Asian Cardiovasc Thorac Ann 2002;10:165-166
© 2002 Asia Publishing EXchange Pte Ltd
Acute Thrombotic Obstruction of Mitral Valve Prosthesis: Low Protein C Level
Toshihiro Ohata, MD,
Tetsuo Sakakibara, MD,
Hiroshi Takano, MD,
Toru Ishizaka, MD
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Department of Cardiovascular Surgery Osaka Police Hospital Osaka, Japan
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Toshihiro Ohata, MD Tel: 81 6 6692 1201 Fax: 81 6 6606 7031 email: tohata{at}aol.comDepartment of Cardiovascular Surgery, Osaka Prefectural Hospital, 3-1-56 Bandai-Higashi, Sumiyoshi-ku, Osaka 558-8558, Japan.
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ABSTRACT
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A 51-year-old female underwent redo mitral valve replacement with a pericardial bioprosthesis because of acute thrombotic obstruction of a mechanical valve, in spite of adequate anticoagulation with warfarin. Her protein C level was 24% of the normal value and protein S was reduced to 54% of normal.
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INTRODUCTION
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Acute thrombotic obstruction of a mechanical valve prosthesis is a rare but serious complication associated with high mortality even if emergency medical and surgical treatment is instituted promptly.1 Other than inadequate or discontinued anticoagulant therapy, which is the most common risk factor, little is known about other factors that might cause or promote prosthetic thrombosis.1,2 A case of mechanical valve thrombosis despite adequate anticoagulation is described.
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CASE REPORT
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A 25-mm St. Jude Medical (SJM) prosthesis (St. Jude Medical, Inc., St. Paul, MN, USA) was used to replace the mitral valve in a 51-year-old woman who had undergone an open mitral commissurotomy for rheumatic mitral valve stenosis 13 years previously. She was dis-charged in good clinical condition on adequate anticoagu-lation with warfarin. Her international normalized ratio was controlled between 2.2 and 2.6. She came to our hospital for an unscheduled examination 3 months after the operation and was readmitted because of heart failure. Physical examination revealed orthopnea, peripheral edema, and coldness of the limbs. Echocardiography showed a large pressure gradient (> 30 mm Hg) across the implanted SJM prosthesis, and little movement of one leaflet, confirming prosthetic valve dysfunction. Sudden hemoptysis occurred during an urgent catheter study. Thrombotic obstruction of the SJM valve was diagnosed and emergency surgery was carried out.
The ascending aorta, superior vena cava, and right atrium were exposed with some difficulty because of severe adhesions, and after cannulation, cardiopulmonary bypass was established. The ascending aorta was crossclamped under moderate systemic hypothermia (28°C). Antegrade and retrograde intermittent cold blood cardioplegia was used for myocardial protection. The SJM prosthesis was thoroughly examined via a superior septal approach. The leaflet of the posteromedial commissure side was almost completely immobilized by a fresh red thrombus on the left atrial side, and fresh thrombi adhered to both hinges and impeded the motion of both leaflets on the left ventricular side (Figure l
). The valve was replaced with a 25-mm Carpentier-Edwards pericardial bioprosthesis (Baxter Healthcare Corp., Irvine, CA, USA) to prevent a recurrence of thrombotic obstruction. The patient was weaned from cardiopulmonary bypass without difficulty and made an unremarkable recovery. She was discharged on postoperative day 24. Her serum levels of protein C and protein S on the 8th postoperative day were signifi-cantly reduced to 24% and 54% of the normal values, respectively. At 4 months after the final operation, the protein C level was 22% and protein S was 47% of the normal value; the other coagulation data and platelet counts were within the normal ranges in the postoperative period, although the levels of factors II, VII, IX, and X were decreased as a result of warfarin anticoagulation. The anticardiolipin antibody level was normal. Patho-logical examination of the resected SJM prosthesis showed fresh and old thrombi, but no pannus formation or bacterial colony. The fresh thrombi were organized with collagen and fibrin deposits.
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Figure 1. Gross appearance of the resected mechanical prosthesis. (A) Left atrial side: the leaflet of the posteromedial commissure side was almost completely immobilized as a result of a fresh red thrombus. (B) Left ventricular side: fresh thrombi adhering to both hinges impeded the motion of both leaflets.
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DISCUSSION
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Acute obstruction is one of the most serious complications of a mechanical prosthetic valve, with an incidence ranging from 0.93% to 4.5% per patient-year.3,4 Because this complication is relatively rare, the mechanism of obstruc-tion and spectrum of presentation are not well defined, and the clinical diagnosis is often missed or made too late. Renzulli and colleagues5 speculated that prosthesis obstruction might be attributable to a primary thrombosis only in cases where it may be prevented by adequate anticoagulation, and that the obstruction is produced by periprosthetic fibroblastic proliferation that might develop in spite of adequate anticoagulation in most cases. This hypothesis does not fit our case because no pannus formation was found in the resected SJM prosthesis. Although the cause of thrombosis unrelated to anticoagu-lation is still unknown, it may be related to an abnormality of coagulation factors, such as a deficiency of proteins with anticoagulant properties.
Protein C, a vitamin K-dependent protein, is a natural anticoagulant synthesized in the liver.6 After activation by thrombin, protein C is a potent inhibitor of the coagulation cascade that stimulates fibrinolysis. Protein S acts as a cofactor in this pathway, increasing fibrinolysis.7 A deficiency of these proteins can cause an increase in coagulation. Miletich and colleagues8 reported that 10 subjects among 5,422 blood donors had protein C levels between 33% and 51% of normal due to a heterozygous deficiency of protein C. The most severe disorder of protein C, the homozygous type, might result in a hypercoagulation state such as unexplained purpura fulminans.8 The level of protein C in our patient was considered to be extremely low. The low protein C and protein S levels may have led to thrombotic valve obstruction in spite of adequate anticoagulation therapy. It is possible that a combination of other abnormalities might increase the risk of thrombosis in patients with protein C deficiency. Further studies are needed to clarify this mechanism. Valve replacement with a bioprosthesis rather than a mechanical prosthesis was preferred because thrombotic reobstruction resulting from metabolic hypercoagulability might occur in such patients. Although we selected surgical management in this case because of sudden hemoptysis and worsening hemodynamics, thrombolysis is regarded as the first choice of treatment in a patient with chronic thrombotic obstruction of a mechanical prosthesis.
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REFERENCES
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Renzulli A, De Luca L, Caruso A, Verde R, Galzerano D, Cotruflo M. Acute thrombosis of prosthetic valves: a multivariate analysis of the risk factors for a life-threatening event. Eur J Cardio-thorac Surg
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Walker FJ. Protein S and the regulation of activated protein C. Thromb Haemost
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Miletich J, Sherman L, Broze G Jr. Absence of thrombosis in subjects with heterozygous protein C deficiency. N Engl J Med
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ABSTRACT
INTRODUCTION
