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Ann Thorac Surg 2001;72:259-261
© 2001 The Society of Thoracic Surgeons

Case report

An unusual case of bioprosthetic mitral valve thrombosis

Boban Thomas, MDa, Francesc Carreras, MDa, Xavier Borras, MDa, Guillem Pons-Lladó, MDa a Service of Cardiology, Hospital de la Santa Creu i Sant Pau, Barcelona, Spain

Accepted for publication May 9, 2000.

Address reprint request to Dr Carreras, Servei de Cardiologia, Hospital de Sant Pau, Sant Antoni M. Claret, 167, 08025 Barcelona, Spain
e-mail: fcarreras{at}hsp.santpau.es


   Abstract
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 Abstract
Introduction
 Comment
 References
 
Bioprosthetic valve thrombosis and related embolism are considered extremely unlikely, thus allowing most patients to avoid long-term anticoagulation. There is, however, limited experience in the diagnosis and treatment of such a condition. We present the case of a patient with a porcine mitral bioprosthesis who presented with acute thrombosis with unusual echocardiographic features. A favorable outcome was observed after conventional anticoagulant treatment.


   Introduction
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 Abstract
 Introduction
Comment
 References
 
Tissue bioprosthetic valves are used extensively because long-term anticoagulation can be avoided as the risk of thrombotic complications after 3 months postoperatively is low [1]. Once anticoagulant treatment has been withdrawn, however, thrombosis should be considered as a potential cause of prosthetic malfunction. To detect this complication transesophageal echocardiography can be used as the features of prosthetic thrombosis in biologic valves have been described previously [2].

An 82-year-old man, operated on at our institution, received Carpentier-Edwards (Irvine, CA) bioprosthetic valves in the aortic (pericardial tissue, model 2900, size 23) and mitral (porcine tissue model 6650, size 27) positions for severe aortic and mitral regurgitation. A routine postoperative Doppler echocardiographic study estimated a mean mitral pressure gradient of 4 mm Hg and a pressure half time of 128 msec; the function of the aortic prosthesis was also normal. When the patient was in normal sinus rhythm, the left atrium was not dilated (39 mm) and the size and function of the left ventricle were within normal limits, so he was advised to stop anticoagulation 3 months postoperatively. A routine echocardiographic study 1 year after the operation showed normal prosthetic function. The patient remained well for another 3 months, after which dyspnea developed over a period of 48 hours. He was admitted to the hospital with a clinical picture of acute pulmonary edema and atrial fibrillation with a rapid ventricular response. The patient was treated with diuretics, and conversion to sinus rhythm occurred after administration of intravenous amiodarone, which improved his clinical condition. A transthoracic echocardiogram with the patient in sinus rythm revealed signs of mitral prosthetic obstruction (mean mitral gradient, 20 mm Hg; pressure half time, 382 msec) and a mildly dilated left atrium (52 mm). A transesophageal echocardiography study showed homogeneously thickened (5 mm) prosthetic mitral leaflets (Fig 1) without valve regurgitation. This finding suggested the presence of a thrombus adhered to the ventricular aspect of the leaflets. A chronic degenerative process of the tissue leaflets or a pannus was not considered, given the normal features of the previous echocardiographic study. Moreover, pannus growth in mitral bioprostheses presents predominantly on the flow surface as a circumferential rim that extends onto the valve cusps and usually is associated with structural abnormalities and mitral regurgitation [3].



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  		Fig 1. Transesophageal echocardiographic view showing abnormal diffuse valve thickening of a biologic mitral prosthesis.

 
Because experience with thrombolytic therapy for thrombotic occlusion of bioprosthetic valves is limited and the clinical condition of the patient improved after conversion to sinus rhythm, initial treatment with thrombolytic agents or surgery was not considered. Intravenous unfractionated heparin at a therapeutic dose (partial thromboplastin time, 2 to 3 times the control) was started. A repeat transthoracic echocardiogram and transesophageal echocardiography 1 week later showed a normal transvalvular mean gradient (4 mm Hg), pressure half time of 146 msec, decreased left atrial size (41 mm), and dramatically reduced leaflet thickness (1.2 mm) (Fig 2). Long-term warfarin treatment was indicated, and the patient had an uneventful clinical course without further signs of prosthetic dysfunction on echocardiography for 1 year after the acute episode.



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  		Fig 2. Image of the valve, in the same view as in Figure 1, obtained after resolution of the thrombus with antithrombotic therapy. Leaflet thickening has disappeared, thus excluding a degenerative process.

 

   Comment
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 Abstract
 Introduction
 Comment
References
 
Freedom from the need for anticoagulation makes bioprosthetic valves an attractive option. However, the potential for thrombus formation and valve dysfunction does remain, as mild abnormalities in blood rheology favoring thrombosis have been described in patients with bioprostheses [4].

Some aspects of this case are remarkable. From the clinical perspective, there was an apparent lack of precipitating factor of the thrombotic process, as the patient had no underlying coagulation abnormality, left ventricular dysfunction, or low cardiac output, which are processes known to cause bioprosthetic thrombosis [5]. Although it cannot be excluded that the valve thrombosis could have been a consequence of the episode of paroxysmal atrial fibrillation, it is more probable that the arrhythmia was secondary to the increased left atrial pressure caused by the prosthetic obstruction. Also interesting was the rapidly evolving left heart failure, which is seen more commonly in acute thrombotic obstruction of mechanical valves. In fact, some reported patients with bioprosthetic thrombosis presented with insidious symptoms of heart failure [2].

Second, the echocardiographic appearance of the prosthetic thrombosis in our case was unusual, with a layered thrombus adhered to the ventricular aspect of the valve leaflets causing a uniform increase in valve thickness (Fig 1). The restricted motion of the leaflets resulted in transient stenosis. Other reports have shown the classic findings of a pedunculated mass on the free edge of the leaflets with an otherwise normal thickness of the valve tissue [2].

Finally, the resolution of the case also deserves comment. Although thrombolytic therapy is an established first-line therapy for high-risk patients with prosthetic valve thrombosis [6], conventional anticoagulant treatment with heparin was instituted as a first therapeutic attempt in our case according to the experience described by others [7] and resulted in an early complete resolution of the process (Fig 2). Heparin therapy has been recommended in patients with prosthetic valve thrombosis and functional class I or II [8], and cases with good outcome after heparin treatment have been reported [2, 7].


   References
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 Abstract
 Introduction
 Comment
 References
 

  1. Stein P.D., Alpert J.S., Dalen J.E., Horstkotte D., Turpie A.G. Antithrombotic therapy in patients with mechanical and biological prosthetic heart valves. Chest 1998;114(Suppl 5):602S-610S.[Free Full Text]
  2. Oliver J.M., Gallego P., Gonzalez A., Dominguez F.J., Gamallo C., Mesa J.M. Bioprosthetic mitral valve thrombosis: clinical profile, transesophageal echocardiographic features, and follow-up after anticoagulant therapy. J Am Soc Echocardiogr 1996;9:691-699.[Medline]
  3. Butany J., Yu W., Silver M.D., David T.E. Morphologic findings in explanted Hancock II porcine bioprostheses. J Heart Valve Dis 1999;8:4-15.[Medline]
  4. Koppensteiner R., Moritz A., Schlick W., et al. Blood rheology after cardiac valve replacement with mechanical prostheses or bioprostheses. Am J Cardiol 1991;67:79-83.[Medline]
  5. Hagley M.T., Lopez-Candales A., Phillips K.J., Daily B.B., Kouchoukos N.T. Thrombosis of mitral valve bioprostheses in patients requiring circulatory assistance. Ann Thorac Surg 1995;60:1814-1816.[Abstract/Free Full Text]
  6. Manteiga R., Carlos Souto J., Altes A., et al. Short-course thrombolysis as the first line therapy for cardiac valve thrombosis. J Thorac Cardiovasc Surg 1998;115:780-784.[Abstract/Free Full Text]
  7. Moujir F., Martín-Durán R., Vázquez de Prada J.A., Trugeda A., Figueroa A., Olalla J.J. Disfuncion por trombosis en bioprotesis de Hancock mitral resuelta con heparina. Rev Esp Cardiol 1989;42:219-221.[Medline]
  8. Lengyel M., Fuster V., Keltai M., 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;30:1521-1526.[Abstract]



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