Document Detail

Prosthetic tricuspid valve thrombosis: three case reports and literature review.
Jump to Full Text
MedLine Citation:
PMID:  23323074     Owner:  NLM     Status:  PubMed-not-MEDLINE    
Abstract/OtherAbstract:
A common complication of prosthetic heart valves is thrombosis. Although the incidence of prosthetic valve thrombosis (PVT) in the tricuspid position is high, there are not enough data on the management of it, in contrast to left-sided PVT. Here, we describe three cases of tricuspid PVT with three different management approaches: thrombolytic therapy; close observation with oral anticoagulants; and surgery. The first case was a woman who suffered from recurrent PVT, for which we successfully used Tenecteplase for second and third episodes. We employed Tenecteplase in this case for the first time in the therapy of tricuspid PVT. The second case had fixed leaflets in open position while being symptomless. At six months' follow-up, with the patient having taken oral anticoagulants, the motion of the leaflets was restricted and she was symptomfree. The last case was a woman who had a large thrombus in the right atrium immediately after mitral and tricuspid valvular replacement. The patient underwent re-replacement surgery and a new biological valve was implanted in the tricuspid position. Also, we review the literature on the pathology, signs and symptoms, diagnosis, and management of tricuspid PVT.
Authors:
Ahmad Yaminisharif; Mohammad Javad Alemzadeh-Ansari; Seyed Hossein Ahmadi
Related Documents :
2602194 - A case of bilateral nursemaid's elbow.
6827354 - Epidural hygroma of the posterior fossa. case report.
22248364 - Isolated granulocytic sarcoma of the pancreas: a tricky diagnostic for primary pancreat...
12754654 - Occupational head injury and subsequent glioma.
9467364 - Granulomatous cheilitis: a study of six cases.
20297864 - Adverse drug reactions in the paediatric population in denmark: a retrospective analysi...
Publication Detail:
Type:  Journal Article     Date:  2012-11-30
Journal Detail:
Title:  The journal of Tehran Heart Center     Volume:  7     ISSN:  1735-5370     ISO Abbreviation:  J Tehran Heart Cent     Publication Date:  2012 Nov 
Date Detail:
Created Date:  2013-01-16     Completed Date:  2013-01-17     Revised Date:  2013-05-30    
Medline Journal Info:
Nlm Unique ID:  101289255     Medline TA:  J Tehran Heart Cent     Country:  Iran    
Other Details:
Languages:  eng     Pagination:  147-55     Citation Subset:  -    
Affiliation:
Tehran Heart Center, Tehran University of Medical Sciences, Tehran, Iran.
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Descriptor/Qualifier:

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

Full Text
Journal Information
Journal ID (nlm-ta): J Tehran Heart Cent
Journal ID (iso-abbrev): J Tehran Heart Cent
Journal ID (publisher-id): JTHC
ISSN: 1735-5370
ISSN: 2008-2371
Publisher: Tehran University of Medical Sciences
Article Information
Download PDF
Copyright © Tehran Heart Center, Tehran University of Medical Sciences
open-access:
Received Day: 24 Month: 1 Year: 2012
Accepted Day: 17 Month: 6 Year: 2012
Electronic publication date: Day: 30 Month: 11 Year: 2012
Print publication date: Month: 11 Year: 2012
Volume: 7 Issue: 4
First Page: 147 Last Page: 155
PubMed Id: 23323074
ID: 3537206
Publisher Id: jthc-7-147

Prosthetic Tricuspid Valve Thrombosis: Three Case Reports and Literature Review
Ahmad Yaminisharif, MD
Mohammad Javad Alemzadeh-Ansari, MD*
Seyed Hossein Ahmadi, MD
Tehran Heart Center, Tehran University of Medical Sciences, Tehran, Iran.
*Corresponding Author: Mohammad Javad Alemzadeh-Ansari, Department of Cardiology, Tehran University of Medical Sciences, Tehran Heart Center, Karegar Street, Tehran, Iran. 1411713138. Tel: +98 21 88029600. Fax: +98 21 88029731. Email: aansari@razi.tums.ac.ir.

Introduction

Since the 1950s, more than 80 models of the prosthetic heart valve have been developed and used.1 Prosthetic valve thrombosis (PVT), however, remains a serious complication and can even prove lethal. Overall, the incidence of thrombosis is reported to be between 0.1% and 5.7% per patient-year.2 The incidence is 0.5% to 6% in the aortic and/or mitral positions and up to 20% in the tricuspid position, whereas the risk of thrombosis in spite of adequate oral anticoagulation has been estimated at between 1% and 4% per year.3 Although inadequate anticoagulant therapy remains the main cause of this complication, it seems that lower pressures on the right side of the heart with a slower blood flow across the tricuspid valve is the most important cause of higher risk of thrombus formation in prosthetic tricuspid valves.4, 5 In contrast to left-sided PVT, there is a paucity of data on the various aspects of tricuspid PVT. We herein present three cases of tricuspid PVT with different management approaches, namely thrombolytic therapy, conservative management, and re-replacement surgery, and then review the relevant literature.


Case Reports
Case # 1

A 32-year-old woman was admitted to our hospital with the complaint of dyspnea (The New York Heart Association [NYHA] factional class III) in January, 2004. Transthoracic echocardiography (TTE) showed left ventricular ejection fraction of 55%, severe mitral stenosis, mild mitral regurgitation, severe aortic regurgitation with moderate to severe aortic stenosis, and severe tricuspid regurgitation with moderate to severe tricuspid stenosis. In April 2004, the patient underwent three valves replacement surgery, during which she received a 24-mm St. Jude Valve (St. Jude Medical, Inc., St. Paul, MN, USA) in the mitral position, a 31-mm St. Jude Valve (St. Jude Medical, Inc., St. Paul, MN, USA) in the tricuspid position, and a 19-mm Regent Mechanical Prosthesis (St. Jude Medical, Inc., St. Paul, MN, USA) in the aortic position. Also, due to persistent atrial fibrillation with a slow ventricular response, she underwent permanent transvenous epicardial pacemaker placement during hospitalization. Twenty-one days after valvular surgery, TTE revealed that the function and gradients of the three prosthetic valves were within the acceptable range and the peak and mean gradients in the prosthetic tricuspid valve were 5 mm Hg and 3 mm Hg, respectively. At the time of discharge, the patient’s international normalized ratio (INR) was 3.9. She was discharged from the hospital with the recommendation to use Warfarin (with goal INR 2.5 - 3.5) plus 80 mg Aspirin daily.

In February, 2006, the patient was re-admitted with the complaint of fatigue and palpitation. The pacemaker had a normal function. At the time of presentation, her INR was 2.5. TTE revealed that the prosthetic aortic and mitral vales had normal functions and gradients, whereas the prosthetic tricuspid valve had malfunction with high gradients. Fluoroscopic evaluation revealed that there was no motion in both leaflets of the prosthetic tricuspid valve, while the motion of both other prosthetic valves was complete and within the normal range. With the diagnosis of tricuspid PVT, the patient was prescribed 250,000 U of Streptokinase via a peripheral vein over thirty minutes, followed by an intravenous infusion of 100,000 U per hour of Streptokinase for forty-eight hours. On the next day, fluoroscopic evaluation showed no evidence of prosthetic tricuspid valve malfunction, and the mobility of both leaflets was completely restored. At discharge, the patient’s INR was 2.6. She was discharged from the hospital with the recommendation to use Warfarin (with goal INR 3.0 - 3.5) plus 80 mg of Aspirin daily.

In November, 2006, the patient was re-admitted to our hospital with the complaint of atypical chest pain. At presentation, her INR was 1.8 and her other laboratory data and also electrocardiogram were unremarkable. TTE revealed that the prosthetic aortic and mitral vales had normal functions and gradients, whereas the prosthetic tricuspid valve had malfunction with high gradients. Fluoroscopic evaluation revealed that both leaflets of the prosthetic tricuspid valve were fixed without any motion, whereas the motion of both other prosthetic valves was complete and within the normal range. With the diagnosis of recurrent tricuspid PVT, the patient was administered a total of 35 mg of Tenecteplase: 15 mg bolus, followed by 20 mg for four hours (the patient’s weight was 64 kg). On the next day, fluoroscopic evaluation showed no evidence of prosthetic tricuspid valve malfunction, and the mobility of both leaflets was completely restored. Twelve days after the administration of Tenecteplase, TTE demonstrated that a significant reduction had occurred in the gradient across the prosthetic tricuspid valve (9.5 mm Hg peak gradient, 4.9 mm Hg mean gradient). At discharge, the patient’s INR was 3.5. She was discharged from the hospital with the recommendation to use Warfarin (with goal INR 3.0 - 3.5) plus 80 mg of Aspirin daily.

Because of the battery depletion of the pacemaker, the patient was re-admitted for generator replacement on October 30, 2011. She had discontinued Aspirin two years previously due to gastrointestinal problems. She complained of atypical chest pain of two months’ duration, but her myocardial perfusion scan was normal. TTE showed left ventricular ejection fraction of 55%, severe increased gradient in the prosthetic tricuspid valve with no paravalvular leakage, and normal function of the mitral and aortic prosthetic valves. Fluoroscopic evaluation of the prosthetic tricuspid valve revealed a severe drop in the motion of both leaflets. The patient was candidated for thrombolytic therapy with the diagnosis of recurrent tricuspid PVT. A single dose of 35 mg of Tenecteplase was administrated via a peripheral vein, according to the dosing regimen used for acute myocardial infarction (the patient’s weight was 65 kg). Fluoroscopic evaluation exhibited no evidence of prosthetic tricuspid valve malfunction, and the mobility of both leaflets was completely restored. Seven days later, TTE demonstrated that a significant reduction had occurred in the gradients across the prosthetic tricuspid valve (9 mm Hg peak gradient, 4 mm Hg mean gradient). She was discharged from the hospital with the recommendation to use Warfarin (with goal INR 3.0 - 3.5) plus 80 mg of Aspirin daily. Table 1 illustrates the three episodes of tricuspid PVT in our patient and the three successful methods for thrombolytic therapy.

Case # 2

A 49-year-old woman was admitted to our hospital for the replacement of the generator of a pacemaker in May 2011. Thirteen years previously in another center, because of severe aortic regurgitation and severe tricuspid regurgitation, she had undergone two valves replacement surgery, during which she received a 31-mm St. Jude Valve (St. Jude Medical, Inc., St. Paul, MN, USA) in the tricuspid position and a 21-mm St. Jude Valve (St. Jude Medical, Inc., St. Paul, MN, USA) in the aortic position. After surgery, due to the presence of complete heart block, she underwent permanent epicardial pacemaker placement during hospitalization. But during this period, she was admitted frequently because of infection at the site of the pacemaker. At the time of recent presentation, her INR was 1.9. TTE revealed that the prosthetic aortic valve had normal function and gradients, whereas the prosthetic tricuspid valve had malfunction with high gradients (15 mm Hg peak gradient, 10 mm Hg mean gradient). Fluoroscopic evaluation revealed that the motion of one leaflet of the prosthetic tricuspid valve was very restricted, while the other leaflet was fixed in an open position. The patient was symptomless. On physical examination, except for a holosystolic murmur at the left lower sternal border, there were no signs of heart failure. With the diagnosis of tricuspid PVT, the patient was administered 250,000 U of Streptokinase via a peripheral vein over thirty minutes, followed by an intravenous infusion of 100,000 U per hour of Streptokinase for forty-eight hours. Fluoroscopic evaluation showed no improvement in the motion of the leaflets. The patient was candidated for tricuspid valve replacement, but because of fungal infection in the pacemaker pocket and lead, replacement of the prosthetic valve or the generator was not performed. She was discharged from the hospital with the recommendation to use antibiotics with Warfarin (with goal INR 3.0 - 3.5) plus 80 mg of Aspirin daily. Six months later, she referred to our clinic; she had no signs or symptoms of heart failure. She was re-admitted for the replacement of the generator of the pacemaker. Before replacement, fluoroscopic evaluation showed no evidence of improvement in the motion of the prosthetic tricuspid valve leaflets. Because the patient was symptom-free, did not respond to thrombolytic therapy, and had a high risk for infection after valve replacement, surgery for valve replacement was not performed. After generator replacement, she was discharged with the recommendation to use Warfarin (with goal INR 3.0 - 3.5) plus 80 mg of Aspirin daily.

Case # 3

A 28-year-old woman was admitted to our hospital with the complaint of orthopnea and dyspnea (NYHA factional class III) in September, 2008. The electrocardiogram revealed atrial fibrillation. TTE showed left ventricular ejection fraction of 40%, severe mitral stenosis, severe tricuspid regurgitation, and a large mobile clot in the left atrium (2.7 × 2.0 cm). She underwent two valves replacement surgery, during which she received a 31-mm St. Jude Valve (St. Jude Medical, Inc., St. Paul, MN, USA) in the tricuspid position and a 29-mm St. Jude Valve (St. Jude Medical, Inc., St. Paul, MN, USA) in the mitral position. Also in the same section of surgery, TEE revealed a large mobile clot in the left atrium without any lesion in the other chambers; the large clot was removed. After surgery, she received an intravenous bolus dose of 5000 U of heparin, followed by intravenous heparin (20000 U per day in divided doses). Because of persistent atrial fibrillation with a low ventricular response after surgery, eleven days later, she underwent permanent transvenous epicardial pacemaker placement. However, during implantation, fluoroscopy revealed that the motion of one leaflet of the prosthetic tricuspid valve was very restricted. With the diagnosis of the malfunction of the prosthetic tricuspid valve, she was transferred to the operating room again. During the removal of the previous prosthetic tricuspid valve, a large clot was seen in the right atrium which was attached to the leaflet. Thus, all of the thrombus was removed and a new 29-mm Hancock II bioprosthesis (Medtronic Inc., Minneapolis, Minn.) was placed in the tricuspid position. Because of the displacement of the transvenous epicardial lead during surgery, a new epicardial lead was placed. After surgery, TEE demonstrated an acceptable gradient across the tricuspid valve (5 mm Hg peak gradient, 2 mm Hg mean gradient). She was discharged with the recommendation to use Warfarin (with goal INR 3.0 - 3.5) plus 80 mg of Aspirin daily.


Discussion
Pathogenesis

Many studies have demonstrated that the leading cause of PVT is subtherapeutic anticoagulation, which chimes in with the findings in our two cases.610 This is most often due to either patient noncompliance or iatrogenic cessation of anticoagulants in preparation for another procedure. Furthermore, valve design and materials influence the incidence of thrombotic complications. Some mechanisms have a role in PVT formation such as molecular interactions and influence of transprosthetic blood flow. Molecular interaction occurs between corpuscular blood components, plasma, and artificial surfaces. The initial adsorption of plasma proteins (fibrinogen, fibronectin, von Willebrand factor, vitronectin, and thrombospondin) on the artificial surface is generally followed by platelet adhesion. The passage of blood through the prosthetic valve creates a turbulent flow with shear stress, which gives rise to a structurally and metabolically damaged endocardium and thus reduces its resistance to thrombosis. Also, subclinical hemolysis with the release of adenosine diphosphatase, platelet factor 4, beta-thromboglobulin, and other proteins triggers the activation of the plasma coagulation system. Other intrinsic factors can progress to thrombus formation; these factors include loss of active atrial contractions (atrial fibrillation), presence of some systemic diseases (e.g. systemic lupus erythematosus) or malignant tumors, and incomplete endothelization of the sewing ring. Use of some drugs such as contraceptives leads to hypercoagulability state3, 1114 Recently, Ricome et al. reported two cases of PVT secondary to heparin-induced thrombocytopenia.15

Type and position of the prosthetic valve and time from surgery can influence thrombus formation (Table 2).1, 13, 16, 17 Additionally, some studies have indicated that season can be correlated with an increased risk for thrombotic events.1820 Piper et al. reported that PVT during winter months occurred more frequently than in the other seasons.13

Signs and Symptoms

In contrast to the acute presentation of left-sided PVT, the onset of the symptoms of tricuspid PVT is usually insidious, and its diagnosis is often delayed. Sometimes symptoms are so slight that the patient is likely to have suffered from them for months or even a year without feeling the need for referral to the hospital.4 Sometimes, the patient even may have no symptoms related to the tricuspid vale thrombosis, and the thrombosis is detected only during routine clinical examination.4, 6 However, the involvement of both leaflets is usually required to produce symptoms.6 The most frequent symptoms related to tricuspid valve malfunction include dyspnea, ascites, peripheral edema, and systemic emboli.4, 6, 21, 22 Also, sometimes the disappearance or attenuation of the prosthetic valve noise may be reported by the patient and/or relatives. Moreover, in some cases where an interatrial communication is present, a pulmonary embolus or a leftsided embolic event may be the presenting manifestation of tricuspid PVT.23, 24

It seems that physical examination may provide important clues for the diagnosis of tricuspid PVT, compared to the thrombosis of the left side, which normally has more severe symptoms.25 Absence or muffling of prosthetic sounds in the tricuspid position might be noted. Other findings include auscultation of a new holosystolic murmur located at the left lower sternal border or in the subxiphoid region that may increase with inspiration or maneuvers that increase venous return (denoting the presence of tricuspid regurgitation), auscultation of a new murmur that is low in frequency, diastolic, located at the lower left sternal border or infraxiphoid area, and increases with inspiration and other maneuvers that increase tricuspid flow velocity (denoting tricuspid stenosis), or auscultation of a combination of murmurs that characterize both of these conditions. Sometimes mid-diastolic and/or pan-systolic murmurs can be heard in the tricuspid area (Zhang DY, Lozier J, Chang R, Sachdev V, Chen MY, Audibert JL, Horvath KA, Rosing DR. Case study and review: Treatment of tricuspid prosthetic valve thrombosis. Int J Cardiol 2011 Oct 14. [Epub ahead of print]).

Diagnosis

The onset of the symptoms of tricuspid PVT is usually insidious and sometimes the patient has nonspecific symptoms or is even symptomless; therefore, suspicion of tricuspid PVT may be raised by physical findings, symptoms of heart failure, or rarely the diagnosis of embolization, especially in patients with poor anticoagulation therapy8, 17, 25 NYHA has classified PVT in functional classes I to IV. The non-obstructive forms of PVT (NYHA functional classes I or II) are usually incidental echocardiographic findings in patients with symptomless, nonspecific symptoms, or thromboembolic events. The obstructive forms (NYHA functional classes III or IV) correspond to obvious hemodynamic repercussions, sometimes including cardiogenic shock, and are often associated with cerebral or peripheral embolism.3, 11, 26

Imaging modalities in patients with suspected PVT are aimed to evaluate leaflet immobilization, cause of leaflet immobilization (thrombus versus pannus or both), and whether thrombolytic therapy attempt in the patient would be successful. Usually the first modality for detecting prosthetic tricuspid valve dysfunction is TTE. Montorsi et al. reported that sensitivity, specificity, and positive and negative predictive values for the diagnosis of PVT in the mitral or aortic position by TTE were 75%, 64%, 57%, and 78%, respectively. TTE, especially in experienced hands, can detect increased transvalvular gradients (mean of 6 mm Hg or higher, and peak of 15 mm Hg or higher), pressure halftime of 230 msec or higher, transvalvular gradients of 50% or higher than that observed before, wide intravalvular jet of tricuspid regurgitation, lower orifice area, visible thrombus on the prosthetic valve, and inability to demonstrate two different mobile echoes representing the valve leaflets in a high quality image. Indirect, nonspecific signs are an enlarged right atrium and engorged inferior vena cava.3, 6, 27

After performance of TTE, the diagnosis should be confirmed by more specific modalities, namely fluoroscopy or TEE.28 Fluoroscopy is a non-invasive method for detecting PVT, especially in patients with bileaflet prosthetic valves, and have high clinical suspicious for PVT and normal Doppler study.29 Sensitivity, specificity, and positive and negative predictive values for the diagnosis of PVT in the mitral or aortic position by fluoroscopy are 87%, 78%, 80%, and 91%.28 Also, fluoroscopy has an important role for detecting the response to thrombolytic therapy. Thrombolysis significantly reduces the mean pressure gradient and improves valve leaflet opening angle. But some patients whose pressure gradient normalizes after thrombolytic infusion tend to continue to have concomitant abnormal leaflet motion at fluoroscopy, suggesting incomplete resolution of valve obstruction (pseudo responders). If lytic infusion is stopped at this time, the remaining thrombus could be the trigger for a late rethrombotic process. Thus, fluoroscopy should be carried out at regular intervals during therapy to confirm Doppler changes.29

TEE can correctly identify opening and closing angles in all patients, regardless of the prosthetic type.30 TEE should be performed in selected patients even if fluoroscopy is negative because TEE is an invasive modality. On the other hand, fluoroscopy and TTE can correctly identify PVT in 85% of all cases. Thus, fluoroscopy and TTE are quick, effective, and complementary diagnostic tools for the diagnosis of PVT in most patients.28 Despite the scarcity of data on the role of TEE in diagnosing tricuspid PVT, it seems that if there is high clinical suspicion and other diagnostic modalities are not helpful, TEE will be help.27 Furthermore, TEE is a superior modality for detecting the etiology of the obstruction (thrombus versus pannus), size, and location of the thrombus compared with TTE and fluoroscopy.31

Magnetic Resonance Imaging (MRI) and cardiac catheterization have limited diagnostic roles, because TEE and fluoroscopy can provide adequate data for decision-making. Since MRI is more expensive and time-consuming than echocardiography, it should be used only when prosthetic-valve regurgitation or paravalvular leakage is suspected but not adequately visualized by echocardiography.1 In contrast, Cardiac Multi-Detector Computer Tomography can provide sharp images to characterize quantitatively the reduced mobility of prosthetic leaflets or even directly visualize and distinguish between thrombus and pannus.3234

Treatment

There are different therapeutic modalities available for PVT such as heparin treatment, thrombolysis, surgery, or even in some cases only watchful waiting. Selecting one of these modalities is largely influenced by the presence of valvular obstruction, valve location (left- or right-sided), and clinical status.6, 35 Surgery is more frequently performed for the treatment of left-sided PVT, not least in patients with either NYHA functional class III–IV symptoms or a large clot burden36 and thrombolytic therapy is more favorable for right-sided PVT, because the risk of systemic embolization and recurrence rate is high by thrombolytic therapy in left-sided PVT.37, 38

The conservative continued anticoagulation approach in patients with tricuspid PVT would only be appropriate if there is no significant hemodynamic compromise or a contraindication to either surgery or pharmacologic intervention is present. Shapira et al. reported that asymptomatic patients with tricuspid PVT who did not respond to thrombolytic therapy might be discharged from the hospital with long-term intensified anticoagulant therapy and close follow-up. The leaflet motion can be fully restored later.6 However, Montorsi et al. proposed that leaflet mobility and duration of prosthetic valve symptoms were important factors in determining successful thrombolytic therapy. It may be because the amount of the thrombus that led to the stuck valve was minimal, thereby improving the chance of successful thrombolytic therapy.29

According the guidelines of the American Heart Association /American College of Cardiology (AHA/ACC) and the American College of Chest physicians (ACCP), in contrast to left-sided PVT, thrombolytic therapy is reasonable for right-sided PVT with NYHA functional class III–IV symptoms or a large clot burden.36, 39 It is due to the high success rate and low incidence of embolism compared to left-sided PVT. The European Society of Cardiology guideline also recommends thrombolytic therapy for tricuspid PVT, but this guideline does not mention the NYHA functional class or clot burden.40 Long-standing symptoms even more than a month should not make one reluctant to use thrombolytic therapy.6 If thrombolytic therapy fails, the presence of a large thrombus or pannus should be considered, which may require surgical intervention (thrombectomy or valve replacement).

In contrast to left-sided PVT, there is limited information about thrombolytic therapy for tricuspid PVT. Various thrombolytic agents have been used for PVT, including streptokinase, urokinases, and tissue-type plasminogen activator (tPA). The choice of the thrombolytic agent depends on several factors, including cost, time to attain maximal pharmacologic effect, half-life of the thrombolytic agent, and hemorrhagic complications. Amongst the above agents, streptokinase is cheaper and has lower cerebral hemorrhage rates. In contrast, tPA has a faster effect reversion and faster reach to maximal pharmacologic effect.3 Roudaut et al. indicated that patients treated by streptokinase had a significantly full success rate compared to patients treated by tPA or urokinases (86%, 68%, and 59%, respectively). Nonetheless, combined therapy improved the results of thrombolytic therapy in all the groups.41 Also, they concluded that full success by thrombolytic therapy was higher in patients in NYHA functional classes I or II; nevertheless, they did not find a significant difference between patients with tilting-discs and bileaflet valves, or between patients with first episode of thrombosis and recurrent thrombotic episodes groups.41 The dosage and route of the administration of thrombolytic therapy are different in various studies. Hering et al. recommended using streptokinase by starting a bolus dose of 250,000 IU over thirty minutes, followed by an intravenous infusion of 100,000 IU per hour (same as the therapy of our patient in the first episode of PVT), urokinase by the same protocol used in patients with acute pulmonary embolism, and t-PA at a dosage of 100 mg given over a period of two to five hours.14 Caceres-Loriga et al. recommended using streptokinase by starting a bolus dose of 250,000 IU over three minutes, followed by an intravenous infusion of 100,000 IU per hour (maximum duration of seventy-two hours), urokinase by starting a bolus dose of 4500 U/kg, followed by an intravenous infusion of 4500 U/kg/h (maximum duration of twenty-four to forty-eight hours), and tPA by starting a bolus dose of 15 mg over five minutes, followed by an intravenous infusion of 95 mg over ninety minutes.3 Manteiga et al. used the short-course of thrombolytic therapy as a first line for PVT: streptokinase by starting a bolus dose of 250,000 IU over twenty minutes, followed by an intravenous infusion of 1,500,000 IU over ninety minutes, or tPA by starting a bolus dose of 10 mg, followed by an intravenous infusion of 90 mg over ninety minutes. They concluded that a successful rate by these regimes was 82%.42 However, Alpert recommended another dose for streptokinase in right-sided PVT (starting a dose of 500,000 IU over twenty minutes, followed by an intravenous infusion of 1,500,000 IU over ninety minutes).43 Some other investigators have used direct intra-atrial infusion of thrombolytic for PVT.44, 45 For the first time, Zhang et al. reported a case of tricuspid PVT, which was successfully treated by an intra-right atrium infusion of tPA.

Recently, Tenecteplase (a genetically engineered variant of tPA which has a longer half-life than tPA and is resistant to inactivation by plasminogen activator inhibitor-146) has been utilized for PVT. Our literature search shows that Tenecteplase has been used in limited case repots for mitral or aortic PVT.4752 Although Tenecteplase has been prescribed in different doses and via different methods, we used this thrombolytic according to the dosing regimen employed for acute myocardial infarction. Data on Tenecteplase for the treatment of PVT are limited. Still, Melandri et al. in a review study about patients with acute myocardial infarction showed that this drug had some advantages compared with tPA. These advantages included being more fibrin-specific, usability in a single bolus dose, and having less non-cerebral bleeding. Be that as it may, mortality rates and intracranial hemorrhage rates were similar to those of tPA.46 For the first time, we reported a successful use of Tenecteplase in our case 1 for the treatment of two episodes of recurrent tricuspid PVT. It seems that this drug might be a suitable alternative for the other types of tPA in the future.

If thrombolytic therapy is successful, a continuous infusion of unfractionated heparin is indicated and should be initiated. Moreover, activated partial thromboplastin time should be maintained at twofold the baseline values, followed by conversion to oral anticoagulation combined with Aspirin (50 to 100 mg per day).39 In contrast to left-sided PVT, guidelines do not provide a recommended INR for prostheses in the tricuspid position.36, 39, 40 For bileaflet prosthetic valves in the mitral position, a range of 2.5 - 3.5 is recommended, 2.0 - 3.0 in the aortic position for patients without additional risk factors for thromboembolism.39 However, Shapira et al. recommended target INR levels of 3.5 - 4.0 for patients with tricuspid prostheses6 and Zhang et al., in order to prevent future thrombotic complications of tricuspid PVT, considered target INR levels of 3.0 - 3.5.

Recurrent tricuspid PVT

A major disadvantage of thrombolytic therapy is the relatively high incidence of recurrent thrombosis during follow-up; however, data are limited about rethrombosis after thrombolytic therapy of tricuspid PVT. Recurrent rates after thrombolytic therapy vary from 11% to 31%.3, 5358 Overall, risk of recurrent thrombosis after thrombolytic therapy in left-sided prosthetic valves is higher than that in the tricuspid position. A meta-analysis showed that while the incidence of recurrent thrombosis in left-sided prosthetic valves was 20%, it was 14% in the tricuspid position.14 As was mentioned earlier, the etiology of recurrent thrombosis is the same as that of the first episode. Also, the coexistence of thrombus and pannus tissue on a prosthetic valve is another factor that can explain the recurrence of PVT after successful thrombolytic therapy in a subset of patients.53, 56 However, some recurrences may be the result of an uncompleted resolution of the initial thrombotic process rather than the result of a new thrombosis. Thus, after successful thrombolytic therapy, it is very important to follow up patients with serial clinical and echocardiographic examinations.27 The results of rethrombolysis after PVT recurrence are comparable to those obtained after the first thrombolytic therapy, which is concordant with our case 1.38, 41, 5862 Therefore, rethrombolysis is safe with a high successful rate and is recommended in patients with recurrent tricuspid PVT.

Choose a prosthetic valve: mechanical or biological

Tricuspid valve replacement is one of the most challenging operations of cardiac surgery. Most cardiac surgeons undertake tricuspid valve surgery infrequently and usually perform tricuspid valve repair. Incidence of tricuspid valve replacement is approximately 0.7% of all valve replacements.63 Although many studies have been performed to determine the preference between mechanical or biological valves in the tricuspid position, they have not reached the same conclusion yet.6369 As was mentioned before, because the risk of thrombosis is high in the tricuspid position and thrombus formation is lower in biological valves,65, 66, 70 we recommend the use of biological valves in the tricuspid position, which is similar to that in re-replacement valve surgery (the same as our case 3).


Conclusion

Thrombosis in tricuspid prosthetic valves is high and in some cases, patients are symptom-free or have a mild complaint. Thus, regular visits after vale replacement are reasonable and if there is suspicion of PVT, other modalities (first TTE) are recommended. Herein, we reported three cases of tricuspid PVT with different conditions. The main cause of PVT in our cases was subtherapeutic anticoagulation. The first case was a woman who suffered from recurrent PVT. In this case we successfully used for the first time Tenecteplase for second and third episodes. Given that this drug can be used in a single dose and has acceptable efficacy compared to the other conventional thrombolytic agents, we would recommend Tenecteplase as a good alternative for PVT treatment. Also, this case shows us that thrombolytic therapy is a good option for recurrent tricuspid PVT, in contrast to left-sided PVT. The second case had fixed leaflets in open position, while the patient was symptomless. Thrombolytic therapy failed in this case; however, due to the patient’s chronic infection, we could not replace her valve. At six months’ follow-up, the motion of the leaflets was restricted and she was symptom-free. Thus, if thrombolytic therapy fails, surgery is not possible, the patient is symptom-free, and hemodynamic is stable, close observation with oral anticoagulant would be a reasonable course of action. The last case was a woman who had a large thrombus in the right atrium immediately after mitral and tricuspid valve replacement. We think that the cause of thrombus formation in this case was inadequate anticoagulation therapy. The patient underwent re-replacement surgery and a new biological valve was implanted in the tricuspid position.


References
1.. Butany J,Ahluwalia MS,Munroe C,Fayet C,Ahn C,Blit P,Kepron C,Cusimano RJ,Leask RL. Mechanical heart valve prostheses: identification and evaluation (erratum)Cardiovascular PathologyYear: 20031232234414630298
2.. Vongpatanasin W,Hillis LD,Lange RA. Prosthetic heart valvesN Engl J MedYear: 19963354074168676934
3.. Caceres-Loriga FM,Perez-Lopez H,Santos-Gracia J,Morlans-Hernandez K. Prosthetic heart valve thrombosis: pathogenesis, diagnosis and managementInt J CardiolYear: 20061101616038994
4.. Thorburn CW,Morgan JJ,Shanahan MX,Chang VP. Long-term results of tricuspid valve replacement and the problem of prosthetic valve thrombosisAm J CardiolYear: 198351112811326837458
5.. Minami K,Horstkotte D,Schulte HD,Bircks W. Thrombosis of two St. Jude Medical prostheses in one patient after triple valve replacement. Case report and review of the literatureEur J Cardiothorac SurgYear: 1988248523078420
6.. Shapira Y,Sagie A,Jortner R,Adler Y,Hirsch R. Thrombosis of bileaflet tricuspid valve prosthesis: clinical spectrum and the role of nonsurgical treatmentAm Heart JYear: 199913772172510097236
7.. Buttard P,Bonnefoy E,Chevalier P,Marcaz PB,Robin J,Obadia JF,Kirkorian G,Touboul P. Mechanical cardiac valve thrombosis in patients in critical hemodynamic compromiseEur J Cardiothorac SurgYear: 1997117107139151042
8.. Lengyel M,Fuster V,Keltai M,Roudaut R,Schulte HD,Seward JB,Chesebro JH,Turpie AG. Guidelines for management of leftsided prosthetic valve thrombosis: a role for thrombolytic therapy. Consensus Conference on Prosthetic Valve ThrombosisJ Am Coll CardiolYear: 199730152115269362411
9.. Deviri E,Sareli P,Wisenbaugh T,Cronje SL. Obstruction of mechanical heart valve prostheses: clinical aspects and surgical managementJ Am Coll CardiolYear: 1991176466501993782
10.. Kawano H,Oda T,Fukunaga S,Tayama E,Kawara T,Oryoji A,Aoyagi S. Tricuspid valve replacement with the St. Jude Medical valve: 19 years of experienceEur J Cardiothorac SurgYear: 20001856556911053818
11.. Silber H,Khan SS,Matloff JM,Chaux A,DeRobertis M,Gray R. The St. Jude valve. Thrombolysis as the first line of therapy for cardiac valve thrombosisCirculationYear: 19938730378419020
12.. Edmunds LH Jr. Thrombotic and bleeding complications of prosthetic heart valvesAnn Thorac SurgYear: 1987444304453310938
13.. Piper C,Hering D,Horstkotte D. Prosthetic valve thrombosis. predisposition and diagnosisEur Heart J SupplementsYear: 20013Q1621
14.. Hering D,Piper C,Horstkotte D. Management of prosthetic valve thrombosisEur Heart J SupplementsYear: 20013Q2226
15.. Ricome S,Provenchere S,Aubier B,Ajzenberg N,Lepage L,Dilly MP,Dufour G,Montravers P,Longrois D. Two cases of valvular thrombosis secondary to heparin-induced thrombocytopenia managed without surgeryCirculationYear: 20111231355135721444894
16.. Cevik C,Izgi C,Dechyapirom W,Nugent K. Treatment of prosthetic valve thrombosis: rationale for a prospective randomized clinical trialJ Heart Valve DisYear: 20101916117020369498
17.. Pibarot P,Dumesnil JG. Prosthetic heart valves: selection of the optimal prosthesis and long-term managementCirculationYear: 20091191034104819237674
18.. Wilhelmsen L,Svardsudd K,Korsan-Bengtsen K,Larsson B,Welin L,Tibblin G. Fibrinogen as a risk factor for stroke and myocardial infarctionN Engl J MedYear: 19843115015056749207
19.. Kannel WB,Wolf PA,Castelli WP,D〉Agostino RB. Fibrinogen and risk of cardiovascular disease. The Framingham StudyJAMAYear: 1987258118311863626001
20.. Alderson M. Season and mortalityHealth TrendsYear: 1985178796
21.. Kao CL,Lu MS,Chang JP,Yang TY,Cheng HW. Thrombotic obstruction of a mechanical prosthetic valve in tricuspid positionTex Heart Inst JYear: 20093626126319568403
22.. Suwansirikul S,Glassman E,Raia F,Spencer FC. Late thrombosis of Starr-Edwards tricuspid ball valve prosthesisAm J CardiolYear: 1974347377404417353
23.. Oxenham H,Bloomfield P,Wheatley DJ,Lee RJ,Cunningham J,Prescott RJ. Twenty year comparison of a Bjork-Shiley mechanical heart valve with porcine bioprosthesesHeartYear: 20038971572112807838
24.. Hammermeister K,Sethi GK,Henderson WG,Grover FL,Oprian C,Rahimtoola SH. Outcomes 15 years after valve replacement with a mechanical versus a bioprosthetic valve: final report of the Veterans Affairs randomized trialJ Am Coll CardiolYear: 2000361152115811028464
25.. Shapira Y,Vaturi M,Sagie A. Obstructive left-sided prosthetic valve thrombosisAcute Card CareYear: 20091116016819562566
26.. Reddy NK,Padmanabhan TN,Singh S,Kumar DN,Raju PR,Satyanarayana PV,Rao DP,Rajagopal P,Raju BS. Thrombolysis in left-sided prosthetic valve occlusion: immediate and follow-up resultsAnn Thorac SurgYear: 1994584624708067850
27.. Zoghbi WA,Chambers JB,Dumesnil JG,Foster E,Gottdiener JS,Grayburn PA,Khandheria BK,Levine RA,Marx GR,Miller FA Jr,Nakatani S,Quiñones MA,Rakowski H,Rodriguez LL,Swaminathan M,Waggoner AD,Weissman NJ,Zabalgoitia M,American Society of Echocardiography〉s Guidelines and Standards CommitteeTask Force on Prosthetic ValvesAmerican College of Cardiology Cardiovascular Imaging CommitteeCardiac Imaging Committee of the American Heart AssociationEuropean Association of EchocardiographyEuropean Society of CardiologyJapanese Society of EchocardiographyCanadian Society of EchocardiographyAmerican College of Cardiology FoundationAmerican Heart AssociationEuropean Association of EchocardiographyEuropean Society of CardiologyJapanese Society of EchocardiographyCanadian Society of EchocardiographyRecommendations for evaluation of prosthetic valves with echocardiography and doppler ultrasound: a report From the American Society of Echocardiography〉s Guidelines and Standards Committee and the Task Force on Prosthetic Valves, developed in conjunction with the American College of Cardiology Cardiovascular Imaging Committee, Cardiac Imaging Committee of the American Heart Association, the European Association of Echocardiography, a registered branch of the European Society of Cardiology, the Japanese Society of Echocardiography and the Canadian Society of Echocardiography, endorsed by the American College of Cardiology Foundation, American Heart Association, European Association of Echocardiography, a registered branch of the European Society of Cardiology, the Japanese Society of Echocardiography, and Canadian Society of EchocardiographyJ Am Soc EchocardiogrYear: 200922975101419733789
28.. Montorsi P,De Bernardi F,Muratori M,Cavoretto D,Pepi M. Role of cine-fluoroscopy, transthoracic, and transesophageal echocardiography in patients with suspected prosthetic heart valve thrombosisAm J CardiolYear: 200085586411078238
29.. Montorsi P,Cavoretto D,Alimento M,Muratori M,Pepi M. Prosthetic mitral valve thrombosis: can fluoroscopy predict the efficacy of thrombolytic treatment?CirculationYear: 2003108II798412970213
30.. Muratori M,Montorsi P,Teruzzi G,Celeste F,Doria E,Alamanni F,Pepi M. Feasibility and diagnostic accuracy of quantitative assessment of mechanical prostheses leaflet motion by transthoracic and transesophageal echocardiography in suspected prosthetic valve dysfunctionAm J CardiolYear: 2006979410016377291
31.. Barbetseas J,Nagueh SF,Pitsavos C,Toutouzas PK,Quiñones MA,Zoghbi WA. Differentiating thrombus from pannus formation in obstructed mechanical prosthetic valves: an evaluation of clinical, transthoracic and transesophageal echocardiographic parametersJ Am Coll CardiolYear: 199832141014179809956
32.. Tsai IC,Lin YK,Chang Y,Fu YC,Wang CC,Hsieh SR,Wei HJ,Tsai HW,Jan SL,Wang KY,Chen MC,Chen CC. Correctness of multi-detector-row computed tomography for diagnosing mechanical prosthetic heart valve disorders using operative findings as a gold standardEur RadiolYear: 20091985786719037643
33.. Teshima H,Hayashida N,Fukunaga S,Tayama E,Kawara T,Aoyagi S,Uchida M. Usefulness of a multidetector-row computed tomography scanner for detecting pannus formationAnn Thorac SurgYear: 20047752352614759431
34.. Habets J,Symersky P,van Herwerden LA,de Mol BA,Spijkerboer AM,Mali WP,Budde RP. Prosthetic heart valve assessment with multidetector-row CT: imaging characteristics of 91 valves in 83 patientsEur RadiolYear: 2011211390139621279515
35.. Roudaut R,Serri K,Lafitte S. Thrombosis of prosthetic heart valves: diagnosis and therapeutic considerationsHeartYear: 20079313714217170355
36.. Bonow RO,Carabello BA,Chatterjee K,de Leon AC Jr,Faxon DP,Freed MD,Gaasch WH,Lytle BW,Nishimura RA,O〉Gara PT,O〉Rourke RA,Otto CM,Shah PM,Shanewise JS,American College of Cardiology/American Heart Association Task Force on Practice Guidelines2008 focused update incorporated into the ACC/AHA 2006 guidelines 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 (Writing Committee to revise the 1998 guidelines for the management of patients with valvular heart disease). Endorsed by the Society of Cardiovascular Anesthesiologists, Society for Cardiovascular Angiography and Interventions, and Society of Thoracic SurgeonsJ Am Coll CardiolYear: 200852e114218848134
37.. Ozkan M,Kaymaz C,Kirma C,Sönmez K,Ozdemir N,Balkanay M,Yakut C,Deligönül U. Intravenous thrombolytic treatment of mechanical prosthetic valve thrombosis: a study using serial transesophageal echocardiographyJ Am Coll CardiolYear: 2000351881181910841239
38.. Lengyel M,Horstkotte D,Völler H,Mistiaen WP,Working Group Infection, Thrombosis, Embolism and Bleeding of the Society for Heart Valve DiseaseRecommendations for the management of prosthetic valve thrombosisJ Heart Valve DisYear: 20051456757516245493
39.. Salem DN,O〉Gara PT,Madias C,Pauker SG,American College of Chest PhysiciansValvular and structural heart disease: American College of Chest Physicians Evidence-Based Clinical Practice Guidelines (8th Edition)ChestYear: 2008133593S629S18574274
40.. Vahanian A,Baumgartner H,Bax J,Butchart E,Dion R,Filippatos G,Flachskampf F,Hall R,Iung B,Kasprzak J,Nataf P,Tornos P,Torracca L,Wenink A,Task Force on the Management of Valvular Hearth Disease of the European Society of CardiologyESC Committee for Practice GuidelinesGuidelines on the management of valvular heart disease: The Task Force on the Management of Valvular Heart Disease of the European Society of CardiologyEur Heart JYear: 20072823026817259184
41.. Roudaut R,Lafitte S,Roudaut MF,Courtault C,Perron JM,Jaïs C,Pillois X,Coste P,DeMaria A. Fibrinolysis of mechanical prosthetic valve thrombosis: a single-center study of 127 casesJ Am Coll CardiolYear: 20034165365812598078
42.. Manteiga R,Carlos Souto J,Altès A,Mateo J,Arís A,Dominguez JM,Borrás X,Carreras F,Fontcuberta J. Short-course thrombolysis as the first line of therapy for cardiac valve thrombosisJ Thorac Cardiovasc SurgYear: 19981157807849576210
43.. Alpert JS. The thrombosed prosthetic valve: current recommendations based on evidence from the literatureJ Am Coll CardiolYear: 20034165966012598079
44.. Desai S,Kavinsky C. Localized left atrial administration of tPA for the treatment of mechanical mitral valve thrombosisCatheter Cardiovasc IntervYear: 20087215115518655116
45.. Seltzer SM,Reed MD,Siwik ES. Intra-atrial tissue plasminogen activator infusion for prosthetic valve thrombosisCatheter Cardiovasc IntervYear: 20066713914116345053
46.. Melandri G,Vagnarelli F,Calabrese D,Semprini F,Nanni S,Branzi A. Review of tenecteplase (TNKase) in the treatment of acute myocardial infarctionVasc Health Risk ManagYear: 2009524925619436656
47.. Maegdefessel L,Issa H,Scheler C,Thäle V,Schlitt A,Hartelt U,Grabitz R,Buerke M. 27-year old pregnant woman with syncope and dyspnea after aortic alloplastic heart valve replacement 15 years agoInternist (Berl)Year: 20084986887218512035
48.. Charokopos N,Antonitsis P,Artemiou P,Rouska E,Foroulis C,Papakonstantinou C. Acute mechanical prosthetic valve thrombosis after initiating oral anticoagulation therapy. Is bridging anticoagulation with heparin required?Interact Cardiovasc Thorac SurgYear: 2009968568719602494
49.. Ferreiro-Gutierrez JL,riza-Sole A,Manas-Jimenez P,Ruiz-Majoral A. Repeated thrombolysis with tenecteplase as a bridge to valvular replacement in a case of preoclusive mitral prosthetic thrombosisMed Clin (Barc)Year: 200913340240319747593
50.. Al-Sarraf N,Al-Shammari F,Al-Fadhli J,Al-Shawaf E. Successful thrombolysis of a thrombosed prosthetic mitral valve using a synthetic tissue plasminogen activator: a case reportJ Med Case RepYear: 2010424120682069
51.. Slaoui M,Cherradi R,Ounzar M,Massou S,Srairi JE. Thrombosis valvular prosthesis of Starr treated successfully by tenecteplase during pregnancyAnn Fr Anesth ReanimYear: 20102950050120573480
52.. Ayyub Ghori M,Bakir S,Ellahham S,Al Nassir A,Al Zubaidi A,Augustin N,Ayman Abdelaziz M,Patrick Turrin N,Al Mahmeed WA. Tenecteplase in prosthetic mitral valve thrombosisJ Saudi Heart AssocYear: 2011239395
53.. Keuleers S,Herijgers P,Herregods MC,Budts W,Dubois C,Meuris B,Verhamme P,Flameng W,Van de Werf F,Adriaenssens T. Comparison of thrombolysis versus surgery as a first line therapy for prosthetic heart valve thrombosisAm J CardiolYear: 201110727527921211605
54.. Gupta D,Kothari SS,Bahl VK,Goswami KC,Talwar KK,Manchanda SC,Venugopal P. Thrombolytic therapy for prosthetic valve thrombosis: short- and long-term resultsAm Heart JYear: 200014090691611099995
55.. Cáceres-Lóriga FM,Pérez-López H,Morlans-Hernández K,Facundo-Sánchez H,Santos-Gracia J,Valiente-Mustelier J,Rodiles-Aldana F,Marrero-Mirayaga MA,Betancourt BY,López-Saura P. Thrombolysis as first choice therapy in prosthetic heart valve thrombosis. A study of 68 patientsJ Thromb ThrombolysisYear: 20062118519016622616
56.. Lengyel M,Vandor L. The role of thrombolysis in the management of left-sided prosthetic valve thrombosis: a study of 85 cases diagnosed by transesophageal echocardiographyJ Heart Valve DisYear: 20011063664911603604
57.. Ozkan M,Kaymaz C,Kirma C,Sönmez K,Ozdemir N,Balkanay M,Yakut C,Deligönül U. Intravenous thrombolytic treatment of mechanical prosthetic valve thrombosis: a study using serial transesophageal echocardiographyJ Am Coll CardiolYear: 2000351881188910841239
58.. Shapira Y,Herz I,Vaturi M,Porter A,Adler Y,Birnbaum Y,Strasberg B,Sclarovsky S,Sagie A. Thrombolysis is an effective and safe therapy in stuck bileaflet mitral valves in the absence of high-risk thrombiJ Am Coll CardiolYear: 2000351874188010841238
59.. Cáceres-Lóriga FM,Pérez-López H,Santos-Gracia J,Morlans-Hernández K,Marrero-Mirayaga MA. Thrombolytic treatment as first option in recurrent tricuspid prosthetic valve thrombosis and Ebstein〉s anomalyJ Pharm Pharm SciYear: 2005833233416124944
60.. Torrado González E,Ferriz Martín JA,Prieto Palomino MA,Rodríguez García JJ,Alvarez Bueno JM,Vera Almazán A,Garrido Alcalde MR,González de Vega N. Thrombolysis of thrombosed heart valve prostheses: presentation of 2 cases and review of the literatureRev Esp CardiolYear: 1990433453512118271
61.. Shapira Y,Herz I,Birnbaum Y,Snir E,Vidne B,Sagie A. Repeated thrombolysis in multiple episodes of obstructive thrombosis in prosthetic heart valves: a report of three cases and review of the literatureJ Heart Valve DisYear: 2000914614910678388
62.. Shapira Y,Vaturi M,Hasdai D,Battler A,Sagie A. The safety and efficacy of repeated courses of tissue-type plasminogen activator in patients with stuck mitral valves who did not fully respond to the initial thrombolytic courseJ Thromb HaemostYear: 2003172572812871407
63.. Ratnatunga CP,Edwards MB,Dore CJ,Taylor KM. Tricuspid valve replacement: UK Heart Valve Registry mid-term results comparing mechanical and biological prosthesesAnn Thorac SurgYear: 199866194019479930473
64.. Rizzoli G,Vendramin I,Nesseris G,Bottio T,Guglielmi C,Schiavon L. Biological or mechanical prostheses in tricuspid position? A meta-analysis of intra-institutional resultsAnn Thorac SurgYear: 2004771607161415111151
65.. Rizzoli G,De Perini L,Bottio T,Minutolo G,Thiene G,Casarotto D. Prosthetic replacement of the tricuspid valve: biological or mechanical?Ann Thorac SurgYear: 199866S62679930419
66.. Kaplan M,Kut MS,Demirtas MM,Cimen S,Ozler A. Prosthetic replacement of tricuspid valve: bioprosthetic or mechanicalAnn Thorac SurgYear: 20027346747311845861
67.. Chang BC,Lim SH,Yi G,Hong YS,Lee S,Yoo KJ,Kang MS,Cho BK. Long-term clinical results of tricuspid valve replacementAnn Thorac SurgYear: 2006811317132316564264
68.. Filsoufi F,Anyanwu AC,Salzberg SP,Frankel T,Cohn LH,Adams DH. Long-term outcomes of tricuspid valve replacement in the current eraAnn Thorac SurgYear: 20058084585016122441
69.. Dalrymple-Hay MJ,Leung Y,Ohri SK,Haw MP,Ross JK,Livesey SA,Monro JL. Tricuspid valve replacement: bioprostheses are preferableJ Heart Valve DisYear: 1999864464810616242
70.. Carrier M,Hébert Y,Pellerin M,Bouchard D,Perrault LP,Cartier R,Basmajian A,Pagé P,Poirier NC. Tricuspid valve replacement: an analysis of 25 years of experience at a single centerAnn Thorac SurgYear: 200375475012537191

Article Categories:
  • Review Article

Keywords: Tricuspid valve, Thrombosis, Thrombolytic therapy, Anticoagulants, Surgical procedures, operative.

Previous Document:  Universal iron fortification of foods: the view of a hematologist.
Next Document:  Increased carotid artery intima-media thickness in pregnant women with gestational diabetes mellitus...