Platelet hyperaggregability and venous thrombosis risk: results from the RETROVE project.
Journal
Blood coagulation & fibrinolysis : an international journal in haemostasis and thrombosis
ISSN: 1473-5733
Titre abrégé: Blood Coagul Fibrinolysis
Pays: England
ID NLM: 9102551
Informations de publication
Date de publication:
01 03 2021
01 03 2021
Historique:
pubmed:
19
12
2020
medline:
27
5
2021
entrez:
18
12
2020
Statut:
ppublish
Résumé
The aim of the study was to determine whether platelet hyperaggregability correlates with short closure times (PFA-100) and if hyperaggregability is associated with the risk of venous thrombosis in a Spanish population. Case--control study (RETROVE project) involving 400 patients with venous thrombosis and 400 healthy controls. We determined platelet aggregation in platelet-rich plasma (PRP) by light transmission aggregometry. Various concentrations of two aggregation agonists [ADP and epinephrine (EPI)] were tested to determine the percentage of maximal aggregation and the percentage area under the curve (AUC). Venous thrombosis risk associated with platelet hyperaggregability was calculated by logistic regression. We estimated the crude and adjusted (by sex and age) odds ratios (OR) for venous thrombosis risk. An agonist concentration of 0.5 μmol/l differentiated between hypo-responders and hyper-responders at the following AUC cut-off values: EPI: the 50th percentile for aggregation with 0.5 μmol/l of EPI (EPI_AUC) was 22.53% (>22.53% = hyper-EPI); the crude risk for venous thrombosis was statistically significant (OR = 1.37; 95% CI 1.03-1.82); ADP: the 75th percentile for aggregation with 0.5 μmol/l of ADP (ADP_AUC) was 29.6% (>29.6% = hyper-ADP), with a significant crude risk for venous thrombosis (OR = 1.44; 95% CI 1.05-1.98). However, after adjustment for confounders (age), the ORs for EPI or ADP aggregation were no longer significant. EPI_AUC and PFA-100 values with the EPI agonist were significantly correlated (R = -0.342, P < 0.01). Only 12% of the PFA-100 values were explained by platelet aggregation. In this case--control study, platelet hyperaggregability was not associated with the risk of developing venous thrombosis.
Identifiants
pubmed: 33337623
doi: 10.1097/MBC.0000000000001006
pii: 00001721-202103000-00007
doi:
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
122-131Informations de copyright
Copyright © 2020 Wolters Kluwer Health, Inc. All rights reserved.
Références
Holiday PL, Mammen E, Gilroy J. Sticky platelet syndrome and cerebral infarction in young adults. Paper presented at: The Ninth International Joint Conference on Stroke and Cerebral Circulation 1983; Phoenix, AZ, USA.
Kubisz P, Stasko J, Holly P. Sticky platelet syndrome. Semin Thromb Hemost 2013; 39:674–683.
Al-Mefty O, Marano G, Rajaraman S, Nugent GR, Rodman N. Transient ischemic attacks due to increased platelet aggregation and adhesiveness. Ultrastructural and function correlation. J Neurosurg 1979; 50:449–453.
Bick RL. Sticky platelet syndrome: a common cause of unexplained arterial and venous thrombosis. Clin Appl Thromb/Hemost 1998; 4:77–81.
Mammen EF. Ten years’experience with the sticky platelet syndrome. Clin Appl Thromb/Hemost 1995; 1:66–72.
Frenkel EP, Mammen EF. Sticky platelet syndrome and thrombocythemia. Hematol Oncol Clin N Am 2003; 17:63–83.
Bick RL. Recurrent miscarriage syndrome due to blood coagulation protein/platelet defects: prevalence, treatment and outcome results. DRW Metroplex Recurrent Miscarriage Syndrome Cooperative Group. Clin Appl Thromb Hemost 2000; 6:115–125.
Mühlfeld AS, Ketteler M, Schwamborn K, et al. Sticky platelet syndrome: an underrecognized cause of graft dysfunction and thromboembolic complications in renal transplant recipients. Am J Transplant 2007; 7:1865–1868.
Hayes C, Kitahara S, Tcherniantchouk O. Decreased threshold of aggregation to low-dose epinephrine is evidence of platelet hyperaggregability in patients with thrombosis. Hematol Rep 2002; 6:325–328.
Yee DL, Sun CW, Bergeron AL, Dong J-F, Bray PF. Aggregometry detects platelet hyperreactivity in healthy individuals. Blood 2005; 106:2723–2729.
Yee DL, Bergeron AL, Sun CW, Dong J-F, Bray PF. Platelet hyperreactivity generalizes to multiple forms of stimulation. J Thromb Haemost 2006; 4:2043–2050.
Berger JS, Becker RC, Kuhn C, Helms MJ, Ortel TL, Williams R. Hyperrreactive platelet phenotypes: relationship to altered serotonin transporter number, transport kinetics and intrinsic response to adrenergic co-stimulation. Thromb Haemost 2013; 109:85–92.
Mammen EF. Sticky platelet syndrome. Semin Thromb Hemost 1999; 25:361–365.
Pujol-Moix N, Martinez-Perez A, Sabater-Lleal M, Llobet D, Vilalta N, Hamsten A, et al. Influence of ABO locus on PFA-100 collagen-ADP closure time is not totally dependent on the Von Willebrand factor. Results of a GWAS on GAIT-2 Project phenotypes. Int J Mol Sci 2019; 20:3221.
Moenen CJI, Vries MJA, Nelemans PJ, van Rooy KJM, Vranken JRRA, Verhezen PWM, et al. Screening for platelet function disorders with multiplate and platelet function analyzer. Platelets 2019; 30:81–87.
Hayward CPM. Practical manual: platelets. Chapter: laboratory diagnosis of platelet disorders.
Vázquez-Santiago M, Vilalta N, Cuevas B, Murillo J, Llobet D, Macho R, et al. Short closure time values in PFA-100 are related to venous thrombotic risk. Results from the RETROVE Study. Thromb Res 2018; 169:57–63.
Jilma B. Platelet function analyzer (PFA-100): a tool to quantify congenital or acquired platelet dysfunction. J Lab Clin Med 2001; 138:152–163.
Favaloro EJ. Clinical utility of the PFA-100. Semin Thromb Hemost 2008; 34:709–733.
Trip MD, Cats VM, van Capelle FJ, Vreeken J. Platelet hyperreactivity and prognosis in survivors of myocardial infarction. N Engl J Med 1990; 322:1549–1554.
Kabbani SS, Watkins MW, Ashikaga T, et al. Platelet reactivity characterized prospectively: a determinant outcome 90 days after percutaneous coronary intervention. Circulation 2001; 104:181–186.
Kabbani SS, Watkins MW, Ashikaga T, Terrien EF, Sobel BE, Schneider DJ. Usefulness of platelet reactivity before percutaneous coronary intervention in determining cardiac risk one year later. Am J Cardiol 2003; 91:876–878.
Konstantopoulos K, Grotta JC, Sills C, Wu KK, Hellums JC. Shear-induced platelet aggregation in normal subjects and stroke patients. Thromb Haemost 1995; 74:1329–1334.
Vanschoonbeek K, Feijge MA, Keuren JF, Coenraad Hemker H, Lodder JJ, Hamulyák K, et al. Thrombin-induced hyperactivity of platelets of young stroke patients: involvement of thrombin receptors in the subject-dependent variability in Ca 2+ signal generation. Thromb Haemost 2002; 88:931–937.
Puurunen MK, Hwang S-J, O’Donnell CJ, Tofler G, Johnson AD. Platelet function as a risk for venous thromboembolism in the Framingham Heart Study. Thromb Res 2017; 151:15157–15162.
Martinez C, Cohen AT, Bamber L, Rietbrock S. Epidemiology of first and recurrent venous thromboembolism: a population-based cohort study in patients without active cancer. Thromb Haemost 2014; 112:255–263.
Kearon C, Ageno W, Cannegieter SC, Cosmi B, Geersing GJ, Kyrle PA. Subcommittees on Control of Anticoagulation, and Predictive and Diagnostic Variables in Thrombotic Disease. Categorization of patients as having provoked or unprovoked venous thromboembolism: guidance from the SSC of ISTH. J Thromb Haemost 2016; 14:1480–1483.
CLSI Standardization of Platelet Fuction testing. CLSI Approved guideline H58-P. Ledford-Kraemer M. 2007
Prandoni P. Venous and arterial thrombosis: two aspects of the same disease? Eur J Intern Med 2009; 20:660–661.
Previtali E, Bucciarelli P, Passamonti SM, Martinelli I. Risk factors for venous and arterial thrombosis. Blood Transfus 2011; 9:120–138.
Favaloro EJ, Franchini M, Lippi G. Aging hemostasis: changes to laboratory markers of hemostasis as we age-a narrative review. Semin Thromb Hemost 2014; 40:621–633.
Weber M, Gerdsen F, Guttensohn K, Schoder V, Eifrig B, Hossfeld DK. Enhanced platelet aggregation with TRAP-6 and collagen in platelet aggregometry in patients with venous thromboembolism. Thromb Res 2002; 107:325–328.
Tekgunduz E, Demir M, Akyol Erikci A, Akpinar S, Ozturk E, Kirkizlar O. Sticky platelet syndrome in patients with uninduced venous thrombosis. Turk J Hematol 2011; 30:48–52.
Campello E, Spieza L, Zabeo E, Maggiolo S, Vettor R, Simioni P. Hypercoagulability detected by whole blood thromboelastometry (ROTEM®) and impedance aggregometry (MULTIPLATE®) in obese patients. Thromb Res 2015; 135:548–553.
Lundström A, Wallén H, von Arbin M, Jörneskog G, Gigante B, Dembrower KH, et al. Clopidogrel resistance after minor ischemic stroke or transient ischemic attack is associated with radiological cerebral small-vessel disease. J Stroke Cerebrovasc Dis 2015; 24:2348–2357.
Lundström A, Laska AC, von Arbin M, Jörneskog G, Wallén H. Glucose intolerance and insulin resistance as predictors of low platelet response to Clopidogrel in patients with minor ischemic stroke or TIA. Platelets 2014; 25:102–110.
Sokol J, Skerenova M, Jedinakova Z, Simurda T, Skonorva I, Stasko J, Kubitz P. Progress in the understanding of sticky platelet syndrome. Semin Thromb Hemost 2017; 43:8–13.
Castilloux JF, Moffat KA, Liu Y, Seecharan J, Pai M, Hayward CPM. A prospective cohort study of light transmission platelet aggregometry for bleeding disorders: is testing native platelet-rich plasma noninferior to testing platelet count adjusted samples? Thromb Haemost 2011; 106:675–682.
Mani H, Luxembourg B, Kläffling C, Erbe M, Lindhoff-Last E. Use of native or platelet count adjusted platelet rich plasma for platelet aggregation measurements. J Clin Pathol 2005; 58:747–750.
Vázquez-Santiago M, Vilalta N, Ziyatdinov A, Cuevas B, Macho R, Pujol-Moix N, et al. Platelet count and plateletcrit are associated with an increased risk of venous thrombosis in females. Results from the RETROVE study. Thromb Res 2017; 157:162–164.
Llobet D, Vallve C, Tirado I, Vilalta N, Murillo J, Cuevas B, et al. VAMP8 and serotonin transporter levels are associated with venous thrombosis risk in a Spanish female population. Results from the RETROVE project. Thromb Res 2019; 181:99–105.