of the valve. This rare occurrence needs to be reported in the literature to forewarn clinicians of an early complication that may not be recognized yet.


    Introduction
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 Abstract
 Introduction
 Case Reports
 Comment
 References
 
The use of tissue valve prosthesis for valve replacement has become standard treatment and is supported by a wealth of clinical data suggesting excellent long-term outcomes from a variety of different valve designs and manufacturers [1–3]. Valve failure has been described as being caused by structural valve degeneration, prosthetic valve endocarditis and nonstructural valve degeneration, usually caused by paravalvular leaks and rarely due to valve dehiscence. The most common reported complication is thromboembolism, which is a recognized complication that has been quoted at 1% per patient year in some reports [4], with actuarial freedom from thromboembolism being reported between 88% and 90% at 10 and 14 years in the aortic position, respectively. However, there are no reports in the literature of acute early tissue valve failure.


    Case Reports
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 Case Reports
 Comment
 References
 
Patient 1
A 67-year-old woman was admitted to the emergency department with palpitations and breathlessness. Clinical examination confirmed biventricular failure and atrial fibrillation. Echocardiography showed hyperdynamic left ventricular function with a dilated right ventricle and evidence of pulmonary hypertension. There was severe posterior mitral valve leaflet prolapse causing severe regurgitation. She did not respond to full medical treatment and intra-aortic balloon pump therapy. Normal coronary arteries were confirmed on urgent angiography.

She underwent urgent mitral valve surgery. A ruptured chordae to P1 & P2 area of the posterior mitral valve leaflet was confirmed intraoperatively. A 27-mm Perimount Plus pericardial tissue valve (model 6900P; Edward Lifesciences, Irvine, CA) was inserted using interrupted suture technique. She was weaned off cardiopulmonary bypass with relative ease supported by low doses of noradrenalin, milrinone, and intra-aortic balloon pump. Her right ventricle showed marked functional improvement. However, an hour after returning to the intensive care unit, her blood pressure dropped necessitating reopening of her chest, cardiac massage, and re-commencement of cardiopulmonary bypass. It was apparent that the right ventricular function was poor and a vein graft was anastomosed to the right coronary artery, but made no improvement. Intraoperative transesophageal echocardiography showed reduced motion of the septal leaflets of the prosthetic mitral valve. The mitral valve was re-explored and found to have extensive deposits of cellular material under the septal leaflet, but no obvious obstruction. This valve was removed and a new size (27-mm mechanical Carbomedics valve, model 700 [Carbomedics Inc, Austin, TX]) was inserted. Several attempts at weaning off bypass were unsuccessful, despite high doses of inotropes and intra-aortic balloon pump. The patient expired on the table.

The explanted valve was returned to Edwards Lifesciences for analysis. The evaluation of the valve found a large amount of thrombotic material on the cusps of the leaflets on the outflow aspect, which had led to stenosis of the valve (Fig 1). There was also extensive material on the inflow aspect of the valve. Pathologic examination of the material found it to be consistent with thrombotic material, which included platelets, red cells, lymphocytes, and fibrin.


Figure 1
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Fig 1. Photograph shows explanted mitral prosthesis covered in extensive thrombotic debris.

 
Patient 2
A 67-year-old woman with a 4-month history of worsening shortness of breath and occasional angina was referred for aortic valve replacement for severe aortic stenosis. The gradient across the valve was measured at 90 mm Hg, with preserved left ventricular function.

In her past medical history, the patient had undergone liver transplantation in 2004 for primary biliary cirrhosis and resection of a Dukes B adenocarcinoma followed by radiotherapy in 1997. Prior to admission she was noted to be neutropenic and her transplant anti-rejection regime of mycophenolate mofetil (MMF) (an inosine 5'-monophosphate dehydrogenase inhibitor) was reduced. She used regular inhalers for chronic obstructive pulmonary disease, and she was on thyroxine replacement therapy for hypothyroidism.

Angiography had shown normal coronary arteries. She was taken to the operating room for an elective, surgical aortic valve replacement. An Aprotonin infusion was used during the procedure and was discontinued at the end of the procedure. The operation was uncomplicated, and a 23-mm Edwards Lifesciences Perimount Magna (model 3000) aortic tissue bioprosthetic valve was placed using interrupted 2.0 Ethibond mattress sutures (Ethicon, Edinburgh, Scotland). The operation was performed using antegrade crystalloid cardioplegia and a cold circuit for myocardial preservation at normothermic bypass. The cross-clamp time was 43 minutes with a bypass time of 50 minutes.

The patient returned to the intensive therapy unit in a stable hemodynamic state and remained in stable condition until her sudden and rapid deterioration 2 hours after the end of her initial operation. There was a rapid and sustained fall in blood pressure, which failed to respond to corrective measures including bolus adrenaline. A decision was made to reopen the patient to exclude tamponade. On reopening there was no evidence of any hemorrhage or tamponade. There was an initial good response to further bolus adrenaline, but this faded away and the patient again became unstable. The surgical team proceeded to establish cardiopulmonary bypass. The aortotomy was reopened and the prosthetic valve was inspected. Deposits of inflammatory cells with the appearance of fibrin were noted covering all three of the valve leaflets, the sewing ring, and the surrounding the left coronary ostia (Fig 2). The valve was therefore explanted and a mechanical valve was placed after irrigation to remove the deposits from the aortic root.


Figure 2
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Fig 2. Photograph shows freshly explanted aortic bioprosthesis with extensive deposition on cusps and sewing ring. An area of the cusp where the deposited fibrin was removed by the explanting surgeon is visible (arrow), showing the degree of material deposition.

 
The patient was weaned from cardiopulmonary bypass with the an infusion of adrenaline after a second bypass run of 63 minutes and a cross-clamp time of 46 minutes. A postoperative transesophageal echocardiogram was satisfactory, showing a well-seated and functioning mechanical aortic valve prosthesis. Her recovery was hindered by the development of Clostridium difficile positive diarrhea and a gram negative bacteremia. She was discharged home on postoperative day 18. Follow-up is complete now 6 months after her operation with a satisfactory outcome.

The explanted valve was returned to Edwards Lifesciences for analysis. A detailed histologic analysis of the deposits on the valve found that they consisted mainly of polymerized fibrin with mild infiltration of white blood cells and foci of red blood cells consistent with thrombus. There was no histologic evidence of any bacterial cells and the leaflet material itself was preserved.


    Comment
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 Abstract
 Introduction
 Case Reports
 Comment
 References
 
These two cases illustrate a rare but potentially lethal early failure of the Edwards perimount pericardial tissue valve (Edwards Lifesciences) in the aortic and mitral position. Edwards valves have a well documented excellent outcome in published series in both the aortic and mitral position [5, 6]. Studies using microsimulation have shown very little difference in the outcome between four major biological valve types [7]. Patient selection and the timing of operation may account for most of the observed differences in prognosis after aortic valve replacement with biological prostheses [7]. Structural valve degeneration is recognized as a major complication of biological valves with the need for reoperation well understood by the implanting surgeon and with proper informed consent by the patient.

Both implanted valves were washed in accordance with manufacturer's guidelines prior to implantation. Aprotonin was used in the aortic valve replacement case, but not in the mitral valve case in which tranexamic acid (2 g) was given during the procedure. There was no use of any sealant or glue in either case. Neither patient bled excessively, received any clotting factors, or any other prothrombotic agents. The unusual appearance of debris on the valve prosthesis may have caused the adverse clinical presentation of these 2 patients by either interfering with the structural function of the valve leaflets, or in the case of the aortic valve, the debris may have caused the acute presentation by obstructing coronary blood flow through the coronary ostia. There is a possibility that the abnormal debris deposition was caused by the patient's immunosuppressive therapy in the form of MMF. However there are no reported complications with bioprosthetic valves and MMF, and this patient's MMF dose had been reduced prior to admission for surgery in view of her recorded neutropenia and appropriate specialist advice. Indeed MMF is an immunosuppressant that should intuitively lead to a decrease in the inflammatory response and activation, and it has been demonstrated to reduce the human leukocyte antigen response to allograft valve replacement in children undergoing valve replacement [8]. Another consideration is that the cellular material is a consequence of the low output state or valve failure rather than its cause. Heparin-induced thrombocytopenic thrombosis has been suggested as a possible cause. Tests to exclude HIT were not performed in either case and can not be ruled out. However, there was no drop in the platelet count of the aortic valve patient, which would indicate a possible HIT leading to thrombosis. Due to the urgent nature of the mitral valve patient, and their rapid demise, a heparin-induced thrombocytopenic thrombosis, which would be a type II reaction, seems unlikely.


    References
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 Abstract
 Introduction
 Case Reports
 Comment
 References
 

  1. Poirer NC, Pelletier LC, Pellerin M, Carrier M. 15-year experience with the Carpentier-Edwards pericardial bioprosthesis Ann Thorac Surg 1998;66(Suppl 6):S57-S61.[Medline]
  2. Borger MA, Ivanov J, Armstrong S, Christie-Hrybinsky D, Feindel CM, David TE. Twenty-year results of the Hancock II bioprosthesis J Heart Valve Dis 2006;15:49-55.[Medline]
  3. Hadjinikolaou L, Boehm MC, Ganner C, Kendall SW, Rosin, MD, Goldsmith IR, Spyt TJ. Aspire porcine bioprosthesis: ten years' experience J Heart Valve Dis 2005;14(1):47-53.[Medline]
  4. Jamieson WR, Fradet GJ, MacNab JS, Burr LH, Stanford EA, Janusz MT, Abel JG, Germann E, Cheung A. Medtronic mosaic porcine bioprosthesis: investigational center experience to six years J Heart Valve Dis 2005;14:54-63.[Medline]
  5. Marchand MA, Aupart MR, Norton R, Goldsmith IR, Pelletier LC, Pellerin M, Dubiel T, Daenen WJ, Herijgers P, Casselman FP, Holden MP, David TE. Fifteen-year experience with the mitral Carpentier-Edwards Perimount pericardial bioprosthesis Ann Thorac Surg 2001;71(Suppl 5):S236-S239.[Medline]
  6. Jamieson WR, Burr LH, Miyagishima RT, Germann E, Macnab JS, Stanford E, Chan F, Janusz MT, Ling H. Carpentier-Edwards supra-annular aortic porcine bioprosthesis: clinical performance over 20 years J Thorac Cardiovasc Surg 2005;130:994-1000.[Abstract/Free Full Text]
  7. Kappetein AP, Takkenberg JJ, Puvimanasinghe JP, Jamieson WR, Eijkemans M, Bogers AJ. Does the type of biological valve affect patient outcome? Interact Cardiovasc Thorac Surg 2006;5:398-402.[Abstract/Free Full Text]
  8. Anderson JB, Fuller TC, Hawkins JA, Brinkman MK, Profaizer T, Shaddy R. Two-year reduction of panel reactive human leukocyte antigen antibodies in children receiving mycophenolate mofetil after valved allograft placement Transplantation 2005;80:414-416.[Medline]




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Jimmy Kim Fatt Hon
Binayak Chanda
Rakesh Uppal
Simon Kendall
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Right arrow Valve disease


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