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European Journal of Echocardiography Advance Access originally published online on April 13, 2007
European Journal of Echocardiography 2008 9(3):399-400; doi:10.1016/j.euje.2007.02.001
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Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2007. For permissions please email: journals.permissions@oxfordjournals.org

An unusual case of late bioprosthetic mitral valve thrombosis successfully managed with anticoagulation

Adel Aminian*, Pascal Lefebvre, Philippe Delmotte and Alain Friart

Division of Cardiology, Tivoli University Hospital, Max Buset Avenue 34, 7100 La Louvière, Belgium

Received 14 September 2006; accepted after revision 4 February 2007; online publish-ahead-of-print 13 April 2007.

* Corresponding author. Tel: +32 64 277391; fax: +32 64 276392. E-mail address: adaminian{at}hotmail.com


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In this report, we present the case of a patient with hemodynamically significant thrombosis of a mitral bioprosthesis occurring 11 years after valve replacement. The diagnosis was suspected on the basis of a subacute increase in the transvalvular gradient seen on transthoracic echocardiography and was con- firmed by transesophageal echocardiography which disclosed unusual features. A hypercoagulable work up showed raised plasma factor VIII levels. The patient was successfully managed with oral anticoagulation.

Keywords: Bioprosthetic; Thrombosis; Anticoagulation


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A 79-year-old woman with a previous history of bioprosthetic mitral valve replacement in 1995 presented at a follow-up visit in February 2006. A transthoracic echocardiography (TTE), with the patient in sinus rhythm, showed signs of mitral valve prosthetic dysfunction (see Table 1). Left ventricular function was preserved. Despite reduced physical activity due to old age, there were no complaints on anamnesis. A transoesophagal echocardiography (TEE) study was performed and revealed abnormal diffuse and homogeneous thickening of the mitral leaflets (Figure 1), causing mild to moderate regurgitation, and suggesting the presence of a thrombotic process. A trial of oral anticoagulation with acenocoumarol (target international normalized ratio between 3 and 4.5) led to a rapid and favorable hemodynamic evolution (Table 1). A control TEE performed 3 months after the beginning of anticoagulation showed a significant regression of the leaflet thickening (Figure 2), confirming the assumption of bioprosthetic thrombosis. A hypercoagulable work up revealed an isolated increase in factor VIII levels (2000 IU/l, normal value 500–1500 IU/l). Long-term anticoagulation was indicated, and the patient remained free of any thrombosis recurrence during follow up.


Figure 1
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Figure 1 Transoesophageal echocardiographic view showing a bioprosthetic mitral valve with abnormal diffuse and homogeneous thickening of the leaflets.

 


Figure 2
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Figure 2 Mitral valve recording obtained after anticoagulation. There is a dramatic decrease in leaflet thickening confirming the diagnosis of bioprosthetic thrombosis.

 


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Table 1 Evolution of hemodynamic data before and after anticoagulation

 

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Unlike mechanical valve prostheses, bioprosthetic valves are associated with a very low rate of thrombosis, approximately 0.03% per year.1 Longterm anticoagulation is thus usually not recommended. When it does occur, it is generally associated with favoring conditions such as thrombophilic disorders, loss of atrial contraction, ventricular dysfunction and low output state. However, in a TEE study, Oliver et al. found bioprosthetic thrombosis in 10 of 161 patients (6.2%) with evidence of bioprosthetic mitral valve dysfunction suggesting that thrombosis could be a more frequent cause of bioprosthetic valve dysfunction than was previously thought.2 Of note, in that study, anticoagulation resulted in complete thrombus resolution in six patients and in long-term symptomatic improvement in seven patients. In this report, we present a case of bioprosthetic mitral valve thrombosis occurring 11 years after valve replacement. Several interesting features of this case deserve comment.

First, since the patient was not symptomatic, prosthetic dysfunction was only diagnosed on the basis of a subacute increase in the transvalvular gradient seen on TTE, but the cause of this increase was unclear. However, suspicion of thrombosis arose after TEE, underscoring its impact on the definition of the cause of prosthetic dysfunction,2 and that allowed starting early anticoagulation before further dysfunction. In this setting, the subacute increase of the transvalvular gradient, as seen in our patient, and due to thrombotic obstruction, must be distinguished from a more gradual increase due to degenerative changes of the prosthetic leaflets. Second, the classical echocardiographic findings reported in bioprosthetic mitral valve thrombosis are a pedunculated or a sessile mass attached to the free edge of the cusps, mainly on the ventricular surface.2 In our patient, we found an unusual appearance of prosthetic thrombosis with an extensive and uniform layered thrombus adhering to the atrial and the ventricular side of both leaflets inducing diffuse valvular thickening and resulting in restricted leaflet motion and stenosis. Only a few reports have described a similar pattern. 3 Interestingly, the result of a hypercoagulable work up showed an isolated increase in factor VIII concentration which is now accepted as an independent marker of thrombotic risk. Finally, the favorable outcome after oral anticoagulation deserves to be emphasized.

In fact, although thombolytic therapy is an established first-line therapy for high-risk patients with mechanical valve thrombosis,4 the optimal treatment of bioprosthetic thrombosis is still a matter of debate. In our patient, given the subacute process and the absence of hemodynamic instability that would have required early surgery, we decided to use conventional oral anticoagulation as a first therapeutic attempt which led to nearly complete thrombus resolution at 3 months.

This case supports the experience described by others2,3 demonstrating that anticoagulation is safe and highly effective in resolving thrombosis on bioprostheses.


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 References
 

  1. Grunkemeier GL, Li HH, Naftel DC, Starr A, Rahimtoola SH. Long-term performance of heart valve prostheses. Curr Probl Cardiol (2000) 25:73–154.[Medline]
  2. Oliver JM, Gallego P, Gonzalez A, Dominguez FJ, Gamallo C, Mesa JM. Bioprosthetic mitral valve thrombosis: clinical profile, transesophageal echocardiographic features, and follow-up after anticoagulant therapy. J Am Soc Echocardiogr (1996) 9:691–9.[CrossRef][Medline]
  3. Thomas B, Carreras F, Borras X, Pons-Llado G. An unusual case of bioprosthetic mitral valve thrombosis. Ann Thorac Surg (2001) 72:259–61.[Abstract/Free Full Text]
  4. Lengyel M, Fuster V, Keltai M, Roudaut R, Schulte HD, Seward JB, et al. Guidelines for management of left-sided prosthetic valve thrombosis: a role for thrombolytic therapy. Consensus Conference on Prosthetic Valve Thrombosis. J Am Coll Cardiol (1997) 30:1521–6.[Abstract]

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This Article
Right arrow Abstract Freely available
Right arrow FREE Full Text (PDF) Freely available
Right arrow All Versions of this Article:
9/3/399    most recent
j.euje.2007.02.001v1
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