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Case Studies

Obstructed Mitral Prosthesis
Brian Walton, Andres Mesa, Efrain Garcia

History of Present Illness

73 year old Hispanic male with a history of rheumatic heart disease requiring mitral and aortic tissue valve replacement in 1980, followed by mitral and aortic mechanical valve replacement 1988, presents to St. Luke's Episcopal Hospital with complaints of progressive shortness of breath and dypsnea on exertion. The patient had been in his usual state of health until the development of these complaints 30 days prior to admission. He reports therapeutic INR levels during the period prior to this evaluation.

Past Medical History

  • Rheumatic heart disease with mitral and aortic tissue valve replacement in 1980.
  • Mitral ( St. Jude #25) and aortic (St. Jude #21) mechanical valve replacement 1988
  • Atrial fibrillation with radiofrequency catheter ablation and VVIR pacemaker placement


  • Coumadin 5 mg po qd
  • Digoxin 0.250 mg po qd
  • Cozaar 50 mg po qd

Vital Signs

  • Heart rate 66
  • Blood pressure 140/60 

Physical Exam

  • HEENT- JVP 3 cm,
  • Heart - S1 S2 with SEM at base and mechanical click, diastolic rumble
  • Lungs - clear
  • Abdomen - benign
  • Extremities - no edema with normal pulses

Pre-admission Transthoracic Echocardiogram

    Click here for color doppler movie showing eccentric MS jet (744 KB).

    M-mode still image. Obstructed mitral prosthesis: peak gradient 35 mm Hg, mean gradient 17 mm Hg, MV TVI 127, pressure time 222


  • Normal ventricular chamber size and function with mild left ventricular hypertrophy.
  • Left ventricular ejection fraction 55-60%.
  • Biatrial dilatation.
  • Normally functioning aortic prosthesis- peak gradient 44 mm Hg, mean gradient 21 mm Hg, AV TVI 57cm, LVOT 17 cm, valve area 1.03 cm2
  • Estimated systolic pulmonary artery pressure 45-50
  • Estimated right atrial pressure 10-15

Hospital Course

    Patient is admitted to St. Luke's Episcopal Hospital for further evaluation of the obstructed mitral valve. Transient symptoms consistent with amaurosis fugax were reported shortly before admission and a neurological evaluation did not reveal any persistent deficits.

     Click here for fluoroscopy revealing a trapped posterior mitral leaflet (544 KB).

    Review of the echocardiographic data suggested thrombus versus pannus was responsible for the obstruction and thrombolysis was initiated. A Retavase infusion of 1unit/ hour was initiated in addition to heparin 500 units/ hour. Serum fibrinogen levels were monitored periodically to ensure adequate fibrinolysis.The patient underwent repeat transthoracic echocardiography on hospital day #2 showing obstructed mitral prosthesis. Peak gradient was 27 mmHg, mean gradient 11 mmHg, MV TVI 86.3cm, pressure time 171.

    Twenty hours after the initiation of thrombolysis our patient reported a global headache and was found by CT scan of the brain to have a left parietal intraparenchymal and interventricular hemorrhage. Both Retevase and heparin were discontinued immediately and cerebral angiography was unrevealing as to a source. The patient's neurological symptoms improved during the next two days.

    Click here for follow-up fluoroscopy on hospital day 7 showing free-moving leaflet (710 KB).

    Follow-up fluoroscopy on hospital day 7 demonstrated resolution of the posterior leaflet obstruction and a normally functioning valve. Transthoracic echocardiography showed normalization of both peak (16 mm Hg) and mean (5 mm Hg) gradients across the mitral valve. His symptoms of dypsnea resolved and his neurologic function returned to baseline. At the time of discharge, our patient was anticoagulated with coumadin and plavix.


    Obstruction of a prosthetic valve is a serious complication of valvular replacement. Obstruction can occur as a result of pannus formation, thrombus formation or a combination of pannus with secondary thrombosis (1). Pannus formation without thrombosis is the most common cause of obstruction and can occur despite therapeutic anticoagulation(2), however, primary thrombosis of mechanical mitral valves has been reported to occur at a rate of 0.63% per patient year (3). Historically, obstruction has been treated by surgical intervention and carries significant mortality risk in the acute setting. The first successful use of thrombolytic therapy for treatment of a mechanical valve obstructed by thrombosis was reported by Luluaga et al (4) in 1971. Since that time thrombolytic therapy for treatment of thrombosed valves has emerged as an alternative to surgical repair in the high risk surgical patient. Silber et al (5) reported successful treatment of 10/12 (83%) patients with thrombosed St. Jude valves with clinical improvement in less than 12 hours using a streptokinase infusion protocol. Similar success rates have been reported with streptokinase and other fibrinolytic agents (6). Major adverse events secondary to thromboembolism and hemorrhage have been reported occur in 19%-30%(5-7) and 6% (8) of cases, respectively. The risk of stroke ranging 5% to10% and recurrent thrombosis occurs in 11% of cases (9). The high clinical success rate and relatively low rate of major adverse events suggest thrombolysis of thrombosed mechanical valves is an alternative to surgery.


  • 1. Vitale N et al. Obstruction of mechanical mitral prostheses: analysis of pathologic findings. Ann Thor Surg 1997;63:1101-6.
  • 2. Renxulli A. Acute thrombosis of prosthetic valves: a multivariate analysis of the risk factors for a life threatening event. Eur J Cardio-thorac Surg 1992;6:412-421.
  • 3. Jamieson WRE et al. Bileaflet mechanical prostheses performance in mitral position. Eur J Cardio-thorac Surg 1999;15:786-794.
  • 4. Luluaga IT et al. Successful thrombolytic therapy after acute tricuspid-valve obstruction. Lancet 1971;1:1067-68.
  • 5. Silber H et al. The St. Jude valve: thrombolysis as the first line of therapy for cardiac valve thrombosis. Circulation 1993;87:30-37.
  • 6. Roudaut R et al. Mechanical cardiac valve thrombosis: is fibrinolysis justified? Circulation 1992;86(suppl II):II-8-II-15.
  • 7. Manteiga R et al. Short-course thrombolysis as the first line of therapy for cardiac valve thrombosis. J Thorac Cardiovasc Surg 1998;115:780-4.
  • 8. Koller PT, Arom KV. Thrombolytic therapy of left-sided prosthetic valve thrombosis. Chest 1995;108:1683-9.
  • 9. Lengyel M et al. Guidelines for management of left-sided prosthetic valve thrombosis: a role for thrombolytic therapy. J Am Coll Cardiol 1997;301521-6.

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