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 2015
2013 / 2014 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
Year

Additional details

5-year impact 1.70
Cited half-life 4.00
Immediacy index 0.30
Eigenfactor 0.01
Article influence 0.49
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

  • Pre-print
    • Author can archive a pre-print version
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  • Conditions
    • Author's pre-print on pre-print servers such as arXiv.org
    • Author's post-print on author's personal website immediately
    • Author's post-print on any open access repository after 12 months after publication
    • Publisher's version/PDF cannot be used
    • Published source must be acknowledged
    • 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
    ​ green

Publications in this journal

  • [Show abstract] [Hide abstract]
    ABSTRACT: Several studies have found a beneficial effect of nicotinic acid on lipid profile, but there remains a limitation in the clinical use of nicotinic acid due to its side effects. In this study, 46 (F/M = 22/24, age = 58.74 ± 10.02 years) patients with Lp(a) ≥500 mg/L and with a previous arterial thrombotic event were treated with nicotinic acid/laropiprant (Tredaptive(®)). We found a significant reduction in the Lp(a) values at T1 (after 12 months), with a decrease of 32.3 % from baseline levels. At T1, 11 patients (23.9 %) showed Lp(a) levels to be <500 mg/L. PAT values were significantly decreased after treatment (2.13 ± 0.81 vs 1.74 ± 0.42, p = 0.001), showing a worsening of endothelial function in 27 (58.6 %) patients. A significantly higher number of patients had RHI <1.5 after the treatment [18 (39.1 %) vs 8 (17.4 %)]. Blood rheology worsened as ED was impaired (p < 0.0001) after 12 months, whereas WHV, plasma viscosity, and red cell aggregation did not show any significant differences in comparison to baseline. Patients with a worsening in microvascular reactivity in comparison to baseline showed a marked impairment in ED (0.3327 ± 0.037 vs 0.3091 ± 0.0351; p < 0.0001), while others showed only a mild, even though significant, reduction (0.3347 ± 0.0299 vs 0.3272 ± 0.0235; p = 0.044). In the light of the results of HPS2-THRIVE study, we may hypothesize that the addition of laropiprant to niacin might be responsible for these negative effects. In turn, these effects might explain, at least in part, the lack of a clinical net benefit of niacin/laropiprant in the trial.
    Journal of Thrombosis and Thrombolysis 08/2015; DOI:10.1007/s11239-015-1256-9
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    ABSTRACT: To investigate the pulmonary angiography and pathology in a canine model with chronic pulmonary thromboembolism (PTE). The cylindrical blood clots were selectively introduced into the left (n = 10) or right (n = 20) lower pulmonary arteries of dogs. Pulmonary arteriography (PA) was performed before or after embolization. The values after embolization and baseline of mean pulmonary arterial pressure, pulmonary vascular resistance, cardiac output had changed. After 1 or 2 weeks' embolization, local PA demonstrated the abrupt cut-off perfusion defects or webs, bands, and abrupt vascular narrowing. 2 weeks after embolization, the pathology showed that the fibrin networks of the thrombi had multiple recanalization channels, and pulmonary artery had the concentric, lamellar (onion-like) intimal hyperplasia, multilayered, irregular arrangements of endothelial cells, and the infiltration of inflammatory cells. After embolectomy-mediated reperfusion, 2 weeks' subgroup showed destroyed and incomplete alveolar structures, and a large number of exudative cells, primarily neutrophils, and exudate. There close concordance between pulmonary angiography and pathology in a canine model with chronic PTE. The LIRI mechanisms after embolectomy-mediated reperfusion involve the destroyed, incomplete alveolar structures, and infiltration of inflammatory cells, primarily neutrophils.
    Journal of Thrombosis and Thrombolysis 08/2015; DOI:10.1007/s11239-015-1268-5
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    ABSTRACT: Atrial fibrillation and obesity are two major growing epidemics in the United States and globally. Obese people are at the increased risk of developing atrial fibrillation. The contribution of obesity as an independent risk factor for stroke in the setting of atrial fibrillation remains unclear. We tested the hypothesis that non-valvular atrial fibrillation (NVAF) patients with increased body mass index (BMI) would be at increased risk for the development of left atrial appendage thrombus (LAAT). Consecutive, anticoagulation naïve patients with NVAF referred for a transesophageal echocardiogram (TEE) between January 1, 2007 and October 21, 2009 were approached for study participation. All clinical, laboratory, and TEE measurement data were collected prospectively. Within a group of 400 anticoagulation naïve NVAF patients (mean age 63 ± 15 years, 28 % women; 17 % with LAAT) the prevalence of LAAT was similar across all BMI categories (normal 13 %, overweight 19 %, obese 16 %, morbidly obese 16 %; p = 0.71). Despite a higher CHADS2 score and a higher prevalence of both hypertension and diabetes mellitus, elevated BMI was not an independent predictor of LAAT when analyzed as either a continuous variable, across BMI WHO categories, a dichotomous variable stratified at values above versus below 27 kg/m(2), or BMI stratified on atrial fibrillation duration. Despite a higher prevalence of major risk factors for thromboembolism, the prevalence of LAAT was not increased in overweight, obese, and morbidly obese patients.
    Journal of Thrombosis and Thrombolysis 08/2015; DOI:10.1007/s11239-015-1266-7
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    ABSTRACT: We analysed time trends in the pulmonary embolism (PE) mortality rates in Germany from 2004 and assessed for an association between the use of anticoagulants and PE caused mortality. We extracted age-specific number of deaths due to PE (ICD-10 I26) from 2004 to 2011 as available from the WHO mortality databases. In addition we derived defined daily dosage (DDD) of prescribed anticoagulants and the low molecular heparin Enoxaparin for the years 2004-2011 from the statutory health insurance-drug-information system reports. Age-standardized PE mortality per 100,000 decreased from 5.9283 in year 2004 to 4.4876 in 2011 (-24.3 %). Amounts of prescribed anticoagulants increased in this period from 271,810.7 × 1000 DDD to 416,611.8 × 1000 DDD (+53.3 %), that of Enoxaparin increased from 27,071.1 × 1000 DDD in 2004 97,276.5 × 1000 DDD in 2011. The PE mortality is negatively correlated with anticoagulants (-0.9463, p = 0.0004) as well as with enoxaparin (-0.9740, p < 0.0001) and of DDD of Enoxaparin per 1000 insured (-0.9682, p < 0.0001). In univariate linear regression model, anticoagulants, Enoxaparin and Enoxaparin per 1000 insured all reach significance (p = 0.0004, p = 4.31 × 10(-5) and p = 0.0001 respectively). Multiple regression models show that Enoxaparin has the most robust effect. Including the time trend in the model does not alter the results. Our study shows that increasing number of prescribed Enoxaparin in an outpatient setting might be one determinant of decreasing PE mortality rate in Germany since 2004.
    Journal of Thrombosis and Thrombolysis 08/2015; DOI:10.1007/s11239-015-1265-8
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    ABSTRACT: Since the introduction of new oral anticoagulants (NOACs), besides vitamin-K antagonists, an additional option for stroke prevention of patients with atrial fibrillation (AF) is available. The objective of this study was to assess AF patients' preferences with regard to the attributes of these different treatment options. We conducted a multicenter study among randomly selected physicians. Preferences were assessed by computer-assisted telephone interviews. We used a discrete-choice-experiment (DCE) with four convenience-related treatment dependent attributes (need of bridging: yes/no, interactions with food/nutrition: yes/no, need of INR controls/dose adjustment: yes/no; frequency of intake: once/twice daily) and one comparator attribute (distance to practitioner: <1 km/>15 km). Preferences measured in the interviews were analyzed descriptively and based on a conditional logit regression model. A total of 486 AF patients (age: 73.9 ± 8.2 years; 43.2 % female; mean CHA2DS2-VASc: 3.7 ± 1.6; current medication: 48.1 % rivaroxaban, 51.9 % VKA) could be interviewed. Regardless of type of medication, patients significantly preferred the attribute levels (in order of patients' importance) "once daily intake" (Level: once = 1 vs. twice = 0; Coefficient = 0.615; p < 0.001), "bridging necessary" (yes = 1 vs. no = 0; -0.558; p < 0.001), "distance to practitioner of ≤1 km (>15 km = 0 vs. ≤1 km = 1; 0.494; p < 0.001), "interactions with food/nutrition" (yes = 1 vs. no = 0; -0.332; p < 0.001) and "need of INR controls/dose adjustment" (yes = 1 vs. no = 0; -0.127; p < 0.001). In our analyses, "once daily frequency of intake" was the most important OAC-attribute for patients' choice followed by "no bridging necessary" and "no interactions with food/nutrition". Thus, patients with AF seem to prefer treatment options which are easier to administer.
    Journal of Thrombosis and Thrombolysis 08/2015; DOI:10.1007/s11239-015-1263-x
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    ABSTRACT: Prognostic stratification of acute pulmonary embolism (PE) remains a challenge in clinical practice. Simplified PESI (sPESI) score is a practical validated score aimed to stratify 30-day mortality risk in acute PE. Whether prognostic value of sPESI score differs according to sex has not been previously investigated. Therefore the aim of our study was to provide information about it. Data records of 452 patients, 180 males (39.8 %) and 272 females (60.2 %) discharged for acute PE from Internal Medicine wards of Tuscany (Italy) were analysed. sPESI was retrospectively calculated. Variables enclosed in sPESI score, all cause in-hospital mortality and overall bleedings were compared between sexes. Moreover, predictive ability of sPESI score as prognosticator of all cause in-hospital mortality mortality was tested and compared between sexes. sPESI score 0 (low risk) was found in 17.7 % of males and 13.6 % of females (p = 0.2323). We didn't find significant difference in sPESI scoring distribution. Age ≥80 years (51.4 vs. 33.8 %, p = 0.0003) and heart rate ≥110 bpm (23.5 vs. 14.4 %, p = 0.0219) were found significantly more prevalent in females, whereas active cancer (23.8 vs. 39.4 %, p = 0.0004) and cardio-respiratory diseases (19.8 vs. 27.7 %, p = 0.0416) were in males. All cause in-hospital mortality was 0 % in both genders for sPESI score 0, whereas it was 5.4 % in females and 13.6 % in males with sPESI score 1-2 (p = 0.0208) and 22 % in females and 19.3 % in males with sPESI score ≥3 (p = 0.7776). Overall bleedings were significantly more frequent in females compared with males (4.77 vs. 0.55 %, p = 0.0189). In females overall bleedings ranged from 2.7 % in sPESI score 0 to 6 % in sPESI score ≥3. Predictive ability of sPESI score as prognosticator of all cause in-hospital mortality was higher in females compared to males (AUC 0.72 vs. 0.67, respectively). In real life different co-morbidity burdens in females compared to males. Females seems to be at lower risk of all cause in-hospital mortality for sPESI score ≤2 but at higher risk of bleeding, irrespective from sPESI scoring. Predictive ability of sPESI score seems better in females.
    Journal of Thrombosis and Thrombolysis 08/2015; DOI:10.1007/s11239-015-1260-0
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    ABSTRACT: It is unclear whether vitamin K antagonists affect stroke severity and outcome in patients with atrial fibrillation (AF). We aimed to evaluate this association. We prospectively studied 539 consecutive patients admitted with acute ischemic stroke (41.2 % males, age 78.9 ± 6.6 years). The severity of stroke was assessed at admission with the National Institutes of Health Stroke Scale (NIHSS). The outcome was assessed with dependency rates at discharge (modified Rankin scale 2-5) and with in-hospital mortality. 177 patients had a history of AF. The median NIHSS at admission did not differ between patients on acenocoumarol with INR 2.0-3.0, on acenocoumarol with INR < 2.0, on single antiplatelet treatment, on dual antiplatelet treatment, or on no treatment [4 (range 0-26), 13 (0-39), 8 (0-33), 3 (2-23) and 7 (0-33), respectively; p = 0.433]. Dependency rates were lower in patients on acenocoumarol with INR 2.0-3.0 or on dual antiplatelet treatment than in those on acenocoumarol with INR < 2.0, single antiplatelet treatment, or no treatment (20.0, 22.2, 61.5, 58.7 and 68.0 %, respectively; p = 0.024). Independent predictors of dependency were age, NIHSS at admission and history of ischemic stroke. In-hospital mortality did not differ between patients on acenocoumarol with INR 2.0-3.0, on acenocoumarol with INR < 2.0, on single antiplatelet treatment, on dual antiplatelet treatment, or on no treatment (7.7, 18.2, 16.1, 16.7 and 22.2 %, respectively; p = 0.822). In conclusion, optimally anticoagulated patients with AF have more favorable functional outcome after stroke and a trend for less severe stroke whereas patients with subtherapeutic anticoagulation have similar stroke severity and outcome with those on no treatment.
    Journal of Thrombosis and Thrombolysis 08/2015; DOI:10.1007/s11239-015-1262-y
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    ABSTRACT: Thrombotic thrombocytopenic purpura (TTP) is an acute, thrombotic microangiopathy with a high mortality rate if left untreated. Plasma exchange (PEX) is the current standard of care. However, a significant number of patients are refractory to this treatment. N-acetylcysteine (NAC) was recently suggested as a potential therapeutic adjunct for patients with TTP. This study reports a series of three patients with TTP successfully treated with NAC in addition to standard therapy. Detailed chart reviews on these patients were conducted. We discuss clinical features, laboratory findings and management of three patients who presented with microangiopathic hemolytic anemia and thrombocytopenia. Anti-ADAMTS13 antibodies and low levels of ADAMTS13 were detected and confirmed the diagnosis of acquired TTP. Based upon their severe presentation or lack of response to initial treatment with PEX, corticosteroids and other immunosuppressive agents, NAC was added. Under this combined treatment, all three patients hada significant clinical improvement of symptoms with concurrent normalization of platelet count and ADAMTS13 activity level. This report highlights the potential therapeutic utility of NAC in the treatment of TTP. Randomized controlled studies will be required to better characterize the risk-to-benefit ratio of NAC in the treatment of TTP.
    Journal of Thrombosis and Thrombolysis 08/2015; DOI:10.1007/s11239-015-1259-6
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    ABSTRACT: Hereditary hemorrhagic telangiectasia (HHT) is an autosomal-dominantly inherited vascular-malformation syndrome associated with gene mutations including ENG, ACVRL1 and SMAD4 gene. Clinically indistinguishable HHT1 and HHT2 are caused by mutations in ENG and ACVRL1 gene, respectively. Generally, pulmonary arteriovenous malformations (PAVMs) and pulmonary arterial hypertension (PAH) are rare manifestations of HHT related to ACVRL1 gene mutations. We described a female patient with HHT2 whose clinical features included epistaxis, mucocutaneous telangiectases, systemic AVMs and PAH. She also suffered from severe iron deficiency anemia and recurrent heart failure. A genetic mutation analysis disclosed a missense mutation in exon 7 of ACVRL1 gene in this patient and her daughter. A nonsense mutation in exon 7 of ACVRL1 gene was detected in her brother and her niece. This case supports that PAVMs and PAH can be rare manifestations of HHT2 patients.
    Journal of Thrombosis and Thrombolysis 08/2015; DOI:10.1007/s11239-015-1253-z
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    ABSTRACT: Unfractionated heparin (UFH) plasma protein binding and elimination might be impaired in patients with chronic kidney disease (CKD-defined as creatinine clearance <60 ml/min). It is currently unknown at which UFH bolus dose persistent prolongation of activated partial thromboplastin time (aPTT) occurs in ST-segment elevation myocardial infarction (STEMI) patients with CKD. We investigated the effect of different UFH bolus doses on the first aPTT measured within 6 and 12 h after PPCI in 1071 STEMI patients with and without CKD undergoing primary percutaneous coronary intervention (PPCI) between 1-1-2003 and 31-07-2008. In the first 6 h after PPCI, aPTT ratio was 5.1 for patients with CKD versus 3.4 for those without (p < 0.001). The proportion of patients with markedly high aPTTs (aPTT ratio ≥ 4 times control) increased with increasing heparin bolus and beyond 130 IU/kg there was a marked difference between patients with and without CKD (74.1 and 42.3 % respectively, p < 0.001). By multivariable analysis, CKD was associated with an increased risk of markedly high aPTTs (odds ratio (OR) 2.04; 95 % confidence interval (CI) 1.27-3.27), driven largely by an increased risk of aPTT prolongation in patients treated with UFH boluses ≥130 IU/kg (OR 3.69; 95 % CI 1.85-7.36; p for interaction = 0.009). In conclusion, CKD is associated with severe persistent aPTT prolongation in STEMI patients undergoing PPCI, possibly due to impaired plasma protein binding and reduced UFH elimination. A lower heparin bolus dose might result in lower aPTTs and less bleeding complications in patients with CKD undergoing PPCI.
    Journal of Thrombosis and Thrombolysis 08/2015; DOI:10.1007/s11239-015-1255-x
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    ABSTRACT: Warfarin is an oral anticoagulant agent with a narrow therapeutic index. There is a marked inter- and intra-patient variability in warfarin dose requirement. All factors influencing warfarin response are not known and this study aims to evaluate if regular physical activity (RPA) is a determining factor. RPA level was collected with the Stanford Brief Activity Survey in 1064 incident warfarin users, as part of the Quebec Warfarin Cohort (QWC), and with the Global Physical Activity Questionnaire in 618 patients from the Montreal Heart Institute (MHI) Biobank. Linear regression was performed to model relationship of warfarin dose after 3 months of therapy in the QWC with RPA, while controlling for height, weight, age, CYP2C9 (*2 and *3 alleles) and VKORC1 (*2 allele) genotype. Warfarin dose of prevalent users was modeled in the MHI Biobank for replication. A higher level of physical activity was associated with higher doses of warfarin in both cohorts. In the QWC, physical activity could explain 5.4 % (P < 0.001) and 0.9 % (P = 3.23 × 10(-5)) of variance in dose, in univariate and multivariable models, respectively. Similarly, RPA was found to be associated with 1.7 % (P = 0.0012) and 0.5 % (P = 0.0391) of inter-individual variability in warfarin dose requirement before and after adjustment for other covariables, respectively. RPA is associated with higher warfarin dose requirement. The relevance of clinical recommendations on RPA to maintain a steady response to warfarin should be assessed in further studies.
    Journal of Thrombosis and Thrombolysis 08/2015; DOI:10.1007/s11239-015-1248-9
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    ABSTRACT: The purpose of this study was to investigate the behavior of platelets (rolling and adhesion) in cerebral microvessels of angiotensin II type-2 receptor-knockout (AT2RKO) mice after transient bilateral carotid artery occlusion using intravital fluorescence microscopy. Twenty AT2RKO mice, consisting of 11 mice in the sham group and 9 mice in the ischemia reperfusion group (reperfusion after 15 min of bilateral, total carotid artery occlusion) were used in this study. The hole traversed the bone and dura mater, but arachnoid, pia mater, and cerebral parenchyma were preserved. Platelets were harvested from donor mice and stained using carboxyfluorescein diacetate succinimidyl ester. The number of platelets showing rolling and adhesion to pial vessels in AT2 deficient mice at 3 and 6 h after cerebral ischemia reperfusion was significantly higher than that in the sham group (P < 0.05). In addition, AT2 receptor has an inhibitory role in platelet rolling and adhesion after cerebral ischemia reperfusion.
    Journal of Thrombosis and Thrombolysis 08/2015; DOI:10.1007/s11239-015-1254-y
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    ABSTRACT: We aimed to characterize the independent predictors of LVT following STEMI and the association with outcomes. The clinical predictors of left ventricular thrombus (LVT) formation after ST-segment elevation myocardial infarction (STEMI) are not well-defined in the contemporary era. We performed a retrospective analysis of STEMI patients at Duke from 2000 to 2011 who had a transthoracic echocardiogram within 90 days post-STEMI and compared patients with and without LVT (LVT+ vs. LVT-). Univariate Cox proportional hazards regression models of baseline characteristics were examined and significant variables were used in a multivariable model to assess adjusted relationships with LVT. A multivariable Cox PH survival model with covariate adjustments was used for assessment of LVT and long-term mortality. Of all eligible patients, 1734 patients met inclusion criteria and 4.3 % (N = 74) had a LVT. LVT+ patients tended to have a history of heart failure (HF) and higher initial troponin compared to LVT- patients. After adjustment, higher heart rate, non-white race, HF severity, and presence of left anterior descending artery (LAD) disease were independent predictors of LVT. There was a trend toward an association between LVT and increased all-cause mortality (HR 1.36; 95 % CI 0.84-2.21, P = 0.22), however this was not statistically significant. LVT was seen in over 4 % of this contemporary post-STEMI population. Several baseline characteristics were independently associated with LVT: Heart rate, HF severity, LAD disease, and non-white race. Prospective studies are warranted to determine whether anticoagulation in patients at increased risk for LVT improves outcomes.
    Journal of Thrombosis and Thrombolysis 07/2015; DOI:10.1007/s11239-015-1252-0
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    ABSTRACT: Rheumatoid arthritis (RA) is a chronic inflammatory autoimmune disorder resulting in the erosion of the cartilage and bone. Systemic involvement including the cardiovascular system with the risk of atherosclerosis may also occur. Calibrated automated thrombogram (CAT), a commercially available thrombin generation assay is suitable for the general assessment of the functionality of coagulation system. In this study we performed CAT assay in RA patients and in non-affected control subjects (matched for age, sex and comorbidities). Among the CAT parameters Velocity Index increased (from 60 to 83 nM/min), Lag Time and Time to Peak decreased (from 3.47 to 2.83 min and from 6.98 to 5.58 min respectively) in RA. On the other hand, Endogenous Thrombin Potential values decreased (from 1242 to 1108 nM min). The observed alterations were not associated with the applied therapy. These results indicate that the velocity of thrombin formation is increased, while the thrombin generating capability is reduced in RA.
    Journal of Thrombosis and Thrombolysis 07/2015; DOI:10.1007/s11239-015-1251-1
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    ABSTRACT: The new oral anticoagulants (NOACs) reduce stroke and systemic embolism in patients with non-valvular atrial fibrillation (AF), but dabigatran may increase risk of coronary ischemic events for unclear reasons. Thus, this study assessed the effects of dabigatran and rivaroxaban on platelet reactivity and inflammatory markers in patients with non-valvular AF. Patients with non-valvular AF planned to begin treatment with NOACs were included. Seventeen patients were prescribed dabigatran and ten rivaroxaban. Platelet function (as assessed by multiple-electrode aggregometry, Impact-R shear-induced platelet deposition, P-selectin expression and plasma RANTES levels) and high-sensitivity C-reactive protein (hs-CRP) were measured at enrollment (prior to initiation of NOAC treatment) and at least 7 days into treatment with either dabigratran or rivaroxaban. Seventeen patients treated with dabigatran (mean age 69 ± 7 years, 35 % women, mean CHADS2 score 2.6 ± 1.2), and ten patients treated with rivaroxaban (mean age 73 ± 9 years, 20 % women, mean CHADS2 score 2.7 ± 1.6) completed the study. In both groups, there were no significant differences in platelet reactivity between the baseline and on-anticoagulant treatment time-points, as measured by each of the platelet-specific assays. There was a trend towards increased platelet reactivity in response to arachidonic acid from baseline to on-treatment in both groups, probably as a result of aspirin discontinuation in 33 % of patients. No significant differences were noted between baseline and on-treatment in hs-CRP in both anticoagulant groups. Treatment with dabigatran and rivaroxaban does not appear to be associated with changes in markers of platelet reactivity or systemic inflammation.
    Journal of Thrombosis and Thrombolysis 07/2015; DOI:10.1007/s11239-015-1245-z
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    ABSTRACT: Some studies have cautioned about the possibility of bleeding complications with routine use of anticoagulants like fondaparinux (FPX) for thrombophylaxis after elective hip surgery. Overdosing or prolonged periods of anticoagulant use should be avoided. We trialed a new regimen using FPX and tranexamic acid (TA) to reduce the risk of bleeding complications while maintaining efficacy in preventing deep vein thrombosis (DVT). The present study evaluated the effectiveness and safety of this regimen in 391 consecutive patients. Each patient was assigned either the FPX group, administered a once-daily subcutaneous injection of 1.5 mg of FPX on postoperative days 2, 3, and 4; or the intermittent pneumatic compression (IPC) group, which used an IPC device continuously for 1-2 days with no administration of any anticoagulant drugs. Ultrasonography was performed to diagnose DVT in all patients. No cases of fatal or symptomatic pulmonary embolism were encountered in either group, but six patients (3.1 %) in the FPX group and nine patients (6.0 %) in the IPC group showed asymptomatic distal DVT. The incidence of DVT tended to be lower (p = 0.19), volumes of intraoperative (p < 0.01) and postoperative (p < 0.01) blood loss were significantly smaller, and hemoglobin level was significantly higher in the FPX group than in the IPC group (p < 0.01). Our new thrombophylactic regimen using FPX and TA appears effective and safe for use after elective hip surgery.
    Journal of Thrombosis and Thrombolysis 07/2015; DOI:10.1007/s11239-015-1249-8
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    ABSTRACT: The Wells score and the revised Geneva score are two most commonly used clinical rules for excluding pulmonary embolism (PE). In this study, we aimed to assess the diagnostic accuracy of these two rules; we also compared the diagnostic accuracy between them. We searched PubMed and Web of science up to April 2015. Studies assessed Wells score and revised Geneva score for diagnosis suspected PE were included. The summary area under the curve (AUC) and the 95 % confidence interval (CI) were calculated. Eleven studies were included in this meta-analysis. For Wells score, the sensitivity ranged from 63.8 to 79.3 %, and the specificity ranged from 48.8 to 90.0 %. The overall weighted AUC was 0.778 (95 % CI 0.740-0.818; Z = 9.88, P < 0.001). For revised Geneva score, the sensitivity ranged from 55.3 to 73.6 %. The overall weighted AUC was 0.693 (95 % CI 0.653-0.736; Z = 11.96, P < 0.001). 95 % CIs of two AUCs were not overlapped, which indicated Wells score was more accurate than revised Geneva score for predicting PE in suspected patients. Meta-regression showed diagnostic accuracy of these two rules was not related with PE prevalence. Sensitivity analysis by only included prospective studies showed the results were robust. Our results showed the Wells score was more effective than the revised Geneva score in discriminate PE in suspected patients.
    Journal of Thrombosis and Thrombolysis 07/2015; DOI:10.1007/s11239-015-1250-2
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    ABSTRACT: The aims of this study were to evaluate the characteristics of hypercoagulable states in patients with membranous nephropathy (MN) via thromboelastography (TEG) and to identify risk factors. 235 MN patients who had undergone TEG examinations from 2011 to 2014 were included. An abnormality in at least two TEG parameters is considered a hypercoagulable state. Patient data was compared between the hypercoagulable and non-hypercoagulable groups. Potential risk factors for hypercoagulability were analyzed by logistic regression models. Subgroup analysis was performed in hypercoagulable patients. Compared to the non-hypercoagulable MN patients, the hypercoagulable patients showed a significantly higher proportion of female patients, urinary protein, platelet count, triglyceride and fibrinogen level, along with more severe hypoproteinemia and a reduction of serum antithrombin III. Correlation analysis showed that hypoproteinemia was the primary risk factor for hypercoagulability in MN patients. Among the hypercoagulable MN patients, a subgroup TEG parameter analysis showed that glucocorticoids-used subgroup and smoker subgroup had shortened time to initial fibrin formation (R value) and increased coagulation index respectively (P < 0.05), indicating a more serious hypercoagulable state. Meanwhile, the time to initial fibrin formation (R value) and time to clot formation (K value) of the statin-used patients were remarkably higher than those of the non-statin patients. TEG examinations facilitated the detection of hypercoagulable states in MN patients, and hypoproteinemia was the most important risk factor for hypercoagulability in these patients. The use of glucocorticoids and smoking may help to aggravate hypercoagulable states, while statin drugs may alleviate hypercoagulability.
    Journal of Thrombosis and Thrombolysis 07/2015; DOI:10.1007/s11239-015-1247-x