Assessment of platelet function assays

Nicholson, Nancy S.; Panzer‐Knodle, Susan G.; Haas, Neal F.; Taite, Beatrice B.; Szalony, James A.; Page, Jimmy D.; Feigen, Larry P.; Lansky, David M.; Salyers, Anita K.

doi:10.1016/s0002-8703(98)70245-5

Cited by 147 publications

(99 citation statements)

References 7 publications

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“…Platelet aggregation was measured by OPA methods 24) . In brief, whole-blood specimens were centrifuged at 200 g for 10 min to obtain platelet-rich plasma.…”

Section: Platelet Aggregation Testingmentioning

confidence: 99%

“…The stable thromboxane metabolite 11-dehydrothromboxane B2 (11-DTXB2) reflects in vivo platelet activation 8) and can be measured in plasma or urine. This metabolite is useful in platelet aggregometry (OPA) 24) , (ii) bleeding time 25) , (iii) platelet function analysis (PFA) 26) , (iv) the VerifyNow Aspirin system 27) , and (v) determination of serum TXB2 or urinary 11-DTXB2 levels 28) . Each method has its own advantages and disadvantages 29,30) .…”

Section: Introductionmentioning

confidence: 99%

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Platelet Response to Aspirin in Chinese Stroke Patients is Independent of Genetic Polymorphisms of COX-1 C50T and COX-2 G765C

Zhou

Lin

et al. 2013

JAT

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Aim: Aspirin resistance (AR) is common in Chinese stroke patients taking antiplatelet medications; however, few studies have documented the role of cyclooxygenase (COX)-1 C50T and COX-2 G765C polymorphisms in AR. The aim of this study was to investigate the prevalence of AR in Chinese stroke patients and the relationships between AR and COX-1 C50T and COX-2 G765C polymorphisms, and to evaluate the effect of these polymorphisms on platelet response to aspirin. Methods: We prospectively enrolled 634 Chinese stroke patients. Platelet aggregation testing was performed before and after aspirin administration. The pre-and post-aspirin levels of 11-dehydrothromboxane B2 (11-dTxB2) were determined in urine samples. COX-1 C50T and COX-2 G765C genotypes were determined by a polymerase chain reaction-allelic restriction assay. Results: AR was detected in 129 patients (20.4%), aspirin semi-resistance (ASR) was detected in 28 patients (4.4%), and aspirin sensitivity (AS) was detected in 477 patients (75.2%). There was no association between COX-1 C50T or COX-2 G765C polymorphisms and ASR＋AR. Aspirin could efficiently reduce 11-dTxB2 production by approximately 75%. In addition, platelet aggregation, both in response to arachidonic acid (AA) and adenosine 5'-diphosphate (ADP), was inhibited by more than 80% and 40%, respectively; however, the percentage reduction in platelet aggregation and 11-dTxB2 levels was not significantly different between the COX-1 C50T and COX-2 G765C genotypes (p＞0.05). Conclusions: There was no association between COX-1 C50T and COX-2 G765C polymorphisms and AR in Chinese stroke patients. In addition, COX-1 C50T and COX-2 G765C polymorphisms had no effect on the platelet response to aspirin. J Atheroscler Thromb, 2013; 20:65-72.

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“…Platelet aggregation was measured by OPA methods 24) . In brief, whole-blood specimens were centrifuged at 200 g for 10 min to obtain platelet-rich plasma.…”

Section: Platelet Aggregation Testingmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Platelet Response to Aspirin in Chinese Stroke Patients is Independent of Genetic Polymorphisms of COX-1 C50T and COX-2 G765C

Zhou

Lin

et al. 2013

JAT

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“…Light transmission aggregometry (LTA) is considered the gold standard in the evaluation of platelet function, but it is costly and time-consuming. 25 Previous studies have compared LTA and other platelet function analyzers, such as VerifyNow, 2,13 PFA-100, 13 and TEG, 2,22 and showed variable results. However, Jeong et al demonstrated a significant correlation between TEG and LTA in 730 patients treated by percutaneous coronary intervention.…”

Section: Discussionmentioning

confidence: 99%

Insufficient platelet inhibition and thromboembolic complications in patients with intracranial aneurysms after stent placement

Yang¹,

Li²,

Jiang³

2016

JNS

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C erebral infarction is one of the major disabling complications of neurovascular stent treatment. During the last decades, many studies have evaluated the safety and efficacy of the technique of stent placement for intracranial aneurysms, which demonstrated a range of 3.7%-21% thromboembolic complications. 4,10,11,29 Dual antiplatelet therapy (aspirin and clopidogrel) has been used as the standard protocol to decrease the incidence of thromboembolic complications in patients with intracranial aneurysms undergoing stent treatment. However, many patients still experience thromboembolic complications after neurovascular intervention, despite being compliant with the standard antiplatelet medication protocol.Previous studies have demonstrated that a low response to antiplatelet medication was associated with the abbreviatioNs AA = arachidonic acid; ADP = adenosine diphosphate; DWI = diffusion-weighted imaging; ICA = internal carotid artery; MA = maximum amplitude; mRS = modified Rankin Scale; TEG = thromboelastography. obJective Insufficient platelet inhibition has been associated with an increased incidence of thromboembolic complications in cardiology patients undergoing percutaneous coronary intervention. Data regarding the relationship between insufficient platelet inhibition and thromboembolic complications in patients undergoing neurovascular procedures remain controversial. The purpose of this study was to assess the relationship of insufficient platelet inhibition and thromboembolic complications in patients with intracranial aneurysm undergoing stent treatment. methods The authors prospectively recruited patients with intracranial aneurysms undergoing stent treatment and maintained the data in a database. MRI with diffusion-weighted sequences was performed within 24 hours of stent insertion to identify acute ischemic lesions. The authors used thromboelastography to assess the degree of platelet inhibition in response to clopidogrel and aspirin. Univariate and multivariate logistic regression analysis was used to identify potential risk factors of thromboembolic complications. results One hundred sixty-eight patients with 193 aneurysms were enrolled in this study. Ninety-one of 168 (54.2%) patients with acute cerebral ischemic lesions were identified by diffusion-weighted MRI. In 9 (5.4%) patients with ischemic lesions, transient ischemic attack or stroke was found at discharge, and these complications were found in 11 (6.5%) patients during the follow-up period. The incidence of periprocedural thromboembolic complications increased with resistance to antiplatelet agents, hypertension, hyperlipidemia, complete occlusion, and aneurysm of the anterior circulation. The multivariate regression analysis demonstrated that the anterior circulation and adenosine diphosphate (ADP) inhibition percentage were independent risk factors of perioperative thromboembolic complications. The maximum amplitude and ADP inhibition percentage were independent risk factors for thromboembolic complications during the follow-up peri...

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“…Furthermore, in our study 8-iso PGF 2a did not potentiate the proaggregatory e ects of either U46619 or collagen. This apparent discrepancy between platelet stimulation in isolated preparations and whole blood may be attributable to proaggregatory alterations in platelets and plasma during separation (Nicholson et al, 1998;Cox, 1998;Kulkarni et al, 2000) and the removal of components of whole blood that inhibit platelet aggregation (Zatta et al, 1990).…”

Section: Discussionmentioning

confidence: 99%

Characterization of the effects of isoprostanes on platelet aggregation in human whole blood

Cranshaw

Evans

Mitchell

2001

British J Pharmacology

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1 We tested the e ects of 11 commercially-available isoprostanes on platelet aggregation directly or when triggered by the thromboxane receptor agonist U46619 or collagen in healthy human citrated blood using a whole blood aggregometer.2 None of the isoprostanes tested triggered aggregation alone, nor facilitated aggregation by a subthreshold dose of U46619 or collagen. Five isoprostanes inhibited aggregation (rank order of potency 8-iso PGE 1 48-iso PGE 2 48-iso PGF 2a 48-iso PGF 3a 48-iso-13,14-dihydro-15-keto PGF 2a ). 3 Blood incubated with LPS to induce a gross in¯ammatory response exhibited a time dependent (2 ± 12 h) reduction in aggregation to U46619 but maintained a consistent response to collagen. Under these conditions, as in control blood, none of the isoprostanes tested induced aggregation. In fact, the inhibitory actions of isoprostanes on U46619-induced aggregation were enhanced in blood treated with LPS. 4 L-NAME inhibited aggregation induced by U46619 in fresh blood and in blood treated with LPS. In the presence of L-NAME, (with or without LPS) none of the isoprostanes tested induced aggregation but retained their inhibitory action. 5 Thus, in human whole blood the action of 8-iso PGE 1 , 8-iso PGE 2 , 8-iso PGF 2a , 8-iso PGF 3a , and 8-iso-13,14-dihydro-15-keto PGF 2a is antiaggregatory. Moreover, this inhibitory capacity is still apparent and may be enhanced in blood subjected to in¯ammatory stimulation.

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Assessment of platelet function assays

Cited by 147 publications

References 7 publications

Platelet Response to Aspirin in Chinese Stroke Patients is Independent of Genetic Polymorphisms of COX-1 C50T and COX-2 G765C

Platelet Response to Aspirin in Chinese Stroke Patients is Independent of Genetic Polymorphisms of COX-1 C50T and COX-2 G765C

Insufficient platelet inhibition and thromboembolic complications in patients with intracranial aneurysms after stent placement

Characterization of the effects of isoprostanes on platelet aggregation in human whole blood

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