Literature DB >> 11729369

Platelet reactivity in coronary ostial blood: a reflection of the thrombotic state accompanying plaque rupture and of the adequacy of anti-thrombotic therapy.

S S Kabbani1, M W Watkins, P A Holoch, E F Terrien, B E Sobel, D J Schneider.   

Abstract

BACKGROUND: Optimal anti-thrombotic therapy for acute coronary syndromes (ACS) should suppress pro-thrombotic activity at the site of plaque rupture. We sought to determine whether platelet reactivity is increased in blood in the immediate vicinity of a ruptured plaque and is apparent even when blood is obtained by sampling from a catheter placed proximal to the lesion.
METHODS: Blood was obtained from a catheter placed in the aorta and from the same catheter after engaging the culprit coronary artery. Platelet reactivity was determined with the use of flow cytometry by surface expression of P-selectin.
RESULTS: In preliminary studies we demonstrated that a marker of thrombin activity, fibrinopeptide A, was similarly increased in blood taken from the coronary sinus and coronary arterial ostium of patients with ACS. Subsequently blood was obtained from the aorta and coronary arterial ostium through a coronary guide catheter for assessment of platelet reactivity in 23 subjects with ACS and 22 subjects with stable angina. The percentage of platelets expressing P-selectin in response to 0.2 microM adenosine diphosphate (ADP) was greater in coronary arterial samples from patients with ACS (aorta=6.1+/-1%, coronary artery=8.8+/-1.6%, p=0.02) compared with that in patients with stable symptoms (aorta=6.9+/-1.2, coronary artery=6.5+/-1.4, p=NS).
CONCLUSIONS: Coronary arterial blood obtained from the ostium through a coronary guide catheter can be used to determine whether thrombin activity and platelet reactivity are increased in the immediate vicinity of a ruptured atherosclerotic plaque. The simplicity of the approach developed should facilitate its use in future studies designed to determine the impact of optimal suppression of platelet reactivity and the pro-thrombotic state before coronary interventions on short- and long-term clinical outcomes.

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Year:  2001        PMID: 11729369     DOI: 10.1023/a:1012927606107

Source DB:  PubMed          Journal:  J Thromb Thrombolysis        ISSN: 0929-5305            Impact factor:   2.300


  24 in total

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2.  Blood clotting in minimally altered whole blood.

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Review 3.  Mechanisms initiating platelet thrombus formation.

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4.  Platelet activation in patients after an acute coronary syndrome: results from the TIMI-12 trial. Thrombolysis in Myocardial Infarction.

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5.  Randomised placebo-controlled trial of effect of eptifibatide on complications of percutaneous coronary intervention: IMPACT-II. Integrilin to Minimise Platelet Aggregation and Coronary Thrombosis-II.

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6.  Differential effects of anticoagulants on the activation of platelets ex vivo.

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8.  Determinants of rebound thrombin activity after cessation of heparin in patients undergoing coronary interventions.

Authors:  M W Watkins; P A Luetmer; D J Schneider; W T Witmer; P T Vaitkus; B E Sobel
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9.  Randomised placebo-controlled and balloon-angioplasty-controlled trial to assess safety of coronary stenting with use of platelet glycoprotein-IIb/IIIa blockade.

Authors: 
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  3 in total

1.  Lack of early augmentation of platelet reactivity after coronary intervention in patients treated with bivalirudin.

Authors:  David J Schneider; Burton E Sobel
Journal:  J Thromb Thrombolysis       Date:  2008-07-08       Impact factor: 2.300

2.  Engagement of platelet toll-like receptor 9 by novel endogenous ligands promotes platelet hyperreactivity and thrombosis.

Authors:  Soumya Panigrahi; Yi Ma; Li Hong; Detao Gao; Xiaoxia Z West; Robert G Salomon; Tatiana V Byzova; Eugene A Podrez
Journal:  Circ Res       Date:  2012-10-15       Impact factor: 17.367

3.  Decreased platelet reactivity in blood anticoagulated with bivalirudin or enoxaparin compared with unfractionated heparin: implications for coronary intervention.

Authors:  Atul Aggarwal; Burton E Sobel; David J Schneider
Journal:  J Thromb Thrombolysis       Date:  2002-06       Impact factor: 2.300

  3 in total

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