open access

Vol 68, No 4 (2010)
Original articles
Published online: 2010-04-23
Submitted: 2012-12-28
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Factors responsible for “aspirin resistance” - can we identify them?

Marek Postuła, Bożena Tarchalska-Kryńska, Krzysztof J. Filipiak, Dariusz Kosior, Agnieszka Serafin, Zenon Huczek, Grzegorz Opolski
Kardiol Pol 2010;68(4):410-418.

open access

Vol 68, No 4 (2010)
Original articles
Published online: 2010-04-23
Submitted: 2012-12-28

Abstract

Background: Aspirin (ASA) is an effective antiplatelet drug that reduces the risk of myocardial infarction, stroke, or death by approximately 25% in patients who are at increased risk of cardiovascular events. However, many patients with cardiovascular disease do not respond to ASA treatment and are deemed ASA resistant. The term “ASA resistance” has been used to describe not only the lack of expected pharmacologic effects of ASA on platelets but also poor clinical outcomes, such as recurrent vascular events, in patients treated with ASA.
Aim: In this prospective observation of patients with stable coronary artery disease (CAD) who received ASA for secondary prevention, we investigated factors responsible for ASA resistance by determining ASA response using the PFA-100 analyser and evaluating relation of ASA resistance to various studied parameters.
Methods: Platelet function tests with the PFA-100 point-of-care system were performed in 92 patients with CAD (mean age 68 ± 8 years, 36 females) who had been taking 75-150 mg of ASA daily for secondary prevention for at least 3 months. Each patient had an angiographically documented CAD with stable angina. ASA resistance was defined as a normal collagen/epinephrine closure time (CEPI-CT) on the PFA-100 (≤ 150 s). Patients with CT ≥ 250 s were defined as ASA responders and patients with CT between 150 and 250 s as semi-responders.
Results: Using a collagen/epinephrine-coated cartridge on the PFA-100, the prevalence of platelet inhibition failure was 29%, while 30% of patients were semi-responders. In our study population, adequate response to ASA was found in 40% of patients. In multivariate logistic regression analysis, parameters independently related to platelet inhibition failure included compliance to ASA therapy [odds ratio (OR) 0.8, 95% confidence interval (CI) 0.20–0.35, p = 0.001], total cholesterol/HDL cholesterol level ratio > 2.99 (OR 0.19, 95% CI 0.05–0.81, p = 0.02), and heart rate > 69 bpm (OR 4.44, 95% CI 1.37-14.38, p = 0.01).
Conclusions: In patients with stable CAD, about one third of the subjects were ASA resistant by PFA-100. Our study shows that non-compliance could be one of the most important risk factors responsible for high residual platelet activity in patients with stable CAD taking ASA. Thus, non-compliant patients should be carefully educated about the mechanism of action of this drug to understand the necessity and long-term benefits of treatment with ASA.

Abstract

Background: Aspirin (ASA) is an effective antiplatelet drug that reduces the risk of myocardial infarction, stroke, or death by approximately 25% in patients who are at increased risk of cardiovascular events. However, many patients with cardiovascular disease do not respond to ASA treatment and are deemed ASA resistant. The term “ASA resistance” has been used to describe not only the lack of expected pharmacologic effects of ASA on platelets but also poor clinical outcomes, such as recurrent vascular events, in patients treated with ASA.
Aim: In this prospective observation of patients with stable coronary artery disease (CAD) who received ASA for secondary prevention, we investigated factors responsible for ASA resistance by determining ASA response using the PFA-100 analyser and evaluating relation of ASA resistance to various studied parameters.
Methods: Platelet function tests with the PFA-100 point-of-care system were performed in 92 patients with CAD (mean age 68 ± 8 years, 36 females) who had been taking 75-150 mg of ASA daily for secondary prevention for at least 3 months. Each patient had an angiographically documented CAD with stable angina. ASA resistance was defined as a normal collagen/epinephrine closure time (CEPI-CT) on the PFA-100 (≤ 150 s). Patients with CT ≥ 250 s were defined as ASA responders and patients with CT between 150 and 250 s as semi-responders.
Results: Using a collagen/epinephrine-coated cartridge on the PFA-100, the prevalence of platelet inhibition failure was 29%, while 30% of patients were semi-responders. In our study population, adequate response to ASA was found in 40% of patients. In multivariate logistic regression analysis, parameters independently related to platelet inhibition failure included compliance to ASA therapy [odds ratio (OR) 0.8, 95% confidence interval (CI) 0.20–0.35, p = 0.001], total cholesterol/HDL cholesterol level ratio > 2.99 (OR 0.19, 95% CI 0.05–0.81, p = 0.02), and heart rate > 69 bpm (OR 4.44, 95% CI 1.37-14.38, p = 0.01).
Conclusions: In patients with stable CAD, about one third of the subjects were ASA resistant by PFA-100. Our study shows that non-compliance could be one of the most important risk factors responsible for high residual platelet activity in patients with stable CAD taking ASA. Thus, non-compliant patients should be carefully educated about the mechanism of action of this drug to understand the necessity and long-term benefits of treatment with ASA.
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Keywords

aspirin resistance; platelets; PFA-100; stable coronary artery disease

About this article
Title

Factors responsible for “aspirin resistance” - can we identify them?

Journal

Kardiologia Polska (Polish Heart Journal)

Issue

Vol 68, No 4 (2010)

Pages

410-418

Published online

2010-04-23

Bibliographic record

Kardiol Pol 2010;68(4):410-418.

Keywords

aspirin resistance
platelets
PFA-100
stable coronary artery disease

Authors

Marek Postuła
Bożena Tarchalska-Kryńska
Krzysztof J. Filipiak
Dariusz Kosior
Agnieszka Serafin
Zenon Huczek
Grzegorz Opolski

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