Publications by authors named "Virginie Barbay"

16 Publications

  • Page 1 of 1

Imaging of Oxford/AstraZeneca® COVID-19 vaccine-induced immune thrombotic thrombocytopenia.

Diagn Interv Imaging 2021 Apr 28. Epub 2021 Apr 28.

Department of Radiology, CHU de Rouen, 76000 Rouen, France; UNIROUEN, Inserm U1096, 76000 Rouen, France.

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http://dx.doi.org/10.1016/j.diii.2021.04.005DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8080133PMC
April 2021

First observation of inhibitor development against efmoroctocog alfa in France.

Transfus Apher Sci 2021 Apr 8:103128. Epub 2021 Apr 8.

Department of Paediatrics, Clinical and Molecular Haemostasis, Frankfurt University Hospital, Frankfurt am Main, Germany.

In patients with severe haemophilia receiving clotting factor concentrates, the risk of immunisation against their usual treatment is still patent and feared. New haemophilia drug treatments with an extended half-life have become available over the past few years. The risk of inhibitor development to these new treatments is unclear. We report the case of a 51-year-old man with severe haemophilia A, who was previously treated with no history of inhibitor development. Soon after a switch in his treatment to efmoroctocog alfa he developed an inhibitor against this recombinant Fc fusion extended half-life FVIII (rFc-FVIII) product. The patient was on an on-demand treatment regimen and was treated for mucosal bleeding. The inhibitor was characterised as type I, with classical epitope mapping. The spontaneous evolution of this inhibitor was favourable, but an anamnestic response led to a switch in his treatment to emicizumab.
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http://dx.doi.org/10.1016/j.transci.2021.103128DOI Listing
April 2021

[Theophylline adenosine dipyridamole (CTAD) and citrate evaluation to survey unfractionated heparin treatment: a delayed centrifugation validation for anti-Xa measurement?].

Ann Biol Clin (Paris) 2020 02;78(1):27-34

Service d'hématologie biologique, CHU Charles Nicolle, Rouen, France, Inserm U1096, CHU Charles Nicolle, Rouen, France.

Unfractionated heparin (UFH) is the main anticoagulante used in intensive care unit. The anticoagulant effect is monitored by activated partial thrombin time (aPTT) and anti-Xa activity (anti-Xa) measurement. However, delayed centrifugation induces platelet factor 4 (PF4) release and anti-Xa decrease. Several studies have concluded that aPTT and anti-Xa measurement should be performed within 2 hours in citrated anticoagulant but may be delayed longer in citrate theophylline adenosine and dypiridamol (CTAD) anticoagulant. The objective of this study was to compare the stability of both aPTT and anti-Xa in citrate and CTAD samples, and to determine the effect of delayed centrifugation on both aPTT, anti-Xa results, and PF4 release in citrate samples only.

Methods: aPTT and anti-Xa were measured in citrate and CTAD anticoagulant samples from 93 patients. Delayed centrifugation was performed in citrate samples from 31 additional patients, with hourly aPTT and anti-Xa measurement from 1 to 6 hours. In 14 of these last patients, PF4 release was also evaluated with Human CXCL4/PF4 Quantikine ELISA Kit.

Results: We observed a significant correlation between citrate and CTAD anticoagulant for aPTT (r=0.94) and anti-Xa (r=0.95). With Bland-Altman correlation, a minor bias was observed for anti-Xa (-0.025±0.041). Delayed centrifugation in citrated anticoagulant showed an excellent concordance from 1 to 4 hours for aPTT (-4.0±5.3 s) and anti-Xa (1.10±0.058 UI/mL) measurements. Moreover, PF4 release was not different between 1 hour (31.5±14.7 ng/mL) and 4 hours (33.8±11.8 ng/mL).

Conclusion: We have demonstrated that anti-Xa measurement for unfractionated heparin should be done 4 hours in citrated plasma and that CTAD was not better than citrate. However, these initial findings require confirmation using other aPTT and calibrated anti-Xa assays.
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http://dx.doi.org/10.1684/abc.2020.1525DOI Listing
February 2020

Is citrate theophylline adenosine dipyridamole (CTAD) better than citrate to survey unfractionated heparin treatment? Has delayed centrifugation a real impact on this survey?

J Thromb Thrombolysis 2019 Aug;48(2):277-283

Rouen University Hospital, Vascular Hemostasis Unit, 76031, Rouen, France.

Unfractionated heparin (UFH) is the main anticoagulant used in intensive care unit. The anticoagulant effect is monitored by activated partial thrombin time (aPTT) and anti-Xa activity (anti-Xa) measurement. However, delayed centrifugation induces platelet factor 4 (PF4) release and anti-Xa decrease. Several studies have concluded that aPTT and anti-Xa measurement should be performed within 2 h in citrated anticoagulant but may be delayed longer in Citrate Theophylline Adenosine and Dypiridamol (CTAD) anticoagulant. The objective of this study was to compare the stability of both aPTT and anti-Xa in citrate and CTAD samples, and to determine the effect of delayed centrifugation on both aPTT, anti-Xa results, and PF4 release in citrate samples only. aPTT and anti-Xa were measured in citrate and CTAD anticoagulant samples from 93 patients. Delayed centrifugation was performed in citrate samples from 31 additional patients, with hourly aPTT and anti-Xa measurement from 1 to 6 h. In 14 of these last patients, PF4 release was also evaluated with Human CXCL4/PF4 Quantikine ELISA Kit. We observed a significant correlation between citrate and CTAD anticoagulant for aPTT (r = 0.94) and anti-Xa (r = 0.95). With Bland-Altman correlation, a minor bias was observed for anti-Xa (- 0.025 ± 0.041). Delayed centrifugation in citrated anticoagulant showed an excellent concordance from 1 to 4 h for aPTT (- 4.0 ± 5.3 s) and anti-Xa (1.10 ± 0.058 UI/ml) measurements. Moreover, PF4 release was not different between 1 h (31.5 ± 14.7 ng/ml) and 4 h (33.8 ± 11.8 ng/ml). We have demonstrated that anti-Xa measurement for unfractionated heparin should be done 4 h in citrated plasma and that CTAD was not better than citrate. However, these initial findings require confirmation using other aPTT and calibrated anti-Xa assays.
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http://dx.doi.org/10.1007/s11239-019-01882-1DOI Listing
August 2019

Thrombin generation profile in non-thrombotic factor V Leiden carriers.

J Thromb Thrombolysis 2019 Apr;47(3):473-477

Normandie Univ, UNIROUEN, INSERM U1096, Rouen University Hospital, Vascular Hemostasis Unit, F 76000, Rouen, France.

Factor V Leiden (FVL) mutation is the most common genetic risk factor for venous thromboembolism. In families with a history of thrombosis, FVL can be present in 18%. Thrombin generation test is commonly used as an evaluation tool of thrombotic risk. The objective of this study was to evaluate the thrombogenic potential of FVL in asymptomatic carriers and in patients with personal or familial history of thrombosis. This was a retrospective single center study including 160 patients. Among them, 43 had personal history of thrombosis and 117 had familial history of thrombosis. Thrombin generation (TG) was realized in frozen platelet poor plasma with 1 pM of tissue factor and 4 µM of phospholipid. FVL mutation was associated with a global increase of TG. No difference was observed between patients with provoked thrombosis and patients with first-degree familial history of thrombosis (endogenous thrombin potential (ETP): 1501.0 ± 316.4 nM min and thrombin peak: 253.4 ± 71.5 nM vs. 1520.4 ± 283.8 nM min and 268.6 ± 68.0 nM). An increase of TG was observed in patients with unprovoked thrombosis (n = 23) and in patients with provoked thrombosis (n = 20) (ETP: 1819.5 ± 319.8 nM min and peak: 332.3 ± 55.8 nM). In the unprovoked thrombosis group, patients with a pulmonary embolism had a higher ETP than patients with deep vein thrombosis (DVT) (2036 ± 343 nM min vs. 1707 ± 261 nM min). With a predictive score formula (s = 0.1315 × Age + 0.0105 × ETP) with a threshold of 22.1 as risk to develop an unprovoked thrombosis among patients with second-degree familial history. The results of our analysis suggest that measurement of thrombin generation in patients with FVL mutation may identify subjects with an increased risk of unprovoked thrombosis. Further studies are needed to examine the usefulness of predicting thrombotic presentation in asymptomatic carriers.
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http://dx.doi.org/10.1007/s11239-019-01821-0DOI Listing
April 2019

Anti-Xa Oral Anticoagulant Plasma Concentration Assay in Real Life: Rivaroxaban and Apixaban Quantification in Emergency With LMWH Calibrator.

Ann Pharmacother 2019 04 31;53(4):341-347. Epub 2018 Oct 31.

1 Rouen University Hospital, France.

Background: Oral anti-Xa inhibitors have demonstrated noninferiority to vitamin K antagonists (VKAs) for the prevention of stroke in patients with atrial fibrillation and recurrent venous thromboembolism. They are associated with a decrease in major bleeding. In contrast with VKA, no coagulation monitoring is required. However, in clinical practice, determination of drug concentration is sometimes necessary.

Objective: The objective of this study was to evaluate a low-molecular-weight heparin (LMWH) calibrated anti-Xa assay for the quantification of rivaroxaban and apixaban plasma concentration in emergency.

Methods: The anti-Xa plasma concentration of rivaroxaban and apixaban were measured in emergency in 210 patients using STA anti-Xa liquid assay. For each plasma concentration <150 ng/mL of rivaroxaban or apixaban, an anti-Xa assay calibrated with LMWH was performed.

Results: We demonstrated a significant correlation between LMWH anti-Xa activity and rivaroxaban ( R = 0.947) or apixaban ( R = 0.959) concentration and a significant correlation between rivaroxaban and apixaban plasma concentration ( R = 0.972). A LMWH anti-Xa activity <0.50 IU/mL could exclude a plasma concentration of rivaroxaban and apixaban >30 ng/mL and indicate the feasibility of invasive procedure. Conclusion and Relevance: In the absence of a specific test, LMWH-calibrated anti-Xa assay could be used to determine the presence and evaluate the plasma concentration of oral anti-Xa inhibitors. However, these initial findings require confirmation using other chromogenic calibrated oral anti-Xa assays.
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http://dx.doi.org/10.1177/1060028018811657DOI Listing
April 2019

Management of dabigatran after overdosage: two case reports and suggestions for monitoring.

Blood Coagul Fibrinolysis 2018 Nov;29(7):653-655

Normandie Univ, UNIROUEN, INSERM U1096, Rouen University Hospital, Vascular Hemostasis Unit.

: Bleeding is the main complication of anticoagulant treatments as dabigatran etexilate. In patients with atrial fibrillation, dabigatran, at certain doses, has been associated with similar rates of stroke and embolism, and a lower rate of major hemorrhage compared to warfarin. Before the recent possibility of reversing the anticoagulant effect of dabigatran with idarucizumab, prothrombin complex concentrate (PCC) was the main available treatment in cases of severe bleeding or emergency surgery . We describe two different cases with very high overdosage in which PCC or idarucizumab was used to reverse the effect of dabigatran etexilate.
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http://dx.doi.org/10.1097/MBC.0000000000000763DOI Listing
November 2018

Thrombin generation test as a marker for high risk venous thrombosis pregnancies.

J Thromb Thrombolysis 2018 Jan;45(1):114-121

Normandie Univ, UNIROUEN, Inserm 1096, Department of Biological Hematology, Rouen University Hospital, F 76000, Rouen, France.

Pregnancy is a well-established risk factor for venous thromboembolism and is associated with a state of hypercoagulability. The use of sensitive and specific biological markers to predict risk factors for thrombosis is essential during pregnancy. Our objective was to investigate the usefulness of thrombin generation test (TGT) as a marker to predict the risk of thrombosis in high risk venous thrombosis (HRVT) pregnancies compared to normal pregnancies. This retrospective study enrolled 134 women with HRVT pregnancies, 78 of whom had monozygotic, spontaneous and untreated pregnancies and formed the study group. The control group comprised 106 women with normal pregnancies. Routine assessment of coagulation activation markers: fibrinogen, D-dimer, prothrombin fragments 1 + 2 (F1 + 2), thrombin-antithrombin complexes (TAT) and fibrin monomer complexes (FMC) was performed every 5 weeks in the study group to detect a possible pathological state of hypercoagulability. TGT was performed using platelet-free plasma, 1 and 5 pM tissue factor (TF), supplemented by phospholipids (PL) ± thrombomodulin. Fibrinogen, D-dimer, F1 + 2, and TAT, but not FMC, increased significantly throughout pregnancy in both groups but no difference was shown between the groups. TGT showed an early increase in thrombin generation in both groups, which stabilized during the second month of pregnancy. No correlation was demonstrated between thrombin generation parameters and coagulation activation markers. Based on our results, TGT did not prove conclusive as a marker to predict the risk of thrombosis in HRVT pregnancies. Finding a sensitive and specific biological marker to predict thrombosis risk requires further investigation.
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http://dx.doi.org/10.1007/s11239-017-1572-3DOI Listing
January 2018

Adjusted value of thromboprophylaxis in hospitalized obese patients: A comparative study of two regimens of enoxaparin: The ITOHENOX study.

Thromb Res 2017 Jul 12;155:1-5. Epub 2017 Apr 12.

Department of internal medicine, vascular and thrombosis unit, Rouen University Hospital, Rouen, France. Electronic address:

Thromboprophylaxis is a mainstay of hospital care in patients at high risk of thrombosis. Fixed doses of low-molecular-weight heparin (LMWH) are recommended for thromboprophylaxis in patients admitted to hospital for an acute medical condition. However, the distribution of LMWH is weight-based, and the efficacy of standard doses in obese patients may be decreased. Data for obese patients are mainly available in bariatric surgery with extremely obese patients who are at greater risk of venous thromboembolism than those hospitalized for a medical condition. We conducted a randomized control trial in medically obese inpatients (BMI≥30kg/m) assessing two regimens of enoxaparin (40mg and 60mg SQ daily) in order to determine whether a stronger dosage would achieve higher anti-Xa level suitable for thromboprophylaxis. Between September 2013 and April 2015, 91 patients were included in the study (mean (±standard deviation) age was 70.4±10.7years, average BMI 37.8±6.4kg/m). Main indications of thromboprophylaxis were mainly acute infection (50%), acute respiratory failure (10%), acute congestive heart failure (9%) and acute rheumatic disorders (18%). Average anti-Xa activity, measured 4h after the third administration of enoxaparin was 0.25±0.09IU/mL in group 1 (enoxaparin 40mg) and 0.35±0.13IU/mL in group 2 (enoxaparin 60mg) (P<10). The proportions of patients with normal anti-Xa activity (between 0.32 and 0.54IU/mL) were 31% (n=11) and 69% (n=24) in group 1 and 2 respectively (P=0.007). The proportions of anti-Xa activity measurement below the normal range were 64% and 36% in group 1 and 2 (P<10) respectively. Subgroup analysis focusing on high weight patients (above 100kg, n=45) showed a marked difference in the proportion of patients with normal anti-Xa activity between group 1 (9%) and 2 (44%) (P=0.009). No venous thromboembolism occurred during the study and one patient in group 1 died because of hemorrhagic shock due to a gastric ulcer. Incidence of adverse events was not different between the two groups (P=0.52). In conclusion, the ITOHENOX study shows in medically obese inpatients that thromboprophylaxis with enoxaparin 60mg provides higher control of anti-Xa activity, without more bleeding complications than the standard enoxaparin regimen. This trial is registered with ClinicalTrials.gov, number NCT01707732.
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http://dx.doi.org/10.1016/j.thromres.2017.04.011DOI Listing
July 2017

Thrombotic thrombocytopenic purpura misdiagnosed as autoimmune cytopenia: Causes of diagnostic errors and consequence on outcome. Experience of the French thrombotic microangiopathies reference centre.

Am J Hematol 2017 Apr 21;92(4):381-387. Epub 2017 Feb 21.

Service de Médecine Interne, Centre Hospitalier Universitaire Charles Nicolle, Rouen, France.

Thrombotic thrombocytopenic purpura (TTP) has a devastating prognosis without adapted management. Sources of misdiagnosis need to be identified to avoid delayed treatment. We studied 84 patients with a final diagnosis of severe (<10%) acquired ADAMTS13 deficiency-associated TTP from our National database that included 423 patients, who had an initial misdiagnosis (20% of all TTP). Main diagnostic errors were attributed to autoimmune thrombocytopenia, associated (51%) or not (37%) with autoimmune hemolytic anemia. At admission, misdiagnosed patients were more frequently females (P = .034) with a history of autoimmune disorder (P = .017) and had organ involvement in 67% of cases; they had more frequently antinuclear antibodies (P = .035), a low/undetectable schistocyte count (P = .001), a less profound anemia (P = .008), and a positive direct antiglobulin test (DAT) (P = .008). In multivariate analysis, female gender (P = .022), hemoglobin level (P = .028), a positive DAT (P = .004), and a low schistocytes count on diagnosis (P < .001) were retained as risk factors of misdiagnosis. Platelet count recovery was significantly longer in the misdiagnosed group (P = .041) without consequence on mortality, exacerbation and relapse. However, patients in the misdiagnosed group had a less severe disease than those in the accurately diagnosed group, as evidenced by less organ involvement at TTP diagnosis (P = .006). TTP is frequently misdiagnosed with autoimmune cytopenias. A low schistocyte count and a positive DAT should not systematically rule out TTP, especially when associated with organ failure.
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http://dx.doi.org/10.1002/ajh.24665DOI Listing
April 2017

A difficult decision: what should we do when malignant tumours are diagnosed in patients supported by left ventricular assist devices?

Eur J Cardiothorac Surg 2015 Sep 18;48(3):e30-6. Epub 2015 Jun 18.

Department of Thoracic and Cardiovascular Surgery, Rouen University Hospital Charles Nicolle, Rouen, France Department of Urology, Andrology and Renal Transplantation, Rouen University Hospital Charles Nicolle, Rouen, France Department of General and Thoracic Surgery, Rouen University Hospital Charles Nicolle, Rouen, France Unit of Vascular Haemostasis, Rouen University Hospital Charles Nicolle, Rouen, France INSERM U1096, Rouen University Hospital, Rouen, France.

Objectives: Left ventricular assist devices (LVADs) are used as a bridge to heart transplantation. During the preimplantation or pretransplantation screening, malignant tumours can be discovered. Owing to the lack of guidelines, the management is difficult. We describe our perioperative approach and the patients' outcomes.

Methods: Between 2006 and 2014, 55 patients underwent implantation of HeartMate II LVAD. Five were diagnosed with malignant tumours: 2 renal, 2 lung and 1 breast tumours. The renal tumours were diagnosed during the preimplantation screening. An LVAD was implanted in both followed by partial nephrectomies 8 and 9 months later. The lung cancers were diagnosed after device implantation, a left pulmonary segmentectomy and a right upper sleeve lobectomy were performed. The breast cancer was diagnosed few months after support and a tumourectomy with lymphadenectomy was performed.

Results: Tumour resection was performed successfully in all patients. Prior to surgery haemostasis, device and heart function were evaluated. During surgery, haemodynamics and anticoagulation were monitored. Reoperations were necessary to evacuate haemothorax after lobectomy and an abdominal haematoma post-nephrectomy. After discussion with oncologists, 3 patients were relisted for heart transplantation. Two were successfully transplanted 2 and 3 years after partial nephrectomy with an actual survival of 56 and 59 months after the cancer diagnosis. The follow-up revealed no cancer recurrences.

Conclusions: Malignant tumours during support with LVAD can be successfully resected. A multidisciplinary evaluation in these high-risk patients is mandatory. After careful evaluation, regaining the patient's heart transplant candidacy is possible.
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http://dx.doi.org/10.1093/ejcts/ezv203DOI Listing
September 2015

Role of M2-like macrophage recruitment during angiogenic growth factor therapy.

Angiogenesis 2015 Apr 24;18(2):191-200. Epub 2014 Dec 24.

UFR Médecine-Pharmacie, Inserm (Institut National de la Santé et de la Recherche Médicale) UMR1096, 22 Boulevard Gambetta, 76183, Rouen Cedex, France.

Therapeutic angiogenesis has yet to fulfill its promise for the clinical treatment of ischemic diseases. Given the impact of macrophages during pathophysiological angiogenesis, we asked whether macrophages may similarly modulate vascular responses to targeted angiogenic therapies. Mouse matrigel plug assay and rat myocardial infarction (MI) model were used to assess angiogenic therapy with either VEGF-A or FGF-2 with HGF (F+H) delivered locally via albumin-alginate microcapsules. The infiltration of classical M1-type and alternative M2-like macrophages was assessed. Clodronate was used to prevent macrophage recruitment, and the VEGFR2 blocking antibody, DC101, to prevent VEGF-A signaling. At 3 weeks after matrigel implantation, the combination therapy (F+H) led to increased total, and specifically M2-like, macrophage infiltration versus control and VEGF-A plugs, correlating with the angiogenic response. In contrast, VEGF-A preferential recruited M1-type macrophages. In agreement with a direct role of M2-like macrophages in F+H-induced vessel growth, clodronate radically decreased angiogenesis. Further, DC101 reduced F+H-induced angiogenesis, without altering macrophage infiltration, revealing macrophage-derived VEGF-A as a crucial determinant of tissue responsiveness. Similarly, increased cardiac M2-like macrophage infiltration was found following F+H therapy post-MI, with strong correlation between macrophage levels and angiogenic and arteriogenic responses. In conclusion, M2-like macrophages play a decisive role, linked to VEGF-A production, in regulation of tissue responsiveness to angiogenic therapies including the combination of F+H. Our data suggest that future attempts at therapeutic revascularization in ischemic patients might benefit from coupling targeted growth factor delivery with either direct or indirect approaches to recruit pro-angiogenic macrophages in order to maximize therapeutic angiogenic/arteriogenic responses.
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http://dx.doi.org/10.1007/s10456-014-9456-zDOI Listing
April 2015

Comparison of markers of coagulation activation and thrombin generation test in uncomplicated pregnancies.

Thromb Res 2013 Sep 2;132(3):386-91. Epub 2013 Aug 2.

Unit of Haemostasis, Rouen University Hospital, Rouen, France.

Introduction: Pregnancy is a well-established risk factor for venous thromboembolism, and is associated with a state of hypercoagulability or parameters of thrombin generation. Currently, there is a lack of consensual data on thrombin generation during pregnancy. This study aimed to find a sensitive and specific biological marker of coagulation activation and to identify parameters of thrombin generation.

Patients And Methods: The population included 101 women with uncomplicated pregnancies. The objective of this study was to correlate thrombin generation test (measured at 5pM tissue factor, 4μM lipids and without thrombomodulin), with fibrinogen and markers of blood coagulation activation: D-dimer, prothrombin fragments 1+2 (F1+2), thrombin-antithrombin complexes (TAT) and fibrin monomer complexes (FMC) in these women. Internal quality control was performed in each set of experiments.

Results: Fibrinogen, D-dimer, F1+2, and TAT concentrations increased significantly throughout pregnancy, and were correlated with term of pregnancy. In our study, thrombin generation seemed to increase early on, and then remained stable throughout normal pregnancy, in contrast with other markers of blood coagulation activation, excepting FMC. The latter are subject to large inter-individual variations, especially during second trimester. No correlation was demonstrated between thrombin generation parameters and other activation markers.

Conclusion: While markers of coagulation activation significantly increased during pregnancy, thrombin generation increased only early on and remains stable during pregnancy. Finding a sensitive and specific biological marker for vascular pregnancy complications, such as FMC and thrombin generation levels, requires further investigation.
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http://dx.doi.org/10.1016/j.thromres.2013.07.022DOI Listing
September 2013

Is anti-platelet therapy needed in continuous flow left ventricular assist device patients? A single-centre experience.

Eur J Cardiothorac Surg 2014 Jan 12;45(1):55-9; discussion 59-60. Epub 2013 May 12.

Department of Thoracic and Cardiovascular Surgery, Rouen University Hospital Charles Nicolle, Rouen, France.

Objectives: We report our 5-year experience of continuous flow left ventricular assist device (LVAD) implantation without the use of anti-platelet therapy.

Methods: Between February 2006 and September 2011, 27 patients (26 men; 1 woman) were implanted with a continuous flow LVAD (HeartMate II, Thoratec Corporation, Pleasanton, CA, USA). The mean age was 55.7 ± 9.9 years. The mean duration of support was 479 ± 436 (1-1555) days with 35.4 patient-years on support. Twenty-one patients were implanted as a bridge to transplantation and 6 for destination therapy. The anticoagulation regimen was fluindione for all patients, with aspirin for only 4 patients. At the beginning of our experience, aspirin was administered to 4 patients for 6, 15, 60 and 460 days. Due to gastrointestinal (GI) bleeding and epistaxis, aspirin was discontinued, and since August 2006, no patients have received anti-platelet therapy.

Results: At 3 years, the survival rate during support was 76%. The most common postoperative adverse event was GI bleeding (19%) and epistaxis (30%) (median time: 26 days) for patients receiving fluindione and aspirin. The mean International Normalized Ratio (INR) was 2.58 ± 0.74 during support. Fifteen patients have been tested for acquired Von Willebrand disease. A diminished ratio of collagen-binding capacity and ristocetin cofactor activity to Von Willebrand factor antigen was observed in 7 patients. In the postoperative period, 2 patients presented with ischaemic stroke at 1 and 8 months. One of these 2 patients had a previous history of carotid stenosis with ischaemic stroke. There were no patients with haemorrhagic stroke, transient ischaemic attack or pump thrombosis. The event rate of stroke (ischaemic and haemorrhagic) per patient-year was 0.059 among the patients without aspirin with fluindione regimen only.

Conclusions: A fluindione regimen without aspirin in long-duration LVAD support appears to not increase thromboembolic events and could lead to a diminished risk of haemorrhagic stroke.
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http://dx.doi.org/10.1093/ejcts/ezt228DOI Listing
January 2014