Journal of Thrombosis and Haemostasis (J THROMB HAEMOST)

Publisher: International Society on Thrombosis and Haemostasis, Wiley

Journal description

The mission of the new Journal of Thrombosis and Haemostasis will be to advance science related to the important medical problems of thrombosis, bleeding disorders and vascular biology through the diffusion and exchange of information and ideas within the international research community. The Journal publishes high quality, original research reports, state-of-the art reviews, invited commentary and debate on timely topics, letters and announcements. Editors invite both laboratory and clinical reports. The Journal of Thrombosis and Haemostasis is now available in print and online.

Current impact factor: 5.55

Impact Factor Rankings

2015 Impact Factor Available summer 2015
2013 / 2014 Impact Factor 5.55
2012 Impact Factor 6.081
2011 Impact Factor 5.731
2010 Impact Factor 5.439
2009 Impact Factor 6.069
2008 Impact Factor 6.291
2007 Impact Factor 5.947
2006 Impact Factor 5.138
2005 Impact Factor 5.262
2004 Impact Factor 4.831
2003 Impact Factor

Impact factor over time

Impact factor

Additional details

5-year impact 6.18
Cited half-life 5.10
Immediacy index 1.17
Eigenfactor 0.05
Article influence 2.06
Website Journal of Thrombosis and Haemostasis website
Other titles Journal of thrombosis and haemostasis, JTH
ISSN 1538-7933
OCLC 48955697
Material type Document, Periodical, Internet resource
Document type Internet Resource, Computer File, Journal / Magazine / Newspaper

Publisher details


  • Pre-print
    • Author can archive a pre-print version
  • Post-print
    • Author cannot archive a post-print version
  • Restrictions
    • 12 months embargo
  • Conditions
    • Some journals have separate policies, please check with each journal directly
    • On author's personal website, institutional repositories, arXiv, AgEcon, PhilPapers, PubMed Central, RePEc or Social Science Research Network
    • Author's pre-print may not be updated with Publisher's Version/PDF
    • Author's pre-print must acknowledge acceptance for publication
    • On a non-profit server
    • Publisher's version/PDF cannot be used
    • Publisher source must be acknowledged with citation
    • Must link to publisher version with set statement (see policy)
    • If OnlineOpen is available, BBSRC, EPSRC, MRC, NERC and STFC authors, may self-archive after 12 months
    • If OnlineOpen is available, AHRC and ESRC authors, may self-archive after 24 months
    • Publisher last contacted on 07/08/2014
    • This policy is an exception to the default policies of 'Wiley'
  • Classification
    ​ yellow

Publications in this journal

  • [Show abstract] [Hide abstract]
    ABSTRACT: The striking coagulopathy in patients with severe sepsis and the increasing insight into the intricate link between inflammation and coagulation has been an inspiration for many researchers and pharmaceutical companies to explore potential therapeutic interventions for severe sepsis [1]. Indeed, in view of the high incidence of severe sepsis and sepsis mortality ranging from 20 to 50%, there is a urgent need for better treatment options [2]. As dysfunctional physiological anticoagulant regulators, such as antithrombin, activated protein C, and tissue factor pathway inhibitor, were shown to be key players in the sepsis-associated activation of coagulation, and animal studies supported the hypothesis that restoration of these pathways resulted in attenuation of coagulopathy and organ dysfunction and reduced mortality, large clinical studies were performed to establish the beneficial effect of these interventions in patients with severe sepsis [2-5]. Although some of these studies demonstrated some advantage in subgroups of patients with most extreme coagulopathies an overall reduction in mortality was not confirmed. This article is protected by copyright. All rights reserved. This article is protected by copyright. All rights reserved.
    Journal of Thrombosis and Haemostasis 02/2015; 13(4). DOI:10.1111/jth.12868
  • Journal of Thrombosis and Haemostasis 09/2014; 12(9):1574-1575. DOI:10.1111/jth.12666
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    ABSTRACT: Thrombosis of a cardiac valve prosthesis is a potentially life threatening but thankfully relatively rare complication following heart valve replacement. Management of this difficult situation is either by repeat surgery or thrombolytic therapy. Not surprisingly, there is no randomized controlled trial evaluating these two treatments and the published guidelines offer no definitive solution with some indicating thrombolysis and others repeat surgery as the primary optimum treatment. This article is protected by copyright. All rights reserved.
    Journal of Thrombosis and Haemostasis 06/2014; 12(8). DOI:10.1111/jth.12640
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    ABSTRACT: Background: Even though the acetylation of platelet cyclooxygenase (COX)-1 at serine-529 is the direct mechanism of action of low-dose aspirin, its antiplatelet effect has been characterized using indirect indexes of COX-1 activity. Objectives: We performed a clinical study with enteric-coated low-dose aspirin (EC-aspirin), in healthy subjects, to evaluate the effects on the extent and duration of platelet COX-1 acetylation, using a novel proteomic strategy for absolute protein quantification (termed AQUA), as compared with traditional pharmacokinetic and pharmacodynamic parameters. Subjects and methods: In a phase I, single-arm, open-label study of EC aspirin (100 mg day(-1)) administered to 24 healthy subjects, we compared, over a 24 h-period on day 1 and 7, % platelet acetylated COX-1 (AceCOX-1) with traditional pharmacokinetic and pharmacodynamics [i.e. serum thromboxane (TX) B-2, platelet function by monitoring CEPI(collagen/epinephrine) closure time (CT) using whole-blood PFA-100 and urinary excretion of 11-dehydro-TXB2] parameters. Results: Acetylation of platelet COX-1 was measurable before detection of aspirin levels in the systemic circulation and increased in a cumulative fashion upon repeated dosing. After the last dose of EC-aspirin, %AceCOX-1, serum TXB2 and CEPI-CT values were maximally and persistently modified throughout 24 h; they averaged 76 +/- 2%, 99.0 +/- 0.4% and 271 +/- 5 s, respectively. EC-aspirin caused 75% reduction in urinary 11-dehydro-TXB2 excretion. After chronic dosing with aspirin, the pharmacokinetics of acetylsalicylic acid was completely dissociated from pharmacodynamics. Conclusions: The demonstrated feasibility of quantifying the extent and duration of platelet COX-1 acetylation will allow characterizing the genetic, pharmacokinetic and pharmacodynamic determinants of the inter-individual variability in the antiplatelet response to low-dose aspirin as well as identifying extra-platelet sites of drug action.
    Journal of Thrombosis and Haemostasis 06/2014; 12(8). DOI:10.1111/jth.12637
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    ABSTRACT: Background: Our previous studies have demonstrated that platelet-specific gene delivery to hematopoietic stem cells can induce sustained therapeutic levels of platelet factor VIII (FVIII) expression in mice with hemophilia A. Objective: In this study, we aimed to enhance platelet FVIII expression while minimizing potential toxicities. Methods: A novel lentiviral vector (LV), which harbors dual genes, the FVIII gene driven by the alpha(IIb) promoter (2bF8) and a drug-resistance gene, the MGMT(P140K) cassette, was constructed. Platelet FVIII expression in mice with hemophilia A was introduced by transduction of hematopoietic stem cells and transplantation. The recipients were treated with O-6 -benzylguanine followed by 1,3-bis-2 chloroethyl-1-nitrosourea monthly three or four times. Animals were analyzed by using polymerase chain reaction (PCR), quantitative PCR, FVIII: C assays, and inhibitor assays. Phenotypic correction was assessed by tail clipping tests and rotational thromboelastometry analysis. Results: Even using a low multiplicity of infection of 1 and a non-myeloablative conditioning regimen, after in vivo selection, the levels of platelet FVIII expression in recipients increased to 4.33 +/- 5.48 mU per 10(8) platelets (n = 16), which were 19.7-fold higher than the levels obtained from the recipients before treatment. Quantitative PCR results confirmed that 2bF8/MGMT-LV-transduced cells were effectively enriched after drug-selective treatment. Fifteen of 16 treated animals survived tail clipping. Blood loss and whole blood clotting time were normalized in the treated recipients. Notably, no anti-FVIII antibodies were detected in the treated animals even after recombinant human B-domain deleted FVIII challenge. Conclusion: we have established an effective in vivo selective system that allows us to enrich 2bF8LV-transduced cells, enhancing platelet FVIII expression while reducing the potential toxicities associated with platelet gene therapy.
    Journal of Thrombosis and Haemostasis 06/2014; 12(8). DOI:10.1111/jth.12633
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    ABSTRACT: We thank Drs. Kjellberg and Hellgren for their letter and for pointing out that the results of their study are consistent with our findings. Space limitations prevented us from more detailed reporting of the methods and results of our systematic review. We are familiar with the study by Kjellberg and colleagues as it was one of the seven full-text articles [1-7] that were retrieved in the systematic review process. Their report was independently assessed by two reviewers (MR, NL) then discussed, leading to the conclusion that the study was not eligible owing to its design. This article is protected by copyright. All rights reserved. This article is protected by copyright. All rights reserved.
    Journal of Thrombosis and Haemostasis 06/2014; DOI:10.1111/jth.12632
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    ABSTRACT: Background: In preclinical hemophilia research, an animal model that reflects both the phenotype and the pathology of the disease is needed. Objectives: Here, we describe the generation and characterization of a novel genetically engineered F8(-/-) rat model. Methods: The rats were produced on a Sprague Dawley background with the zinc finger nuclease technique. A founder with a 13-bp deletion in exon 16 causing a premature translational stop in the C-terminal part of the A3 domain of factor VIII was selected, and a breeding colony was established. Results: Seventy per cent of the homozygous rats had clinically manifest spontaneous hemorrhagic episodes that needed treatment. The F8(-/-) rats had no detectable FVIII activity, and had a significantly prolonged activated partial thromboplastin time (APTT) and clot formation time as compared with wild-type (WT)/WT rats. In vitro spiking of rat plasma with human recombinant FVIII resulted in dose-dependent normalization of the APTT. Conclusion: On the basis of the targeted deletion in F8, and the distinct physical and analytic characteristics of the rat, we conclude that an FVIII-deficient rat strain has been generated that has the potential to contribute greatly to translational research.
    Journal of Thrombosis and Haemostasis 06/2014; 12(8). DOI:10.1111/jth.12635
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    ABSTRACT: The development of factor VIII neutralizing alloantibodies (inhibitors) is a major complication of the treatment with factor VIII concentrates in hemophilia A and the etiology is still poorly understood. The low-affinity Fc gamma receptors (FcγR), which are expressed on immune cells, provide an important link between cellular and humoral immunity by interacting with IgG subtypes. Genetic variations of the genes encoding FcγRs (FCGR genes) have been associated with susceptibility for infectious and autoimmune diseases.
    Journal of Thrombosis and Haemostasis 06/2014; 12(8). DOI:10.1111/jth.12631
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    ABSTRACT: We read with interest the report by Rodger et al [1] on thrombophilia associated with placenta-mediated pregnancy complications. The statistical rigor with which this multicentric study was carried out deserves critical acclaim. For the first time, the authors have tried to dissect different placental components of pregnancy related complications and associate them with two thrombophilia markers in a large cohort of patients which is in contrast to other studies in literature, where these complications of pregnancy are merged under a single term of "recurrent pregnancy loss (RPL)" or "adverse pregnancy complications". However, when one increases the rigor of the study, one progressively loses sight of the challenges posed in the real world by these patients. Each of the conditions analyzed by the authors can lead to RPL or associated conditions in an interlinked manner. This article is protected by copyright. All rights reserved.
    Journal of Thrombosis and Haemostasis 06/2014; DOI:10.1111/jth.12630
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    ABSTRACT: Background: Drug interaction references report that initiation of levothyroxine potentiates the effects of warfarin, and recommend more frequent International Normalized Ratio (INR) monitoring, but the mechanism is not well understood. Objective: To assess the impact of levothyroxine initiation on INR response. Patients/Methods: A retrospective, self-controlled study was performed on patients aged >= 18 years receiving chronic warfarin therapy who were started on levothyroxine between 1 January 2006 and 30 June 2013, and who were followed for 90 days prior to and after levothyroxine initiation. The included patients had at least one elevated thyroid-stimulating hormone laboratory value in the pre-period, continuous warfarin therapy for 100 days prior to levothyroxine initiation, no purchases of medications known to interact with warfarin, no procedures requiring warfarin interruption, and no bleeding or thromboembolic event during the study period. The primary outcome was a comparison of the warfarin dose/INR ratio recorded before the initiation of levothyroxine with the ratio recorded during the post-period after two consecutive INRs with no warfarin dose change. Results: One hundred and two patients were included in the primary outcome. The mean warfarin dose/INR ratios in the pre-period and post-period were equivalent (P = 0.825). Although the mean warfarin dose was numerically lower in the post-period than in the pre-period, this difference did not reach statistical significance (P = 0.068). Conclusion: No difference in the mean warfarin dose/INR ratio before and after initiation of levothyroxine was detected. The results suggest that there is not a clinically significant interaction between warfarin and levothyroxine, and so additional monitoring may not be necessary.
    Journal of Thrombosis and Haemostasis 06/2014; 12(8). DOI:10.1111/jth.12626
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    ABSTRACT: We thank Professor Girard and colleagues for their interesting comments on the diagnosis of pulmonary embolism (PE) in patients with renal cell carcinoma and residual tumor thrombus/embolism [1]. Their manuscript highlights the difficulty in differentiating between bland and tumor thrombus in cancer patients presenting with suspected PE and diagnosed with a filling defect within a pulmonary artery on computed tomography pulmonary angiography (CTPA). The radiological diagnosis of tumor embolism can be challenging and depends on the size of the involved pulmonary artery. This article is protected by copyright. All rights reserved.
    Journal of Thrombosis and Haemostasis 06/2014; 12(8). DOI:10.1111/jth.12625
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    ABSTRACT: Background: Recombinant factor VIIa (rFVIIa) is an FX-cleaving coagulation enzyme licensed for the treatment of bleeding episodes in hemophiliacs with inhibitory antibodies. Even though the optimal dosing and comparative dose efficacy of rFVIIa remain poorly understood, genetic or chemical modifications of rFVIIa have been proposed, with the goal of achieving faster and longer hemostatic action. No ongoing trial is currently comparing rFVIIa variants with each other. Objectives and methods: We used mathematical modeling to compare the pharmacokinetics, dose-response (pharmacodynamics) and dose-effect duration (pharmacokinetics/pharmacodynamics) of rFVIIa variants to predict their optimal doses. The pharmacodynamic (PD) model of FXa generation by FVIIa in complexes with tissue factor (TF) and procoagulant lipids (PLs) was validated against published ex vivo and in vitro thrombin generation (TG) experiments. To compare variants' safety profiles, the highest non-thrombogenic doses were estimated from the clinical evidence reported for the licensed rFVIIa product. Results: The PD model correctly described the biphasic TF-dependent and PL-dependent dose response observed in TG experiments in vitro. The pharmacokinetic/PD simulations agreed with published ex vivo TG data for rFVIIa and the BAY 86-6150 variant, and explained the similar efficacies of a single dose of 270 mu g kg(-1) (as reported in the literature) and repeated doses of 90 mu g kg(-1) of unmodified rFVIIa. The duration of the simulated hemostatic effect after a single optimal dose was prolonged for rFVIIa variants with increased TF affinity or extended half-lives, but not for those with modulated PL activity. Conclusions: Some modifications of the rFVIIa molecule may not translate into a prolonged hemostatic effect.
    Journal of Thrombosis and Haemostasis 06/2014; 12(8). DOI:10.1111/jth.12628
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    ABSTRACT: Background: Airline pilots may be at increased risk of venous thromboembolism (VTE) because air travel has recently been established as a risk factor for VTE. Objectives: The aim of this study was to assess the risk of VTE in a cohort of Dutch airline pilots. Patients/Methods: Airline pilots who had been active members of the Dutch aviation society (VNV) were questioned for the occurrence of VTE, presence of risk factors for VTE and number of flight hours per year and rank. Incidence rates among pilots were compared with those of the general Dutch population and with a population of frequently flying employees of multinational organizations. Results and Conclusions: A total of 2630 male pilots were followed-up for a total of 20420 person-years (py). Six venous thromboses were reported, yielding an incidence rate of 0.3 per 1000 py. The standardized morbidity ratio, comparing these pilots with the general Dutch population adjusted for age, was 0.8. Compared with the international employee cohort, the standardized morbidity ratio was 0.7 when all employees were included and 0.6 when only the frequently travelling employees were included. The incidence rate did not increase with number of flight hours per year and did not clearly vary by rank. We conclude that the risk of VTE is not increased amongst airline pilots.
    Journal of Thrombosis and Haemostasis 06/2014; 12(8). DOI:10.1111/jth.12627
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    ABSTRACT: Blood platelets are small anucleated cell fragments generated from bone marrow megakaryocytes (MKs) by a cytoskeleton-driven process. Thereby, mature MKs form long cytoplasmic protrusions (pro-platelets), which extend into the sinusoids within the bone marrow and finally release platelets. Podosomes are F-actin rich matrix contacts that have been suggested to play an important role in cell migration, but also for pro-platelet formation by MKs. Phospholipase D (PLD) has been proposed to contribute to the regulation of actin dynamics through the local generation of phosphatidic acid but its role in platelet formation is unknown.
    Journal of Thrombosis and Haemostasis 06/2014; 12(8). DOI:10.1111/jth.12623