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Platelet Inhibition (platelet + inhibition)
Selected AbstractsThe effects of vasoactive agents, platelet agonists and anticoagulation on thrombelastographyACTA ANAESTHESIOLOGICA SCANDINAVICA, Issue 9 2007J. Kawasaki Background:, Platelet activation is a critical step in primary hemostasis and clot formation. We tested a hypothesis that platelet stimulating effects of vasoactive agents or platelet agonists could be shown using thrombelastography (TEG®) as faster onset or increased clot strength. We further examined if TEG® could be modified to evaluate activated platelets as a reversal of anticoagulation in the presence of partial thrombin inhibition. Methods:, Blood samples were obtained from 126 non-cardiac surgical patients. Effects of vasoactive agents on TEG® and aggregometry were examined using epinephrine, norepinephrine, vasopressin, desmopressin acetate, milrinone and olprinone (Experiment I). Platelet agonists (epinephrine, ADP and collagen) were separately tested on TEG® (Experiment II). Effects of platelet agonists (ADP and collagen) on TEG® under anticoagulation in the absence or presence of abciximab were studied (Experiment III). We also tested antiplatelet effects of milrinone and olprinone in the presence of anticoagulants on TEG® (Experiment IV). Results:, Neither vasoactive agents nor platelet agonists affected TEG® or aggregometry results except for milrinone and olprinone on aggregometry (Experiment I, II). Platelet agonists facilitated clotting in the presence of anticoagulants (Experiment III). Abciximab-treated platelets still exhibited procoagulant effects in the presence of heparin, while not in the presence of argatroban (Experiment III). Platelet inhibition on the modified TEG® was more extensive with milrinone than olprinone, and it was dose dependent (Experiment IV). Conclusion:, Modified TEG® using heparin or argatroban might delineate the procoagulant effects of platelets by adding platelet specific agonist. [source] Initiating and potentiating role of platelets in tissue factor-induced thrombin generation in the presence of plasma: subject-dependent variation in thrombogram characteristicsJOURNAL OF THROMBOSIS AND HAEMOSTASIS, Issue 3 2004K. Vanschoonbeek Summary., The hemostatic activity of plasma is determined by platelet activation and coagulation, which processes are mutually stimulatory. We studied this interaction by measuring the cleavage of fluorescent thrombin substrate in platelet-rich plasma (PRP), using the calibrated thrombogram method. In freshly isolated human plasma, thrombin formation triggered by tissue factor was fully dependent on the presence of platelets. It was abolished by annexin A5, indicating dependence on phosphatidylserine (PS) exposure at activated platelets. Comparison of plasmas from various subjects showed considerable interindividual variation in total amount of thrombin generation, regardless of whether platelets or PS-containing phospholipids were present. Integrin ,IIb,3 antagonists and ADP receptor blockage, but not aspirin, decreased the rate of thrombin generation (thrombin peak level) and extended the time of onset. Platelet inhibition with cAMP-elevating agents decreased the thrombin-forming rate, but surprisingly shortened the onset time. Stimulation of platelets with agonists of Gi/q-coupled receptors and, to a larger extent, with collagen or Ca2+ -ionophore increased the rate of thrombin generation and shortened its onset. In PRP from donors with low and high generation, platelet inhibitors and activators were similarly effective. Taken together, these results indicate that, in tissue factor-triggered PRP, PS exposure on activated platelets regulates both onset and rate of thrombin generation. However, coagulant activity rather than platelet activation determines the total amount of thrombin formed, i.e. the endogenous thrombin potential. Thus, kinetics of thrombin generation in PRP are controlled by platelet inhibitors and agonists, but the process is restricted in amount by the subject-dependent variation in coagulation. [source] Antiplatelet therapy after endovascular intervention: Does combination therapy really work and what is the optimum duration of therapy?,,CATHETERIZATION AND CARDIOVASCULAR INTERVENTIONS, Issue S1 2009Richard V. Milani MD Abstract The number of patients undergoing peripheral interventions has increased in recent years, highlighting the need for a safe and effective protective antithrombotic therapy. Platelet inhibition following coronary intervention is associated with a significantly reduced risk of graft occlusion, and has been acknowledged to be safe and effective in patients with peripheral arterial disease. Monotherapy with either aspirin or clopidogrel, reduces the rate of stroke, myocardial infarction, and cardiovascular death in patients suffering from peripheral arterial disease. Limited data from clinical trials investigating combination therapy of aspirin with ticlopidine or clopidogrel in patients undergoing endovascular interventions, have suggested the potential for a reduction in cardiovascular events. Nevertheless, the optimal duration of postintervention antiplatelet therapy remains to be defined. © 2009 Wiley-Liss, Inc. [source] Endothelin attenuates endothelium-dependent platelet inhibition in manACTA PHYSIOLOGICA, Issue 4 2010R. E. Malmström Abstract Aim:, The vascular endothelium produces several substances, including nitric oxide (NO) and endothelin-1 (ET-1), which participate in the regulation of vascular tone in humans. Both these substances may exert other actions of importance for cardiovascular disease, e.g. effects on vascular smooth muscle cell proliferation and inflammation, and NO inhibits platelet function. Experiments were designed to investigate the effect of ET-1 on endothelium-dependent vasodilatation and attenuation of platelet activation. Methods:, In 25 healthy male subjects (25 ± 1 years), forearm blood flow was measured by venous occlusion plethysmography, and platelet activity was assessed by whole blood flow cytometry (platelet fibrinogen binding and P-selectin expression) in unstimulated and adenosine diphosphate (ADP)-stimulated samples during administration of ET-1, the endothelium-dependent vasodilator acetylcholine and the NO synthase inhibitor l -NMMA. Results:, Acetylcholine increased forearm blood flow and significantly inhibited platelet activation in both unstimulated and ADP-stimulated samples. In samples stimulated with 0.3 ,m ADP, fibrinogen binding decreased from 41 ± 4% to 31 ± 3% (P < 0.01, n = 11) after acetylcholine administration. The vasodilator response to acetylcholine was significantly impaired during infusions of ET-1 and l -NMMA. ET-1 did not affect platelet activity per se, whereas l -NMMA increased platelet P-selectin expression. Both ET-1 and l -NMMA attenuated the acetylcholine-induced inhibition of platelet activity. Conclusions:, Our study indicates that, further to inhibiting endothelium-dependent vasodilatation, ET-1 may also attenuate endothelium-dependent inhibition of platelet activation induced by acetylcholine. An enhanced ET-1 activity, as suggested in endothelial dysfunction, may affect endothelium-dependent platelet modulation and thereby have pathophysiological implications. [source] Aggressive chronic platelet inhibition with prasugrel and increased cancer risks: revising oral antiplatelet regimens?FUNDAMENTAL & CLINICAL PHARMACOLOGY, Issue 4 2009Victor L. Serebruany Abstract The TRITON-TIMI 38 was a head-to-head trial to assess the efficacy and safety of the experimental antiplatelet agent prasugrel vs. standard care with clopidogrel on top of aspirin. Besides some ischemic protection at expense of overwhelming bleeding disadvantage, prasugrel treated patients experienced three times higher rate of colonic neoplasms then after clopidogrel, and this difference was significant. Importantly, known gastrointestinal bleeding preceded the diagnosis of colonic neoplasms only in half of the patients. Three potential mechanisms responsible for such harmful association are reviewed, namely: (i) direct hazard of the experimental drug on cancer occurrence and progression; (ii) indirect modulation of tumor growth; and (iii) enhanced metastatic dissemination due to instability of platelet-tumor cell aggregates, or/and inability to keep the disease locally due by much more potent long-term platelet inhibition should be considered. Significant excess of cancer after prasugrel is alarming, and can be reasonably explained, with critical clinical implications not only for prasugrel further development, but also for existing and future chronic antiplatelet strategies. If the hypothesis that oral aggressive platelet inhibition cause higher cancer risks will turn out to be true, then intensity of platelet inhibition, and especially duration of chronic antiplatelet therapy should be reconsidered. More delicate platelet inhibition, and shorter exposure to oral antiplatelet agents will prevail. [source] Smoking behaviour modulates pharmacokinetics of orally administered clopidogrelJOURNAL OF CLINICAL PHARMACY & THERAPEUTICS, Issue 4 2008A.-M. Yousef PhD Summary Background and objectives:, Clopidogrel is an important antiplatelet drug that is effective in preventing thrombotic events, especially for patients undergoing percutaneous coronary intervention. The therapeutic usefulness of clopidogrel has been limited by documented inter-individual heterogeneity in platelet inhibition, which may be attributable to known clopidogrel pharmacokinetic variability. The objective of this study was to assess the influence of smoking cigarettes and abnormal body weight on the pharmacokinetics of clopidogrel. Methods:, Seventy-six healthy adult male volunteers were selected randomly. Each subject received a single 75 mg oral dose of clopidogrel after overnight fast. Clopidogrel carboxylate plasma levels were measured and non-compartmental analysis was used to determine peak plasma concentration (Cmax), time to peak plasma concentration (Tmax), elimination half-life (t1/2e), and area under the curve (AUC0,,). Results:, One-third of volunteers were smokers (n = 27) and one-half had abnormal body weight (n = 39). Smokers had lower AUC0,, (smokers: 6·24 ± 2·32 ,g/h/mL vs. non-smokers: 8·93 ± 3·80 ,g/h/mL, P < 0·001) and shorter half-life (smokers: 5·46 ± 2·99 vs. non-smokers: 8·43 ± 4·26, P = 0·001). Smoking behaviour had no influence on Cmax (P = 0·3) and Tmax (P = 0·7). There was no statistically significant difference in Cmax, AUC0,,, Tmax and t1/2e between volunteers with abnormal body weight and normal body weight. However the difference in body weight of the two groups was relatively narrow (mean ± SE; 26·93 ± 0·16 vs. 23·11 ± 0·27). In general, the pharmacokinetic parameters were characterized by considerable inter-individual differences (Cmax = 3·09 ± 0·99 ,g/mL, CV = 32%), (Tmax =0·76 ± 0·24 h, CV = 31·6%), (AUC0,, = 7·98 ± 3·58 ,g/h/mL, CV = 44·8%), and (t1/2e = 7·38 ± 4·10 h, CV = 55·6%). Conclusion:, Smoking is a significant factor affecting the pharmacokinetics of clopidogrel, following administration of a single 75 mg dose in healthy young volunteers. The study supports smoking-cessation recommendations. Further studies are required to evaluate the influence of smoking and body weight on the pharmacokinetics of the active metabolite of clopidogrel and on the clinical effects of any differences observed. [source] The Rationale for and Comparisons of Different Antiplatelet Treatments in Acute Coronary SyndromeJOURNAL OF INTERVENTIONAL CARDIOLOGY, Issue 2008PAUL A. GURBEL M.D. Fundamentally, acute coronary syndromes are platelet-centric diseases, resulting from platelet-rich thrombi that develop at the site of vessel wall injury. In addition to aggregation, platelets modulate a plethora of other important pathophysiologic processes, including inflammation and coagulation. Therefore, a primary goal of therapy in the acute setting should be treatment with agents that provide predictable and superior platelet inhibition to prevent further ischemic events that develop from unchecked high platelet reactivity. Translational research studies of patients undergoing percutaneous revascularization have clearly demonstrated that adverse thrombotic outcomes are associated with high platelet reactivity and the latter is now emerging as a potent measurable cardiovascular risk factor. The intensity of antithrombotic therapy is influenced by patient risk. In the highest risk patients with elevated cardiac biomarkers indicative of myonecrosis, current guidelines support the use of early therapy with glycoprotein IIb/IIIa inhibition, aspirin, and clopidogrel. [source] Measurement of Antiplatelet Inhibition during Neurointerventional Procedures: The Effect of Antithrombotic Duration and Loading DoseJOURNAL OF NEUROIMAGING, Issue 1 2010DJ Pandya MD ABSTRACT BACKGROUND/OBJECTIVE Symptomatic thromboembolic events are the most common complications associated with aneurysm coiling, and carotid and intracranial stenting. Our objective is to assess the effect of aspirin (ASA) and clopidogrel dose and duration on platelet inhibition using a point of care assay in neurointerventional (NI) suite. METHOD The dose, duration, and point of care platelet function assay data for clopidogrel and aspirin therapy were prospectively collected between February 2006 and November 2007. Inadequate platelet inhibition for ASA was defined as ,550 ASA reaction units (ARU), and for clopidogrel was defined as ,50% inhibition of the P2Y12/ADP receptor RESULTS We collected data from 216 consecutive patients. Inadequate platelet inhibition was noted in 13% of patients on aspirin and 66% of patients on clopidogrel (P -value < .0001). Patients taking clopidogrel 75 mg for ,7 days, 300 mg for 24 hours, and 600 mg same day load had a mean P2Y12/ADP inhibition of 45%, 35% (P- value = .09), and 16%, respectively (P -value = .005). CONCLUSION Premedication with clopidogrel, in contrast to aspirin, does not achieve adequate platelet inhibition in about two-third of the patients. Same day antiplatelet loading may be insufficient to achieve adequate platelet inhibition and should be avoided if clinically feasible. J Neuroimaging 2010;20:64-69. [source] The Residual Platelet Aggregation after Deployment of Intracoronary Stent (PREDICT) scoreJOURNAL OF THROMBOSIS AND HAEMOSTASIS, Issue 1 2008T. GEISLER Summary.,Background:,Recent studies suggest a high interindividual variability of response to clopidogrel associated with adverse cardiovascular outcome. Different clinical factors are considered to influence a persistent residual platelet aggregation (RPA) despite conventional antiplatelet therapy. Objectives:,To investigate clinical factors that affect RPA after 600-mg clopidogrel loading in a large unselected cohort of patients with symptomatic CAD. Methods:,The study population included a consecutive cohort of 1092 patients treated with coronary stenting for stable angina and acute coronary syndromes (ACS). Residual platelet activity was assessed by ADP (20 ,mol L,1)-induced platelet aggregation , 6 h after LD. Eleven clinical factors were included in the primary analysis. Results:,In multivariate regression analysis increased RPA was significantly influenced by ACS, reduced LV-function, diabetes mellitus, renal failure (creatinine > 1.5 mg dL,1), and age > 65 years. In a factor-weighed model the risk for high RPA increased with higher score levels (OR for patients with a score of 1,3, 1.21, 95% CI 0.7,2.1; score 4,6, OR 2.0, 95% CI 1.17,3.5; P = 0.01; score 7,9, OR 3.3, 95% CI 1.8,6.0). During a 30-day follow-up the incidence of major adverse events was higher in patients with RPA in the upper tertile (4.8% vs. 2.5% in the 2nd and 1.5% in the 1st tertile; P < 0.05). Conclusions:,The PREDICT score provides a good tool to estimate residual platelet activity after clopidogrel LD by easily available patient details. Additionally, we demonstrate its association with short-term outcome. Thus, patients with a high score may benefit from intensified antiplatelet therapy by improved platelet inhibition and risk reduction for thromboischemic events. [source] Orbofiban: An orally active GPIIb/IIIa platelet receptor antagonistMEDICINAL RESEARCH REVIEWS, Issue 3 2001Nancy S. Nicholson Abstract A key role has been established for platelet activation and thrombus formation in the pathogenesis of acute coronary syndromes, and restenosis after percutaneous interventions. Antiplatelet agents that have a wider spectrum of activity than aspirin, and clopidogrel would be expected to provide improved antithrombotic protection. Preclinical studies were used to predict clinical efficacy of orally active GPIIb/IIIa antagonists such as xemilofiban, sibrafiban, lefradafiban, and orbofiban. While clinical trials have shown potent and sustained platelet inhibition, outcomes of trials with these first generation GPIIb/IIIa compounds have been disappointing. The active moiety of orbofiban is a potent and specific inhibitor of fibrinogen binding to GPIIb/IIIa, leading to inhibition of platelet aggregation to a wide variety of agonists. Studies comparing inhibition of aggregation and bleeding suggest that chronic inhibition of platelet aggregation can be achieved without major bleeding side effects. Thrombus formation is prevented in canine models of thrombosis. Orbofiban is approximately 28% bioavailable with a t1/2 of 18,hr. The high bioavailability, long half-life, and potential safety suggest orbofiban would be suitable for chronic oral administration. Clinical data demonstrate that orally administered orbofiban has the desired pharmacodynamic effect of inhibiting platelet aggregation but does not demonstrate clinical benefit when examined in large-scale trials. © 2001 John Wiley & Sons, Inc. Med Res Rev, 21, No. 3, 211,226, 2001 [source] Etomidate and thiopental inhibit platelet function in patients undergoing infrainguinal vascular surgeryACTA ANAESTHESIOLOGICA SCANDINAVICA, Issue 4 2001A. Gries Background: Postoperative platelet hyperaggregability following general anesthesia has been reported in patients undergoing major vascular surgery. In contrast, since anesthetic agents inhibited platelet function both in vitro and in vivo, an increased risk for postoperative bleedings due to prolonged platelet dysfunction has been discussed. Nevertheless, data describing platelet-affecting properties of induction agents such as etomidate and thiopental in patients undergoing major vascular surgery are lacking. Methods: Platelet function was determined at 0, 2, 20, and 200 ,g/ml thiopental and at 0, 0.2, 2, 20 ,g/ml etomidate in vitro in blood samples drawn from 16 patients suffering from severe occlusive arterial disease. In addition, 30 patients undergoing vascular surgery were investigated before (PRE) and after anesthesia induction (T0) either with etomidate (ETO group, n=16) or thiopental (THIO group, n=14), and 2 h after the beginning of surgery (T2). Platelet function was determined according to platelet aggregation, in vitro bleeding time, and flow cytometric measurements. Results:In vitro, P-selectin expression was inhibited by etomidate at 2 and 20 ,g/ml (,28% and ,38%, respectively) and also by thiopental at 200 ,g/ml (,27%). In patients undergoing vascular surgery, anesthesia induction in the ETO group resulted in a 31% prolongation of the in vitro bleeding time and an inhibition of ADP- and collagen-induced platelet aggregation (,30% and ,17%, respectively) and of P-selectin expression (,25%) at T0. In the THIO group, only ADP-induced platelet aggregation was affected (,16%). At T2, all parameters had reached PRE level again in both groups. Furthermore, in comparison with the THIO group, operation time was significantly prolonged and transfusion volume was significantly increased in the ETO group. In addition, platelet count and hematocrit significantly decreased at T2, whereas levels of tPA, PAI-1, fibrinogen and antithrombin III and partial thromboplastin time remained unchanged in both groups during the study period. Conclusions: In the present study, etomidate and, to a minor extent, thiopental offered significant platelet inhibitory properties. Anesthetic-induced platelet inhibition may lead to higher transfusion rates and prolonged operation times. Therefore, anesthetic-related platelet inhibitory properties should be considered when searching for the anesthetic agent of choice, especially in patients with compromised hemostasis and co-existing bleeding disorders. [source] Tirofiban and Activated Protein C Synergistically Inhibit the Instant Blood Mediated Inflammatory Reaction (IBMIR) from Allogeneic Islet Cells Exposure to Human BloodAMERICAN JOURNAL OF TRANSPLANTATION, Issue 7 2009S. Akima Instant blood mediated inflammatory reaction (IBMIR) occurs when islets are exposed to blood and manifests clinically as portal vein thrombosis and graft failure. The aim of this study was to determine the impact of recombinant human activated protein C (rhAPC) and platelet inhibition on IBMIR in order to develop a better targeted treatment for this condition. Five thousand human islet cell equivalents (IEQ) were mixed in a PVC loop system with 7 mL of ABO compatible human blood and incubated with rhAPC, either alone or in combination with tirofiban. Admixing human islets and blood caused rapid clot formation, consumption of platelets, leukocytes, fibrinogen, coagulation factors and raised d -dimers. Islets were encased in a fibrin and platelet clot heavily infiltrated with neutrophils. Tirofiban monotherapy was ineffective, whereas rhAPC monotherapy prevented IBMIR in a dose-dependent manner, preserving islet integrity while maintaining platelet and leukocyte counts, fibrinogen and coagulation factor levels, and reducing d -dimer formation. The combination of tirofiban and low-dose rhAPC inhibited IBMIR synergistically with an efficacy equal to high dose rhAPC. Tirofiban and rhAPC worked synergistically to preserve islets, suggesting that co-inhibition of the platelet and coagulation pathways' contribution to thrombin generation is required for the optimal anti-IBMIR effect. [source] Reduced Blood Platelet Sensitivity to Aspirin in Coronary Artery Disease: Are Dyslipidaemia and Inflammatory States Possible Factors Predisposing to Sub-optimal Platelet Response to Aspirin?BASIC AND CLINICAL PHARMACOLOGY & TOXICOLOGY, Issue 5 2006Leszek Markuszewski Platelet non-responsiveness to aspirin is associated with an increased risk of serious cardiovascular events. Several environmental and hereditary factors are reportedly involved in sub-optimal acetylsalicylic acid response. Forty-five coronary artery disease patients and 45 non-coronary artery disease controls received acetylsalicylic acid at a daily dose of 75,150 mg. Controls were examined twice: on the day of entering the study and 10 days later. Urinary 11-dehydrothromboxane B2 was assessed as the marker of platelet thromboxane generation. Aggregation was studied in platelet-rich plasma using turbidimetric aggregometry with collagen and arachidonic acid. Fifty to seventy percent of coronary artery disease patients showed an extent of collagen-induced aggregation above the upper quartile of the reference range compared with 8,15% in controls (P<0.003). For arachidonic acid-activated aggregation these proportions were 45,50% in coronary artery disease versus 7% in controls (P<0.007). In coronary artery disease patients, the acetylsalicylic acid-mediated platelet inhibition positively correlated with increased triglycerides (in arachidonic acid-stimulated platelets, r=0.30, P=0.0018), total cholesterol (r=0.33, P<0.0001 in coll and arachidonic acid-activated platelets) and elevated serum C-reactive protein (CRP) (r=0.27, P=0.0024). In coronary artery disease patients urine 11-dehydrothromboxane B2 concentrations were significantly increased compared to controls after 10 day acetylsalicylic acid intake (563; 313,728 pg/mg creatinine versus 321; 246,488 pg/mg creatinine, P=0.04). The incidence of suboptimal acetylsalicylic acid response incidence was more common in patients with coronary artery disease. Acetylsalicylic acid inhibition of blood platelet reactivity and thromboxane generation was less effective in these patients. Dyslipidaemia and chronic inflammatory states may promote suboptimal acetylsalicylic acid response in coronary artery disease patients. [source] Thromboembolic events after carotid endarterectomy are not prevented by aspirin, but are due to the platelet response to adenosine 5,-diphosphateBRITISH JOURNAL OF SURGERY (NOW INCLUDES EUROPEAN JOURNAL OF SURGERY), Issue 4 2000P. D. Hayes Background: Aspirin therapy fails to prevent a number of postprocedural thrombotic events, yet it still remains the standard antiplatelet regimen in most vascular surgical centres. After carotid endarterectomy (CEA), thrombosis of the endarterectomized vessel is preceded by increasing numbers of microemboli that can be detected with transcranial Doppler (TCD). The number and rate of emboli is highly predictive of thrombotic stroke. It was hypothesized that a preoperative test of platelet function might identify the mechanism(s) underlying post-CEA thrombosis. Methods: Blood was taken from 120 patients using a standardized phlebotomy technique. Platelet fibrinogen binding was measured by whole blood flow cytometry, in unstimulated samples, and in response to adenosine 5,-diphosphate (ADP) (10,5,10,7 mol l,1) and thrombin (0·02,0·16 units ml,1). Platelet aggregation was measured using ADP (4,20 × 10,7 mol l,1). The ability of aspirin to inhibit platelets was assessed by the aggregation induced by arachidonic acid. For the first 3 h after operation, the number of emboli occurring was quantified using TCD. Results: Of the 120 patients studied, 110 were monitored by TCD. These were divided into patients with more than 25 postoperative emboli (n = 22) and those with fewer than 25 emboli (n = 88). The degree of platelet inhibition induced by aspirin was not significantly different between the two groups (P = 0·89). However, platelets from the group with high rates of embolization bound 58 per cent more fibrinogen on flow cytometry in response to stimulation with a physiological dose of ADP (10,7 mol l,1) (P = 0·006). Aggregation of platelets from this group was also increased in response to ADP (35 per cent) relative to the group with few emboli (P = 0·001). ADP also induced more rapid aggregation in the patients with more than 25 emboli (P = 0·04). There was no difference in the activity of resting platelets (P = 0·4) or platelets stimulated by thrombin (P = 0·43), between the two groups of patients. Conclusion: These data suggest that it is the platelet response to ADP which is important in arterial thrombotic complications rather than products of the cyclo-oxygenase pathway. This observation could have significant therapeutic implications for other vascular or interventional procedures in which the endothelium is disrupted. © 2000 British Journal of Surgery Society Ltd [source] Point-of-care testing shows clinically relevant variation in the degree of inhibition of platelets by standard-dose abciximab therapy during percutaneous coronary interventionCATHETERIZATION AND CARDIOVASCULAR INTERVENTIONS, Issue 2 2004Michael J. Ray PhD Abstract Administration of GP IIb/IIIa inhibitors during percutaneous coronary intervention (PCI) has proven clinical benefit, but is administered at a dose allowing for the patients' weight but not other variables. This study of 75 patients evaluated platelet inhibition achieved by standard-dose abciximab therapy during PCI as measured by two point-of-care (POC) instruments, Plateletworks (PW) and whole blood aggregation (WB). Results were related to the decrease of platelet activation produced as well as patients' return of angina within 30 days. Flow cytometric measurement showed abciximab suppressed platelet-monocyte aggregates (P < 0.001) and activated glycoprotein IIb/IIIa (P < 0.001) but not P-selectin. Greater POC-measured inhibition corresponded to less postabciximab expression of platelet-monocyte aggregates (P < 0.01). Patients above the lowest quartile of POC inhibition with PW demonstrated a relative risk of experiencing return of angina within 30 days of 0.48 (0.23,0.99). In conclusion, POC measurements reflect platelet activation suppression, higher PW measurements being associated with a decreased risk of return of angina. Catheter Cardiovasc Interv 2004;62:150,154. © 2004 Wiley-Liss, Inc. [source] | ||||||||||||||||||||||