Bioprosthetic Valve Thrombosis Research Articles

Comparison of apixaban versus aspirin for the prevention of latent bioprosthetic aortic valve thrombosis: study protocol for a prospective randomized trial.

The optimal antithrombotic strategy early after aortic valve replacement surgery with a biological valve remains controversial due to lack of high-quality evidence. Either oral anticoagulants or acetylsalicylic acid should be considered for the first 3 months. Hypo-attenuated leaflet thickening on cardiac computed tomography has been associated with latent bioprosthetic valve thrombosis and may be prevented with anticoagulation. We hypothesize that anticoagulation with apixaban is superior to single antiplatelet therapy with acetylsalicylic acid in reducing hypo-attenuated leaflet thickening of bioprosthetic aortic valve prostheses. In this prospective, open-label, randomized trial, patients undergoing isolated aortic valve replacement surgery with rapid deployment bioprosthetic valves will be randomized. The treatment group will receive 5 mg of apixaban twice a day for the first 3 months and 100 mg of acetylsalicylic acid thereafter. The control group will be administered 100 mg of acetylsalicylic acid once a day, indefinitely. After the 3-month treatment period, a contrast-enhanced electrocardiogram-gated cardiac computed tomography will be performed to identify hypo-attenuated leaflet thickening of the bioprosthetic valve. The primary objective of the study is to assess the impact of apixaban on the prevention of hypo-attenuated leaflet thickening at 3 months. The secondary and exploratory endpoints will be clinical outcomes and safety profiles of the two strategies. Antithrombotic therapy after aortic valve replacement is used to prevent valve thrombosis and systemic thromboembolism. Latent bioprosthetic valve thrombosis is a precursor of clinically significant prosthetic valve dysfunction or thromboembolic events. The hallmark feature of latent bioprosthetic valve thrombosis is hypo-attenuated leaflet thickening on cardiac computed tomography. Subclinical leaflet thrombosis occurs frequently in bioprosthetic aortic valves, more commonly in transcatheter than in surgical valves. There is no evidence on the effect of direct oral anticoagulants on the incidence of hypo-attenuated leaflet thickening after surgical aortic valve replacement with rapid deployment bioprostheses. ClinicalTrials.gov NCT06184113. Registered on December 28, 2023.

Thrombosis of Prosthetic Tricuspid Valve During Veno-Arterial Extracorporeal Membrane Oxygenation Support: A Case Report

Extracorporeal membrane oxygenation (ECMO) is frequently used for severe postcardiotomy cardiogenic shock in patients with bioprosthetic valves. Acute prosthetic valve thrombosis (PVT) is a rare complication after valve replacement surgery and significantly increases morbidity and mortality. Patients who develop PVT on ECMO could significantly influence the long-term durability of the bioprosthetic valves. However, previous studies only analyzed risk factor and treatment of the mitral valve thrombosis during ECMO support. The mechanism of thrombosis on the tricuspid valve was still unknown. Here we describe the symptoms and treatment of a valve replacement patient who developed bioprosthetic tricuspid valve thrombosis during veno-arterial extracorporeal membrane oxygenation (VA-ECMO). Meanwhile, the patient’s mechanical prosthetic mitral valve functioned normally. An emergency re-do tricuspid prosthesis replacement was performed, and the patient finally developed the successful decannulation. At 6 months follow-up, the patient showed asymptomatic and had a reasonable quality of life. The pathophysiology of tricuspid valve thrombosis may be different from the left heart. Our case highlights that the risk of thrombosis associated with a prosthesis in the tricuspid position can be even higher in the setting of VA-ECMO support. In such patients, promoting forward blood flow across the prosthesis and improving levels of anticoagulation may be particularly important.

Abstract 16163: Low Dose Alteplase for Treatment of Pacemaker Lead Associated Thrombosis

Multiple previously published case reports highlighted the thromboembolic risks associated with permanent transvenous pacemaker leads. Even though mostly clinically silent, pacemaker lead associated thrombosis has been linked to fatal outcomes via pulmonary or paradoxical embolism in the case of large mobile RA or RV thrombi formation. There is a lack of consensus on the optimal strategy for managing this condition. Oral and IV anticoagulation, thrombolysis, surgical and percutaneous thrombectomy have been attempted previously with mixed results. A 72 year old gentleman with a history of CAD requiring PCI, paroxysmal atrial fibrillation, and AV node ablation with subsequent biventricular pacemaker implant was admitted to our hospital with a few weeks of worsening dyspnea, now present at rest. Surface echocardiogram showed multiple mobile echo densities in the right ventricle and right atrium, attached to the pacemaker leads, confirmed by TEE, most likely thrombi. The venous duplex was positive for right lower extremity DVT. Bilateral pulmonary emboli with mild right-sided heart strain were noted on CTA chest. The patient was initially treated with IV unfractionated heparin. We subsequently decided to start low-dose tPA infusion for 24 hrs, similar to current off-label protocols for mechanical prosthetic valves or bioprosthetic valve thrombosis. After an initial IV bolus of 5 mg, 1 mg/hour of alteplase was continued for 24 hours. Our team has decided to use percutaneous thrombectomy as a last resort.Follow-up ECHO immediately post tPA infusion showed complete thrombi resolution. The patient was asymptomatic at this point. He was discharged the following day on Lovenox and Coumadin. To our knowledge, this is the first case demonstrating complete resolution of pacemaker lead-associated thrombi by using a 24 hr low dose tPA infusion in addition to IV anticoagulation. This can be entertained as a simple conservative initial strategy in stable patients with pacemaker lead/catheter-associated intracardiac thrombi.

Early 6 months usage of single anTiplAtelet OR anTicoAgulant followed by single antiplatelet after transcatheter aortic valve replacement: protocol for a multicentre, open-label, randomised controlled clinical trial

IntroductionThe strategy for initiating antithrombotic therapy to prevent bioprosthetic valve thrombosis (BPVT) after transcatheter aortic valve replacement (TAVR) remains uncertain. There is still lacking evidence on the efficacy and safety...

Coronary embolism due to probable clinical bioprosthetic aortic valve thrombosis: a case report

BackgroundCoronary embolism is a relatively rare but important non-atherosclerotic cause of acute coronary syndrome, mainly caused by atrial fibrillation and mechanical heart valve thrombosis due to subtherapeutic anticoagulation. There have been increasing reports of bioprosthetic valve thrombosis (BPVT), but thromboembolic events are rare and mainly affect the cerebrovascular system. Coronary embolism is an extremely rare complication of BPVT.Case presentationA 64-year-old male presented with non-ST-Elevation myocardial infarction (NSTEMI) to an Australian regional health service. Three years ago, he had undergone Bentall procedure with bioprosthetic aortic valve replacement for severe aortic regurgitation and significant aortic root dilatation. Diagnostic coronary angiography revealed embolic occlusion of first diagonal branch in the absence of underlying atherosclerosis. Prior to NSTEMI presentation, the patient was clinically asymptomatic apart from the progressive increase in transaortic mean pressure gradient on transthoracic echocardiography which was first detected seven months after surgical aortic valve replacement. Transoesophageal echocardiography showed restrictions of the aortic leaflet opening but no evidence of mass or vegetation. After eight weeks of warfarin therapy, the raised aortic valve gradient returned to normal. Lifelong warfarin was prescribed, and patient remained clinically well at 39-month follow-up.ConclusionWe experienced a case of coronary embolism in a patient with probable BPVT. Reversible bioprosthetic valve hemodynamic deterioration after anticoagulation strongly supports the diagnosis in the absence of histopathology. Early moderate-to-severe hemodynamic valve deterioration warrants further investigations, including cardiac computed tomography and sequential echocardiography, to investigate for probable BPVT and consideration of timely anticoagulation initiation to prevent thromboembolic events.

Intravenous thrombolysis for bioprosthetic valve thrombosis.

A 77-year-old woman experienced new-onset dyspnoea on exertion 1 year after alcohol septal ablation and transcatheter aortic valve implantation (TAVI) with a balloon-expandable valve for symptomatic severe aortic stenosis and basal septal hypertrophy. Transthoracic echocardiographic assessment (TTE) revealed an incremental transvalvular peak velocity from 2.9 m/s 3 days after TAVI to 4.3 m/s. Multislice computed tomography (MSCT) demonstrated hypoattenuated leaflet thickening (HALT) of all leaflets and reduced leaflet motion (RLM) of one leaflet (Panel A). Her antithrombotic regimen was changed from apixaban 5 mg bi-daily to acenocoumarol with a target international normalized ratio (INR) of 2.5–3.5. Six weeks later, symptoms persisted and the transvalvular peak velocity was 3.9 m/s (Panel B). A decision was made to attempt to resolve the thrombus with repeated intravenous infusions of alteplase.1,2 Four sequential infusions of 25 mg alteplase/25 h resulted in an uneventful but stepwise decrease of the transvalvular peak velocity to 2.8 m/s (Panel C–F). Multislice computed tomography confirmed normalization of leaflet motion with some residual remaining leaflet thickening (Panel F). MSCT cine images before and after alteplase infusion are available in the Supplementary data online (Videos S1 and S2).

Medium-Term Outcomes of the Different Antithrombotic Regimens After Transcatheter Aortic Valve Implantation

Bioprosthetic valve thrombosis is associated with accelerated bioprosthesis degeneration and valve re-replacement. Whether 3-month warfarin use after transcatheter aortic valve implantation (TAVI) protects against such consequences is unknown. We aimed to investigate if 3-month warfarin treatment after TAVI is associated with better outcomes than dual antiplatelet therapy (DAPT) and single antiplatelet therapy (SAPT) at medium-term follow-up. Adults who underwent TAVI were identified retrospectively (n = 1,501) and classified into warfarin, DAPT, and SAPT groups based on antithrombotic regimen received. Patients with atrial fibrillation were excluded. Outcomes and valve hemodynamics were compared between the groups. Annualized change from baseline in mean gradients and effective orifice area at last follow-up echocardiography was calculated. Overall, 844 patients were included (mean age: 80 ± 9 years, 43% women; 633 receiving warfarin, 164 DAPT, and 47 SAPT). Median time to follow-up was 2.5 (interquartile range 1.2 to 3.9) years. There were no differences in the adjusted outcome end points of ischemic stroke, death, valve re-replacement/intervention, structural valve degeneration, or their composite end point at follow-up. Annualized change in aortic valve area was significantly higher in DAPT (−0.11 [0.19] cm2/year) than warfarin (−0.06 [0.25] cm2/y, p = 0.03), but annualized change in mean gradients was not different (p >0.05). In conclusion, antithrombotic regimen, including warfarin, after TAVI was associated with marginally lower decrease in aortic valve area but no difference in medium-term clinical outcomes compared with DAPT and SAPT. Bioprosthetic valve thrombosis is associated with accelerated bioprosthesis degeneration and valve re-replacement. Whether 3-month warfarin use after transcatheter aortic valve implantation (TAVI) protects against such consequences is unknown. We aimed to investigate if 3-month warfarin treatment after TAVI is associated with better outcomes than dual antiplatelet therapy (DAPT) and single antiplatelet therapy (SAPT) at medium-term follow-up. Adults who underwent TAVI were identified retrospectively (n = 1,501) and classified into warfarin, DAPT, and SAPT groups based on antithrombotic regimen received. Patients with atrial fibrillation were excluded. Outcomes and valve hemodynamics were compared between the groups. Annualized change from baseline in mean gradients and effective orifice area at last follow-up echocardiography was calculated. Overall, 844 patients were included (mean age: 80 ± 9 years, 43% women; 633 receiving warfarin, 164 DAPT, and 47 SAPT). Median time to follow-up was 2.5 (interquartile range 1.2 to 3.9) years. There were no differences in the adjusted outcome end points of ischemic stroke, death, valve re-replacement/intervention, structural valve degeneration, or their composite end point at follow-up. Annualized change in aortic valve area was significantly higher in DAPT (−0.11 [0.19] cm2/year) than warfarin (−0.06 [0.25] cm2/y, p = 0.03), but annualized change in mean gradients was not different (p >0.05). In conclusion, antithrombotic regimen, including warfarin, after TAVI was associated with marginally lower decrease in aortic valve area but no difference in medium-term clinical outcomes compared with DAPT and SAPT.

Cardiovascular computed tomography in the evaluation of post-TAVI prosthesis dysfunction: the thin line between hypo attenuated leaflet thickening and clinical valve thrombosis.

It is accepted that hypo attenuated leaflet thickening (HALT) can be detected in 12% and 32% of transcatheter aortic valve implantation (TAVI) patients on oral anticoagulation or dual antiplatelet therapy at 3 months, respectively.1 Clinically relevant TAVI thrombosis is rare, with up to 1% incidence.2 We present the case of an 86-year-old male with a history of ischemic cardiomyopathy, atrial fibrillation (on apixaban 5 mg BID), and 4 months post-TAVI (Sapien 3–29 mm) who presented to the Emergency Department with worsening dyspnea and elevated cardiac biomarkers: HS-Tn (1689 ng/L) and NT-proBNP (>5000 pg/mL). Echocardiogram showed new severe systolic dysfunction (left ventricular EF = 30%) and elevated gradients (compared to the basal post-TAVI study) with limited visualization of the valve (central figure, Panels A and B). He underwent invasive coronary angiography, which showed no coronary artery disease progression as to explain the clinical changes. Given the rapidly worsening clinical status, a cardiovascular computed tomography (CCT) was ordered over transesophageal echocardiogram for better evaluation. The CCT was acquired using retrospective gating without ECG dose modulation (IQon, Philips) for high-quality full-cycle images (Panels C–F). There was severe symmetrical tri-leaflet thickening with sparing of the distal tips (meniscal shape), classically described in HALT.3 The Hounsfield units were more consistent with thrombus (<100 HU) (Panel C), and significantly reduced tri-leaflet motion was also noted on functional images (see Supplementary data online, Video S1). Despite being treated with i.v. heparin and guideline-directed medical therapy for HFrEF, the patient developed refractory cardiogenic shock and expired. The best antithrombotic regimen for patients undergoing TAVI remains controversial.4 Bioprosthetic valve thrombosis involves a spectrum with different grades of clinical manifestation. The CCT is paramount for establishing the etiology of the dysfunction and providing prognostic information for patient management.5

194 THROMBOEMBOLIC ACUTE ST ELEVATION MYOCARDIAL INFARCTION AFTER TRANSCATHETER VALVE IMPLANTATION

Abstract Transcatheter aortic valve implantation (TAVI) is an established treatment of severe symptomatic aortic valve stenosis and is an effective and less invasive treatment option compared with conventional surgical aortic valve replacement (SAVR) for patients considered inoperable or at high surgical risk. Thromboembolic and bleeding complications negatively impact recovery and survival after TAVI. This case describes one of the few reported TAVI-associated myocardial infarction due to thrombosis of the prosthetic aortic valve. A 82-years-old woman, suffering from severe symptomatic aortic stenosis, underwent TAVI. Before the procedure, coronary artery disease was excluded by invasive coronary angiography. Since the time of the discharge the patient didn't assume any therapy with aspirin or other antithrombotic drugs. A month after TAVI she complained persistent epigastric pain and was admitted to our department for anterior ST elevation myocardial infarction. Coronary angiography highlighted a monovascular coronary artery disease with thrombotic occlusion of the first diagonal and of the distal left anterior descending coronary artery. In consideration of the thrombotic load thyrofiban was started and it was performed a chest contrast CT which confirmed the diagnostic suspicion of bioprosthetic valve thrombosis. She was first treated with unfractionated heparin (UFH) and then oral anticoagulant therapy with warfarin was started. Echocardiograms (echo) showed a severely reduced systolic function (EF 25%) and high trans-prosthetic gradients (mean transprosthetic pressure gradient of 30 mmHg). On the 8th day after hospitalization she complained chest pain with evidence of moderate pericardial effusion. Epistenocardica pericarditis was therefore diagnosed and the patient started acetylsalicylic acid therapy with progressive clinical, instrumental and laboratory improvement. After 10 days of anticoagulation therapy, she underwent a transesophageal echocardiogram which turned out negative for bioprosthetic valve thrombosis. The predischarge transthoracic echocardiography showed severely reduced systolic function (EF 30%) with a mean transprothesic gradient of 12 mmHg; the circumferential pericardial effusion was mild-moderate but not haemodynamically significative. Therapy at discharged included warfarin and aspirin. Ten days after an echo showed a reduction of the pericardial effusion, an improved systolic function (EF 42%) and mean transprothesic gradient not changed significantly since discharge. Prosthetic valve thrombosis has been reported in up to 40% of patients after TAVI and this case hightlights the importance of antithrombotic therapy after this procedure. Therapeutic anticoagulation appears to be the only non-invasive treatment for resolving valve thrombosis but it is not clear how long this therapy should last for the prevention of prosthetic valve thrombosis.

Postoperative prosthetic mitral valve occlusion due to left atrial thrombus during veno-arterial extracorporeal membrane oxygenation: a case report

BackgroundAnticoagulation using heparin is generally used to prevent thrombus formation during mechanical circulatory support, such as veno-arterial extracorporeal membrane oxygenation (VA-ECMO). However, during the early period following cardiac surgery, anticoagulation becomes more difficult due to the greater risk of critical bleeding complications.Case presentationA 71-year-old man presented with acute prosthetic valve occlusion caused by left atrial thrombus formation and bioprosthetic valve thrombosis during peripheral VA-ECMO following mitral valve replacement (MVR) despite continuous heparin administration and loading of antiplatelet agents. The VA-ECMO flow rate decreased 10 h after the intensive care unit (ICU) admission after MVR. Exploratory transesophageal echocardiography (TEE) examination revealed a left atrial thrombus, prosthetic valve obstruction by the thrombus, and an intrapericardial hematoma.ConclusionsIntracardiac thrombus formation might occur during VA-ECMO despite appropriate anticoagulation and loading of antiplatelet agents. Exploratory TEE examination was helpful in the detection of intra-atrial thrombus formation after cardiac surgery and surgical decision-making.

Abstract 9831: Antithrombotic Regimens After Transcatheter Aortic Valve Replacement: Comparison of Medium-Term Outcomes

Introduction: Bioprosthetic valve thrombosis is a recognized cause of bioprosthetic valve dysfunction. It was found to be associated with accelerated bioprosthetic degeneration and higher rates of valve re-replacement. Hypothesis: Warfarin for 3 months after transcatheter aortic valve replacement (TAVR) protects against accelerated valve degeneration and is therefore associated with better outcomes compared to dual antiplatelet (DAPT) and single antiplatelet therapies (SAPT). Methods: Adult patients who underwent TAVR (2012-2019) were identified retrospectively (n=1,501). Patients with atrial fibrillation were excluded (n=657). Patients were classified into warfarin, DAPT, and SAPT groups based on antithrombotic regimen. Structural valve degeneration (SVD) was considered when patients developed new ≥ moderate trans-prosthetic regurgitation, increase in mean gradients ≥10 mmHg from baseline, or when gradients exceeded 20 mmHg. Discharge date was considered time zero. Results: Overall, 844 patients [mean age 80 (±9), 43% females, mean Society of Thoracic Surgeons risk score 6.7 (±5.0)] were included. Warfarin was used in 633 (75%) patients, DAPT in 164 (19%), and SAPT in 47 (6%). Median follow-up time was 2.5 (IQR 1.2-3.9) years. There was no difference in outcomes of ischemic stroke, death, valve re-intervention, SVD, their composite endpoint, or hemorrhagic stroke and hemorrhagic stroke/RBC transfusion events (Figures 1 &amp; 2), even after adjustment for confounders. Conclusion: Warfarin after TAVR was not associated with better clinical or hemodynamic outcomes or with worse adverse events compared to DAPT and SAPT.

Abstract 11101: Q Fever Endocarditis Combined With Thrombus and Antiphospholipid Syndrome

A 63-year-old-man presented to our institution with dyspnea. Transthoracic echocardiography (TTE) showed severe degenerative aortic stenosis with regurgitation and decreased left ventricular contractility. Subsequent transesophageal echocardiography (TEE) and cardiac computed tomography (CT) revealed an outpouching structure at aortomitral intervalvular fibrosa (AMIVF) (Fig A to D), which was compatible with pseudoaneurysm and suggested sequelae of previous infective endocarditis. On surgery, thickened AV leaflets were noted, especially on NCC and LCC (Fig E). When extracting the AV leaflets, subannular pouching was seen without evidence of active inflammation or infection (Fig F). AV replacement with 25-mm Sorin Mitroflow was performed.One-year TTE follow-up showed markedly increased transAV pressure gradient. TEE and cardiac CT revealed symmetric nodular thickening of bioprosthetic AV leaflets with opening limitation (Fig G to J). The patient was admitted on the diagnosis of subclinical bioprosthetic valve thrombosis, and anticoagulation with warfarin and aspirin was started. During the hospitalization, the patient had persistent fever with bicytopenia and hepatosplenomegaly, but repetitive blood cultures were negative. There was no definite fever focus even in 18F-FDG PET CT (Fig K). Since the patient worked on a farm in Dangjin, Chungcheongnam-Do, South Korea, where Q fever is prevalent, an indirect immunofluorescence assay for Coxiella burnetii was conducted and the result turned out to be positive. Additional coagulopathy laboratory findings showed positive for lupus anticoagulant, anti-cardiolipin IgM, and anti-beta2 GPI IgM. Finally, the patient was diagnosed with Q fever endocarditis combined with antiphospholipid syndrome and treated with doxycycline with hydroxychloroquine and maintained anticoagulation. Recent follow-up of TTE and cardiac CT showed complete resolution of prosthetic AV thrombus.

Contact pathway in surgical and transcatheter aortic valve replacement.

BackgroundAortic valve replacement is the gold standard treatment for severe symptomatic aortic stenosis, but thrombosis of bioprosthetic valves (PVT) remains a concern.ObjectiveTo analyze the factors involved in the contact pathway during aortic valve replacement and to assess their impact on the development of thromboembolic complications.MethodsThe study was conducted in 232 consecutive patients who underwent: transcatheter aortic valve replacement (TAVR, N = 155), and surgical valve replacement (SAVR, N = 77) (MUVITAVI project). Demographic and clinical data, outcomes including a combined end point (CEP) of thrombotic events, and imaging controls were recruited. Samples were collected 24 h before and 48 h after valve replacement. FXII, FXI and (pre)kallikrein were evaluated by Western Blot and specific ELISA with nanobodies.ResultsThe CEP of thrombotic events was reached by 19 patients: 13 patients presented systemic embolic events and 6 patients subclinical PVT. Valve replacement did not cause FXII activation or generation of kallikrein. There was a significant reduction of FXI levels associated with the procedure, which was statistically more pronounced in SAVR than in TAVR. Cases with reductions of FXI below 80% of basal values had a lower incidence of embolic events during the procedure than patients in whom FXI increased above 150%: 2.7 vs. 16.7%; p: 0.04.ConclusionTAVR or SAVR did not significantly activate the contact pathway. A significant reduction of FXI, was observed, particularly in SAVR, associated with lower incidence of thrombotic events. These results encourage evaluating the usefulness and safety of FXI-directed antithrombotic treatments in these patients.

A bioprosthetic heart valve material prepared by copolymerization of 2-Amino-4-pentanoic acid modified pericardium and N, N-Dimethylacrylamide

Bioprosthetic heart valve thrombosis (BHVT) is no longer considered a rare clinical entity in recent years and could cause valve motion abnormalities, which requires reoperation. Currently reported modifications of bioprosthetic heart valves (BHVs) mainly focused on improving the anti-calcification property. However, it was hard to improve their anti-thrombogenicity and crosslinking efficiency at the same time. Here we reported a method that combines improved hemocompatibility, crosslinking efficiency, cytocompatibility, and anti-calcification property for BHVs. Porcine pericardia (PPs) and 2-amino-4-pentanoic acid (APA) were first co-crosslinked with glutaraldehyde to introduce allyl moieties to the PPs, then poly(N, N-dimethylacrylamide) (PDMAA) was covalently immobilized on PPs through radical polymerization. In vitro and in vivo studies demonstrated that the structural stability of PDMAA modified PPs was much superior than that of traditional glutaraldehyde crosslinked PPs (GA). The PDMAA modified PPs exhibited enhanced antithrombogenic performance with a 75% decrease of platelet adhesion compared with GA. Moreover, the calcium content accumulated on the modified PPs after 90-day rat subcutaneous implantation decreased 93.5% compared with that on GA. The PDMAA modified PPs may alleviate BHVT and calcification, offering a potential option for BHVs fabrication in the future.

Efficacy of Cardiac Computed Tomography for Diagnostic and Therapeutic Evaluation of Bioprosthetic Valve Thrombosis

Efficacy of Cardiac Computed Tomography for Diagnostic and Therapeutic Evaluation of Bioprosthetic Valve Thrombosis

A PEGylation method of fabricating bioprosthetic heart valves based on glutaraldehyde and 2-amino-4-pentenoic acid co-crosslinking with improved antithrombogenicity and cytocompatibility

With the development of diagnostic techniques, the incidence of bioprosthetic heart valve thrombosis (BHVT) is found to be seriously underestimated. Developing bioprosthetic heart valves (BHVs) that have good hemocompatibility without sacrificing other properties such as hydrodynamics and durability will be an effective strategy to alleviate BHVT. In this study, we developed a PEGylation method by co-crosslinking and subsequent radical polymerization. 2-amino-4-pentenoic acid was used to introduce carbon-carbon double bonds for glutaraldehyde crosslinked pericardia. Then poly (ethylene glycol) diacrylate (PEGDA) was immobilized on pericardia by radical polymerization. A comprehensive evaluation of the modified pericardia was performed including structural characterization, hemocompatibility, cytocompatibility, mechanical properties, component stability, hydrodynamic performance and durability of the BHVs. The modified pericardia significantly reduced platelet adhesion by more than 75% compared with traditional glutaraldehyde crosslinked pericardia. Cell viability in the modified pericardia group was nearly 5-fold higher than that in glutaraldehyde crosslinked pericardia. The hydrodynamic performance met the requirements of ISO 5840–3 under physiological aortic valve conditions and its durability was proved after 200 million cycles of accelerated fatigue test. In conclusion, PEGDA modified pericardia exhibited improved antithrombogenicity and cytocompatibility properties compared with glutaraldehyde crosslinked pericardia. Statement of significanceBioprosthetic valve (BHV) implantation requires BHV to be structurally stable as well as biocompatible in vivo. Traditional glutaraldehyde crosslinking method prepared BHV suffers from severe cytotoxicity, thrombosis, and calcification. BHV modification methods that have simultaneously improved structural stability and biocompatibility were rarely reported. Here, we proposed a PEGylation method for BHV based on co-crosslinking strategy that could improve its structural stability as well as hemocompatibility. We take the advantage of high efficiency of glutaraldehyde crosslinking and demonstrate the feasibility and superiority of the PEGylated strategy, offering a promising option in glutaraldehyde-based BHV fabrication in the future.

An Extreme Case of Bioprosthetic Valve Thrombosis in a Patient With Systemic Lupus Erythematosus and Antiphospholipid Antibody Syndrome

A young woman presented with increasing fatigue, dyspnea, lightheadedness, and intermittent chest pain. She had a history of systemic lupus erythematosus, antiphospholipid antibody syndrome, and Libman-Sacks endocarditis, resulting in a bioprosthetic aortic valve replacement 6 months before presentation. A bioprosthetic valve was chosen at that time over a mechanical valve because of inability to consistently maintain therapeutic anticoagulation levels with warfarin. Transthoracic echocardiography was performed and showed severe aortic valve prosthetic stenosis with a mean gradient of 69 mm Hg and thickened leaflets (Figure A) with reduced mobility, consistent with bioprosthetic valve thrombosis (BPVT).

Bioprosthetic mitral valve thrombosis.

Bioprosthetic mitral valve thrombosis.

A Case of Bioprosthetic Valve Thrombosis: Is it Time to Revise Our Thinking?

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.

Bioprosthetic Mitral Valve Thrombosis: A Multifaceted and Challenging Clinical and Imaging Spectrum

Bioprosthetic Mitral Valve Thrombosis: A Multifaceted and Challenging Clinical and Imaging Spectrum