Desmopressin<i>in vitro</i>effects on platelet function, monitored with Multiplate, ROTEM and Sonoclot

Jensen, Hanna; Kander, Thomas; Schött, Ulf

doi:10.3109/00365513.2016.1149615

Cited by 12 publications

(5 citation statements)

References 39 publications

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“…If this had had any reversal effect on ASA-mediated platelet inhibition it could not be measured with MEA. This is in line with a previous study by Pearson et al that failed to demonstrate an effect of DDAVP added invitro [20]. Weber et al used MEA with ASPItest® to investigate the effect of intravenously administered DDAVP in patients currently not treated with platelet inhibitors but who had suspected postoperative platelet dysfunction after coronary artery bypass grafting [47].…”

Section: Discussionsupporting

confidence: 83%

“…A p-value of <0.05 was considered significant. As gender has been described to affect platelet function, [20] a subgroup analysis with a Mann Whitney test of gender differences was also performed, analyzing Delta differences between before ASA and at 120 minutes for ASPItest®, COLtest®, and ASPI® with DDAVP.…”

Section: Statisticsmentioning

confidence: 99%

“…Desmopressin has also been used to reverse ASA effects on platelets [19]. DDAVP has also been proposed to have direct effects on platelets, but in a study from our laboratory, MEA failed to demonstrate any in vitro effect of desmopressin on whole blood platelet aggregation in healthy volunteers with no platelet inhibiting drugs [20].…”

Section: Introductionmentioning

confidence: 95%

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Time to peak effect of aspirin-induced platelet inhibition and ex vivo effects of desmopressin: an observational study

Schött¹,

Sigurjonsdóttir²,

Thomas³

et al. 2021

J Integr Cardiol

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Objective: To investigate the time to maximal platelet inhibition after an oral loading dose of ASA. The effect of ex vivo reversal platelet inhibition by desmopressin (DDAVP) was also studied.Methods: Ten healthy volunteers were given a 300 mg ASA-tablet. Blood was sampled at 0, 15, 30, 60, 120, and 180 minutes. DDAVP was added to the samples taken at 120 minutes.Samples were analyzed with a Multiplate® platelet aggregometer (MEA) using arachidonic acid (AA), collagen, and thrombin aggregation agonists.Results: Platelet inhibition was observed in the sample activated by AA at 15 minutes but not until 120 minutes in the samples activated by collagen. No platelet inhibition was seen in the samples activated by thrombin. The median time to maximal AA-induced platelet inhibition of <30 U was 30 (interquartile range 15-90) minutes. Ex vivo DDAVP did not reverse platelet inhibition. Subgroup analysis did not show any gender differences.Conclusions: ASA induces a strong platelet inhibition within 30 minutes of oral ingestion, with no gender differences. Ex vivo DDAVP did not reverse ASA's platelet inhibition.

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Section: Discussionsupporting

confidence: 83%

Section: Statisticsmentioning

confidence: 99%

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Time to peak effect of aspirin-induced platelet inhibition and ex vivo effects of desmopressin: an observational study

Schött¹,

Sigurjonsdóttir²,

Thomas³

et al. 2021

J Integr Cardiol

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“…Identification of impaired platelet function with a PFA-100® [834] or MEA [835] might be helpful in the identification of patients who could benefit from desmopressin therapy. In contrast, desmopressin did not improve platelet function measured with three different devices (MEA, ROTEM® and Sonoclot®) in vitro [836].…”

Section: Resultsmentioning

confidence: 99%

The European guideline on management of major bleeding and coagulopathy following trauma: fifth edition

et al. 2019

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Background: Severe traumatic injury continues to present challenges to healthcare systems around the world, and post-traumatic bleeding remains a leading cause of potentially preventable death among injured patients. Now in its fifth edition, this document aims to provide guidance on the management of major bleeding and coagulopathy following traumatic injury and encourages adaptation of the guiding principles described here to individual institutional circumstances and resources. Methods: The pan-European, multidisciplinary Task Force for Advanced Bleeding Care in Trauma was founded in 2004, and the current author group included representatives of six relevant European professional societies. The group applied a structured, evidence-based consensus approach to address scientific queries that served as the basis for each recommendation and supporting rationale. Expert opinion and current clinical practice were also considered, particularly in areas in which randomised clinical trials have not or cannot be performed. Existing recommendations were reexamined and revised based on scientific evidence that has emerged since the previous edition and observed shifts in clinical practice. New recommendations were formulated to reflect current clinical concerns and areas in which new research data have been generated. Results: Advances in our understanding of the pathophysiology of post-traumatic coagulopathy have supported improved management strategies, including evidence that early, individualised goal-directed treatment improves the outcome of severely injured patients. The overall organisation of the current guideline has been designed to reflect the clinical decision-making process along the patient pathway in an approximate temporal sequence. Recommendations are grouped behind the rationale for key decision points, which are patient-or problem-oriented rather than related to specific treatment modalities. While these recommendations provide guidance for the diagnosis and treatment of major bleeding and coagulopathy, emerging evidence supports the author group's belief that the greatest outcome improvement can be achieved through education and the establishment of and adherence to local clinical management algorithms. Conclusions: A multidisciplinary approach and adherence to evidence-based guidance are key to improving patient outcomes. If incorporated into local practice, these clinical practice guidelines have the potential to ensure a uniform standard of care across Europe and beyond and better outcomes for the severely bleeding trauma patient.

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“…9 10 Horstman et al reported on the formation of platelet-derived microparticles (PMPs) and the initiation of a procoagulant state. 11 More recently, Pearson et al 12 observed that DDAVP did not increase normal platelet coagulation functions (thromboelastography, Multiplate and Sonoclot) in vitro . Besides, Swieringa et al 13 showed that in vivo administration of DDAVP caused an increase in collagen-dependent thrombus formation and phosphatidylserine exposure.…”

Section: Introductionmentioning

confidence: 99%

Effect of DDAVP on Platelet Activation and Platelet-Derived Microparticle Generation

et al. 2021

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Background The way by which 1-deamino-8-D-arginine vasopressin (DDAVP) acts on platelets remains unclear. Data from the literature tend to show that there is no definite effect on platelet activation, but recent work has suggested that a subtype of platelets, activated by the combined action of collagen and thrombin, was triggered by DDAVP. Moreover, platelet microparticles (PMPs), which have been shown to be procoagulant, have rarely been studied in this context. The goal of this study was to analyze the effects of DDAVP on PMPs' release through platelet activation. Methods Fifteen out of 18 consecutive patients undergoing a therapeutic test with DDAVP were included. They were suffering from factor VIII deficiency or from von Willebrand disease. The expression of P-selectin and PAC-1 binding on platelets and the numbers of circulating PMPs were evaluated ex vivo before and after DDAVP infusion. Peripheral blood was collected on CTAD to limit artifactual platelet activation. Results DDAVP induced a significant decrease of platelet counts and volume. Only small changes of P-selectin expression and PAC-1 binding were observed. Considering PMPs, two populations of patients could be defined, respectively, with (120%, n = 6) or without (21%, n = 7) an increase of PMPs after DDAVP. The decrease in platelet counts and volume remained significant in the group of responders. Conclusion This study shows that DDAVP induces the generation/release of PMPs in some patients with factor VIII deficiency and von Willebrand disease 1 hour after DDAVP infusion.

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Desmopressinin vitroeffects on platelet function, monitored with Multiplate, ROTEM and Sonoclot

Cited by 12 publications

References 39 publications

Time to peak effect of aspirin-induced platelet inhibition and ex vivo effects of desmopressin: an observational study

Time to peak effect of aspirin-induced platelet inhibition and ex vivo effects of desmopressin: an observational study

The European guideline on management of major bleeding and coagulopathy following trauma: fifth edition

Effect of DDAVP on Platelet Activation and Platelet-Derived Microparticle Generation

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