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- Alehagen, Urban, 1951-, et al.
(author)
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Elevated D-dimer level is an independent risk factor for cardiovascular death in out-patients with symptoms compatible with heart failure
- 2004
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In: Thrombosis and Haemostasis. - 0340-6245 .- 2567-689X. ; 92:6, s. 1250-1258
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Journal article (peer-reviewed)abstract
- D-dimer, a marker of fibrin turnover, exhibits many interesting properties as a biological marker of thrombosis. Some of the properties of D-dimer might also be used to provide additional information about patients with heart failure. In this study, we evaluate the prognostic information acquired from D-dimer concerning increased risk of cardiovascular mortality in an elderly population with symptoms associated with heart failure. A cardiologist examined 458 elderly patients, out of 548 invited, attending primary care for symptoms of dyspnoea, fatigue and/or peripheral oedema and assessed NYHA functional class and cardiac function. Abnormal systolic function was defined as EF <40% on Doppler echocardiography. Abnormal diastolic function was defined as reduced E/A ratio and/or an abnormal pattern of pulmonary venous flow. Blood samples were drawn, and BNP and D-dimer were analysed. D-dimer was analysed using an automated micro-latex assay. A statistical analysis was performed to identify the prognostic value of increased plasma concentration of D-dimer. Results showed that during a median follow-up period of 5.5 years, 68 (14%) patients died of cardiovascular disease. No gender difference was noted. A plasma concentration of D-dimer >0.25mg/L increased the risk almost 4-fold. In conclusion, D-dimer is an independent risk factor for cardiovascular mortality that may be used to risk-stratify patients with heart failure. © 2004 Schattauer GmbH, Stuttgart.
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| 3. |
- Hillarp, Andreas, et al.
(author)
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Local INR calibration of the Owren type prothrombin assay greatly improves the intra- and interlaboratory variation
- 2004
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In: Thrombosis and Haemostasis. - 0340-6245 .- 2567-689X. ; 91:2, s. 300-307
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Journal article (peer-reviewed)abstract
- In 1999, a simplified procedure for calibration of the Owren prothrombin time (Owren PT) assay was introduced by a working group of the organisation for national quality assurance in laboratory medicine in Sweden. The new protocol allowed local calibration by means of only two lyophilised national plasma calibrators and expression of results as an international normalized ratio (INR). This is our report of a three-year follow-up involving the analysis of data from all laboratories, in hospitals (n=88 in 2002) and primary health care units (n=246 in 2002) that perform the Owren PT assay in Sweden. The interlaboratory variation was significantly improved after the introduction of the new calibration procedure. For the larger hospital-based laboratories, the mean coefficient of variation (CV) was reduced from 7.9% to 5.2% (p<0.0001) when analysing test materials with INR range 2-4. In the higher INR range (>4), the CV was reduced even further, from 10.4% to 6.8% (p<0.0001). The corresponding results from smaller laboratories in the primary health care units showed a similar decrease in CV from 8.2% to 5.7% in the INR range 2-4 (p<0.0001). At the INR range >4, the CV was reduced from 9.5% to 7.8%. The intralaboratory variation was also improved for both types of laboratory categories. This study shows an improved precision, with CV less than 6% at the therapeutic INR range, for both hospital-based laboratories and smaller laboratories in the primary health care system. The results indicate that the Owren PT assay is well suited for local INR calibration employing only two calibrant plasmas in a simplified procedure.
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| 7. |
- Ramström, Sofia, 1973-, et al.
(author)
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Platelet phosphatidylserine exposure and procoagulant activity in clotting whole blood : different effects of collagen,TRAP and calcium ionophore A23187
- 2003
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In: Thrombosis and Haemostasis. - 0340-6245 .- 2567-689X. ; 89:1, s. 132-141
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Journal article (peer-reviewed)abstract
- We have studied the effects of different platelet agonists onphosphatidylserine (PS) exposure and clotting times in bloodwithout anticoagulants. Similar reductions in clotting time wereobtained for collagen, TRAP-6 or calcium ionophore A23187(50 µmol/L), in spite of huge differences in PS expression[6.7 ± 2.4%, 2.3 ± 0.5% and 99.9 ± 0.1%, respectively (mean ±SD, n = 5)]. Furthermore, the clotting times were much longerfor samples with A23187 exposing the same amounts of PS assamples with collagen or TRAP-6. Annexin V reversed theclotting time reduction, but could not prevent coagulation.Addition of phospholipid vesicles containing 20% PS neitheraffected the clotting times nor induced clotting in recalcified,platelet-free plasma.We conclude that platelet PS exposure is necessary, but notsufficient, for the coagulation amplification observed whenplatelets are stimulated via physiological receptors in a wholeblood environment.
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| 8. |
- Tunströmer, Kjersti, 1986-, et al.
(author)
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Quantification of Platelet Contractile Movements during Thrombus Formation
- 2018
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In: Thrombosis and Haemostasis. - New York : Georg Thieme Verlag KG. - 0340-6245 .- 2567-689X. ; 118:09, s. 1600-1611
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Journal article (peer-reviewed)abstract
- Imaging methods based on time-lapse microscopy are important tools for studying the dynamic events that shape thrombus formation upon vascular injury. However, there is a lack of methods to translate the vast amount of visual data generated in such experiments into quantitative variables describing platelet movements that can be subjected to systematic analysis. In this study, we developed experimental and computational protocols allowing for a detailed mathematical analysis of platelet movements within a developing thrombus. We used a flow chamber-based model of thrombosis wherein a collagen strip was used to initiate platelet adhesion and activation. Combining the use of a platelet staining protocol, designed to enable identification of individual platelets, and image processing, we tracked the movements of a large number of individual platelets during thrombus formation and consolidation. These data were then processed to generate aggregate measures describing the heterogeneous movements of platelets in different areas of the thrombus and at different time points. Applying this model and its potential, to a comparative analysis on a panel of platelet inhibitors, we found that total platelet intra-thrombus movements are only slightly reduced by blocking the interactions between glycoproteins IIb/IIIa and Ib and their ligands or by inhibiting thromboxane synthesis or P2Y12 signalling. In contrast, whereas 30 to 40% of the platelets movements (for the CD42a-labelled platelets) and 20% (for the pro-coagulant platelets), within a thrombus, are contractile, i.e., towards the centre of the thrombus, this contractile component is almost totally abolished in the presence of agents inhibiting these pathways.
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| 10. |
- Vretenbrant, Karin, 1979-, et al.
(author)
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Platelet activation via PAR4 is involved in the initiation of thrombin generation and in clot elasticity development
- 2007
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In: Thrombosis and Haemostasis. - 0340-6245 .- 2567-689X. ; 97:3, s. 417-424
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Journal article (peer-reviewed)abstract
- Thrombin is a pivotal enzyme formed in the coagulation cascade and an important and potent platelet activator. The two protease-activated thrombin receptors on human platelets are denoted PARI and PAR4. The physiological relevance of PAR4 is still unclear, as both aggregation and secretion can be accomplished by PAR1 activation alone. In the present study we have investigated the role of PARS in platelet activation, blood coagulation, clot elasticity and fibrinolysis. Flow cytometry, free oscillation rheometry and thrombin generation measurements were used to analyze blood or platelet-rich plasma from healthy individuals. Maximum PAR1 activation with the peptide SFLLRN gave fewer fibrinogen-binding platelets with lower mean fluorescent intensity than maximum PAR4 activation with AYPGKF. Inhibition of any of the receptors prolonged clotting times. However, PAR1 is more important for fibrinolysis, inhibition of this receptor prolonged all the steps in the fibrinolytic process. Clot elasticity decreased significantly when the PAR4 receptor was inhibited. In the thrombin generation measurements, PAR4 inhibition delayed the thrombin generation start and peak, but did not affect the total amount of thrombin generated. PAR1 inhibition had no significant impact on thrombin generation. We found that PAR4 is most likely activated by low concentrations of thrombin during the initial phase of thrombin generation and is of importance to the clotting time. Furthermore, we suggest that the PAR4 receptor may have a physiological role in the stabilisation of the coagulum.
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