Effect of low-intensity warfarin anticoagulation on level of activity of the hemostatic system in patients with atrial fibrillation. BAATAF Investigators.

Kistler, J P; Singer, Daniel E.; Millenson, MM; Bauer, Kenneth A.; Gress, Daryl R.; Barzegar, Samad; Hughes, Robert A.; Sheehan, Mary A.; Maraventano, S W; Oertel, Lynn B.

doi:10.1161/01.str.24.9.1360

Cited by 58 publications

(31 citation statements)

References 24 publications

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“…Sherman et al [17] found that patients with the greatest risk of embolism were those with hypertension on the basis of their AF. Large, prospective studies [3,18,19] have shown that the risk for thromboembolism does not differ between patients with paroxysmal AF and those with chronic AF. Advanced age and AF in the absence of anticoagulation were the factors that were independently associated with stroke occurrence.…”

Section: Discussionmentioning

confidence: 99%

The role of high-sensitivity C-reactive Protein, interleukin-6 and cystatin C in ischemic stroke complicating atrial fibrillation

You

Wang

et al. 2010

J. Huazhong Univ. Sci. Technol. [Med. Sci.]

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This study examined the role of high-sensitivity C-reactive protein (hsCRP), interleukin-6 (IL-6) and cystatin C in ischemic stroke complicating atrial fibrillation (AF) and the relationship of systemic inflammation with this disease in order to identify AF patients who are at high risk of stroke and need optimal anticoagulant therapy. A total of 103 AF patients, simple (n=75) or complicated by ischemic stroke (n=28), and 112 control subjects were recruited. IL-6 level was detected by using enzyme linked immunosorbent assay. Cystatin C and hsCRP levels were measured by means of a particle-enhanced immunonephelometric assay. The results showed that the AF patients had higher levels of hsCRP (P=0.004), IL-6 (P=0.000), and cystatin C (P=0.000) than control subjects. Plasma hsCRP level was increased in the AF patients with ischemic stroke as compared to the patients with simple AF (P=0.036). The AF patients who had the level of hsCRP exceeding 3.83 mg/L were at a higher risk than those with hsCRP level lower than 3.83 mg/L (P=0.030). After adjusting for other factors, cystatin C remained positively associated with IL-6 (r=0.613) and hsCRP (r=0.488). It was concluded that hsCRP is positively correlated with ischemic stroke complicating AF and may be a risk factor independent of other risk factors for AF. Elevated cystatin C level is also indicative of the increased risk of AF.

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Section: Discussionmentioning

confidence: 99%

The role of high-sensitivity C-reactive Protein, interleukin-6 and cystatin C in ischemic stroke complicating atrial fibrillation

You

Wang

et al. 2010

J. Huazhong Univ. Sci. Technol. [Med. Sci.]

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“…19,20 In addition, oral anticoagulants suppress thrombin generation with a significant reduction in F1+2. 21,22 Although it has been suggested that among patients with a hypercoagulable state, higher levels of F1+2 could identify a subgroup of patients with higher risk of thrombosis, this observation remains to be proven. Therefore, although we documented an increase in F1+2 and TAT levels in patients receiving G-CSF, the clinical significance of this finding remains unclear.…”

Section: Discussionmentioning

confidence: 99%

A prospective study of G-CSF effects on hemostasis in allogeneic blood stem cell donors

LeBlanc

Roy

Demers

et al. 1999

Bone Marrow Transplant

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Summary:Granulocyte colony-stimulating factor (G-CSF) is used in healthy donors of peripheral blood stem cells (PBSC) for allogeneic transplantation. However, some data have recently suggested that G-CSF may induce a hypercoagulable state, prompting us to study prospectively 22 PBSC donors before and after G-CSF 5 g/kg twice daily. We sought evidence for changes in the following parameters: platelet count, von Willebrand factor antigen (vWF:Ag) and activity (vWF activity), ␤-thromboglobulin (␤-TG), platelet factor 4 (PF-4), platelet activation markers (GMP-140 and PAC-1), activated partial thromboplastin time (aPTT), prothrombin time (PT), coagulant factor VIII (FVIII:C), thrombin-antithrombin complex (TAT), prothrombin fragment 1+2 (F1+2), thrombomodulin (TM) and tissue plasminogen activator antigen (tPA:Ag) prior to G-CSF and immediately before leukapheresis. ADP-induced platelet aggregation studies were also performed. G-CSF administration produced only mild discomfort. We found a significant increase in vWF:Ag (from 0.99 ؎ 0.32 U/ml to 1.83 ؎ 0.69 U/ml; P Ͻ 0.001), in vWF activity (from 1.04 ؎ 0.34 U/ml to 1.78 ؎ 0.50 U/ml; P Ͻ 0.001) and in FVIII:C (from 1.12 ؎ 0.37 U/ml to 1.73 ؎ 0.57 U/ml; P Ͻ 0.001) after G-CSF. Of note, four donors with low baseline vWF had a two-to three-fold increase after receiving G-CSF. G-CSF had no impact on the platelet count, ␤-TG, PF-4, GMP-140 or PAC-1. The final% of platelet aggregation decreased from 73 ؎ 22% to 37 ؎ 26% after G-CSF (P Ͻ 0.001). We found a significant decrease in aPTT after G-CSF (29.9 ؎ 3.1 s to 28.3 ؎ 3.3 s; P = 0.004), but the PT was unaffected. In addition, we also observed a significant increase in TAT, F1+2 and TM, but not in tPA:Ag. Our data suggest that G-CSF may possibly induce a hypercoagulable state by increasing levels of FVIII:C and thrombin generation. In contrast to this information, we found reduced platelet aggregation after G-CSF administration. The clinical implications of these findings remain unclear and larger studies are definitely required.

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“…it is expected that there will be a higher mean FI + 2 value in WARSS patients who have recurrent stroke, thus providing a hematologic marker of stroke risk. Based on the findings in the Boston Area Anticoagulation Trial for Atrial Fibrillation study [50], a lower mean FI + 2 level is expected in the coumadin-trcatcd patients as com pared to those on aspirin. The secondary' aim s of HAS are to analyze the natural history of FI + 2 levels over time, correlate these values with data obtained in APASS and PICSS, and correlate FI + 2 values with other vascular risk factors.…”

Section: The Hem Ostatic Syste M Activation Stu D Y (Has)mentioning

confidence: 99%

The Feasibility of a Collaborative Double-Blind Study Using an Anticoagulant

Faber¹,

Troost²,

Vermes³

et al. 1997

Cerebrovasc Dis

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We present the methodology and data indicating the feasibility of a five-study collaborative stroke trial. The core study, the Warfarin-Aspirin Recurrent Stroke Study (WARSS), is a prospective, randomized, double-blind multicenter trial comparing warfarin and aspirin in preventing the recurrence of ischemic stroke. The WARSS primary endpoint is the earlier of death or symptomatic ischemic stroke recurrence. The primary null hypothesis is that, over 2 years, warfarin therapy will not differ in frequency of death or ischemic stroke recurrence compared with platelet antiaggregant therapy (aspirin). The target sample size is 1,920. Four related studies use the WARSS data. The Antiphospholipid Antibodies and Stroke Study (APASS) investigates the significance of antiphospholipid antibodies in ischemic stroke; the Patent Foramen Ovale in Cryptogenic Stroke Study (PICSS) assesses the risk of stroke recurrence or systemic embolization in medically treated cryptogenic stroke patients with and without patent foramen ovale; and the Hemostatic System Activation Study (HAS) studies the F1 + 2 fractions of prothrombin in a subgroup of patients to allow comparison between the international normalized ratio (INR) and the evidence of prothrombin split products activity. The Genes in Stroke Study (GENESIS) investigates whether the double deletion genotype of the angiotensin converting enzyme is a risk factor for stroke. Features of the collaboration are cost savings in research arising from the use of a common data base; standardization through use of one central laboratory for processing of INR values, and double blinding by fabrication of INR values for aspirin patients. WARSS randomization began June 22, 1993. Cumulative patient recruitment through June 1, 1996 exceeds 1,400 at 50 sites.

show abstract

Effect of low-intensity warfarin anticoagulation on level of activity of the hemostatic system in patients with atrial fibrillation. BAATAF Investigators.

Cited by 58 publications

References 24 publications

The role of high-sensitivity C-reactive Protein, interleukin-6 and cystatin C in ischemic stroke complicating atrial fibrillation

The role of high-sensitivity C-reactive Protein, interleukin-6 and cystatin C in ischemic stroke complicating atrial fibrillation

A prospective study of G-CSF effects on hemostasis in allogeneic blood stem cell donors

The Feasibility of a Collaborative Double-Blind Study Using an Anticoagulant

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