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Ann Thorac Surg 1997;64:255-257
© 1997 The Society of Thoracic Surgeons
Departments of Interventional Cardiology and Nuclear Medicine, St. Georg Hospital Leipzig, Leipzig, Germany
Accepted for publication March 5, 1997.
| Abstract |
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| Introduction |
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Thrombosis of a valvular prosthesis is a rare but potentially lethal condition. Most reports on prosthetic valve thrombosis describe patients with valves implanted in the aortic or mitral position. We present our experience with a thrombosis of a pulmonary prosthetic valve, where the clinical management might be different than in left ventricular prosthetic valves.
A 22-year-old woman complained of left-sided chest pain and exertional dyspnea for 2 weeks. According to her medical records pulmonary atresia and a ventricular septal defect were diagnosed at the age of 6 years. Additionally, the aortic valve was overriding the ventricular septal defect with about two thirds of its orifice. At that time the right ventricular outflow tract was surgically enlarged using a Dacron patch. Simultaneously a St. Jude Medical (St. Paul, MN) bileaflet prosthetic valve (size 23 mm) was inserted in the pulmonary valve position, and the ventricular septal defect was closed by an approximately 25 mm triangular Dacron patch. Thereafter oral anticoagulation was started. Four years later, the ventricular septal defect had to be reoperated on due to recurrence of a left-to-right shunt. When the patient was 14 years of age, a DDD pacemaker was implanted for treatment of high-grade atrioventricular block. For the following years the patient was feeling well. Seven years ago, oral anticoagulation was terminated on recommendation of her pediatric cardiologist, and the patient was told to take aspirin, 300 mg a day, which was reduced to 100 mg 4 years later.
Nine weeks before the current visit, the patient was seen routinely at another outpatient clinic, where a maximum Doppler gradient of 45 mm Hg was measured for the prosthetic pulmonary valve.
On physical examination blood pressure was 110/70 mm Hg in both arms. Heart rate was 60 beats per minute. Auscultation revealed a grade 4 ejection murmur with peak intensity over the second left intercostal space. The valve clicks were not audible. The electrocardiogram showed a regular sinus rhythm with a pulse rate of 64 per minute. Ventricular complexes were initiated by pacing spikes followed by a QRS complex with left bundle-branch configuration. Doppler echocardiography demonstrated a peak gradient of 70 mm Hg for the valve prosthesis. Large thrombotic masses situated within the prosthetic valve could be excluded by two-dimensional transthoracic echocardiography.
To further evaluate the function of the pulmonary valve, we performed fluoroscopy and right heart catheterization. Fluoroscopy showed a standstill of both leaflets in the systolic position (Fig 1
AC). Right ventricular pressure was 60/0/5 mm Hg. Mean right atrial pressure was 3 mm Hg. Right ventricular angiography showed a slightly dilated right ventricle with preserved systolic function. At that time arterial oxygen saturation was 96%.
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| Comment |
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The patient was receiving aspirin as the sole antithrombotic agent for 7 years. Aspirin as an antiplatelet agent without oral anticoagulation was recently recommended as a safe treatment for the prevention of prosthetic valve thrombosis in selected patients with replacements of the aortic or mitral valve [6]. These patients were characterized by sinus rhythm, left atrial size less than 55 mm, and no previous thromboembolic episodes [6]. However, the current case suggests that such a therapeutic regimen should not be recommended in patients with a St. Jude bileaflet prosthesis in the pulmonary position. Furthermore, an earlier case report observed thrombosis of a St. Jude valve prosthesis in the pulmonary position even during correct and adequate oral anticoagulation. The authors of that report therefore concluded that aspirin should be added to oral anticoagulation in these patients [4].
An earlier report [1] on a thrombosed St. Jude prosthesis in the tricuspid position described crossing of the prosthetic valve by a Swan-Ganz catheter to determine the transvalvular pressure gradient. There exists, however, a report on a lethal outcome after entrapment of a cardiac catheter in a prosthetic heart valve [7]. Therefore we did not try to confirm the echocardiographically obtained transvalvular pressure gradient of the thrombosed valve during cardiac catheterization.
Thrombolytic therapy for thrombosis of prosthetic valves carries a substantial risk of embolism, reaching an average of 17% in a recently published literature review [2]. On the other hand, reoperation has a mortality rate between 8% and 42%, depending on the functional stage of the patient [1]. In the patient presented here, the risk of a third operation was considered higher than the risk of the occurrence of a major pulmonary embolism during thrombolysis, especially because large pulmonary embolism was not expected due to echocardiographic and angiographic exclusion of large thrombotic masses. In previous work, successful thrombolytic therapy was still observed when the duration of symptoms did not exceed 14 days [3]. Therefore we decided to initiate systemic urokinase therapy at this comparatively late stage after the beginning of the suspected thrombosis. We applied a dose that is used for treatment of pulmonary embolism [8]. The risks of thrombolysis-related bleeding complications were considered minimal in our young, otherwise healthy patient.
We cannot exclude that the observed pulmonary embolism already occurred before thrombolytic therapy. Therefore, future cases of thrombolytic therapy in thrombotic right heart prosthetic valves should consider a lung perfusion scan both before and after thrombolysis.
In conclusion, thrombolytic therapy can be considered as a first-line regimen for the treatment of a thrombosed prosthetic pulmonary valve. Aspirin as a substitute for oral anticoagulation after prosthetic replacement of a pulmonary valve carries a substantial risk of valve thrombosis.
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