+ Site Statistics
References:
54,258,434
Abstracts:
29,560,870
PMIDs:
28,072,757
+ Search Articles
+ PDF Full Text Service
How our service works
Request PDF Full Text
+ Follow Us
Follow on Facebook
Follow on Twitter
Follow on LinkedIn
+ Subscribe to Site Feeds
Most Shared
PDF Full Text
+ Translate
+ Recently Requested

Platelet count, not oxidative stress, may contribute to inadequate platelet inhibition by aspirin



Platelet count, not oxidative stress, may contribute to inadequate platelet inhibition by aspirin



International Journal of Cardiology 143(1): 43-50



Several patient characteristics have been shown to increase the risk of inadequate platelet inhibition by aspirin, yet underlying mechanisms remain mostly unknown. We explored whether oxidative stress, via isoprostane formation, was associated with inadequate platelet response to aspirin. Additionally, we sought to investigate whether individual pre-selected demographic, hematological or biochemical parameters further increased the risk of inadequate platelet response to aspirin. Two hundred consecutive subjects suffering from stable coronary artery disease and under daily aspirin therapy were enrolled in our study. Inadequate platelet response to aspirin was defined as residual platelet aggregation>or=20% per arachidonic acid-induced light transmission aggregometry. Morning urinary samples were used to determine levels of isoprostanes (8-iso-PGF2alpha) using an enzyme immunoassay. Eight subjects were deemed to present inadequate platelet response to aspirin. Wide intersubject variability was observed in urinary 8-iso-PGF2alpha levels. However, levels were similar between aspirin responders and non-responders. Patients with inadequate platelet response to aspirin had higher platelet counts and received the lowest daily aspirin dose when compared to responders, suggesting subtherapeutic aspirin therapy due to increased platelet production. Only platelet count remained independently predictive of inadequate platelet response to aspirin in a multiple logistic regression model. Urinary 8-iso-PGF2alpha levels, a reflection of systemic oxidative stress, did not appear to contribute to impaired platelet responsiveness to aspirin, while increased platelet production may partly explain this phenomenon.

Please choose payment method:






(PDF emailed within 0-6 h: $19.90)

Accession: 055025874

Download citation: RISBibTeXText

PMID: 19215991

DOI: 10.1016/j.ijcard.2009.01.037


Related references

Platelet activation and platelet-monocyte aggregate formation contribute to decreased platelet count during acute simian immunodeficiency virus infection in pig-tailed macaques. Journal of Infectious Diseases 208(6): 874-883, 2013

Platelet and Red Blood Cell Counts, as well as the Concentrations of Uric Acid, but Not Homocysteinaemia or Oxidative Stress, Contribute Mostly to Platelet Reactivity in Older Adults. Oxidative Medicine and Cellular Longevity 2019: 9467562, 2019

The Ratio of ADP- to TRAP-Induced Platelet Aggregation Quantifies P2Y12-Dependent Platelet Inhibition Independently of the Platelet Count. Plos One 11(2): E0149053, 2016

Platelet count evaluation using three automated haematology analysers compared with the immunoplatelet reference method, and estimation of possible inadequate platelet transfusion. International Journal of Laboratory Hematology 31(3): 298-306, 2008

Platelet cyclooxygenase inhibition by low-dose aspirin is not reflected consistently by platelet function assays: implications for aspirin "resistance". Journal of the American College of Cardiology 53(8): 667-677, 2009

High platelet count in platelet-rich plasma reduces measured platelet inhibition by abciximab but not tirofiban nor eptifibatide glycoprotein IIb/IIIa receptor antagonists. Journal of Thrombosis and Thrombolysis 9(2): 149-155, 1999

The role of platelet count, mean platelet volume, and the mean platelet volume/platelet count ratio in predicting postoperative vomiting in children after deep sedation. Saudi Medical Journal 37(10): 1082-1088, 2017

Total platelet count, adhesive platelet count, platelet adhesiveness in normal menstrual cycle and functional uterine bleeding: a comparative study. Asia-Oceania Journal of Obstetrics and Gynaecology 9(3): 265-269, 1983

Incomplete inhibition of platelet function as assessed by the platelet function analyzer (PFA-100) identifies a subset of cardiovascular patients with high residual platelet response while on aspirin. Platelets 22(3): 179-187, 2011

Platelet count and platelet associated immuno globulin g in 123 consecutive pregnancies relationship of maternal factors to neo natal platelet count. Pediatric Researchpart 2: 241a, 1984

A study of total platelet count, adhesive platelet count and platelet adhesiveness in various phases of normal menstrual cycles. Journal of Obstetrics and Gynaecology of India 25(6): 797-800, 1975

The effect of the normal menstrual cycle on the total platelet count, adhesive platelet count and platelet adhesiveness. Journal of Obstetrics and Gynaecology of the British Commonwealth 75(3): 357-359, 1968

Platelet count, mean platelet volume, platelet distribution width, and plateletcrit do not correlate with optical platelet aggregation responses in healthy volunteers. Journal of Thrombosis and Thrombolysis 22(3): 161-164, 2006

Aspirin inhibition of platelet deposition at angioplasty sites: demonstration by platelet scintigraphy. Radiology 151(2): 487-490, 1984

Effect of platelet antigen polymorphism on platelet inhibition by aspirin, clopidogrel, or their combination. Journal of the American College of Cardiology 47(3): 541-546, 2006