Monitoring of antiplatelet therapy

2011 ◽  
Vol 31 (01) ◽  
pp. 41-51 ◽  
Author(s):  
H. Seidel ◽  
M. M. Rahman ◽  
R. E. Scharf
Keyword(s):  
Antiplatelet Therapy ◽  
Platelet Function ◽  
Platelet Reactivity ◽  
Point Of Care ◽  
High Sensitivity ◽  
Antiplatelet Agents ◽  
Daily Practice ◽  
Adenosine Diphosphate ◽  
Poor Responders ◽  
Platelet Aggregometry

SummaryScreening of platelet function can be performed by point-of-care testing followed by platelet aggregometry in response to agonists such as collagen, adenosine diphosphate, epinephrine, and arachidonic acid. Despite in use for decades, this technique is not well standardized. Monitoring of antiplatelet therapy is increasingly applied in patients at high risk for re-thrombosis or bleeding. To assess pharmacological inhibition of platelet function, agonist-induced platelet aggregation, thromboxane B2 (TxB2) and vasodilator-stimulated protein phosphorylation (VASP) are being measured. While serum TxB2 levels of < 2 ng/ml reflect aspirin-induced inhibition of cyclo-oxygenase-1 activity with high sensitivity, VASP exhibits a wide variability upon treatment with clopidogrel or prasugrel. Multiple studies reveal an association between high residual platelet reactivity and adverse cardiovascular events in patients on antiplatelet therapy. However, despite the plethora of platelet function assays currently under investigation, their use in daily practice cannot be recommended. This is due to several reasons: (i) there is no consensus on the method and a respective cut-off value associated with clinical adverse outcome, and (ii) data demonstrating any benefit of tailored antiplatelet therapy and its monitoring (based on assessment of platelet functions) are still limited. Thus, appropriate identification of ‘resistant’ or ‘poor responders’ to antiplatelet agents remains challenging in clinical practice.

Mechanisms of platelet activation: Need for new strategies to protect against platelet-mediated atherothrombosis

2009 ◽  
Vol 102 (08) ◽  
pp. 248-257 ◽  
Author(s):  
Lisa Jennings
Keyword(s):  
Antiplatelet Therapy ◽  
Platelet Activation ◽  
Platelet Reactivity ◽  
Thrombus Formation ◽  
Antiplatelet Agents ◽  
Bleeding Risk ◽  
Adenosine Diphosphate ◽  
Adp Receptor ◽  
Activation Pathways ◽  
New Strategies

SummaryPlatelets are central mediators of haemostasis at sites of vascular injury, but they also mediate pathologic thrombosis. Activated platelets stimulate thrombus formation in response to rupture of an atherosclerotic plaque or endothelial cell erosion, promoting atherothrombotic disease. They also interact with endothelial cells and leukocytes to promote inflammation, which contributes to atherosclerosis. Multiple pathways contribute to platelet activation, and current oral antiplatelet therapy with aspirin and a P2Y12 adenosine diphosphate (ADP) receptor antagonist target the thromboxane A2 and ADP pathways, respectively. Both can diminish activation by other factors, but the extent of their effects depends upon the agonist, agonist strength, and platelet reactivity status. Although these agents have demonstrated significant clinical benefit, residual morbidity and mortality remain high. Neither agent is effective in inhibiting thrombin, the most potent platelet activator. This lack of comprehensive inhibition of platelet function allows continued thrombus formation and exposes patients to risk for recurrent thrombotic events. Moreover, bleeding risk is a substantial limitation of antiplatelet therapy, because these agents target platelet activation pathways critical for both protective haemostasis and pathologic thrombosis. Novel antiplatelet therapies that provide more complete inhibition of platelet activation without increasing bleeding risk could considerably decrease residual risk for ischemic events. Inhibition of the protease-activated receptor (PAR)-1 platelet activation pathway stimulated by thrombin is a novel, emerging approach to achieve more comprehensive inhibition of platelet activation when used in combination with current oral antiplatelet agents. PAR-1 inhibition is not expected to increase bleeding risk, as this pathway does not interfere with haemostasis.

Individualised Antiplatelet Therapy – Is There a Role for Platelet Function Testing in Routine Clinical Practice?

2010 ◽  
Vol 5 (1) ◽  
pp. 96 ◽  
Author(s):  
Collet Jean-Philippe ◽  
Jochem Wouter van Werkum ◽  
◽  
Keyword(s):  
Clinical Practice ◽  
Antiplatelet Therapy ◽  
Platelet Function ◽  
Platelet Reactivity ◽  
Point Of Care ◽  
Coronary Intervention ◽  
Platelet Function Testing ◽  
Increased Risk ◽  
Coronary Syndromes ◽  
Function Testing

Antiplatelet therapies are often used to minimise complications in patients with acute coronary syndromes or who are undergoing percutaneous coronary intervention with stenting. However, the occurrence of ‘high on-treatment platelet reactivity’ associated with the gold standard treatments aspirin and clopidogrel in a subset of individuals limits the efficacy of these drugs. This lack of response, which has been attributed to a genetic polymorphism, is associated with an increased risk of subsequent atherothrombotic events. In recent years, platelet function assays have been used to monitor antiplatelet inhibition. Various tests have been introduced that allow physicians to evaluate pharmacological response and potentially permit risk stratification of patients. While some of these assays have proved to be labour-intensive, the development of point-of-care assays may ease the time burden in clinical practice. Preliminary findings demonstrate the effectiveness of altering therapy based on assay results in terms of improving clinical outcomes, suggesting an important role for platelet function testing in the future of antiplatelet therapy.

scholarly journals Sensitivity of Viscoelastic Tests to Platelet Function

2020 ◽  
Vol 9 (1) ◽  
pp. 189 ◽  
Author(s):  
Marco Ranucci ◽  
Ekaterina Baryshnikova
Keyword(s):  
Platelet Function ◽  
Light Transmission ◽  
Platelet Reactivity ◽  
Point Of Care ◽  
Dynamic Assessment ◽  
Antiplatelet Agents ◽  
Protease Activated Receptors ◽  
Specific Test ◽  
Clot Strength ◽  
P2y12 Inhibitors

Viscoelastic tests provide a dynamic assessment of coagulation, by exploring the time to clot formation and the clot strength. Using specific activators or inhibitors, additional factors can be explored, like the fibrinogen contribution to clot strength. Since the early days, various attempts have been done to measure platelet function with viscoelastic test. In general, the difference between the maximum clot strength and the fibrinogen contribution is considered an index of platelet contribution. However, this parameter does not clearly split platelet count from function; additionally, the extensive thrombin generation of standard activated viscoelastic tests activates platelet through the protease activated receptors, bypassing the other pathways. For this reason, standard viscoelastic tests cannot be used to assess platelet reactivity under the effects of aspirin or P2Y12 inhibitors. To overcome this limitation, a specific test was developed (thromboelastography platelet mapping). This test has been compared with the gold standard of light transmission aggregometry and with other point-of-care tests, with conflicting results. In general, the use of viscoelastic tests to assess the effects of antiplatelet agents is still limited. Conversely, platelet contribution to clot strength in the setting of coagulopathic bleeding is considered an important parameter to trigger platelet transfusion or desmopressin.

Individualised Antiplatelet Therapy – Is There a Role for Platelet Function Testing in Routine Clinical Practice?

2010 ◽  
Vol 6 (1) ◽  
pp. 41 ◽  
Author(s):  
Collet Jean-Philippe ◽  
Jochem Wouter van Werkum ◽  
◽  
Keyword(s):  
Clinical Practice ◽  
Antiplatelet Therapy ◽  
Platelet Function ◽  
Platelet Reactivity ◽  
Point Of Care ◽  
Coronary Intervention ◽  
Platelet Function Testing ◽  
Increased Risk ◽  
Coronary Syndromes ◽  
Function Testing

Antiplatelet therapies are often used to minimise complications in patients with acute coronary syndromes or who are undergoing percutaneous coronary intervention with stenting. However, the occurrence of ‘high on-treatment platelet reactivity’ associated with the gold standard treatments aspirin and clopidogrel in a subset of individuals limits the efficacy of these drugs. This lack of response, which has been attributed to a genetic polymorphism, is associated with an increased risk of subsequent atherothrombotic events. In recent years, platelet function assays have been used to monitor antiplatelet inhibition. Various tests have been introduced that allow physicians to evaluate pharmacological response and potentially permit risk stratification of patients. While some of these assays have proved to be labour-intensive, the development of point-of-care assays may ease the time burden in clinical practice. Preliminary findings demonstrate the effectiveness of altering therapy based on assay results in terms of improving clinical outcomes, suggesting an important role for platelet function testing in the future of antiplatelet therapy.

Comparison of methods for monitoring residual platelet reactivity after clopidogrel by point-of-care tests on whole blood in high-risk patients

2010 ◽  
Vol 104 (08) ◽  
pp. 587-292 ◽  
Author(s):  
Emilia Antonucci ◽  
Niccolò Maggini ◽  
Marco Miranda ◽  
Anna Gori ◽  
Rossella Marcucci ◽  
...  
Keyword(s):  
High Risk ◽  
Antiplatelet Therapy ◽  
Whole Blood ◽  
Dual Antiplatelet Therapy ◽  
Light Transmission ◽  
Platelet Reactivity ◽  
Point Of Care ◽  
Platelet Aggregometry ◽  
Risk Patients ◽  
Artery Disease

SummaryCardiovascular events are more frequent in high-risk coronary artery disease (CAD) patients on dual antiplatelet therapy with a residual platelet reactivity (RPR) than in those showing inhibition of ADP-inducible platelet activation. It is known that post-interventional RPR is a clinically important entity confirming it as a risk factor for thrombo-is-chaemic events. Multiple electrode platelet aggregometry (MEA) on whole blood has been recently proposed as a rapid tool to evaluate RPR in high-risk CAD patients on clopidogrel therapy. It was the aim of this study to detect RPR in 801 high-risk CAD patients on dual antiplatelet therapy comparing MEA with the VerifyNow P2Y12 assay on whole blood and classical light transmission aggregation (LTA) on plateletrich plasma. ADP (10 μM) was employed as agonist for MEA and LTA. The prevalence of RPR was 20.6% by MEA, 16.1% by LTA and 30.8% by VerifyNow. MEA showed a significant correlation (rho=0.62, p<0.0001) with VerifyNow and a moderate agreement (k=0.52, p<0.001) with 81.5% of concordant values. A significant correlation was found between MEA and LTA (rho=0.71, p<0.001) with a good agreement (k=0.63, p<0.001) and 88.8% of concordant values. MEA in relation to LTA showed a sensitivity of 80% and a specificity of 91%. MEA might represent a reliable method and valid alternative in comparison with other available platelet function assays. It might help to guide antiplatelet therapy and thus improve clinical outcome of high-risk CAD patients.

scholarly journals Optimal platelet function test for in-stent tissue protrusion following carotid artery stenting

2018 ◽  
Vol 46 (5) ◽  
pp. 1866-1875 ◽  
Author(s):  
Masanori Tsujimoto ◽  
Yukiko Enomoto ◽  
Masafumi Miyai ◽  
Yusuke Egashira ◽  
Toru Iwama
Keyword(s):  
Carotid Artery ◽  
Platelet Function ◽  
Carotid Artery Stenting ◽  
Platelet Reactivity ◽  
Point Of Care ◽  
Adenosine Diphosphate ◽  
Light Transmittance ◽  
Projection Area ◽  
Platelet Function Test ◽  
Function Test

Purpose To determine the best platelet function test for in-stent tissue protrusion following carotid artery stenting (CAS). Methods Patients who underwent CAS were recruited prospectively in this observational study. Combination of aspirin 100 mg/day and clopidogrel 75 mg/day was administered for a minimum of 7 days prior to procedure. Platelet aggregation was measured by light transmittance aggregometry (LTA) following stimulation by adenosine diphosphate (ADP), collagen, and thrombin receptor activating peptide (TRAP) and by the point of care assay, VerifyNow which measures aspirin and thienopyridine reaction units. Results In-stent tissue protrusion with maximum projection area of ≥1 mm2 was detected by optical coherence tomography (OCT) in 10/28 (36%) patients. Baseline characteristics were not significantly different between the two in-stent size groups (i.e., ≥1 mm2 vs. <1 mm2) but after stimulation by collagen at 10 and 20 μg/ml, platelet reactivity as measured by LTA was significantly higher in the ≥1 mm2 group compared with the <1 mm2 group. No other differences in platelet function were detected. Conclusions Collagen-induced platelet reactivity was related to in-stent tissue protrusion size following CAS.

scholarly journals Correlation between PlateletWorks® and PFA-100® for Measuring Platelet Function before Urgent Surgery in Patients with Chronic Antiplatelet Therapy

2021 ◽  
Vol 10 (2) ◽  
pp. 255
Author(s):  
Rafael Anaya ◽  
Mireia Rodriguez ◽  
José María Gil ◽  
Noelia Vilalta ◽  
Angela Merchan-Galvis ◽  
...  
Keyword(s):  
Antiplatelet Therapy ◽  
Platelet Function ◽  
Point Of Care ◽  
Antiplatelet Agents ◽  
Kappa Coefficient ◽  
Function Evaluation ◽  
Cohen’S Kappa ◽  
Platelet Function Test ◽  
Cohen's Kappa ◽  
Cohen’S Kappa Coefficient

Hemostasis is crucial for reducing bleeding during surgical procedures. The points-of-care based on the platelet function test could be useful to minimize the complications related to chronic antiplatelet therapy during surgery. The present study is aimed at comparing two point-of-care platelet function devices—Platelet Function Analyzer PFA-100® (Siemens Canada, Mississauga, ON, Canada) and Plateletworks®(Helena Laboratories, Beaumont, TX, USA). Our objective is to evaluate if they provide comparable and useful information to manage anti-aggregate patients before surgery. We included patients with a femoral fracture receiving chronic antiplatelet therapy and a median age of 89 years (range from 70 to 98). A platelet function evaluation was performed on all patients before surgery using both devices—Plateletworks® and PFA-100®. The correlation between Plateletworks® and PFA-100® was performed using Cohen’s Kappa coefficient. Twenty consecutive patients participated in the trial; 16 patients were under treatment with 75 mg/day of clopidogrel, three with >300 mg/day of acetylsalicylic acid (ASA), and only one was in treatment with both antiplatelet agents. Cohen’s Kappa coefficient was 0.327 comparing PFA-100®-ADP (adenosine diphosphate) and Plateletworks® and, 0.200 comparing PFA-100®-EPI (epinephrine) and Plateletworks®. In conclusion, we found a weak concordance comparing PFA-100® and Plateletworks®. This could partially be due to the advanced age of the included patients. However, given the limited sample size, more studies are necessary to confirm these results.

High on-treatment platelet reactivity – definition and measurement

2013 ◽  
Vol 109 (05) ◽  
pp. 792-798 ◽  
Author(s):  
Marco Cattaneo
Keyword(s):  
At Risk ◽  
Platelet Function ◽  
Platelet Reactivity ◽  
Antiplatelet Agents ◽  
Antiplatelet Drug ◽  
Major Adverse Cardiovascular Events ◽  
Poor Responders ◽  
Patient Response ◽  
Increased Risk ◽  
Patients At Risk

SummaryIn the last decade, several studies revealed inter-patient response variability to antiplatelet agents: patients who display negligible or no responses to these drugs are considered poor responders, or “resistant” to treatment. In order to identify poor responders to an antiplatelet drug, laboratory tests of platelet function that specifically explore the platelet activation pathway that is targeted by the drug should be utilised. In addition, they should be performed both at baseline and during treatment: however, most studies explored platelet function during antiplatelet treatment, in order to identify those patients with “high on-treatment platelet reactivity” (HPR), which exposes them to increased risk of major adverse cardiovascular events (MACE). Many tests of platelet function have been used, most of which are able to identify patients at risk of MACE. Unfortunately, universal cut-off values for HPR have not been clearly established yet. In addition, the concordance among different tests in the identification of patients at risk is very poor and the most effective and safe treatment for patients at risk is still unknown.

scholarly journals Advances in Our Understanding of “Resistance” to Antiplatelet Agents for Prevention of Ischemic Stroke

2013 ◽  
Vol 2013 ◽  
pp. 1-7 ◽  
Author(s):  
Philip B. Gorelick ◽  
Muhammad U. Farooq
Keyword(s):  
Ischemic Stroke ◽  
Clinical Practice ◽  
Antiplatelet Therapy ◽  
Platelet Function ◽  
Platelet Reactivity ◽  
Antiplatelet Agents ◽  
Patient Characteristics ◽  
Therapy Resistance ◽  
Test Methods ◽  
Platelet Function Test

We review the role of aspirin and clopidogrel for prevention of ischemic stroke and explore the concept of antiplatelet therapy resistance both from a laboratory and clinical perspective and genetic polymorphisms that might influence platelet reactivity with clopidogrel administration. Debates have raged over the years about the application of platelet function tests in clinical practice. We conclude that platelet function testing is not indicated in routine clinical practice. This recommendation is supported by clinical guideline statements, a lack of a global platelet function measure, and limitations of current platelet function test methods as applied in practice. We discuss a recently hypothesized hierarchy of patient characteristics in relation to which patients are most likely to benefit from platelet function studies based on acuity (i.e., risk) of cardiovascular disease. A focus of antiplatelet therapy administration should include emphasis on compliance/adherence and in the example of aspirin, use of well-absorbed forms of aspirin and avoidance of drugs that may interact with aspirin to inhibit its mechanism of action (e.g., certain nonsteroidal anti-inflammatory drugs).

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