Enhanced platelet aggregation with TRAP-6 and collagen in platelet aggregometry in patients with venous thromboembolism

Weber, Martin; Gerdsen, Frank; Gutensohn, K.; Schoder, Volker; Eifrig, B.; Hossfeld, Dieter K.

doi:10.1016/s0049-3848(02)00351-1

Cited by 22 publications

(23 citation statements)

References 17 publications

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“…In parts, these fi ndings are consistent with our previous investigations [18] . Using platelet aggregometry with high agonist concentrations, we found no platelet hyperreagibility at comparable amounts of ADP in the same populations of patients and normal donors [18] . Only TRAP-6 at a lower concentration of 2 M was able to signifi cantly differentiate between the investigated groups.…”

Section: Discussionsupporting

confidence: 94%

Platelet Activation Markers in Patients with Venous Thromboembolism without Predisposing Factors

Gerdsen¹,

Weber²,

Eifrig³

et al. 2005

Pathophysiol Haemos Thromb

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A constant in vitro hypersensitivity of platelets (adenosine diphosphate) has been suggested as a risk factor for arterial and even venous thrombosis. Our aim was to determine phenotypic and functional alterations of platelets by flow cytometry as potential prothrombotic risk factors in patients with a history of unexplained spontaneous venous thrombosis. Forty-nine patients with a history of spontaneous venous thrombosis and no inherited or acquired thrombophilic risk factors were compared with a reference group of 39 healthy volunteers. Flow cytometry (FACS) was used to analyze the surface expression of CD62 (P-selectin) and CD63 in nonactivated platelets and after in vitro stimulation with adenosine diphosphate and thrombin receptor activator peptide 6. Mean fluorescence intensity of CD62 and CD63 surface expression as well as percentage of CD62 and CD63 positive cells and binding index differed in patients with a history of thrombosis compared with the reference group, but failed to reach statistical significance. Similar results were observed after in vitrostimulation with adenosine diphosphate and thrombin receptor activator peptide 6. In conclusion, the expression of CD62 and CD63 of resting and in vitro activated platelets could not be established as a risk factor for spontaneous venous thromboembolism.

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Section: Discussionsupporting

confidence: 94%

Platelet Activation Markers in Patients with Venous Thromboembolism without Predisposing Factors

Gerdsen¹,

Weber²,

Eifrig³

et al. 2005

Pathophysiol Haemos Thromb

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“…Notably, Weber et al studied patients with unexplained VTE (n=34) for 3 doses each of ADP, epinephrine, collagen and TRAP-6 (a thrombin receptor activating peptide) versus healthy individuals (n=53). [9] They found that ADP (0.58, 1.17, or 2.34 u M) or epinephrine (0.55, 1.1, 11.0 u M) aggregation were not associated with VTE at any of the doses examined. Aggregation to moderate or higher doses of collagen (0.1, 0.25 u M) and TRAP-6 (5.0, 7.5 u M) were not associated with VTE.…”

Section: Discussionmentioning

confidence: 99%

“…However, higher percent aggregation to low dose collagen (0.05 u M) was associated VTE (P=0.00076), as was higher aggregation to low dose TRAP-6 (2.0 u M) (P=0.006). In our current study we did not have data available to evaluate thrombin or low dose collagen effects in order to compare to the results of Weber et al [9], and these pathways of activation were not evaluated by Hayes et al [8]…”

Section: Discussionmentioning

confidence: 99%

“…[6,7] Several small studies have variously reported an exaggerated platelet aggregation response to epinephrine, collagen or thrombin in patients with thrombosis but have not been completely consistent. [8,9] However, to our knowledge, no studies on platelet aggregation measures as prospective predictors of VTE risk have been published to date. Our aim is to describe the role of platelet function at baseline in the development of VTE in the community-based Framingham Heart Study (FHS) cohort.…”

Section: Introductionmentioning

confidence: 99%

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Platelet function as a risk factor for venous thromboembolism in the Framingham Heart Study

Puurunen

Hwang

O’Donnell

et al. 2017

Thrombosis Research

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Introduction The relationship of venous thromboembolism (VTE) with platelet reactivity is unclear. Platelet function plays a key role in arterial thrombosis. Evidence suggests antiplatelet agents also effects in reducing VTE. Our aim is to describe the role of baseline platelet function in development of VTE in the community-based Framingham Heart Study (FHS) cohort. Materials and Methods Participants in the Framingham Offspring cohort fifth examination and Omni cohort first examination were eligible. We used light transmission aggregometry to measure platelet aggregation in response to collagen and a range of ADP and epinephrine doses. The study population consisted of 2831 participants [average age 54.3 y; 57% female]. Results and Conclusions During a median follow-up of 20.4 years, we observed 138 incident VTE events. In age-, sex- and cohort-adjusted analysis an increase in collagen lag time was associated with increased risk for incident VTE (HR 1.01 [1.00–1.02]; p=0.049). Increased maximal aggregation to low dose epinephrine (1.0uM) was associated with lower VTE risk (HR 0.84 [0.71–0.99]; p=0.042]. However, additional multivariable analyses attenuated the collagen-VTE and epinephrine-VTE associations to trends, primarily due to adjustment for baseline body mass index (BMI), a VTE risk factor and potential modifier of platelet function. Secondary analyses considering varying follow-up periods, cancer incidence and interim aspirin use did not dramatically affect the collagen and epinephrine trends observed. Baseline platelet aggregability was only weakly associated with incident VTE, and in a paradoxical direction, in a community-based population. Other markers of platelet function and hemostasis could prove to be more useful predictors.

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“…Although inhibitory effects of statins on platelet function assessed with ex vivo tests of platelet aggregation have been described in patients at risk for cardiovascular disease, the effects of statins on platelet function in patients with a history of VT are unclear [15][16][17]. As enhanced platelet aggregation has been reported in patients with VT [18], and the VerifyNow assay can measure TxA 2 -mediated platelet activation and aggregation, we decided to investigate the effect of rosuvastatin on platelet aggregation in patients with a history of confirmed deep vein thrombosis or pulmonary embolism as measured with the VerifyNow assay.…”

Section: Introductionmentioning

confidence: 99%

Platelet reactivity in patients with venous thrombosis who use rosuvastatin: a randomized controlled clinical trial

Biedermann

Cannegieter

Roest

et al. 2016

Journal of Thrombosis and Haemostasis

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To cite this article: Biedermann JS, Cannegieter SC, Roest M, van der Meer FJM, Reitsma PH, Kruip MJHA, Lijfering WM. Platelet reactivity in patients with venous thrombosis who use rosuvastatin: a randomized controlled clinical trial. J Thromb Haemost 2016; 14: 1404-9. Essentials• Statins, especially rosuvastatin, may reduce venous thrombosis risk, but the mechanism is unclear.• We performed a randomized trial investigating the effect of rosuvastatin on platelet reactivity.• Thromboxane-A2 mediated platelet aggregation was measured before and after rosuvastatin therapy.• Rosuvastatin did not inhibit thromboxane-mediated platelet aggregation in venous thrombosis patients.Summary. Background: Statins may exert a protective effect against the risk of venous thrombosis (VT), but the mechanism is unclear. Objectives: In this open-label, randomized clinical trial (www.clinicaltrials.gov NCT01613794), we aimed to determine the ex vivo effect of rosuvastatin on platelet reactivity in patients with a history of VT. Methods: Platelet reactivity, in platelet reaction units (PRUs), was measured at baseline and after 28 days with VerifyNow, which uses arachidonic acid to determine thromboxane-mediated platelet aggregation, in 50 consecutive patients included in our study (25 receiving rosuvastatin and 25 without intervention). Results: Forty-seven of 50 (94.0%) consecutively enrolled patients had two valid PRU measurements. The mean PRUs in rosuvastatin users were 609 at baseline and 613 at the end of the study (mean change 5; 95% confidence interval [CI] À 18 to 27). The mean PRUs in non-users were 620 at baseline and 618 at the end of the study (mean change À 2; 95% CI À 15 to 12). The mean difference in PRU change between users and non-users was 6 (95% CI À 20 to 33). After exclusion of patients who used antiplatelet medication, or had thrombocytopenia, similar results were obtained, i.e. no apparent effect of rosuvastatin on PRUs, with a mean difference in PRU change between users and non-users of À 1 (95% CI À 20 to 19). Conclusions: Rosuvastatin does not affect platelet reactivity when arachidonic acid is used as an agonist in patients with a history of VT.

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Enhanced platelet aggregation with TRAP-6 and collagen in platelet aggregometry in patients with venous thromboembolism

Cited by 22 publications

References 17 publications

Platelet Activation Markers in Patients with Venous Thromboembolism without Predisposing Factors

Platelet Activation Markers in Patients with Venous Thromboembolism without Predisposing Factors

Platelet function as a risk factor for venous thromboembolism in the Framingham Heart Study

Platelet reactivity in patients with venous thrombosis who use rosuvastatin: a randomized controlled clinical trial

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