Relation between inhibition of platelet aggregation and clinical outcomes☆,☆☆,★
Section snippets
Measurement of Biological Effect
When treating patients with antithrombotic therapy, it is common to measure some parameter of the hemostatic system to assess the biological effect of the agent. Such assays typically quantitate the ability of the agent to interrupt the hemostatic system. The assumption is made that a certain level of inhibition is desirable in producing a balance between providing efficacy and remaining safe. Examples of this include measurement of the activated partial thromboplastin time and the activated
Summary and Conclusions
Despite a clinical trials experience in excess of 30,000 randomized patients, there is no definitive answer or agreement as to the relation between the level of inhibition of platelet aggregation and clinical outcome. Work with abciximab in the setting of percutaneous intervention would suggest that a level of platelet inhibition in excess of 80% provides the most favorable clinical benefit. Whether this applies to the small molecule inhibitors such as eptifibatide, tirofiban, and lamifiban is
References (39)
- et al.
Immediate and reversible platelet inhibition after intravenous administration of a peptide glycoprotein IIb/IIIa inhibitor during percutaneous coronary intervention
Am J Cardiol
(1995) - et al.
Expression of ligand-induced binding sites on glycoprotein IIB/IIIa complexes and the effect of various inhibitors
Am Heart J
(1998) - et al.
Clinical pharmacology of eptifibatide
Am J Cardiol
(1997) - et al.
Relation between systemic anticoagulation as determined by activated partial thromboplastin time and heparin measurements and in-hospital clinical events in unstable angina and non-Q wave myocardial infarction
Am Heart J
(1996) Collaborative overview of randomised trials of antiplatelet therapy, II: maintenance of vascular graft or arterial patency by antiplatelet therapy
Br Med J
(1994)- et al.
Platelet glycoprotein IIb/IIIa receptors in cardiovascular medicine
N Engl J Med
(1995) - et al.
Antiplatelet and antithrombin therapies in the acute coronary syndromes
Curr Opin Cardiol
(1997) - et al.
Monitoring the coagulation system after thrombolytic therapy
- et al.
Activated partial thromboplastin time and outcome after thrombolytic therapy for acute myocardial infarction: results from the GUSTO-I trial
Circulation
(1996) - et al.
Activated partial thromboplastin time and clinical outcome among patients with unstable angina or non-Q-wave MI treated with intravenous heparin [abstract]
Circulation
(1996)
An analysis of the lowest effective intensity of prophylactic anticoagulation for patients with nonrheumatic atrial fibrillation
N Engl J Med
Platelet aggregation, II: some results from a new method of study
J Clin Pathol
Use of a monoclonal antibody directed against the platelet glycoprotein IIb/IIIa receptor in high-risk coronary angioplasty
N Engl J Med
Platelet glycoprotein IIb/IIIa receptor blockade and low-dose heparin during percutaneous coronary revascularization
N Engl J Med
Randomised placebo-controlled trial of abciximab before and during coronary intervention in refractory unstable angina: the CAPTURE study
Lancet
Randomised placebo-controlled trial of effect of eptifibatide on complications of percutaneous coronary intervention: IMPACT II
Lancet
Effects of platelet glycoprotein IIb/IIIa blockade with tirofiban on adverse cardiac events in patients with unstable angina or acute myocardial infarction undergoing coronary angioplasty
Circulation
Meeting highlights: XIXth Congress of the European Society of Cardiology
Circulation
Meeting highlights: 46th annual scientific sessions of the American College of Cardiology
Circulation
Cited by (29)
Preincisional peritonsillar vs. intravenous lornoxicam for posttonsillectomy analgesia: A clinical and platelet aggregometry comparative study
2012, Egyptian Journal of AnaesthesiaCitation Excerpt :Secondly, the inhibition in platelet aggregation presented in intravenous group did not result in increased bleeding episodes. A future research question arises about the relation between the level of platelet aggregation inhibition and clinical presentation [39]. Thirdly, patients in the placebo controls showed mild significant reductions in platelet functions.
Facts and controversies of aspirin and clopidogrel therapy
2009, American Heart JournalCitation Excerpt :In the laboratory, resistance theoretically encompasses the drug's failure to attain a particular level of platelet inhibition in ex vivo studies. Although platelet testing was originally developed to identify patients at risk for platelet dysfunction,42 there has been considerable focus on using ex vivo platelet testing to identify patients whose platelets may be poorly responsive to antiplatelet therapy. Several platelet function tests are available, including bleeding time, optical aggregometry, PFA-100, and VerifyNow (Table III).
- ☆
From the aDivisions of Cardiology and Hematology, Duke University Medical Center; the bDivision of Cardiology, Baylor College of Medicine.
- ☆☆
Reprint requests: Robert A. Harrington, MD, Duke Clinical Research Institute, P.O. Box 17969 Durham, NC 27715.
- ★
4/0/93433