A new method for measuring inhibition of platelet function by nonsteroidal antiinflammatory drugs

Schwartz, Kenneth A.; Schwartz, Dianne E.; Pittsley, Richard A.; Mantz, Sandra L.; Ens, Gordon; Sami, Amer; Davis, John M.

doi:10.1067/mlc.2002.121855

Cited by 16 publications

(15 citation statements)

References 26 publications

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“…When compared to light transmission aggregometry (LTA) using AA, the VerifyNow assay demonstrated 91.4% sensitivity and 100% specificity (VerifyNow-ASA package insert). Although a previous generation of the VerifyNow device did use propyl gallate (PG) as the agonist, Schwartz et al (3) demonstrated that PG detects aspirin-induced inhibition of platelets with 100% sensitivity and differentiates the degree of aspirininduced inhibition of platelet function produced by single doses of 81 mg and 325 mg, and hence is a specific activator of the aspirin-inhibited COX-1 pathway. Most importantly, results of the VerifyNow assay have been correlated to clinical outcome in several studies, including one published in JACC (4 -6).…”

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confidence: 98%

Platelet Aspirin Resistance Detection and Validation

Hillman¹

2006

Journal of the American College of Cardiology

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confidence: 98%

Platelet Aspirin Resistance Detection and Validation

Hillman¹

2006

Journal of the American College of Cardiology

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“…The slope gradually increases over 72 hours toward baseline (Figure 4). 42 This assay is useful in a semiquantitative sense to measure variations in the amount of aspirin-induced platelet inhibition. Aspirin inhibition of platelets decreases platelet function.…”

Section: Platelet Prostaglandin Agonist-stimulated Light Aggregometrymentioning

confidence: 99%

“…After a single 325 mg aspirin, platelet aggregation to AA stimulation is inhibited for 72 hours, while platelets not exposed to aspirin will aggregate normally (Figure 4). 42 Arachidonic acid-induced light aggregometry is useful as a qualitative assay to determine whether platelets are or are not inhibited by aspirin.…”

Section: Arachidonic Acid-stimulated Light Aggregometry (A Qualitativmentioning

confidence: 99%

“…Both ADP and PPA were directly compared as agonists for light aggregometry (Figure 6). 42 Participants were tested off aspirin and 2 hours after observed ingestion of 325 mg of aspirin. The slope of the PPA aggregation curve allowed 100% separation of the on and off aspirin platelet responses.…”

Section: Adenosine Diphosphate-and Collagen-stimulated Light Aggregommentioning

confidence: 99%

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Aspirin Resistance

Schwartz

2011

The Neurohospitalist

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Aspirin is an inexpensive, readily available medication that reduces the risk of subsequent vascular disease by about 25% in patients with known occlusive vascular disease. Aspirin's beneficial effect is mediated via inhibition of arachidonic acid (AA) activation of platelets and is detected by demonstrating a decrease in platelet function and/or a decrease in prostaglandin metabolites. Patients who are assumed to be taking their aspirin, but who do not demonstrate an aspirin effect are labeled as, ''aspirin resistant.'' This is an unfortunate designation as the vast majority of patients labeled as ''aspirin resistant'' are noncompliant. Noncompliance is demonstrated in multiple studies that use repeat testing for platelet inhibition in patients with an initial inadequate response to aspirin. When the test is repeated under condition where ingestion of the test aspirin is assured, the patients' platelets are inhibited. Instead of using the term ''aspirin resistance,'' this review will use ''inadequate response to aspirin.'' Patients with an inadequate aspirin response have an increased likelihood for subsequent vascular events. Detection and treatment of an inadequate aspirin response would be facilitated by the development of a bedside assay that uses whole blood, is technically simple, inexpensive, sensitive, specific, reproducible, and provides an answer in a few minutes. Future research in patients with an inadequate response to aspirin should focus on mechanisms to improve compliance, which should decrease their risk of future vascular events.

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“…Cationic propyl gallate is a novel platelet activator used to detect and monitor the amount of platelet inhibition induced by platelet prostanoid antagonists, including aspirin and other nonsteroid anti-infl ammatory drugs [11] . The Ultegra device is a turbidometric optical detection system, which measures platelet-induced aggregation as an increase in light transmittance.…”

Section: Ultegramentioning

confidence: 99%

Dipyridamole Decreases Protease-Activated Receptor and Annexin-V Binding on Platelets of Poststroke Patients with Aspirin Nonresponsiveness

Serebruany

Malinin

Ziai³

et al. 2006

Cerebrovasc Dis

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Background: Although controversial, the phenomenon of aspirin resistance (AR) has been correlated in some small studies with poor clinical outcomes in patients with coronary artery disease. Even less is known regarding the role of AR in the poststroke population. The reason for and the underlying mechanism of AR is unknown. We hypothesized that excessive formation of thrombin on the platelet surface may contribute to this phenomenon and assessed how dipyridamole affects multiple platelet and thrombin generation biomarkers in AR patients after ischemic stroke. Methods: Whole blood samples from 20 poststroke AR patients were pretreated with dipyridamole, simulating the therapeutic range, and then incubated for 45 min at 37°C. Platelet characteristics were assessed by aggregometry, cartridge-based analyzer, and receptor expression by flow cytometry. Markers of thrombin generation were measured in the autologous plasma by ELISA. Results: Pretreatment of blood with dipyridamole resulted in 22–26% diminished expression of intact PAR-1 receptor (p = 0.021 and p = 0.024) and 28–31% decrease of annexin V binding (p = 0.031 and p = 0.02) after incubation with 2 µg/ml and 4 µg/ml of dipyridamole, respectively. Platelet aggregation and thrombin generation markers were not affected in vitro by dipyridamole. Conclusions: Dipyridamole may be capable of overcoming increased prothrombinase complex formation and be in part able to compensate for AR in patients with moderate carotid stenosis. This phenomenon may explain the clinical advantages of Aggrenox^®, known to reduce ischemic events in poststroke patients as proven in clinical trials, though an additional antithrombotic benefit beyond the platelet inhibition by aspirin alone.

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A new method for measuring inhibition of platelet function by nonsteroidal antiinflammatory drugs

Cited by 16 publications

References 26 publications

Platelet Aspirin Resistance Detection and Validation

Platelet Aspirin Resistance Detection and Validation

Aspirin Resistance

Dipyridamole Decreases Protease-Activated Receptor and Annexin-V Binding on Platelets of Poststroke Patients with Aspirin Nonresponsiveness

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