Point-of-Care Determination of Baseline Platelet Function as a Predictor of Clinical Outcomes in Patients who Present to the Emergency Department with Chest Pain

Selvaraj, C; Graaff, Eric John Van De; Campbell, Charles L.; Abels, Brad S.; Marshall, John; Steinhubl, Steven R.

doi:10.1007/s11239-004-0207-7

Cited by 6 publications

(3 citation statements)

References 26 publications

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“…In vitro responsiveness to clopidogrel is classically assessed by adenosine diphosphate (ADP)-induced light transmission platelet aggregometry (LTA) [4,5]. A number of alternative tests have now become available, including the rapid platelet function assay (RPFA, using VerifyNow Ò P2Y12 cartridges) [6] and vasodilator-stimulated phosphoprotein [7]. In contrast, the platelet function analyzer (PFA)-100 Ò system is considered largely unsuitable for monitoring clopidogrel, as variable but often normal closure times (CT) have been observed on both collagen/ADP (CADP) and collagen/epinephrine (CEPI) cartridges in samples from patients receiving clopidogrel therapy [8][9][10][11][12][13].…”

mentioning

confidence: 99%

Can the PFA‐100® be modified to detect P2Y12 inhibition?

Pidcock

Harrison

2006

Journal of Thrombosis and Haemostasis

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concentration between those patients co-prescribed simvastatin and those taking warfarin alone. Although dietary vitamin K intake influences warfarin dose requirements, a parameter not assessed in this study, it can be assumed that the two patient groups had similar dietary intakes as there was no significant difference between their mean fasting plasma vitamin K concentrations.In conclusion, we have found that concurrent simvastatin therapy results in alterations in warfarin pharmacokinetics, most likely through inhibition of the P450 enzymes CYP3A4 and CYP2C9 responsible for the metabolism of R-and S-warfarin respectively, rather than by modification of its pharmacodynamics. Clinicians should be aware of the interaction between these commonly co-prescribed drugs and patients receiving warfarin should be monitored carefully when concurrent therapy with simvastatin is initiated to avoid overanticoagulation. References

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confidence: 99%

Can the PFA‐100® be modified to detect P2Y12 inhibition?

Pidcock

Harrison

2006

Journal of Thrombosis and Haemostasis

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“…Moreover, the clinical condition of the patient [i.e. acute coronary syndrome (ACS)] can have a significant effect on the degree of baseline platelet activation [23].…”

Section: Patient‐related Factorsmentioning

confidence: 99%

Antiplatelet ‘resistance’ and ‘non‐responders’: what do these terms really mean?

Serebruany

Eisert

Atar³

et al. 2009

Fundamemntal Clinical Pharma

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The term ‘resistance’ should be restricted to very specialized physiologic circumstances, if not abandoned altogether. The term ‘non‐responder’ needs to be placed in the context of the question: ‘Non‐responder to what?’ Even if we would somehow magically know what an optimal response to antiplatelet therapy was, it will still be challenging to demonstrate an ‘inadequate’ response to antiplatelet therapy. At present there are two alternatives – give more drug or give additional drugs. Both strategies may work in further inhibiting platelet function, but both strategies can also be associated with an increased risk of bleeding. The trick, for the future, much as with our antihypertensive and lipid‐lowering armamentaria, will be to know in whom to do what with which drug, and why. Single isolated measurements are not useful – if you don't know where you started, how we would know that antiplatelet drug is producing an ‘adequate’ clinical effect? There is no evidence of any sort of absolute ‘threshold’ that must be exceeded for treatment to be effective, and in the absence of this, if we are to evaluate the effect of a given drug, we have to have baseline values (off drug), therapeutic values (on drug), and some sort of assessment of both resting (unstimulated) and agonist‐provoked (stimulated) platelet function. Moreover, given all of the different things that platelets do, the ideal assessment of platelet function and drug responsiveness will need to incorporate more than one agonist and some sort of assessment of both platelet activation and platelet aggregation. No one man (or test) tells us everything; it is the totality of the information that gives us the most complete picture. And, ultimately, we need to more firmly establish how the variability in platelet function and drug‐associated changes in that function correlates with long‐term, hard‐endpoint clinical events.

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“…The Ultegra RPFA (Accumetrics; San Diego, CA) has been used in research studies of subjects receiving therapy with aspirin, clopidogrel, and antagonists of GP aIIbb3. [48][49][50][51][52] The Platelet Reactivity Index, Plateletworks (Helena Laboratories Corp; Beaumont, TX), and other whole-blood, single-platelet counting methods have been used to follow aggregate formation in whole-blood samples, predominately in research on drug-induced platelet dysfunction. 30,48,[53][54][55][56][57] The assessment of platelet function by the hemoSTATUS (Medtronic Inc, Minneapolis, MN), involves comparing data for a modified activated clotting time, performed with or without added platelet activating factor.…”

Section: Quality Assurance and The Assessment Of Drug-induced Platelementioning

confidence: 99%

Platelet Function Testing: Quality Assurance

Hayward¹,

Eikelboom²

2007

Semin Thromb Hemost

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Platelet function tests are widely used for the diagnosis of platelet disorders. In recent years there has been increasing interest in the use of platelet function tests to monitor antiplatelet drug therapy. Quality assurance is important to optimize the performance of laboratory assays but it has not been widely applied to platelet function tests. This deficiency likely reflects the need to use freshly collected blood samples for platelet function tests, and the complex, time-consuming nature of some assays such as aggregation studies. Platelet function testing lacks guidelines, is poorly standardized between laboratories, and rarely is evaluated by internal and external quality assurance exercises. The sensitivity, specificity, and diagnostic utility of some newer, simplified assays of platelet function have been evaluated in a range of clinical settings but corresponding quality assurance data for many established as well as emerging platelet function assays are lacking. Quality assurance issues relevant to testing platelet function are reviewed in this article, with a focus on their application to established and to new and emerging tests.

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Point-of-Care Determination of Baseline Platelet Function as a Predictor of Clinical Outcomes in Patients who Present to the Emergency Department with Chest Pain

Abstract: Point-of-care testing of platelet function deserves further study for risk assessment and individualized therapy in the future.

Cited by 6 publications

References 26 publications

Can the PFA‐100® be modified to detect P2Y12 inhibition?

Can the PFA‐100® be modified to detect P2Y12 inhibition?

Antiplatelet ‘resistance’ and ‘non‐responders’: what do these terms really mean?

Platelet Function Testing: Quality Assurance

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