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J Thorac Cardiovasc Surg 2006;132:1464-1465
© 2006 The American Association for Thoracic Surgery
Brief Communication |
Department of Cardiothoracic Surgery, National Heart Centre, Singapore.
Received for publication July 21, 2006; accepted for publication August 8, 2006. * Address for reprints: Nakao Masakazu, National Heart Centre, Singapore, Department of Cardiothoracic Surgery, Mistri Wing, 17 Hospital Ave, Singapore 168752, Singapore. (Email: mnakao{at}singnet.com.sg).
Bioprosthetic valves are the preferred option for mitral valve replacement in the elderly because there is a low risk of thromboembolic complications compared with mechanical valves. Current consensus is that long-term anticoagulation can be avoided in patients with bioprosthetic valve replacement because postoperative thromboembolic risk after 3 months is extremely low.1
Once anticoagulation is withdrawn, thrombosis causing bioprosthetic valve dysfunction is extremely rare.
A 69-year-old man with a history of stroke 14 years before surgical intervention underwent mitral valve replacement with a 31-mm Hancock II porcine bioprosthesis (Medtronic, Inc, Minneapolis, Minn) and the radiofrequency maze procedure for severe mitral regurgitation and chronic atrial fibrillation. He was started on warfarin, and the international normalized ratio was kept within a therapeutic range of 2.0 to 2.5. Postoperative transthoracic echocardiography (TTE) showed normal bioprosthetic valve function with a mean mitral pressure gradient (PG) of 4.0 mm Hg.
Warfarin was discontinued at 1
years postoperatively because there was no recurrence of atrial fibrillation on follow-up electrocardiography and 24-hour Holter tests. Aspirin was continued for minor coronary artery disease. TTE before cessation of warfarin confirmed normal mitral valve function with a mean PG of 6.0 mm Hg. Ratio of early filling velocity to atrial contraction velocity (E/A ratio) was 1.58, implying active atrial contraction. Left ventricular ejection fraction (LVEF) was 62%. Left atrial diameter was 6.0 cm.
One month after warfarin was stopped, the patient was admitted with fever, shortness of breath, and loss of appetite for 3 days. Blood culture was sterile. Chest radiography revealed acute pulmonary edema. TTE demonstrated severe mitral stenosis with a mean mitral PG of 24 mm Hg and pressure half-time (PHT) of 187 ms. The mitral valve leaflets were thickened, and leaflet motion was restricted. There was no change in LVEF or left atrial diameter. The E/A ratio was 1.4. Transesophageal echocardiography (TEE) confirmed the findings on TTE. No discrete intracardiac thrombus was visualized. Valve thickness on TEE was 6.5 mm (Figures 1 and 2).
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A repeat TTE 1 week later showed a decreased mean mitral PG of 11 mm Hg. PHT had also decreased to 107 ms. Two weeks after treatment was commenced, TTE demonstrated normal mitral bioprosthetic valve function with a mean mitral PG of 6.2 mm Hg and a PHT of 114 ms. Three months after discharge, TEE revealed a mean mitral valve PG of 4.0 mm Hg and a valve thickness of 1.2 mm.
The patient was maintained on warfarin and was well on follow-up 6 months later.
Bioprosthetic mitral valve thrombosis is a rare cause of prosthetic valve dysfunction postoperatively. Low cardiac output,1 large left atrium,1 prior history of thromboembolic events,1 low transvalvular flow caused by atrial fibrillation,2,3 and abnormality in blood rheology4 are most commonly cited as predisposing factors.
In this case there were no obvious risk factors for thrombosis: LVEF was normal, the left atrium was only mildly enlarged, and there was no hypercoagulable diathesis, although the patient did have a history of stroke 14 years before the operation. Surgical intervention had also successfully been used to treat the problem of atrial fibrillation, and he had been in sinus rhythm for 1 years. His E/A ratio was 1.58 before warfarin was withdrawn. He was also taking aspirin, and it has been reported that aspirin alone can reduce the risk of postoperative thromboembolic complications after bioprosthetic valve implantation in the mitral position.1 Radiofrequency maze lesion lines were unlikely to be a source leading to propagation onto the valve leaflets because there were no intra-atrial clots and thrombus was laminar along all the valve leaflets.
Intravenous heparin was started in this patient with a plan to commence thrombolytic therapy if heparin alone was ineffective. Although thrombolytic therapy is an established first-line treatment, this patient responded to heparin anticoagulation followed by warfarin. Several studies have reported good resolution of bioprosthetic thrombus after conventional anticoagulation.2-5 Concurring with these studies, we had a favorable result after 1 week of heparin and subsequent warfarinization.
Clinically significant bioprosthetic valve thrombosis is rare, although the reported incidence in the study by Oliver and colleagues5 is 6.2%. It should be considered a possible cause of valve dysfunction when there is increasing transvalvular pressure gradient after anticoagulation is terminated. Treatment with conventional anticoagulation is unavoidable in such a setting.
References
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