Assessment of platelet function in patients with stroke using multiple electrode platelet aggregometry: a prospective observational study.

Ahmed Sabra,Sharon Storton,Mushtaq Wani,John F Potter,Lindsay D’Silva,Sophia N Stanford,Roger H K Morris,Phillip A Evans,Matthew Lawrence,Vanessa Evans

doi:10.1186/s12883-016-0778-x

Abstract

BackgroundThere is a link between high on-treatment platelet reactivity (HPR) and adverse vascular events in stroke. This study aimed to compare multiple electrode platelet aggregometry (MEA), in healthy subjects and ischaemic stroke patients, and between patients naive to antiplatelet drugs (AP) and those on regular low dose AP. We also aimed to determine prevalence of HPR at baseline and at 3–5 days after loading doses of aspirin.MethodsPatients with first ever ischaemic stroke were age and sex-matched to a healthy control group. Three venous blood samples were collected: on admission before any treatment given (baseline); at 24 h and 3–5 days after standard treatment. MEA was determined using a Mutliplate® analyser and agonists tested were arachidonic acid (ASPI), adenosine diphosphate (ADP) and collagen (COL).ResultsSeventy patients (mean age 73 years [SD 13]; 42 men, 28 women) were age and sex-matched to 72 healthy subjects. Thirty-three patients were on antiplatelet drugs (AP) prior to stroke onset and 37 were AP-naive. MEA results for all agonists were significantly increased in AP-naive patients compared to healthy subjects: ADP 98 ± 31 vs 81 ± 24, p < 0.005; ASPI 117 ± 31 vs 98 ± 27, p < 0.005; COL 100 ± 25 vs 82 ± 20, p < 0.005. For patients on long term AP, 33% (10/30) of patients were considered aspirin-resistant. At 3–5 days following loading doses of aspirin, only 11.1% were aspirin resistant based on an ASPI cut-off value of 40 AU*min.ConclusionsMany patients receiving low dose aspirin met the criteria of aspirin resistance but this was much lower at 3–5 days following loading doses of aspirin. Future studies are needed to establish the causes of HPR and potential benefits of individualizing AP treatment based on platelet function testing.

Highlights

There is a link between high on-treatment platelet reactivity (HPR) and adverse vascular events in stroke
Stroke patients were matched for sex and age with 72 healthy subjects recruited from the same population as the stroke patients
The emergence of new P2Y12 antagonists and ongoing uncertainties of platelet function testing dictate the need for larger Randomised control trial (RCT) to answer these questions and investigate the clinical benefit of antiplatelet drugs (AP) switching strategy in stroke patients based on multiple electrode platelet aggregometry (MEA) results

Summary

Introduction

There is a link between high on-treatment platelet reactivity (HPR) and adverse vascular events in stroke. Despite the effectiveness of aspirin in the primary and secondary prevention of atherothrombotic disease, patients continue to suffer recurrent thromboembolic vascular events whilst on AP treatment [16]. This recurrence has been associated with high on-treatment platelet reactivity (HPR), with up to more than 60% of subjects being reported to be resistant to antiplatelet therapy (aspirin or clopidogrel) [17, 18]. This study aimed to compare platelet function, as determined by MEA, in healthy subjects and stroke patients prior to treatment initiation and between patients naive to AP therapy and those on regular low dose aspirin or clopidogrel

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