ArticleThe journal of trauma and acute care surgery2020
Identification of injury and shock driven effects on ex vivo platelet aggregometry: A cautionary tale of phenotyping.
Article in The journal of trauma and acute care surgery, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 21 citations in OpenAlex.
- Platelets and inflammation-insights from platelet non-coding RNA content and release in the Bruneck study and the PACMAN-AMI trial.Cardiovascular research · 2025Trial
- CD63 Immunological Activation Versus Hemostatic Function: Platelet Alterations After Polytrauma.Current issues in molecular biology · 2025Article
- Microfluidics in Assessing Platelet Function.Journal of visualized experiments : JoVE · 2024Article
- Blood failure: traumatic hemorrhage and the interconnections between oxygen debt, endotheliopathy, and coagulopathy.Clinical and experimental emergency medicine · 2024Article
- Severe Trauma-Induced Coagulopathy: Molecular Mechanisms Underlying Critical Illness.International journal of molecular sciences · 2023Review
- How to manage coagulopathies in critically ill patients.Intensive care medicine · 2023Review
- Effects of the circulating environment of COVID-19 on platelet and neutrophil behavior.Frontiers in immunology · 2023Article
- "Importance of catecholamine signaling in the development of platelet exhaustion after traumatic injury": Reply.Journal of thrombosis and haemostasis : JTH · 2022Article
- Importance of catecholamine signaling in the development of platelet exhaustion after traumatic injury.Journal of thrombosis and haemostasis : JTH · 2022Article
- Review
- Platelet-mimicking procoagulant nanoparticles augment hemostasis in animal models of bleeding.Science translational medicine · 2022Article
- Trauma-induced coagulopathy.Nature reviews. Disease primers · 2021Review
- Platelet Proteomes, Pathways, and Phenotypes as Informants of Vascular Wellness and Disease.Arteriosclerosis, thrombosis, and vascular biology · 2021Review
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
backgroundPlatelet behavior in trauma-induced coagulopathy is poorly understood. Injured patients have impaired platelet aggregation (dysfunction) in ex vivo agonist-stimulated platelet aggregometry (PA). However, PA assumes that platelets are inactivated before ex vivo stimulated aggregation, which may be altered by injury. We hypothesized that following trauma, platelet aggregation (area under the curve) is decreased regardless of injury burden, but that (1) minor injury is associated with an increased baseline electrical impedance, characteristic of a functional platelet phenotype (platelets that activate in response to injury), and that (2) severe injury is not associated with an increased baseline electrical impedance, characteristic of a dysfunctional phenotype (platelets that do not activate well in response to injury) compared with healthy controls.
methodsBlood from 458 trauma patients and 30 healthy donors was collected for PA. Baseline electrical impedance (Ω); platelet aggregation stimulated by adenosine diphosphate, collagen, thrombin, and arachidonic acid; and rotational thromboelastometry were measured. Multivariate regression was performed to identify associations of PA measures with blood transfusion.
resultsCompared with healthy controls, injured patients had impaired platelet aggregation in response to ex vivo stimulation, regardless of injury burden. However, minorly injured patients had increased endogenous platelet activation (baseline electrical impedance, Ω: with shock, p = 0.012; without shock, p = 0.084), but severely injured patients did not have significant increases in endogenous platelet activation (baseline electrical impedance, Ω: with shock, p = 0.86; without shock, p = 0.37). For every 10 Ω increase in baseline electrical impedance, there was an 8% decrease in units of blood transfused in the first 24 h (-0.08; confidence interval, -0.14 to -0.02; p = 0.015).
conclusionInjury and shock confer differential patterns of platelet aggregation in PA. Minor injury overestimates the presence of platelet dysfunction, while severe injury induces a truly dysfunctional phenotype-platelets that do not activate nor aggregate appropriately after injury. This is consequential in improving accurate phenotyping of postinjury platelet behavior for platelet-based therapeutics. LEVEL OF EVIDENCE: Prognostic, level IV.
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