Asian Cardiovasc Thorac Ann 1998;6:179-182
© 1998 Asia Publishing EXchange Pte Ltd
Prosthetic Cardiac Valve Replacement: Management Problems
Navneet Sharma, MD,
Anil Grover, DM1,
Bishan Das Radotra, MD2
Department of Internal Medicine
1 Department of Cardiology
2 Department of Pathology Postgraduate Institute of Medical Education and Research Chandigarh, India
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For reprint information contact: Anil Grover, DM Department of Cardiology Postgraduate Institute of Medical Education and Research Chandigarh 160012, India Tel: 91 172 54 1032 Ext. 380 Fax: 91 172 54 0401 Email: medinst{at}pgi.chd.nic.net.in.
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ABSTRACT
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Altered states of coagulability can be precarious for patients with valvular prostheses. Prosthetic valvular thrombosis can produce devastating hemodynamic changes wherein surgical intervention might be high risk. We describe the cases of 4 patients with prosthetic cardiac valve replacements to highlight some of the problems that might be encountered. The first patient suffered prosthetic valve thrombosis following withdrawal of her anticoagulants during labor. She was treated with urokinase but failed to survive. The second young female suffered two episodes of valvular thrombosis and was successfully treated with streptokinase on the first occasion but succumbed one year later during the second episode. The third patient was an elderly male who suffered an intracerebral hemorrhage as a result of an increase in anticoagulant dosage. He was successfully managed with low molecular weight heparin. In the fourth case, a young female with a prosthetic mitral valve had a favorable clinical outcome in spite of withdrawal of anticoagulants during labor.
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INTRODUCTION
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Replacement of a diseased and deformed cardiac valve with a prosthesis is a common mode of treatment for patients with hemodynamically significant cardiac valvular lesions. In spite of improvement in the quality of life for the patient, valve prostheses carry an inherent risk of complications, mainly thromboembolism and infection. Treatment of the acquired risk of thrombosis with the lifelong use of oral anticoagulant drugs has prevented morbidity to an extent. However, the many improvements in the design and quality of prosthetic valves have not overcome the risk of thrombotic complications. The following cases illustrate the problems faced in 4 patients.
CASE 1
A 23-year-old female diagnosed with chronic rheumatic heart disease underwent mitral valve replacement with a Medtronic valve (Medtronic Inc., Minneapolis, MN, USA). She was prescribed oral anticoagulation with 2 mg acenocoumarol daily. One year later, she conceived. At the 8th month of gestation, she was admitted for a change from oral anticoagulant therapy to intravenous heparin therapy. The coagulation profile showed that her international normalized ratio (INR) was 2.5. On echocardiography, a normally functioning prosthetic mitral valve was visualized. Oral acenocoumarol was discontinued and intravenous heparin was started in adequate doses to maintain the partial kaolin thromboplastin time at 1.5 to 1.8 times the control value. She went into spontaneous labor and heparin was withheld in the second stage of labor. While in labor, the patient developed breathlessness and cyanosis, she was noted to have tachycardia, tachypnea, and hypotension. On auscultation, there was muffling of the prosthetic valvular sounds and basal crepitations over the lung bases. She was treated for pulmonary edema. After delivery, her symptoms worsened. Intravenous heparin was administered and thrombolytic therapy with urokinase was started. The patient continued to deteriorate in spite of maximal doses of inotropic agents and soon succumbed to her illness. The clinical diagnosis of prosthetic valve thrombosis was confirmed at autopsy (Figure 1
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Figure 1. Atrial aspect of the thrombosed mitral valve prosthesis from patient no. 1. The open arrow indicates the valve prosthesis while the closed arrow indicates the thrombosis.
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CASE 2
A 16-year-old female underwent mitral valve replacement with a Sorin valve (Sorin Biomedical Inc., Irvine, CA, USA) for chronic rheumatic heart disease. She was taking 3 mg acenocoumarol daily and did not report for follow-up in the outpatient clinic for supervision of her anticoagulation. She was admitted twice with prosthetic valve thrombosis. On the first occasion, she presented with acute onset breathlessness and diminished acuity of her prosthetic valvular sounds. Fluoroscopy revealed a diminished opening of the tilting-disc valve. Thrombolytic therapy with streptokinase was administered with successful results. A complete subsidence of her symptoms was noted. One year later, she was hospitalized again with acute breathlessness. She admitted to having discontinued acenocoumarol intake. A Doppler evaluation showed an end-diastolic gradient of 18.5 mm Hg across the prosthetic mitral valve and fluoroscopy showed a reduced opening of the tilting disc. Her INR was 1.6. Thrombolytic therapy with a streptokinase drip was started but she developed cardiogenic shock and died.
CASE 3
A 59-year-old male had undergone mitral and aortic valve replacement for chronic rheumatic heart disease with a Starr-Edwards prosthesis (Baxter Healthcare, Edwards CVS Division, Santa Ana, CA, USA) 5 years previously. He presented to the emergency services with headache, vomiting, slurring of speech, and giddiness. He had been admitted earlier to a primary care hospital with a diagnosis of thrombotic stroke. A computed tomography scan at this time revealed two hypodense areas in the left parietal lobe. He was discharged on an increased dose of 6 mg acenocoumarol daily. On referral to our unit one month later, his INR was 6.2. A computed tomography scan of the brain revealed cerebellar hemorrhage and hypodense areas in the left parietal lobe with no surrounding edema. Treatment with mannitol and furosemide was started to prevent cerebral edema, vitamin K and fresh frozen plasma were administered intravenously, and acenocoumarol intake was discontinued. The prothrombin time normalized with these measures and all signs of raised intracranial pressure subsided. He was started on low molecular weight heparin (parnaparin sodium) in a dose of 3200 units twice daily, 9 days after his admission. He was discharged in a stable condition on 3 mg of acenocoumarol.
CASE 4
A 28-year-old female who had undergone mitral valve replacement for chronic rheumatic heart disease 2 years previously, was admitted for a change from oral anticoagulation therapy to heparin therapy in the 7th month of pregnancy. She had been treated with oral acenocoumarol 3 mg daily since her valve replacement and her INR had been maintained at 2.5. She was taking acenocoumarol regularly. A successful change to heparin therapy in sufficient doses to maintain the partial thromboplastin time at 1.5 to 1.8 times the control value was accomplished. Echocardiography showed trivial mitral regurgitation with an insignificant end-diastolic gradient across the mitral prosthesis. She went on to a full-term pregnancy and heparin was withheld during second stage of labor. She delivered a live baby and was discharged on the 10th day after delivery with an INR of 3.0 on 3 mg of acenocoumarol.
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DISCUSSION
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Prosthetic valve thrombosis is the occlusion of a valvular prosthesis by noninfective thrombotic material and not by pannus, entrapment of the occluder, infective vegetations, or cardiac structures.l Valve thrombosis includes all new permanent or transient events until evidence is obtained to the contrary at surgery or by clinical investigation.2 Thrombotic occlusion of prosthetic cardiac valves has been reported to occur in 1% to 13% of cases following the implantation of most types of valves including tilting-discs, ball-and-cage valves, and also rarely, bioprostheses.3,4 In ball-and-cage prosthetic cardiac valves, the function is gradually compromised by progressive fibrous in-growth and thrombus formation. Such mechanical obstruction causes an increased gradient across the prosthetic valve and profound alteration of hemodynamic parameters. When thrombotic occlusion occurs on the high-precision dynamics of tilting-disc valves, sudden malfunction and hemodynamic collapse necessitates prompt diagnosis and emergency management.4 Karp and colleagues5 used an actuarial method to estimate the cumulative risk of thrombotic occlusion after Björk-Shiley valve replacement and estimated that at 4 years after surgery the risk of thrombosis for the aortic, mitral, and combined aortic and mitral valves was 3%, 13%, and 13% respectively. The risk of thrombosis for prosthesis in the mitral position is greater than for prosthesis in the aortic position.6 This is due to the low velocity of blood flow across the mitral valve, the small mitral annulus, atrial fibrillation, left atrial enlargement, and left atrial thrombus at the time of surgery.7
The mechanism of intracardiac thrombus formation in the presence of a valvular prosthesis depends on 4 factors. Firstly, there is the interaction between plasma proteins such as fibrinogen and the artificial surface of the valves. The initial deposition of fibrinogen is followed by adherence of thrombocytes.8,9 Secondly, there is the influence of transmitral blood flow. Thirdly, the slight hemolysis and platelet destruction at areas of turbulence causes a release of adenosine diphosphate, platelet factor 4, and beta-thromboglobulin that further promote the thrombotic cycle.9 Lastly, a local hypercoagulable state occurs in the area of the replaced valve, which promotes local clotting and platelet deposition. Many factors are responsible for the genesis and maintenance of this hypercoagulable state: inadequate anticoagulation; loss of atrial contraction; drugs such as oral contraceptives and estrogens; other systemic diseases; and the presence of nonbacterial thrombotic vegetations.10,11 All 4 of our patients had a prosthesis in the mitral position and patient no. 3 also had an aortic valve prosthesis. Patients no. 1 and 2 developed prosthetic valve thrombosis whereas patients no. 3 and 4 did not suffer any adverse outcome even on withdrawal of anticoagulation.
The recommended treatment for thrombosis of prosthetic cardiac valves is surgical replacement. Reoperation on prosthetic cardiac valves carries a high perioperative mortality ranging from 8% to 20% for urgent cases and 37% to 54% for emergency cases.12 This high perioperative mortality is attributed to the poor preoperative condition of these patients. Significant experience has accumulated on the medical management of these patients with thrombolytic therapy. Thrombolytic therapy may become the primary modality of treatment to restabilize the valvular orifice and also to reduce operative risk if the patient requires surgery. A study by Birdi and colleagues13 of 158 patients with left-sided prosthetic valve thrombosis showed that the success rate of thrombolysis depended on the adequacy of anticoagulation, prosthesis in the aortic position, the New York Heart Association functional class, and the type of mechanical prosthesis (tilting-disc or bileaflet valve). The success rate of thrombolytic therapy in this review was calculated as 68% and was better for prostheses in the aortic position and the tilting-disc type. However, rethrombosis occurred in 17% of patients.
Experience of thrombolytic therapy with streptokinase in the Indian subcontinent is restricted to case reports and two relatively small analyses of 16 (13 mitral and 3 aortic prostheses) and 12 patients (2 aortic, 6 mitral, and 4 tricuspid prostheses).14,15 These analyses showed successful thrombolysis in 100% and 92% of cases respectively. In the first study, 2 patients developed minor systemic embolism and another 2 developed rethrombosis (mitral position) on follow-up, which necessitated surgical intervention. Two of our patients (no. 1 and 2) underwent thrombolysis with urokinase or streptokinase. While case 1 had a dismal outcome, thrombolysis with streptokinase in case 2 was successful on the first occasion. The catastrophic outcome during the second admission of patient no. 2 was related to failure to adhere to oral anticoagulant therapy, previous use of streptokinase, and a late arrival at the hospital.
Pregnancy in patients with valvular prostheses is a frequently encountered problem. Many of the earlier case reports of pregnancies in women with mechanical valves arose in the United States where over-anticoagulation was frequent with the use of thromboplastins of low responsiveness.l6 With the advent of the internationalized normalized ratio, this problem has been circumvented but to date there are only a few studies analysing the outcome of pregnancies in women on oral anticoagulants with mechanical valvular prostheses. One such study by Hanania and colleagues17 of 155 pregnancies in 133 patients (95 with mechanical and 60 with bioprosthetic valves) found 16 thromboembolic events associated with mechanical prosthesis in 108 pregnancies and thrombosis was 4 times more frequent with the use of oral anticoagulants. Further analysis revealed that the rate of miscarriages was higher in those on oral anticoagulants. The success rate of pregnancy in patients with a mechanical prosthesis was 53%.17 Another retrospective study of 204 pregnancies in 184 women (151 pregnancies in 133 women with mechanical prostheses) found a success rate of 73% in women with a mechanical prosthesis; there were 13 valve thrombosis, 8 embolic events, and 7 hemorrhages associated with mechanical prostheses. Most of these complications occurred with the use of heparin.18 Neither of these studies found any increase in the incidence of embryopathies associated with the use of oral anticoagulants. Our two cases of pregnancy (no. l and 4) also did not show any malformations of the fetus. The dismal outcome in the first case draws attention to the immediate postpartum period when these patients are most vulnerable to thrombosis on sudden discontinuation of heparin therapy. The state of pregnancy causes an increase in the blood coagulability by elevating factor II, V, and VII levels.19 This increase in blood coagulability coupled with discontinuation of heparin therapy can have catastrophic consequences on the prosthetic valve. In contrast, there was an optimal outcome in case 4 suggesting that factors other that hypercoagulability may be at play.
Optimal antithrombotic therapy in patients with prosthetic heart valves is another pertinent problem. Anticipation and treatment of the risk of thrombosis through the lifelong use of oral anticoagulant drugs to raise the INR to 2.5 to 4.0 is the standard practice. However, the use of these drugs carries a substantial risk of hemorrhage. In a Dutch study on patients with well-controlled anticoagulation, there was a log-linear relationship between increasing INR and hematuria.20 In a study of major bleeding (bleeding causing death or necessitating hospital admission), the majority of patients had an INR well above the intended therapeutic range, or a comorbid condition predisposing to bleeding, or both.21 Our patient no. 3 had an INR well above the therapeutic range, which led to cerebral hemorrhage.
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CONCLUSION
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In conclusion, mechanical prosthetic valve replacement should be carried out with sufficient patient education about the inherent risk of the thrombotic potential that it poses. The use of oral anticoagulation following prosthetic valve replacement is for life and any failure of compliance can have disastrous consequences. Prosthetic valve thrombosis requires investigation for a hypercoagulable state to allow early medical and surgical intervention. Thrombolytic therapy is an effective therapeutic modality but caution is required. Judicious monitoring of oral anticoagulant therapy with adjustment according to the INR is essential.
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ABSTRACT
INTRODUCTION
