Journal of Thrombosis and Thrombolysis (J Thromb Thrombolysis)

Publisher: LINK (Springer), Springer Verlag

Journal description

The Journal of Thrombosis and Thrombolysis is a long-awaited resource for contemporary cardiologists hematologists and clinician-scientists actively involved in treatment decisions and clinical investigation of thrombotic disorders involving the cardiovascular and cerebrovascular systems. Its principal focus centers on the pathobiology of thrombosis and the use of anticoagulants platelet antagonists and thrombolytic agents in scientific investigation and patient care. The journal publishes original work that interlinks basic scienctific principles with clinical investigation thus creating a unique forum for interdisciplinary dialogue. Published works will advocate the development of solid platforms for planned clinical research and precise clinically-applicable benchwork. The Journal of Thrombosis and Thrombolysis 's comprehensive and interdisciplinary design will expand the reader's knowledge base and provide important insights for the most rapidly growing field in medicine. The journal seeks original manuscripts devoted to laboratory investigation and clinical studies. State-of-the-art reviews and editorials will be summoned by invitation. The journal will closely follow new trends on the cutting edge of the field and highlight drugs in the early stages of development which may warrant testing in the clinical arena. Updates of major national and international clinical trials will also be provided as will a forum of guidelines for interpreting the results of these trials from a patient care perspective. The Journal will publish an ongoing educational series of topics applicable to clinician scientists that will include such topics as: 'Seminars in Thrombosis Thromboysis and Vascular Biology' and a 6-part series on 'Hematology for the Cardiologist'. Manuscripts submitted must not be under consideration by an other journal and should not have been published elsewhere in similar form. All articles will be refereed by two qualified referees. All clinical trials being considered for publication will also be reviewed by a statistician. A response will be provided within four weeks of receipt.

Current impact factor: 2.17

Impact Factor Rankings

2015 Impact Factor Available summer 2016
2014 Impact Factor 2.169
2013 Impact Factor 2.039
2012 Impact Factor 1.985
2011 Impact Factor 1.476
2010 Impact Factor 1.539
2009 Impact Factor 1.846
2008 Impact Factor 2.266
2007 Impact Factor 1.432
2006 Impact Factor 1.155
2005 Impact Factor 1.093
2004 Impact Factor 0.909
2003 Impact Factor 1.066
2002 Impact Factor 1.067
2001 Impact Factor 1.055
2000 Impact Factor 0.785

Impact factor over time

Impact factor

Additional details

5-year impact 1.83
Cited half-life 4.20
Immediacy index 0.50
Eigenfactor 0.01
Article influence 0.57
Website Journal of Thrombosis and Thrombolysis website
Other titles Journal of thrombosis and thrombolysis (En ligne)
ISSN 1573-742X
OCLC 300185160
Material type Periodical, Internet resource
Document type Internet Resource, Journal / Magazine / Newspaper

Publisher details

Springer Verlag

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    • Author's post-print on any open access repository after 12 months after publication
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    • Must link to publisher version
    • Set phrase to accompany link to published version (see policy)
    • Articles in some journals can be made Open Access on payment of additional charge
  • Classification

Publications in this journal

  • [Show abstract] [Hide abstract]
    ABSTRACT: Platelet reactivity, an important factor in hemostasis and chronic disease, has widespread inter-individual variability with a substantial genetic contribution. Previously, our group performed a genome-wide association study of platelet reactivity identifying single nucleotide polymorphisms (SNPs) associated with ADP- and epinephrine- induced aggregation, including SNPs in MRVI1, PIK3CG, JMJD1C, and PEAR1, among others. Here, we assessed the association of these previously identified SNPs with ADP-, thrombin-, and shear- induced platelet aggregation. Additionally, we sought to expand the association of these SNPs with blood cell counts and hemostatic factors. To accomplish this, we examined the association of 12 SNPs with seven platelet reactivity and various hematological measures in 1300 middle-aged men in the Caerphilly Prospective Study. Nine of the examined SNPs showed at least suggestive association with platelet reactivity. The strongest associations were with rs12566888 in PEAR1 to ADP-induced (p = 1.51 × 10(-7)) and thrombin-induced (p = 1.91 × 10(-6)) reactivity in platelet rich plasma. Our results indicate PEAR1 functions in a relatively agonist independent manner, possibly through subsequent intracellular propagation of platelet activation. rs10761741 in JMJD1C showed suggestive association with ADP-induced reactivity (p = 1.35 × 10(-3)), but its strongest associations were with platelet-related cell counts (p = 1.30 × 10(-9)). These associations indicate variation in JMJD1C influences pathways that modulate platelet development as well as those that affect reactivity. Associations with other blood cell counts and hemostatic factors were generally weaker among the tested SNPs, indicating a specificity of these SNPs' function to platelets. Future genome-wide analyses will further assess association of these genes and identify new genes important to platelet biology.
    Journal of Thrombosis and Thrombolysis 10/2015; DOI:10.1007/s11239-015-1290-7
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    ABSTRACT: We present the case of a healthy, young Caucasian female who presented to an outside hospital with phlegmasia cerulea dolens of both lower extremities. Computed tomography angiography revealed inferior vena cava (IVC) occlusion. She was initiated on heparin infusion and transferred to University of Virginia Medical Center. Our evaluation revealed aplasia of the IVC from the infrahepatic segment to the confluence of the common iliac veins and acute bilateral iliac vein thromboses. An extensive network of collateral veins was noted. These findings were consistent with IVC agenesis. She was not pregnant or using contraception. Primary thrombophilia workup was negative. She underwent bilateral iliac vein thrombolysis and was started on anticoagulation. While IVC agenesis is rare, it carries risk for development of thrombotic sequelae and bears consideration when evaluating young patients with unexplained deep vein thrombosis, especially if extensive and bilateral.
    Journal of Thrombosis and Thrombolysis 10/2015; DOI:10.1007/s11239-015-1289-0
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    ABSTRACT: This study deciphered the molecular mechanisms of the inhibition of MMP-9 expression using rosuvastatin in cultured human umbilical vein endothelial cells (HUVECs) and apoE knockout mice and whether the combination of rosuvastatin and probucol enhanced this effect. The role that microRNA (miR)-497 plays in the regulation of MMP-9 expression was evaluated in cultured HUVECs and apoE knockout mice using quantitative real-time reverse transcription polymerase chain reaction and Western blotting. First, TNFα significantly increased mitogen-activated protein kinases/extracellular signal-regulated kinase (MAPK/ERK) signaling and MMP-9 levels, and the transfection of miR-497 prevented this increase. The converse results were obtained after miR-497 suppression. Second, the administration of rosuvastatin or the combination of two drugs decreased MAPK/ERK signaling and MMP-9 levels, and the suppression of miR-497 upregulated these levels. Third, the administration of rosuvastatin or the combination of two drugs increased miR-497 expression levels in the aortas of apoE knockout mice, but the levels of serum lipids and plaque areas decreased, which improved plaque components and decreased the MAPK/ERK signaling and MMP-9 levels. Finally, the combination of the two drugs was more effective than the use of rosuvastatin alone. Rosuvastatin inhibits MMP-9 expression by upregulating miR-497 in HUVECs and apoE knockout mice, and the combination of rosuvastatin and probucol enhances this effect.
    Journal of Thrombosis and Thrombolysis 10/2015; DOI:10.1007/s11239-015-1291-6
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    ABSTRACT: Over the past several years, non-vitamin K oral anticoagulants (NOACs) have been introduced into clinical practice for the treatment of venous thromboembolism and prevention of stroke in patients with nonvalvular atrial fibrillation. Clinical trials have shown these agents to have similar or less risk of major bleeding as compared to warfarin therapy. Moreover, when patients do experience a major bleeding event administration of advanced factor products is rare, and post-bleed outcomes are similar in those receiving a NOAC compared to those receiving warfarin. However, there are situations where urgent reversal of NOAC anticoagulation would be desirable. The following review focuses on the outcomes and management strategies for patients experiencing a major bleed with warfarin or NOAC agents and describes the rationale for the development of therapies capable of targeted NOAC-reversal.
    Journal of Thrombosis and Thrombolysis 10/2015; DOI:10.1007/s11239-015-1296-1
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    ABSTRACT: Thrombelastographic methods have been recently introduced to detect iron mediated hypercoagulability in settings such as sickle cell disease, hemodialysis, mechanical circulatory support, and neuroinflammation. However, these inflammatory situations may have heme oxygenase-derived, coexistent carbon monoxide present, which also enhances coagulation as assessed by the same thrombelastographic variables that are affected by iron. This brief report presents a novel, Sonoclot-based method to detect iron enhanced coagulation that is independent of carbon monoxide influence. Future investigation will be required to assess the sensitivity of this new method to detect iron mediated hypercoagulability in clinical settings compared to results obtained with thrombelastographic techniques.
    Journal of Thrombosis and Thrombolysis 10/2015; DOI:10.1007/s11239-015-1293-4
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    ABSTRACT: Anticoagulant thromboprophylaxis with low molecular weight heparin is widely used in nonsurgical settings. To obtain best estimates of the effects of nadroparin for the prevention of venous thromboembolism (VTE) in nonsurgical patients, we conducted a systematic review and meta-analysis. Data sources were Medline, Embase, and Cochrane Library supplemented with conference abstracts, without language restrictions. Selection criteria were randomized controlled trials with nadroparin at prophylactic dose in adult nonsurgical patients. Main efficacy outcomes were major VTE (the composite of symptomatic deep vein thrombosis, symptomatic pulmonary embolism, asymptomatic proximal deep vein thrombosis and VTE-related death) and symptomatic VTE. The main safety outcome was major bleeding. We expressed treatment effects as risk ratios. Ten studies (4 vs. placebo or no treatment, 4 vs. UFH, 1 vs. fondaparinux and 1 vs. warfarin) enrolling a total of 7658 patients were included. In comparison with placebo, nadroparin reduced major VTE by about one-half (RR 0.48, 95% CI 0.24-0.97) with a consistent effect on symptomatic VTE (RR 0.69, 95% CI 0.46-1.05) and no increase in major bleeding (RR 1.51, 95% CI 0.40-5.79). In comparison with other pharmacological prophylaxis, nadroparin was similarly efficacious for prevention of major VTE (RR 1.14, 95% CI 0.63-2.10) and symptomatic VTE (RR 1.10, 95% CI 0.51-2.35) and produced similar effects on major bleeding (RR 0.60, 95% CI 0.25-1.50). Five studies were open label, and for three of these the adjudication method was not described or not blinded. In nonsurgical populations at risk of VTE, nadroparin reduced VTE by about one half compared with placebo or no treatment and appeared similarly effective and safe as other prophylactic anticoagulants.
    Journal of Thrombosis and Thrombolysis 10/2015; DOI:10.1007/s11239-015-1294-3

  • Journal of Thrombosis and Thrombolysis 10/2015; DOI:10.1007/s11239-015-1286-3
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    ABSTRACT: We performed a meta-analysis to evaluate gender differences of venous thromboembolism (VTE) risk after total hip (THA) and total knee arthroplasty (TKA). We searched PubMed and Web of Knowledge from their beginning to 25 July 2015. Pooled odds ratio (OR) and 95 % confidence interval (CI) for VTE risk were calculated. Twenty studies with 7,892,585 patients were included in our study. The VTE incidence ranged from 0.27 to 61.0 %. The sex ratio (male/female) was 0.623 (3,016,648/4,839,785) in no VTE group versus 0.492 (11,926/24,226) in VTE group. The pooled OR was 1.184 (95 % CI 1.070-1.310; Z = 3.28, P = 0.001). The Begg's test (z = 1.46, P = 0.144) and the Egger's test (t = 0.58, P = 0.571), and the funnel plot suggested there was no significant publication bias. Sensitivity analysis by omitted a study with largest simple size showed the pooled OR was 1.166 (95 % CI 1.051-1.294; Z = 2.91, P = 0.004) by random-effects model. Meta-regression showed VTE risk was not related with THA and TKA incidence (t = 0.35, P = 0.732). Our meta-analysis showed female patients have slightly higher risk of VTE than male patients after THA and TKA.
    Journal of Thrombosis and Thrombolysis 10/2015; DOI:10.1007/s11239-015-1283-6
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    ABSTRACT: Venous thrombosis (VT) is a preventable cause of death in hospitalized patients. The main strategy to decrease VT incidence is timely thromboprophylaxis in at-risk patients. We sought to evaluate the reliability of risk assessment model (RAM) data, the incremental usefulness of additional variables and the modelling of an adjusted score (the NAVAL score). We used the RAM proposed by Caprini for initial assessment. A 5 % systematic sample of data was independently reviewed for reliability. We evaluated the incremental usefulness of six variables for VT during the score modelling by logistic regression. We then assessed the NAVAL score for calibration, reclassification and discrimination performances. We observed 11,091 patients with 37 (0.3 %) VT events. Using the Caprini RAM, high-risk and moderate-risk patients were respectively associated with a 17.4 (95 % confidence interval [CI] 6.1-49.9) and 4.2 (95 % CI 1.6-11.0) increased VT risk compared with low-risk patients. Four independent variables were selected for the NAVAL score: "Age", "Admission clinic", "History of previous VT event" and "History of thrombophilia". The area under the receiver-operating-characteristic curve for the NAVAL score was 0.72 (95 % CI 0.63-0.81). The Net Reclassification Index (NRI) for the NAVAL score compared with the Caprini RAM was -0.1 (95 % CI -0.3 to 0.1; p = 0.28). We conclude that the NAVAL score is a simplified tool for the stratification of VT risk in hospitalized patients. With only four variables, it demonstrated good performance and discrimination, but requires external validation before clinical application. We also confirm that the Caprini RAM can effectively stratify VT risk in hospitalized patients in our population.
    Journal of Thrombosis and Thrombolysis 10/2015; DOI:10.1007/s11239-015-1277-4
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    ABSTRACT: Abnormal platelet reactivity is associated with recurrent ischemia and bleeding following percutaneous coronary intervention (PCI). Protease-activated receptor-1 (PAR1), encoded by F2R, is a high affinity thrombin receptor on platelets and the target of the antiplatelet drug vorapaxar. The intronic single nucleotide polymorphism F2R IVS-14 A/T affects PAR1 receptor density and function. We hypothesized that carriers of the T allele, who have been shown to have decreased platelet reactivity, would be at lower risk for thrombotic events, but higher risk for bleeding following PCI. Using BioVU, the Vanderbilt DNA repository linked to the electronic medical record, we studied 660 patients who underwent PCI for unstable or stable coronary artery disease. Primary outcome measures were major adverse cardiovascular events (MACE, composite of revascularization, MI, stroke, death) and bleeding (assessed by Bleeding Academic Research Consortium scale) over 24 months. The minor allele (T) frequency was 14.8 %. There were no genotypic differences in the frequency of MACE (33.7, 28.8, and 31.6 % for A/A, A/T, and T/T respectively, P = 0.50) or bleeding (15.7, 14.7, and 18.8 % for A/A, A/T, and T/T respectively, P = 0.90). In a Cox regression model, fully adjusted for age, race, sex, BMI, and smoking status, carrying a T allele was not associated with MACE (HR 1.19, 95 % CI 0.89-1.59, P = 0.23) or bleeding (HR 0.73, 95 % CI 0.37-1.4, P = 0.34). In conclusion, in our population, F2R IVS-14 PAR1 variability does not affect risk of MACE or bleeding following PCI.
    Journal of Thrombosis and Thrombolysis 10/2015; DOI:10.1007/s11239-015-1285-4
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    ABSTRACT: Copeptin (COP) was reported to have prognostic value in various cardiovascular diseases. We hypothesized that COP levels reflect the severity of acute pulmonary embolism (PE) and may be useful in prognostic assessment. Plasma COP concentrations were measured on the Kryptor Compact Plus platform (BRAHMS, Hennigsdorf, Germany). The study included 107 consecutive patients with diagnosed acute PE (47 males, 60 females), with median age of 65 years (range 20-88). High risk PE was diagnosed in 3 patients (2.8 %), intermediate risk in 69 (64.5 %), and low risk PE in 35 (32.7 %) patients. Control group included 64 subjects (25 males, 39 females; median age 52.5 year, range 17-87). Four patients (3.7 %) died during 30-day observation. Complicated clinical course (CCC) was experienced by 10 (9.3 %) patients. COP level was higher in PE patients than in controls [11.55 pmol/L (5.16-87.97), and 19.00 pmol/L (5.51-351.90), respectively, p < 0.0001], and reflected PE severity. COP plasma concentration in low risk PE was 14.67 nmol/L (5.51-59.61) and in intermediate/high risk PE 19.84 mol/L (5.64-351.90) p < 0.05. Median COP levels in nonsurvivors was higher than in survivors, 84.6 (28.48-351.9) pmol/L and 18.68 (5.512-210.1) pmol/L, respectively, p = 0.009. Subjects with CCC presented higher COP levels than patients with benign clinical course 53.1 (17.95-351.9) pmol/L and 18.16 (5.51-210.1) pmol/L, respectively, p = 0.001. Log-transformed plasma COP was the significant predictor of CCC, OR 16.5 95 % CI 23.2-111.9, p < 0.001. AUC-for prediction of CCC using plasma COP was 0.811 (95 % CI 0.676-0.927). The COP cut off value of 17.95 nmol/l had sensitivity of 100 %, specificity 49.5 %, positive predictive value of 16.9 % and negative predictive value of 100 %. We conclude that plasma COP levels can be regarded for promising marker of severity of acute PE and show potential in risk stratification of these patients.
    Journal of Thrombosis and Thrombolysis 10/2015; DOI:10.1007/s11239-015-1284-5
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    ABSTRACT: Thrombelastography (TEG) measures coagulation in venous blood. We hypothesized that TEG, by reflecting clot subtype and ex vivo fibrinolysis, might predict fibrinolytic response to tPA as reflected by rapid clinical improvement or hemorrhagic transformation of the infarct. 171 acute ischemic stroke patients treated with tPA were prospectively enrolled. Venous blood for TEG was drawn before and 10 min after tPA bolus. We measured rapid clinical improvement (RCI = 8 point improvement on NIHSS or total NIHSS of 0, 1 at 36 h), Hemorrhagic transformation (HT = any blood on imaging within 36 h), and hyperdense middle cerebral artery sign (HDMCA = biomarker for erythrocyte-rich clot). Multivariable regression models compared TEG parameters after adjusting for potential confounders. No differences in pre- or post-tPA TEG were found between patients with or without RCI. Also, there was no correlation between TEG and HDMCA. Clotting was slightly prolonged in patients with HT (p = 0.046). We failed to find a robust association between TEG and clinical response to tPA. It is likely that arterial clot lysis is determined by factors unrelated to coagulation status as measured by TEG in the venous circulation. It is unlikely that TEG will be useful to predict clinical response to tPA, but may help predict bleeding.
    Journal of Thrombosis and Thrombolysis 09/2015; DOI:10.1007/s11239-015-1280-9
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    ABSTRACT: In addition to degrading fibrinogen as a source of consumptive coagulopathy, purified fractions of southern copperhead (Agkistrodon contortrix contortrix; A. c. contortrix) venom has been demonstrated to enhance fibrinolysis. The goal of this investigation was to characterize the kinetic fibrinolytic profile of A. c. contortrix venom in the absence and presence of tissue-type plasminogen activator (tPA) to determine if intact venom had tPA independent fibrinolytic properties. Utilizing thrombelastographic methods, the coagulation and fibrinolytic kinetic profiles of human plasma exposed to A. c. contortrix venom (0-6 μg/ml) were determined in the absence or presence of tPA (0-100 IU/ml). Then, plasma was exposed to 0-6 μg/ml of venom without tPA added and coagulation observed for 3 h. Venom significantly prolonged the onset of coagulation, decreased the velocity of thrombus growth but did not significantly decrease clot strength. In the presence of tPA, venom significantly decreased clot strength, shortened the time of onset of fibrinolysis, decreased clot lysis time but did not significantly affect the maximum rate of lysis. Lastly, while venom exposure in the absence of tPA significantly prolonged the onset of coagulation and decreased the velocity of clot growth, venom exposure did not result in detectable fibrinolysis over the 3 h observation period. A. c. contortrix venom enhances tPA mediated fibrinolysis by degrading plasma coagulation kinetics. Intact A. c. contortrix venom does not possess sufficient fibrinolytic activity to cause fibrinolysis in human plasma at the concentration tested.
    Journal of Thrombosis and Thrombolysis 09/2015; DOI:10.1007/s11239-015-1287-2
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    ABSTRACT: Although the non-vitamin K antagonist oral anticoagulants (NOACs) do not require routine monitoring, there are special circumstances in which laboratory measurement may be warranted. The objectives of this review are to summarize evidence on the influence of the NOACs on coagulation tests and provide practical guidance to clinicians on measurement and interpretation of coagulation assays in NOAC-treated patients. Selection of an appropriate assay for NOAC measurement depends on the drug, clinical objective, and assay availability. Separate suggestions for assay selection are provided depending on whether specialized assays are available or whether choice is limited to conventional coagulation assays such as the prothrombin time (PT) and activated partial thromboplastin time (APTT). The dilute thrombin time (TT) and ecarin-based assays are able to quantify dabigatran across a broad range of concentrations, but are not widely available. A normal TT excludes clinically relevant levels. A normal APTT probably excludes excess levels of dabigatran, but does not rule out typical on-therapy drug concentrations. The PT is insufficiently sensitive to dabigatran to be useful in most situations. Factor Xa inhibitors may be quantified with an anti-Xa assay calibrated with drug-specific standards. A normal PT probably excludes excess levels of rivaroxaban and edoxaban, but not typical on-therapy levels of these agents. The PT is less sensitive to apixaban. Depending on the sensitivity of the thromboplastin reagent, a normal PT may not exclude excess levels of apixaban. The APTT has inadequate sensitivity to factor Xa inhibitors and is not recommended for their measurement.
    Journal of Thrombosis and Thrombolysis 09/2015; DOI:10.1007/s11239-015-1282-7
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    ABSTRACT: Anterior spinal artery syndrome (ASAS) often leads to complete motor paralysis with poor clinical outcome. There is a lack of controlled clinical trials on acute treatment strategies in ASAS. However, systemic thrombolysis with recombinant tissue-plasminogen activator (rt-PA) might be a useful therapeutic option in ASAS. We report the management of a patient with ASAS below thoracic level 10, who was treated with intravenous thrombolysis. An 81 year old patient presented with flaccid paraplegia. After exclusion of aortal dissection, spinal tumour or haemorrhage, the patient was treated with intravenous rt-PA 3 h 40 min after symptom onset. The follow up magnetic resonance imaging (MRI) showed spinal infarction below thoracic segment 10. In the clinical course, the patient partially recovered lower limb muscle strength and was able to walk with assistance. To the best of our knowledge, this is the first case in the literature of ASAS with MRI-proven spinal ischemia and the application of rt-PA. Systemic thrombolysis seems to be justifiable in patients with ASAS after the rule-out of aortal dissection and spinal bleeding.
    Journal of Thrombosis and Thrombolysis 09/2015; DOI:10.1007/s11239-015-1281-8
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    ABSTRACT: Heparin is a glycosaminoglycan with anticoagulant properties and antiinflammatory effects. The discovery of heparin approaches its 100th year and its antiinflammatory properties still draws much attention and anticipation to new possibilities of use and the likelihood of developing heparin-like drugs that lacked the anticoagulation effects. It is known that heparins limit the embolization and the extension of the thrombus, although they do not promote its complete lysis in most cases. The complexity and pleiotropic characteristics of these glycosaminoglycans still challenge science, to the point in which approaches hitherto unusual appear repeatedly in the literature. New indications, accompanied by longtime consecrated others, dismantle the idea of an outdated medication and create high expectations for the near future. The objective of this review is to analyze the pleiotropic effects of heparin and its use in several diseases, highlighting its safety and effectiveness.
    Journal of Thrombosis and Thrombolysis 09/2015; DOI:10.1007/s11239-015-1261-z