Background: Poststenting ischemic events occur despite dual-antiplatelet therapy, suggesting that a "one size fits all" antithrombotic strategy has significant limitations. Ex vivo platelet function measurements may facilitate risk stratification and personalized antiplatelet therapy.
Methods: We investigated the prognostic utility of the strength of adenosine diphosphate (ADP)-induced (MA(ADP)) and thrombin-induced (MA(THROMBIN)) platelet-fibrin clots measured by thrombelastography and ADP-induced light transmittance aggregation (LTA(ADP)) in 225 serial patients after elective stenting treated with aspirin and clopidogrel.
The objective of the study was to determine the relation of platelet reactivity, hypercoagulability and inflammation in various stages of coronary artery disease acuity (CAD). Thrombin-induced platelet-fibrin clot strength (MA), time to initial platelet-fibrin clot formation (R), C-reactive protein (CRP), prothrombotic factors, activated GPIIb/IIIa receptor expression and other biomarkers were studied in patients with asymptomatic stable CAD (AS), in patients undergoing PCI for stable (SA) and unstable angina (UA). MA and R were measured by thrombelastography, GPIIb/IIIa expression by flow cytometry and all other markers by fluorokine multianalyte profiling assays.
View Article and Find Full Text PDFHeightened thrombogenicity and biomarker evidence of inflammation have been independently associated with ischemic risk in patients with coronary artery disease. However, a study examining their relation has not been reported. We analysed the relation between measurements of thrombogenicity and biomarkers in patients undergoing stenting and followed for 24 months recurrent ischemic events.
View Article and Find Full Text PDFObjectives: The primary objective of this study was to compare the effect of therapy with bivalirudin alone versus bivalirudin plus eptifibatide on platelet reactivity measured by turbidometric aggregometry and thrombin-induced platelet-fibrin clot strength (TIP-FCS) measured by thrombelastography in percutaneous coronary intervention (PCI) patients. The secondary aim was to study the relation of platelet aggregation and TIP-FCS to the occurrence of periprocedural infarction.
Background: Bivalirudin is commonly administered alone to clopidogrel naïve (CN) patients and to patients on maintenance clopidogrel therapy (MT) undergoing elective stenting.
Platelets play a central role in the genesis of post-percutaneous coronary intervention (PCI) ischemic events. High post-procedural platelet reactivity to adenosine diphosphate (HPR(ADP)) may be a risk factor for ischemic events after PCI. The study was designed to evaluate a cutpoint of platelet reactivity that is associated with the occurrence of ischemic events after PCI.
View Article and Find Full Text PDFObjectives: The purpose of this study was to examine the effect of cigarette smoking on the platelet response to clopidogrel.
Background: Response variability to clopidogrel therapy has been demonstrated. Clopidogrel is metabolically activated by several hepatic cytochrome P450 (CYP) isoenzymes, including CYP1A2.
Background: The study rationale was to compare the biomarker profile of metalloproteinases (MMPs) and inflammation markers (IMs) in patients requiring revascularization with that of patients with long-term, clinically quiescent coronary artery disease (CAD).
Methods: Seventy-eight patients with symptomatic CAD (S-CAD) (7 patients with myocardial infarction and 71 patients with stable angina) and 67 patients with asymptomatic CAD (A-CAD) were enrolled. Plasma samples were analyzed for MMPs, MMP inhibitors (MMPIs), IMs, coagulation factors, and apolipoproteins by use of the fluorokine multianalyte profiling assay.
The routine off-label use of drug-eluting stents (DESs) has been associated with a higher prevalence of stent thrombosis in clinical practice than was suggested in US Food and Drug Administration (FDA) preapproval studies. Consequently, the early identification of patients at risk for stent thrombosis has become a major goal in cardiology. Although a number of factors may be involved in DES thrombosis, the biologic cascade begins with local platelet activation and culminates in platelet aggregation, the generation of coagulation factors, the formation of a fibrin network, and the creation of a stable occlusive thrombus.
View Article and Find Full Text PDFObjective: Diabetic patients may have a higher prevalence of platelet aspirin resistance than nondiabetic patients. Our goal was to analyze platelet aspirin responsiveness to various aspirin doses in diabetic and nondiabetic patients.
Research Design And Methods: We examined the effect of aspirin (81, 162, and 325 mg/day for 4 weeks each) on platelet aspirin responsiveness in 120 stable outpatients (30 diabetic patients and 90 nondiabetic patients) with coronary artery disease (CAD) using light transmittance aggregometry (LTA), VerifyNow, platelet function analyzer (PFA)-100, and levels of urinary 11-dehydro-thromboxane B(2) (11-dh-TxB(2)).
Selected aspirin treated patients may exhibit high platelet reactivity to agonists other than arachidonic acid. This study aimed to determine whether the VerifyNow identifies generalized high platelet reactivity supported by correlations with other established methods that stimulate platelets with various agonists. Stable outpatients with coronary artery disease (n = 110) were treated with aspirin in a two 3 x 3 Latin square design (81, 162 and 325 mg/day for 4 weeks each).
View Article and Find Full Text PDFBackground: The antiplatelet effect of aspirin is attributed to platelet cyclooxygenase-1 inhibition. Controversy exists on the prevalence of platelet resistance to aspirin in patients with coronary artery disease and effects of aspirin dose on inhibition. Our primary aim was to determine the degree of platelet aspirin responsiveness in patients, as measured by commonly used methods, and to study the relation of aspirin dose to platelet inhibition.
View Article and Find Full Text PDFObjectives: We sought to determine whether patients receiving chronic clopidogrel therapy undergoing nonemergent stenting who display high on-treatment preprocedural platelet aggregation measured by standard light transmittance aggregometry and thrombelastography (TEG) will be at increased risk for poststenting ischemic events.
Background: Patients exhibiting heightened platelet reactivity to adenosine diphosphate (ADP) might be at increased risk for recurrent ischemic events after coronary stenting.
Methods: A total of 100 consecutive patients receiving chronic antiplatelet therapy consisting of aspirin (325 mg qd) and clopidogrel (75 mg qd) were studied before undergoing nonemergent stenting.