Relationship between acute stroke outcome, aspirin resistance, and humoral factors

Lai, Ping-Tsun; Chen, Shu‐Yi; Lee, Yu-Sun; Chiang, Yi-Ying; Hsu, Hung‐Yi

doi:10.1016/j.jcma.2012.07.005

Cited by 13 publications

(20 citation statements)

References 40 publications

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“…While well described in the prevention of stroke related to atherosclerosis, APDs have also been shown to reduce the risk of cardioembolic stroke and small deep infarct [13] . This benefit could be related to an inhibition of the first phase of coagulation and reduction of microthrombi [14,15] and partly explain the trend toward an increased frequency of cardioembolic stroke in APDR patients observed in this study as well as by Lai et al [7] . Interestingly, we confirmed the potential increase in stroke severity in patients resistant to APD previously as reported by Zheng et al [16] .…”

Section: Discussionsupporting

confidence: 74%

“…Another reason may be the presence of non-atherothrombotic causes of cerebrovascular events that are not expected to be efficiently prevented by APD, such as cardioembolic diseases or lipohyalinosis [3] . Few studies investigated the association between stroke subtype and APD biological efficacy, and they provided heterogeneous results [6][7][8] . All of them used the TOAST classification to describe stroke mechanism [9] .…”

Section: Introductionmentioning

confidence: 99%

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Interest of Antiplatelet Drug Testing after an Acute Ischemic Stroke

Coignion

Poli²,

Sagnier

et al. 2015

Eur Neurol

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Background: Stroke occurrence despite chronic antiplatelet drug (APD) treatment is frequent. We aimed at evaluating the relevance of platelet aggregation testing in the identification of stroke etiology in this context. Methods: Patients admitted for a suspected acute ischemic stroke, while under APD (aspirin and/or clopidogrel), were prospectively included. The efficacy of the APD was evaluated using a Multiplate™ assay. Resistance was confirmed using light transmission aggregometry. A standardized diagnostic work-up was performed to identify stroke mechanism according to the TOAST and the ASCO classifications. We evaluated the influence of APD functional status on stroke severity and identified potential determinants of resistance. Results: APD resistance was observed in 53 of the 287 patients (18.5%). No difference in stroke mechanism depending on APD efficacy was observed. Patients sensitive to APD had less severe initial stroke severity (mean National Institutes of Health Stroke Scale 3.9 ± 5.6 vs. 7.2 ± 6.8; p < 0.01). Main determinants for APD resistance were a worse control of the diabetes and higher baseline levels of inflammation (mean CRP 26.4 ± 56.0 vs. 9.3 ± 21.0; p < 0.01). Conclusions: Platelet function testing does not provide orientation concerning stroke mechanism in patients who were previously on APDs. However, the high frequency of APD resistance and its association with inflammation and stroke severity are confirmed.

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Section: Discussionsupporting

confidence: 74%

Section: Introductionmentioning

confidence: 99%

Interest of Antiplatelet Drug Testing after an Acute Ischemic Stroke

Coignion

Poli²,

Sagnier

et al. 2015

Eur Neurol

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“…None of the studies published to date have been adequately powered to definitively comment on whether ex vivo HTPR status on platelet function testing in CVD patients predicts the risk of recurrent vascular events. Evidence pertaining to the relationship between antiplatelet-HTPR status and functional outcome, stroke severity and mortality on antiplatelet therapy following TIA or stroke is emerging, but available data from small-medium sized studies need to be validated in larger studies [51,64,66,92,93]. Furthermore, with the exception of three studies [45,51,64], duration of clinical follow-up has been relatively short.…”

Section: Discussionmentioning

confidence: 99%

“…Lai et al prospectively recruited 269 Taiwanese patients within 7 days of ischaemic stroke onset who were on 100 mg aspirin daily for 45 days before assessment [66]. Thirty-one per cent of patients had aspirin-HTPR on the C-EPI cartridge using a cross-sectional definition of HTPR in 3.8% citrate-anticoagulated blood.…”

mentioning

confidence: 99%

Platelet function testing in transient ischaemic attack and ischaemic stroke: A comprehensive systematic review of the literature

et al. 2015

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The majority of patients with ischaemic cerebrovascular disease (CVD) are not protected from further vascular events with antiplatelet therapy. Measurement of inhibition of platelet function ex vivo on antiplatelet therapy, using laboratory tests that correlate with the clinical effectiveness of these agents, would potentially enable physicians to tailor antiplatelet therapy to suit individuals. A systematic review of the literature was performed to collate all available data on ex vivo platelet function/reactivity in CVD patients, especially those treated with aspirin, dipyridamole or clopidogrel. Particular emphasis was paid to information from commonly available whole blood platelet function analysers (PFA-100 Õ , VerifyNow Õ and Multiplate Õ ). Data on pharmacogenetic mechanisms potentially influencing high on-treatment platelet reactivity (HTPR) on antiplatelet therapy in CVD were reviewed. Two-hundred forty-nine potentially relevant articles were identified; 93 manuscripts met criteria for inclusion. The prevalence of ex vivo HTPR in CVD varies between 3-62% with aspirin monotherapy, 8-61% with clopidogrel monotherapy and 56-59% when dipyridamole is added to aspirin in the early, subacute or late phases after TIA/stroke onset. The prevalence of HTPR on aspirin was higher on the PFA-100 than on the VerifyNow in one study (p50.001). Furthermore, the prevalence of HTPR on aspirin was lower when one used 'novel longitudinal' rather than 'cross-sectional, case-control' definitions of HTPR on the PFA early after TIA or stroke (p ¼ 0.003; 1 study). Studies assessing the influence of genetic polymorphisms on HTPR in CVD patients are limited, and need validation in large multicentre studies. Available data illustrate that an important proportion of CVD patients have ex vivo HTPR on their prescribed antiplatelet regimen, and that the prevalence varies depending on the definition and assay used. Large, adequately-sized, prospective multicentre collaborative studies are urgently needed to determine whether comprehensive assessment of HTPR at high and low shear stress with a range of user-friendly whole blood platelet function testing platforms, in conjunction with pharmacogenetic data, improves our ability to predict the risk of recurrent vascular events in CVD patients, and thus enhance secondary prevention following TIA or ischaemic stroke.

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“…13,14 In the current issue of the Journal of the Chinese Medical Association, Lai et al report a relationship between biochemical AR and functional outcome following an acute ischemic stroke. 15 Demographic data, vascular risk factors, and inflammatory biomarkers were analyzed prospectively in 269 patients. Biochemical AR after 5 days of aspirin use was assessed using a PFA-100 instrument equipped with an epinephrine/collagen cartridge.…”

mentioning

confidence: 99%