scholarly journals Relationship Between the Serum sCD40L Level and Aspirin-Resistant Platelet Aggregation in Patients With Stable Coronary Artery Disease

2008 ◽  
Vol 72 (1) ◽  
pp. 61-66 ◽  
Author(s):  
Burak Pamukcu ◽  
Huseyin Oflaz ◽  
Imran Onur ◽  
Kenan Midilli ◽  
Gulden Yilmaz ◽  
...  
Keyword(s):  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Platelet Aggregation ◽  
Stable Coronary Artery Disease ◽  
Artery Disease ◽  
Scd40l Level

Thrombopoietin and platelet aggregation in patients with stable coronary artery disease

Platelets ◽  
2017 ◽  
Vol 28 (8) ◽  
pp. 822-824
Author(s):  
Sanne Bøjet Larsen ◽  
Erik Lerkevang Grove ◽  
Søs Neergaard-Petersen ◽  
Morten Würtz ◽  
Anne-Mette Hvas ◽  
...  
Keyword(s):  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Platelet Aggregation ◽  
Stable Coronary Artery Disease ◽  
Artery Disease

Greater reduction of platelet activation markers and platelet-monocyte aggregates by prasugrel compared to clopidogrel in stable coronary artery disease

2008 ◽  
Vol 100 (10) ◽  
pp. 626-633 ◽  
Author(s):  
Christoph arenhorst ◽  
Stefan James ◽  
John T. Brandt ◽  
Joseph A. Jakubowski ◽  
Kenneth J. Winters ◽  
...  
Keyword(s):  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Platelet Aggregation ◽  
Platelet Activation ◽  
Maintenance Dose ◽  
Stable Coronary Artery Disease ◽  
Loading Dose ◽  
Activation Markers ◽  
Fluorescent Intensity ◽  
Artery Disease

SummaryPrasugrel, a novel P2Y12 ADP-receptor antagonist, has been reported to achieve greater inhibition of platelet aggregation compared to clopidogrel as assessed by light transmission aggregometry. It was the objective of this study to investigate the effect of prasugrel on alternative markers of platelet activation in comparison to a high loading dose and the approved maintenance dose of clopidogrel. One hundred ten aspirintreated patients with stable coronary artery disease were randomized to a loading dose (LD, day 1)/ maintenance dose (MD, days 2–29) of prasugrel 60 mg/10 mg or clopidogrel 600 mg/75 mg. Platelet activation markers were analyzed by whole blood flow cytometry pre-dose and at 2 and 24 hours after LD and pre-dose at 14 and 29 days. After stimulation with 20 µM ADP, 2 hours after LD, significantly lower expression of activated GPIIb/IIIa (4.3 vs. 21.8 [mean fluorescent intensity (MFI)], p < 0.001) and P-selectin (2.0 vs. 11.7 MFI, p < 0.001) along with decreased formation of platelet-monocyte aggregates (16.4% vs.29.6% positive cells, p < 0.001) was observed with prasugrel versus clopidogrel. All these effects were maintained through 24 hours and during the MD period. In conclusion, prasugrel 60 mg LD and 10 mg MD inhibit several markers of platelet activation and the formation of platelet-monocyte aggregates more effectively than a 600 mg LD and 75 mg MD of clopidogrel. Attenuated platelet aggregation and reduced expression of platelet procoagulant and pro-inflammatory markers with prasugrel suggest the potential to reduce cardiovascular events both in the acute setting and in longterm treatment.

Pharmacological Resistance to Aspirin In Patients with Stable Coronary Artery Disease.

Blood ◽  
2010 ◽  
Vol 116 (21) ◽  
pp. 1100-1100
Author(s):  
Davinder S Chadha ◽  
Sumana Budha ◽  
Jaya Prasad V ◽  
Arun S. Shet
Keyword(s):  
Coronary Artery Disease ◽  
Arachidonic Acid ◽  
Coronary Artery ◽  
Platelet Aggregation ◽  
Stable Coronary Artery Disease ◽  
Aspirin Resistance ◽  
Aspirin Therapy ◽  
Laboratory Parameters ◽  
History Of ◽  
Artery Disease

Abstract Abstract 1100 Introduction: Aspirin is the cornerstone of antiplatelet therapy in patients with coronary artery disease (Lancet 1997; 350: 437–439). However, a substantial proportion of patients manifest “breakthrough” events despite regular intake of aspirin suggesting therapeutic resistance to aspirin. Unfortunately, aspirin resistance remains a poorly defined term. There are conflicting reports on the prevalence of aspirin resistance in India. Materials and Methods: We evaluated the prevalence of pharmacological resistance to aspirin therapy in patients with stable and unstable coronary artery disease at a tertiary center in India. One hundred and twenty six patients aged ≥21 with recorded history of previous myocardial infarction (MI) and/or angiographically proven coronary artery disease undergoing routine outpatient cardiac care were enrolled in the study. Eligible patients were recruited 7days after ensuring compliance with a single formulation of aspirin (enteric coated aspirin 150 mg). Compliance was determined by obtaining a history of drug ingestion and performing a pill count. Patients with history of bleeding disorders and those consuming clopidogrel, dipyridamole, or non-steroidal anti- inflammatory drugs were excluded from study. Platelet function analysis was performed using the technique of optical aggregometry (Chronolog 490D, PA, USA). The following agonists (concentrations in parenthesis) were used: ADP (5 μM), Arachidonic acid (0.5 mg/mL), Collagen (2 μg/mL), and Epinephrine (5 μM). A healthy control was run every time a batch of tests was run for subjects. Pharmacological aspirin resistance was defined as the combined demonstration of mean platelet aggregation of ≥ 70% with ADP and a mean aggregation of ≥20% with Arachidonic acid in patients compliant with aspirin therapy. Patients satisfying either one of the above criteria were considered semi-responders (Am J Cardiol 2001; 88:230-5). Results: Out of a total of 126 patients with stable CAD, 64 % were responders, 36 % were non responders (semi-responders = 34% and resistant = 2%). All the patients with acute coronary syndrome (n = 7) were found to be semi-responders. Aspirin resistance did not show any statistically significant correlation with CAD risk factors like history of smoking, diabetes, obesity and hypertension. Of the laboratory parameters, only the total leukocyte count was significantly associated with the presence of aspirin resistance (p<0.03). Surprisingly, this relationship did not extend to either the absolute lymphocyte or neutrophil count. The other laboratory parameters such as hemoglobin, platelet count, hematocrit, mean cell volume, total protein, and albumin did not show any significant statistical relationship with aspirin resistance. To overcome the influence of preanalytical variables, platelet aggregation studies were repeated randomly on 50% of the study population. Paired analysis did not reveal any major changes among the responders and semi responders although the two resistant patients became semi-responders. Conclusion: Pharmacological resistance or semi-responsiveness to aspirin is prevalent in Indian patients with stable coronary artery disease. Long term follow up of these patients to ascertain their clinical outcome will assist in determining the clinical importance of this phenomenon. Disclosures: No relevant conflicts of interest to declare.

P804The AB0 gene locus is associated with increased platelet aggregation in stable coronary artery disease patients

2018 ◽  
Vol 39 (suppl_1) ◽  
Author(s):  
M K Christiansen ◽  
S B Larsen ◽  
M Nyegaard ◽  
S Neergaard-Petersen ◽  
M Wurtz ◽  
...  
Keyword(s):  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Platelet Aggregation ◽  
Gene Locus ◽  
Stable Coronary Artery Disease ◽  
Artery Disease

Effect of different aspirin doses on platelet aggregation in patients with stable coronary artery disease

2003 ◽  
Vol 33 (8) ◽  
pp. 350-354 ◽  
Author(s):  
S. Malhotra ◽  
Y. P. Sharma ◽  
A. Grover ◽  
S. Majumdar ◽  
S. M. Hanif ◽  
...  
Keyword(s):  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Platelet Aggregation ◽  
Stable Coronary Artery Disease ◽  
Artery Disease

Clopidogrel but not Aspirin prevents acute smoking-induced platelet aggregation in patients with stable coronary artery disease

2009 ◽  
Vol 123 (4) ◽  
pp. 640-643 ◽  
Author(s):  
Faouzi Addad ◽  
Tahar Chakroune ◽  
Ayed Asma ◽  
Fatma Abderazek ◽  
Dridi Zohra ◽  
...  
Keyword(s):  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Platelet Aggregation ◽  
Stable Coronary Artery Disease ◽  
Artery Disease
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