|INTERESTING CASE REPORT
|Year : 2022 | Volume
| Issue : 1 | Page : 59-62
A Case of Bioprosthetic Valve Thrombosis: Is it Time to Revise Our Thinking?
Ramkumar Rajappan, PR Vydianathan, R Shanmuga Sundaram
Department of Cardiology, GKNM Hospital, Coimbatore, Tamil Nadu, India
|Date of Submission||23-Dec-2020|
|Date of Acceptance||12-Apr-2021|
|Date of Web Publication||29-Apr-2022|
Dr. Ramkumar Rajappan
Department of Cardiology, GKNM Hospital, P. N. Palayam, Coimbatore - 641 037, Tamil Nadu
Source of Support: None, Conflict of Interest: None
Surgical valve replacement is a time-tested modality of treatment in patients with significant valvular heart disease. Bioprosthetic valves (BPVs) are preferred among certain patients because of less thrombogenicity which warrants only a short duration of anticoagulation as recommended by guidelines. Subclinical thrombosis as well as symptomatic BPV thrombosis is being increasingly recognized nowadays, more because of improvement in diagnostic modalities and increasing awareness. Our case report highlights the occurrence of BPV thrombosis in a patient who underwent surgical BPV implantation and was on anticoagulation for guideline recommended duration. This report also highlights the need for regular periodic echocardiographic screening of these patients to detect BPV thrombosis at an early stage.
Keywords: Anticoagulation, bioprosthetic valve thrombosis, paravalvular regurgitation
|How to cite this article:|
Rajappan R, Vydianathan P R, Sundaram R S. A Case of Bioprosthetic Valve Thrombosis: Is it Time to Revise Our Thinking?. J Indian Acad Echocardiogr Cardiovasc Imaging 2022;6:59-62
|How to cite this URL:|
Rajappan R, Vydianathan P R, Sundaram R S. A Case of Bioprosthetic Valve Thrombosis: Is it Time to Revise Our Thinking?. J Indian Acad Echocardiogr Cardiovasc Imaging [serial online] 2022 [cited 2023 Jun 10];6:59-62. Available from: https://jiaecho.org/text.asp?2022/6/1/59/344314
| Introduction|| |
Valvular heart disease requiring prosthetic valve replacement constitutes a considerable number of patients in our clinical practice. Bioprosthetic valves (BPVs), though less durable, are preferred in certain groups of patients because of less thrombogenicity. Structural valve degeneration (SVD) of the BPV is more common than valve thrombosis. Subclinical BPV thrombosis (BPVT) is not commonly recognized because of less stringent screening protocols. If BPVT is identified and treated appropriately at an earlier stage, redo surgery can be avoided.
| Clinical Presentation|| |
A 61-year-old male, a known case of mitral valve prolapse, systemic hypertension, and bronchial asthma, was admitted with acute onset breathlessness in 2017. On evaluation, he was diagnosed to have chordal rupture of mitral valve apparatus and severe mitral regurgitation. He underwent mitral valve replacement with a 27 mm Hancock II valve with total chordal preservation. Baseline transthoracic echocardiogram (TTE) after surgery revealed normal prosthetic valve function with a peak gradient of 13 mmHg and a mean gradient of 4 mmHg and no prosthetic valve regurgitation. He was started on oral anticoagulation (warfarin) which was continued for 3 months. Ten months after surgery, he developed New York Heart Association Class II dyspnea on exertion. TTE revealed moderate paravalvular BPV regurgitation with normal antegrade flow velocities across the BPV (peak gradient was 11 mmHg and mean gradient was 5 mmHg). Transesophageal echocardiogram (TEE) did not reveal any vegetation. With the optimization of diuretics, he became asymptomatic and was advised medical follow-up.
Currently, he presented to the outpatient department with a month history of progressively worsening dyspnea in September 2020. He was breathless at rest and was tachypneic. Electrocardiogram showed sinus rhythm with an incomplete right bundle branch block. Chest X-ray showed Grade 2 pulmonary venous hypertension. TTE revealed diffusely thickened BPV leaflets (5 mm) with increased gradients across the mitral valve prosthesis (peak gradient – 50 mmHg and mean gradient – 27 mmHg at a heart rate of 44 beats per min [bpm]; pressure half time was 285 ms), moderate intravalvular as well as paravalvular regurgitation with mild tricuspid regurgitation and pulmonary hypertension [Figure 1]. Differential diagnosis of BPVT versus accelerated SVD was considered. He was started on parenteral diuretics for decongestion. Complete blood count was normal. Blood culture did not grow any organism. TEE done after stabilization revealed thickened BPV leaflets with restricted mobility and soft echodense structures attached to the ventricular surface of BPV leaflets [Figure 2]. TEE also revealed moderate intravalvular, and paravalvular BPV regurgitation. No vegetations or evidence of paravalvular infection was noticed. In view of increased thickness of the valve leaflets with high gradients within 5 years of the BPV implantation, a provisional diagnosis of BPVT with paravalvular and intravalvular regurgitation was made.
|Figure 1: Transthoracic echocardiogram images at baseline. (a-c) Thickened bioprosthetic valves leaflets, (d) Continuous wave Doppler with increased gradients|
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|Figure 2: Transesophageal echocardiography images at baseline- thickened bioprosthetic valves leaflets (a and b), soft-tissue echogenic structure attached to its ventricular surface (c) and moderate intra- and paravalvular regurgitation (d)|
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Since he was hemodynamically stable, heparin infusion was started and continued for more than 48 h with a target activated partial thromboplastin time of 1.5–2 times the control. Repeat TTE done after heparin infusion showed a reduction in the thickness of BPV leaflets. TTE also showed a significant reduction in the mitral inflow gradients (peak inflow gradient of 22 mmHg and a mean gradient of 15 mmHg at a heart rate of 60 bpm, pressure half time of 160 ms), moderate intravalvular, and moderate paravalvular regurgitation [Figure 3]. He was started on oral anticoagulation and the dose was titrated to maintain a target international normalized ratio (INR) of 2.5–3. He was also started on clopidogrel at a dose of 75 mg per day. His dyspnea improved and he was discharged. Re-evaluation with TTE after a month of anticoagulation showed normal BPV thickness with further reduction in the gradients (peak inflow gradient of 15 mmHg and a mean gradient of 6 mmHg at a heart rate of 68 bpm, pressure half time 170 ms), moderate intravalvular as well as paravalvular regurgitation [Figure 4]. He was planned for conservative management for paravalvular regurgitation since he was documented to have regurgitation during the previous evaluation in 2018 itself, which did not progress further. Left ventricular dimensions and systolic function were normal.
|Figure 3: Transthoracic echocardiography images after heparin infusion showing reduced valve leaflet thickness (a) and gradients (b)|
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|Figure 4: Transthoracic echocardiography images after 1 month of anticoagulation showing reduced valve leaflet thickness (a) and gradients across the prosthesis (b); (c and d) moderate regurgitation|
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| Discussion|| |
BPVT is a clinical entity that is being recognized more often now because of increasing awareness and improvement in imaging technologies. The reported incidence varies depending upon the modality of evaluation (echocardiography vs. computerized tomography [CT]) as well as the clinical scenario- whether it was noticed in asymptomatic patients during routine evaluation or in patients with symptomatic prosthetic valve dysfunction. Its incidence is reported to be varying between 0.04% and 6.2% per year.
Diagnosis of BPVT is challenging, more often because of the lack of proper definition of this entity. In published reports, valve thrombosis is considered any thrombosis unrelated to infection, attached to or within close proximity of the valve, interfering with valve function or sufficiently large so as to warrant treatment. Egbe et al. have proposed a model for diagnosis of this entity combining clinical, echocardiographic, and CT features. Paroxysmal atrial fibrillation, depressed ejection fraction, subtherapeutic INR, recent withdrawal of anticoagulants, and hypercoagulability are some of the risk factors for BPVT. BPVT should be suspected in the presence of valve dysfunction within 5 years of implantation. Patients may be asymptomatic or may present with progressive dyspnea, syncope, or heart failure. Our patient developed symptoms within 3 years after surgery. He was on anticoagulation for 3 months post surgery.
TTE may underdiagnose BPVT. Hence, TEE is recommended when this condition is suspected clinically., Direct visualization of valve thrombosis, 50% increase in mean gradient compared with the initial postoperative evaluation, increased cusp thickness (>2 mm), especially on the downstream aspect of the BPV (ventricular side for mitral and tricuspid prostheses, arterial side for aortic and pulmonary prostheses) reduced leaflet mobility, and regression of BPV abnormalities with anticoagulation, usually within 1–3 months of initiation of anticoagulation therapy, are the echocardiographic features of this entity. CT features suggestive of BPVT include reduced leaflet motion on four-dimensional CT and hypo-attenuated leaflet thrombus. Echocardiography in our patient showed an increase in cusp thickness (5 mm) and increased mean valve gradients. TEE showed thrombus on the downstream aspect of the valve leaflet and within a month of anticoagulation, the valve abnormalities decreased. He did not have clinical as well as serological features of underlying connective tissue disorders. Workup for other prothrombotic states was planned during follow-up.
Treatment options available for BPVT are surgical valve replacement, thrombolysis, and anticoagulation. For large left-sided nonobstructive BPVT, intravenous heparin is preferred. Surgical options need to be considered if anticoagulation fails. For smaller thrombi (<5 mm), oral anticoagulation is preferred. Our patient was treated with intravenous heparin infusion followed by oral anticoagulation. He improved clinically. Echocardiography showed a reduction in valve leaflet thickness as well as gradients across BPV during follow-up.
European Society of Cardiology guidelines recommend TTE at 1 year after valve implantation and annually thereafter, whereas American College or Cardiology/American Heart Association guidelines recommend TTE only after 10 years of BPV implantation. However, studies have shown that 85% of BPVT cases occurr within 5 years. Hence, periodic evaluation of the prosthetic valve function with echocardiography will help in earlier identification of this entity.
After implantation of the BPV, guidelines recommend 3 months of anticoagulation followed by antiplatelets. Our patient did not receive antiplatelets after an initial period of anticoagulation. The optimal duration of anticoagulation after BPV remains unknown. The optimal duration of anticoagulation after an episode of BPVT also remains unknown. Some studies have also shown that malfunctioning BPV with regurgitation are potentially thrombogenic.
| Conclusion|| |
BPVT is a major cause of early prosthetic valve dysfunction. The diagnosis of subclinical BPVT by timely imaging is important, by which treatment can be initiated early and redo surgery can be avoided in many cases. Whether extended oral anticoagulation beyond the guideline-recommended duration will be helpful to prevent subclinical as well as symptomatic BPVT needs to be validated by further randomized studies.
Declaration of patient consent
The authors certify that they have obtained all appropriate patient consent forms. In the form, the legal guardian has given his consent for images and other clinical information to be reported in the journal. The guardian understands that names and initials will not be published and due efforts will be made to conceal identity, but anonymity cannot be guaranteed.
Financial support and sponsorship
Conflicts of interest
There are no conflicts of interest.
| References|| |
Butnaru A, Shaheen J, Tzivoni D, Tauber R, Bitran D, Silberman S. Diagnosis and treatment of early bioprosthetic malfunction in the mitral valve position due to thrombus formation. Am J Cardiol 2013;112:1439-44.
Akins CW, Miller DC, Turina MI, Kouchoukos NT, Blackstone EH, Grunkemeier GL, et al
. Guidelines for reporting mortality and morbidity after cardiac valve interventions. J Thorac Cardiovasc Surg 2008;135:732-8.
Egbe AC, Pislaru SV, Pellikka PA, Poterucha JT, Schaff HV, Maleszewski JJ, et al
. Bioprosthetic valve thrombosis versus structural failure: Clinical and echocardiographic predictors. J Am Coll Cardiol 2015;66:2285-94.
Córdoba-Soriano JG, Puri R, Amat-Santos I, Ribeiro HB, Abdul-Jawad Altisent O, del Trigo M, et al
. Valve thrombosis following transcatheter aortic valve implantation: A systematic review. Rev Esp Cardiol (Engl Ed) 2015;68:198-204.
Daniel WG, Mügge A, Grote J, Hausmann D, Nikutta P, Laas J, et al
. Comparison of transthoracic and transesophageal echocardiography for detection of abnormalities of prosthetic and bioprosthetic valves in the mitral and aortic positions. Am J Cardiol 1993;71:210-5.
Pislaru SV, Pellikka PA, Schaff HV, Connolly HM. Bioprosthetic valve thrombosis: The eyes will not see what the mind does not know. J Thorac Cardiovasc Surg 2015;149:e86-7.
Roudaut R, Serri K, Lafitte S. Thrombosis of prosthetic heart valves: Diagnosis and therapeutic considerations. Heart 2007;93:137-42.
Vahanian A, Alfieri O, Andreotti F, Antunes MJ, Barón-Esquivias G, Baumgartner H, et al
. Guidelines on the management of valvular heart disease (version 2012): The joint task force on the management of valvular heart disease of the European Society of Cardiology (ESC) and the European Association for Cardio-Thoracic Surgery (EACTS). Eur J Cardiothorac Surg 2012;42:S1-44.
Nishimura RA, Otto CM, Bonow RO, Carabello BA, Erwin JP, Guyto RA, et al
. 2014 AHA/ACC guideline for the management of patients with valvular heart disease: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. J Am Coll Cardiol 2014;63:e57-185.
Yong MS, Grant R, Saxena P, Yadav S. Recurrent bioprosthetic valve thrombosis-Should long-term anticoagulation be considered? Heart Lung Circ 2018;27:e70-2.
Prandoni P, Pengo V, Boetto P, Zambon G, Menozzi L. Do malfunctioning bioprosthetic heart valves represent a potential thrombogenic focus? Haemostasis 1985;15:337-44.
[Figure 1], [Figure 2], [Figure 3], [Figure 4]