Is There a Role for Platelet Function Testing In Patients Receiving P2Y12 Inhibitors?

Strong Biological Plausibility to Measure Platelet Function

Indisputable evidence from multiple areas of research provides a powerful rationale for platelet function testing in patients with high-risk coronary artery disease (CAD). Mathematical models using hybrid dissipative particle dynamics/partial differential equation model and animal models using platelet-labeling techniques and confocal microscopy have confirmed the pivotal role of platelets during occlusive thrombus generation.1-4 Histological studies have demonstrated platelet thrombi at the site of coronary occlusion and distally in the microvasculature of patients with unstable angina prior to death.5,6 Sustained platelet activation has been reported following the index myocardial ischemic event.7 By expressing adhesion molecules, activated platelets bind to dysfunctional endothelium and facilitate the adhesion and internalization of macrophages, thereby playing a key role in the initiation and progression of atherothrombosis.8,9 Platelets have been shown to oxidize low-density lipoprotein (LDL) cholesterol. Oxidized LDL is a major contributor to plaque vulnerability.10,11 Intravascular imaging techniques have demonstrated an independent association between high platelet reactivity to adenosine diphosphate (ADP) and atherosclerosis burden, periprocedural myocardial infarction (MI), and vessel calcification.12,13 High platelet reactivity has been also independently linked to culprit lesion burden and adverse plaque morphology.14 Taken together, all these observations strongly support a fundamental relationship between platelet reactivity and activation and cardiovascular (CV) risk.

P2Y12 Plays a Central Role in Amplifying the Response to Other Agonists

Continuous downstream signaling from the P2Y12 receptor is essential for the amplification of platelet aggregation in response to all agonists that degranulate the platelet and release ADP, leading to irreversible and stable platelet-rich thrombus generation (Figure 1).15 In this line, P2Y12 has recently been shown to inhibit RASA3, an important GTPase-activating protein that inhibits platelet activation and maintains GP IIb/IIIa in an inactive state.16 The latter observation further solidifies the key role for P2Y12 receptor during occlusive thrombosis generation and supports the measurement of the reactivity to ADP as an important marker of CV risk.

Figure 1. P2Y12 Plays a Central Role in Amplifying the Response to Other Agonists

Figure 1
After vascular injury, platelets adhere to injury site and undergo activation. Platelet activation results in the release of three important platelet agonists: thromboxane A2 (TxA2), ADP, and thrombin. Thrombin protease-activated receptor-1, TxA2-thromboxane receptor, and ADP-P2Y12 receptor pathways amplify the response to platelets, resulting in sustained platelet aggregation via activated GP IIb/IIIa receptor. The ADP-P2Y12 interaction plays a central role in platelet aggregation and subsequent ischemic event occurrences. Finally, formation of occlusive platelet-rich thrombus formation at the site of plaque rupture is mainly responsible for the occurrence of arterial thrombotic event occurrences, such as MI, stent thrombosis, and stroke.

Link of High Platelet Reactivity to Thrombosis in Percutaneous Coronary Intervention Patients: Observational Studies

Earlier small observational studies demonstrated a strong relation of high platelet reactivity to ADP phenotype to both short- and long-term ischemic event occurrences, including periprocedural MI and stent thrombosis.17-19 Subsequent observational studies using various methods to measure platelet reactivity to ADP have further reinforced the earlier findings.20 The magnitude of the association between platelet reactivity and ischemic risk is strongly dependent on the level of CV risk in clopidogrel-treated patients. Platelet reactivity to ADP allowed the reclassification of 44% of the total population of clopidogrel-treated patients to a different risk level for the outcome of major adverse clinical events, mostly in intermediate or high-risk patients.21 In the ADAPT-DES (Platelet reactivity and clinical outcomes after coronary artery implantation of drug-eluting stents) registry of 8,583 patients, high platelet reactivity to ADP as measured by the VerifyNow assay was independently associated with 30-day and 2-year definite/probable stent thrombosis and MI.22,23 Further analyses demonstrated a monotonic association between successively higher P2Y12 reaction units quintiles (less platelet inhibition) and stent thrombosis with the lowest P2Y12 reaction units quintile (more platelet inhibition) with the greatest risk for clinically relevant bleeding.23 The latter findings in a large patient population strongly support the concept of a "therapeutic window" during which platelet reactivity to ADP is associated with both ischemic event occurrence (upper threshold) and bleeding risk (lower threshold).24

Therapy With More Potent P2Y12 Inhibitors Than Clopidogrel: Less Thrombosis

Clopidogrel is the most widely used P2Y12 receptor blocker to prevent recurrent ischemic events in high-risk patients with CAD. However, it is associated with major limitations such as delayed onset of action, wide inter-individual variability, and low response or nonresponse as indicated by high platelet reactivity in nearly one third of patients that is associated with post-percutaneous coronary intervention (PCI) ischemic event occurrences.24 These limitations provided a strong rationale for the development and use of more potent P2Y12 inhibitors such as prasugrel and ticagrelor. In two prospective large-scale clinical trials in high-risk CAD patients, the therapy with the latter agents was associated with a nearly 20% relative-risk reduction in the occurrence of thrombotic events versus clopidogrel.25,26 These findings further solidify the "platelet hypothesis" that states that pharmacologic treatment strategies associated with lower platelet reactivity to ADP as determined by ex vivo methods translates into fewer thrombotic event occurrences.27 There is no stronger biologically plausible explanation than greater P2Y12 inhibition for the latter large-scale clinical trial results. However, increased bleeding in patients treated with ticagrelor and prasugrel further indicate that instead of blanket use of these potent agents, platelet function testing may assist in selecting patients who are most likely to benefit from treatment with these potent P2Y12 receptor blockers.

Personalized Antiplatelet Therapy Trials

Small, prospective studies with tailored antiplatelet therapy provided initial evidence that high platelet reactivity may not be just a diagnostic marker but also a modifiable risk factor for post-PCI ischemic event occurrence. These trials used either tailored incremental clopidogrel loading doses (LDs) before PCI to overcome high platelet reactivity or selective GP IIb/IIIa receptor blocker administration in patients who had high platelet reactivity following clopidogrel loading. The latter approaches to overcoming high platelet reactivity were effective in reducing periprocedural as well as long-term ischemic outcomes.28-31

Encouraged by the positive results of the latter studies, two large-scale personalized antiplatelet therapy studies explored the utility of modifying antiplatelet therapy based on platelet function testing to improve clinical outcomes: The GRAVITAS (Gauging Responsiveness With A VerifyNow Assay-Impact On Thrombosis And Safety) trial (n = 2,214) and the ARCTIC (Double Randomization of a Monitoring Adjusted Antiplatelet Treatment Versus a Common Antiplatelet Treatment for DES Implantation, and Interruption Versus Continuation of Double Antiplatelet Therapy, One Year After Stenting) study (n = 2,440) (Figure 2).32,33

Figure 2. Randomized Trials of Personalized Antiplatelet Therapy

Study (Ref)

 Patients (n)

Treatment regimen to address high platelet reactivity



Bonello et al. 28

Patients with coronary stenting, vasodilator stimulated phosphoprotein (VASP)  phosphorylation (PRI) >50% on 600 mg clopidogrel (VASP-guided group = 78 vs. control = 84)

Repeated clopidogrel LD to decrease VASP-Index <50%

1 month CV death, angiographically confirmed ST, recurrent acute coronary syndrome (ACS):
0% vs. 10%, p = 0.007
Major and minor bleeding: 5% vs. 4%, p = 1.0

Low n

Bonello et al. 29

Patients undergoing stenting (50% ACS), VASP-PRI>50% on 600mg clopidogrel LD
(VASP-guided group = 215 vs. control = 214)

Repeated clopidogrel LD to decrease VASP-Index <50%

<30 day definite stent thrombosis:
0.5% vs. 4.2%, p <  0.01
CV death, recurrent ACS and urgent revascularization by coronary angioplasty or bypass surgery
0.5% vs. 8.9%
Bleeding, 2.8% vs. 3.7%, p = 0.8

Despite a 2,400-mg LD of clopidogrel, 8% of patients in the VASP-guided group had VASP-PRI  > 50%

Campo et al. 30

Patients undergoing PCI and treated with 600/300 mg clopidogrel (n = 826)

GP IIb/IIIa inhibitor

Periprocedural MI was associated with poor responsiveness, hazard ratio = 1.25.
GP IIb/IIIa inhibitor reduced periprocedural MI in poor responders (21.2% vs. 3.47%, p = 0.02), not in responders (6.3% vs. 6.5%, p = 0.8).

Comparatively low-risk patients with silent ischemia, stable angina, and low-risk unstable angina

Cuisset et al. 31

Elective PCI patients with 10 mcM ADP-induced aggregation >70%

GP IIb/IIIa inhibitor arm, n = 74
Conventional arm, n = 75

1 month any death, periprocedural MI, acute or subacute definite or probable ST, and recurrent ACS, 19% vs. 40%, p = 0.006

Low n


Stable (60%) and non-ST elevation ACS (40%) patients with P2Y12 reaction units >230 on clopidogrel (n = 2,214)

600 mg LD/150 mg maintenance dose or 75 mg maintenance dose for 6 months

6 month CV death, nonfatal MI, or stent thrombosis 2.3% vs. 2.3%

Mainly low-risk patients, low event rate
High-dose clopidogrel is not sufficient to reduce high platelet reactivity
VerifyNow P2Y12 assay to determine high platelet reactivity


63% stable CAD + 27% non-ST elevation MI treated drug-eluting stent (n = 2,440)

VerifyNow assay
High platelet reactivity was >550 aspirin reaction units or >235 P2Y12 reaction units (total ~40%)
GP IIb/IIIa inhibitor (30 during PCI) + additional ≥600mg clopidogrel (83%) or 60 mg prasugrel (2.3%)

1 year death, MI, ST, or urgent revascularization (mainly driven by MI)
34% vs. 31%, p = 0.1
No difference in bleeding

Mainly stable CAD patients
VerifyNow assay
Twice more patients were lost to follow up in the conventional arm than in the monitoring arm (3.8% vs. 1.9%).
The event rate was mainly driven by
periprocedural MI that was assessed by nonuniform methodology postprocedure.
Prasugrel was administered in only <10% of patients.

These investigations failed to demonstrate the utility of platelet function testing in reducing the post-PCI ischemic risk. However, both investigations used the VerifyNow P2Y12 assay to identify high platelet reactivity, included a population of patients who had low postdischarge event rates irrespective of platelet reactivity, and largely used the suboptimal remedy of high-dose clopidogrel to overcome high platelet reactivity. In addition, low postdischarge event rates resulted in trials that were not adequately powered to prove or disprove the utility of platelet function testing in personalizing antiplatelet therapy.

Role of Platelet Function Testing in Determining Eligible Patients for Long-Term Dual Antiplatelet Therapy

The results of the DAPT Study (Dual Antiplatelet Therapy Study) and the PEGASUS-TIMI 54 (Prevention of Cardiovascular Events in Patients With Prior Heart Attack Using Ticagrelor Compared to Placebo on a Background of Aspirin-Thrombolysis in Myocardial Infarction 54) trial support long-term dual antiplatelet therapy without interruption in selected patients at high risk for ischemic events and lower risk for bleeding.34,35 In this scenario, objective measurement of platelet function may improve the identification of candidates who are more likely to benefit from prolonged dual antiplatelet therapy.36

Personalized Antiplatelet Therapy in Patients Undergoing Cardiac Bypass Surgery

Current guidelines recommend 5-7 days discontinuation of P2Y12 receptor inhibitor treatment in patients undergoing coronary artery bypass grafting to allow adequate platelet function recovery, thereby avoiding excessive perioperative bleeding. Recent studies have demonstrated that preoperative platelet function testing in these patients may assist in optimizing the timing of surgery to reduce perioperative bleeding.37 The utility of platelet function testing in patients undergoing coronary artery bypass grafting and PCI patients has been acknowledged in recent guidelines.37-42


High platelet reactivity is consistent with the proposed Wilson-Jungner requirements43 for a meaningful risk marker because 1) it has biological plausibility because it is a measure of the potential for platelet aggregation in vivo, which is the physiological process being targeted by the P2Y12 inhibitor; 2) there is a strong, consistent association of high platelet reactivity with worse outcome across multiple studies, including observational studies, analyses of randomized clinical trials, and meta-analyses; 3) high platelet reactivity precedes the event; and 4) there is evidence of a dose-response relationship between the degree of platelet reactivity and outcome. In addition, there is evidence of a "therapeutic window" of P2Y12 receptor reactivity that provides a rationale for measuring platelet function to assess both ischemic and bleeding risk. A potential explanation for the neutral results in the recent prospective personalized antiplatelet therapy trials may be related to the assay itself. Platelet agglutination to fibrinogen-coated beads in anticoagulated blood in the VerifyNow P2Y12 assay may not optimally discriminate high-risk patients. In this line, other point-of-care assays such as analyzers that are based on impedance aggregometry and thrombelastography that measures platelet-fibrin clot strength may be more effective in discriminating risk. In the ongoing TROPICAL-ACS (Testing Responsiveness to Platelet Inhibition on Chronic Antiplatelet Treatment For Acute Coronary Syndromes Trial) (n = 2,600), an analyzer-guided approach is being used to personalize antiplatelet therapy in patients with ACS who are treated with PCI.

Current evidence suggests that platelet function testing may be useful in the following scenarios: 1) Identification of PCI patients at increased risk for CV complications; 2) monitoring response to antiplatelet agents to assist in personalizing antiplatelet therapy in selected high-risk patients undergoing PCI and also select high-risk patients for prolonged dual antiplatelet therapy; and 3) assessment of pharmacodynamic effects to optimally time surgical procedures to reduce wait time and bleeding.


  1. Tosenberger A, Ataullakhanov F, Bessonov N, Panteleev M, Tokarev A, Volpert V. Modelling of platelet-fibrin clot formation in flow with a DPD-PDE method. J Math Biol 2016;72:649-81.
  2. Stalker TJ, Welsh JD, Tomaiuolo M, et al. A systems approach to hemostasis: 3. Thrombus consolidation regulates intrathrombus solute transport and local thrombin activity. Blood 2014;124:1824-31.
  3. Hoefer T, Armstrong PC, Finsterbusch M, Chan MV, Kirkby NS, Warner TD. Drug-Free Platelets Can Act as Seeds for Aggregate Formation During Antiplatelet Therapy. Arterioscler Thromb Vasc Biol 2015;35:2122-33.
  4. Gurbel PA, Tantry US. Inhibited and Uninhibited Platelet Deposition Within a Thrombus: Does It Depend on the Antiplatelet Drug? Arterioscler Thromb Vasc Biol 2015;35:2081-2.
  5. Falk E. Unstable angina with fatal outcome: dynamic coronary thrombosis leading to infarction and/or sudden death. Autopsy evidence of recurrent mural thrombosis with peripheral embolization culminating in total vascular occlusion. Circulation 1985;71:699-708.
  6. Davies MJ, Thomas AC, Knapman PA, Hangartner JR. Intramyocardial platelet aggregation in patients with unstable angina suffering sudden ischemic cardiac death. Circulation 1986;73:418-27.
  7. Ault KA, Cannon CP, Mitchell J, et al. Platelet activation in patients after an acute coronary syndrome: results from the TIMI-12 trial. Thrombolysis in Myocardial Infarction. J Am Coll Cardiol 1999;33:634-9.
  8. Schulz C, Schäfer A, Stolla M, et al. Chemokine fractalkine mediates leukocyte recruitment to inflammatory endothelial cells in flowing whole blood: a critical role for P-selectin expressed on activated platelets. Circulation 2007;116:764-73.
  9. Gawaz M, Stellos K, Langer HF. Platelets modulate atherogenesis and progression of atherosclerotic plaques via interaction with progenitor and dendritic cells. J Thromb Haemost 2008;6:235-42.
  10. Carnevale R, Bartimoccia S, Nocella C, et al. LDL oxidation by platelets propagates platelet activation via an oxidative stress-mediated mechanism. Atherosclerosis 2014;237:108-16.
  11. Navarese EP, Kolodziejczak M, Kereiakes DJ, Tantry US, O'Connor C, Gurbel PA. Proprotein Convertase Subtilisin/Kexin Type 9 Monoclonal Antibodies for Acute Coronary Syndrome: A Narrative Review. Ann Intern Med 2016;164:600-7.
  12. Mangiacapra F, De Bruyne B, Muller O, et al. High residual platelet reactivity after clopidogrel: extent of coronary atherosclerosis and periprocedural myocardial infarction in patients with stable angina undergoing percutaneous coronary intervention. JACC Cardiovasc Interv 2010;3:35-40.
  13. Chirumamilla AP, Maehara A, Mintz GS, et al. High platelet reactivity on clopidogrel therapy correlates with increased coronary atherosclerosis and calcification: a volumetric intravascular ultrasound study. JACC Cardiovasc Imaging 2012;5:540-9.
  14. Yun KH, Mintz GS, Witzenbichler B, et al. Relationship Between Platelet Reactivity and Culprit Lesion Morphology: An Assessment from the ADAPT-DES Intravascular Ultrasound Substudy. JACC Cardiovasc Imaging 2016 Feb 10 [Epub ahead of print].
  15. Dorsam RT, Kunapuli SP. Central role of the P2Y12 receptor in platelet activation. J Clin Invest 2004;113:340-5.
  16. Stefanini L, Bergmeier W. RAP1-GTPase signaling and platelet function. J Mol Med (Berl) 2016;94:13-9.
  17. Gurbel PA, Bliden KP, Guyer K, et al. Platelet reactivity in patients and recurrent events post-stenting: results of the PREPARE POST-STENTING Study. J Am Coll Cardiol 2005;46:1820-6.
  18. Gurbel PA, Antonino MJ, Bliden KP, et al. Platelet reactivity to adenosine diphosphate and long-term ischemic event occurrence following percutaneous coronary intervention: a potential antiplatelet therapeutic target. Platelets 2008;19:595-604.
  19. Gurbel PA, Bliden KP, Samara W, et al. Clopidogrel effect on platelet reactivity in patients with stent thrombosis: results of the CREST Study. J Am Coll Cardiol 2005;46:1827-32.
  20. Bonello L, Tantry US, Marcucci R, et al. Consensus and future directions on the definition of high on-treatment platelet reactivity to adenosine diphosphate. J Am Coll Cardiol 2010;56:919-33.
  21. Reny JL, Fontana P, Hochholzer W, et al. Vascular risk levels affect the predictive value of platelet reactivity for the occurrence of MACE in patients on clopidogrel. Systematic review and meta-analysis of individual patient data. Thromb Haemost 2016;115:844-55.
  22. Stone GW, Witzenbichler B, Weisz G, et al. Platelet reactivity and clinical outcomes after coronary artery implantation of drug-eluting stents (ADAPT-DES): a prospective multicentre registry study. Lancet 2013;382:614-23.
  23. Kirtane AJ, Parikh PB, Stuckey TD, et al. Is There an Ideal Level of Platelet P2Y12-Receptor Inhibition in Patients Undergoing Percutaneous Coronary Intervention?: "Window" Analysis From the ADAPT-DES Study (Assessment of Dual AntiPlatelet Therapy With Drug-Eluting Stents). JACC Cardiovasc Interv 2015;8:1978-87.
  24. Tantry US, Bonello L, Aradi D, et al. Consensus and update on the definition of on-treatment platelet reactivity to adenosine diphosphate associated with ischemia and bleeding. J Am Coll Cardiol 2013;62:2261-73.
  25. Wiviott SD, Braunwald E, McCabe CH, et al. Prasugrel versus clopidogrel in patients with acute coronary syndromes. N Engl J Med 2007;357:2001-15.
  26. Wallentin L, Becker RC, Budaj A, et al. Ticagrelor versus clopidogrel in patients with acute coronary syndromes. N Engl J Med 2009;361:1045-57.
  27. Gurbel PA, Bliden KP, Hayes KM, Tantry U. Platelet activation in myocardial ischemic syndromes. Expert Rev Cardiovasc Ther 2004;2:535-45.
  28. Bonello L, Camoin-Jau L, Arques S, et al. Adjusted clopidogrel loading doses according to vasodilator-stimulated phosphoprotein phosphorylation index decrease rate of major adverse cardiovascular events in patients with clopidogrel resistance: a multicenter randomized prospective study. J Am Coll Cardiol 2008;51:1404-11.
  29. Bonello L, Camoin-Jau L, Armero S, et al. Tailored clopidogrel loading dose according to platelet reactivity monitoring to prevent acute and subacute stent thrombosis. Am J Cardiol 2009;103:5-10.
  30. Campo G, Fileti L, de Cesare N, et al. 3T/2R Investigators. Long-term clinical outcome based on aspirin and clopidogrel responsiveness status after elective percutaneous coronary intervention: a 3T/2R (tailoring treatment with tirofiban in patients showing resistance to aspirin and/or resistance to clopidogrel) trial substudy. J Am Coll Cardiol 2010;56:1447-55.
  31. Cuisset T, Frere C, Quilici J, et al. Glycoprotein IIb/IIIa inhibitors improve outcome after coronary stenting in clopidogrel nonresponders: a prospective, randomized study. JACC Cardiovasc Interv 2008;1:649-53.
  32. Price MJ, Berger PB, Teirstein PS, et al. Standard- vs high-dose clopidogrel based on platelet function testing after percutaneous coronary intervention: the GRAVITAS randomized trial. JAMA 2011;305:1097-105.
  33. Collet JP, Cuisset T, Rangé G, et al. Bedside monitoring to adjust antiplatelet therapy for coronary stenting. N Engl J Med 2012;367:2100-9.
  34. Mauri L, Kereiakes DJ, Yeh RW, et al. Twelve or 30 months of dual antiplatelet therapy after drug-eluting stents. N Engl J Med 2014;371:2155-66.
  35. Bonaca MP, Bhatt DL, Steg PG, et al. Ischaemic risk and efficacy of ticagrelor in relation to time from P2Y12 inhibitor withdrawal in patients with prior myocardial infarction: insights from PEGASUS-TIMI 54. Eur Heart J 2016;37:1133-42.
  36. Gurbel PA, Tantry US. Deciding about prolonged ticagrelor therapy in coronary clot formers: an ongoing dilemma. Eur Heart J 2016;37:1143-4.
  37. Mahla E, Suarez TA, Bliden KP, et al. Platelet function measurement-based strategy to reduce bleeding and waiting time in clopidogrel-treated patients undergoing coronary artery bypass graft surgery: the timing based on platelet function strategy to reduce clopidogrel-associated bleeding related to CABG (TARGET-CABG) study. Circ Cardiovasc Interv 2012;5:261-9.
  38. Jneid H, Anderson JL, Wright RS, et al. 2012 ACCF/AHA focused update of the guideline for the management of patients with unstable angina/non-ST-elevation myocardial infarction (updating the 2007 guideline and replacing the 2011 focused update): a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. J Am Coll Cardiol 2012;60:645-81.
  39. Hamm CW, Bassand JP, Agewall S, et al. ESC Guidelines for the management of acute coronary syndromes in patients presenting without persistent ST-segment elevation: The Task Force for the management of acute coronary syndromes (ACS) in patients presenting without persistent ST-segment elevation of the European Society of Cardiology (ESC). Eur Heart J 2011;32:2999-3054.
  40. Levine GN, Bates ER, Blankenship JC, et al. 2011 ACCF/AHA/SCAI Guideline for Percutaneous Coronary Intervention: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines and the Society for Cardiovascular Angiography and Interventions. Circulation 2011;124:e574-651.
  41. Ferraris VA, Saha SP, Oestreich JH, et al. 2012 update to the Society of Thoracic Surgeons guideline on use of antiplatelet drugs in patients having cardiac and noncardiac operations. Ann Thorac Surg 2012;94:1761-81.
  42. Roffi M, Patrono C, Collet JP, et al. 2015 ESC Guidelines for the management of acute coronary syndromes in patients presenting without persistent ST-segment elevation: Task Force for the Management of Acute Coronary Syndromes in Patients Presenting without Persistent ST-Segment Elevation of the European Society of Cardiology (ESC). Eur Heart J. 2016;37:267-315.
  43. Wilson JM, Jungner YG. [Principles and practice of mass screening for disease]. Bol Oficina Sanit Panam 1968;65:281-393.

Clinical Topics: Acute Coronary Syndromes, Cardiac Surgery, Dyslipidemia, Heart Failure and Cardiomyopathies, Invasive Cardiovascular Angiography and Intervention, Stable Ischemic Heart Disease, Vascular Medicine, Atherosclerotic Disease (CAD/PAD), ACS and Cardiac Biomarkers, Aortic Surgery, Cardiac Surgery and Heart Failure, Cardiac Surgery and SIHD, Lipid Metabolism, Nonstatins, Novel Agents, Heart Failure and Cardiac Biomarkers, Interventions and ACS, Interventions and Coronary Artery Disease, Interventions and Vascular Medicine, Chronic Angina

Keywords: Acute Coronary Syndrome, Adenosine, Adenosine Diphosphate, Agglutination, Angina, Stable, Angina, Unstable, Angioplasty, Aspirin, Atherosclerosis, Blood Platelets, Cholesterol, LDL, Coronary Artery Bypass, Coronary Artery Disease, Coronary Occlusion, Drug-Eluting Stents, Electric Impedance, Endothelium, Fibrin, Fibrinogen, GTPase-Activating Proteins, Macrophages, Microscopy, Confocal, Microvessels, Myocardial Infarction, Percutaneous Coronary Intervention, Phenotype, Phosphoproteins, Phosphorylation, Physiological Processes, Platelet Activation, Platelet Aggregation, Platelet Aggregation Inhibitors, Platelet Function Tests, Platelet Membrane Glycoprotein IIb, Prospective Studies, Randomized Controlled Trials as Topic, Receptor, PAR-1, Receptors, Thromboxane A2, Prostaglandin H2, Registries, Risk Factors, Risk Reduction Behavior, Stroke, Thrombelastography, Thrombin, Thrombosis, Thromboxane A2, Ticlopidine, Vascular System Injuries, Vasodilator Agents

< Back to Listings