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      The impact of blood shear rate on arterial thrombus formation

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          Abstract

          The shear rate and corresponding shear stress have impacts on arterial thrombus formation. In particular, the effects of increasing concentration of platelets at the vessel wall and activation of platelets at this site increase the growth and stability of the thrombi which may result in a fatal narrowing of the arterial lumen. The efficacy of many antithrombotic agents is shear dependent as well. It is apparent that there is a need for a point-of-care device to rapidly monitor the risk for arterial thrombosis and to optimize antithrombotic therapy in vitro. The present review focuses on the essential role of shear rate on arterial thrombus formation in native human blood drawn directly from an antecubital vein.

          Abstract

          Arterial thrombosis formation is to a large extent determined by the physical parameters of arterial blood flow, that is, shear rate and shear stress. In addition, the efficacy of many antithrombotic agents is dependent upon the shear. Consequently, there is a medical need for a rapid global assay to assess prothrombotic risk and antithrombotic treatment that is performed under arterial blood flow conditions, using native blood, which has not been in vitro anticoagulated.

          Most cited references54

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          Aspirin plus dipyridamole versus aspirin alone after cerebral ischaemia of arterial origin (ESPRIT): randomised controlled trial.

          Jan Van Lunzen, Peter J Koudstaal, A Algra … (2006)
          Results of trials of aspirin and dipyridamole combined versus aspirin alone for the secondary prevention of vascular events after ischaemic stroke of presumed arterial origin are inconsistent. Our aim was to resolve this uncertainty. We did a randomised controlled trial in which we assigned patients to aspirin (30-325 mg daily) with (n=1363) or without (n=1376) dipyridamole (200 mg twice daily) within 6 months of a transient ischaemic attack or minor stroke of presumed arterial origin. Our primary outcome event was the composite of death from all vascular causes, non-fatal stroke, non-fatal myocardial infarction, or major bleeding complication, whichever happened first. Treatment was open, but auditing of outcome events was blinded. Primary analysis was by intention to treat. This study is registered as an International Standard Randomised Controlled Trial (number ISRCTN73824458) and with (NCT00161070). Mean follow-up was 3.5 years (SD 2.0). Median aspirin dose was 75 mg in both treatment groups (range 30-325); extended-release dipyridamole was used by 83% (n=1131) of patients on the combination regimen. Primary outcome events arose in 173 (13%) patients on aspirin and dipyridamole and in 216 (16%) on aspirin alone (hazard ratio 0.80, 95% CI 0.66-0.98; absolute risk reduction 1.0% per year, 95% CI 0.1-1.8). Addition of the ESPRIT data to the meta-analysis of previous trials resulted in an overall risk ratio for the composite of vascular death, stroke, or myocardial infarction of 0.82 (95% CI 0.74-0.91). Patients on aspirin and dipyridamole discontinued trial medication more often than those on aspirin alone (470 vs 184), mainly because of headache. The ESPRIT results, combined with the results of previous trials, provide sufficient evidence to prefer the combination regimen of aspirin plus dipyridamole over aspirin alone as antithrombotic therapy after cerebral ischaemia of arterial origin.
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            Analysis of shear stress and hemodynamic factors in a model of coronary artery stenosis and thrombosis.

            D Brands, J Strony, Caroline B. Adelman … (1993)
            Shear stress and alterations in blood flow within a stenosed artery promote platelet-dependent thrombosis. Using the Folts model of coronary thrombosis, we evaluated morphology, histology, and the hemodynamic properties of the stenosed vessel in 18 animals. The average stenosis created was 58 +/- 8%, with stenosed vessel diameters ranging from 0.084 to 0.159 cm. Histological examination of the stenosed vessel demonstrated that thrombi were composed primarily of platelets and formation occurred 1.0 mm downstream from the apex of the constriction, propagating distally. Peak shear stress occurred just upstream from the apex of the stenosis and varied from 520 to 3,349 dyn/cm2. Only small differences in shear forces were noted when blood viscosity was calculated using Newtonian and non-Newtonian properties. In contrast, shear stress computed for Poiseuille flow with use of the stenosis diameter underestimated the apical shear stress. Blood flow remained laminar within the stenosis with a Reynolds number range of 292-534. Our data indicate that the geometry of the stenosis inflow region must be considered in the evaluation of platelet activation and thrombus formation within a stenosed artery.
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              Early potent antithrombotic effect with combined aspirin and a loading dose of clopidogrel on experimental arterial thrombogenesis in humans.

              Y Cadroy, K S Sakariassen, B Boneu … (2000)
              We conducted a double-blind, randomized, crossover study to assess the antithrombotic effects of the combination of aspirin (acetylsalicylic acid, ASA) and clopidogrel, with or without a loading dose, versus ASA alone in a model of arterial thrombosis in humans. Eighteen male volunteers received the following 3 regimens for 10 days separated by a 1-month period: (1) 325 mg ASA daily, (2) 325 mg ASA+75 mg clopidogrel daily, (3) 325 mg ASA daily+300-mg clopidogrel loading dose on day 1 and +75 mg clopidogrel per day on days 2 to 10. The antithrombotic effect was measured 1.5, 6, and 24 hours after drug intake on day 1 and 6 hours after drug intake on day 10. Arterial thrombus formation was induced ex vivo by exposing a collagen-coated coverslip in a parallel-plate perfusion chamber to native blood for 3 minutes at an arterial wall shear rate. Without a loading dose, clopidogrel+ASA developed an antithrombotic effect within 6 hours after the first intake. It was superior to that produced by ASA, but it was moderate (P
              Article 0 comments Cited 27 times – based on 0 reviews     Review now
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                Author and article information

                Journal
                Journal ID (nlm-ta): Future Sci OA
                Journal ID (iso-abbrev): Future Sci OA
                Journal ID (publisher-id): FSO
                Title: Future Science OA
                Publisher: Future Science Ltd (London, UK )
                ISSN (Electronic): 2056-5623
                Publication date Collection: November 2015
                Publication date (Electronic): 01 November 2015
                Volume: 1
                Issue: 4
                Electronic Location Identifier: FSO30
                Affiliations
                [1 ]KellSa s.a.s., Str. Campo e Zampo 12, I-13900 Biella, BI, Italy
                [2 ]Alere Technologies AS, POB 6863 Rodelokka, N-0504 Oslo, Norway
                [3 ]Illinois Institute of Technology, 3440 S. Dearborn Street, Chicago, IL 60616, USA
                Author notes
                *Author for correspondence: kjell.sakariassen@ 123456kellsa.com
                Article
                DOI: 10.4155/fso.15.28
                PMC ID: 5137878
                PubMed ID: 28031903
                SO-VID: bf180349-8f60-4bb4-a446-3170dae34595
                Copyright © © KS Sakariassen
                License:

                This work is licensed under a Creative Commons Attribution 4.0 License

                History
                Categories
                Subject: Review

                Keywords: arterial stenosis,platelet activation,platelet adhesion,platelet aggregation,shear rate,shear stress
                Data availability:
                Keywords: arterial stenosis, platelet activation, platelet adhesion, platelet aggregation, shear rate, shear stress

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