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At least 1,657 records · Page 92Linked to original sources
PubMed2004

[Acetylsalicylic acid resistance--clinical diagnosis with unclear mechanism].

A review on the subject of aspirin resistance and its role in vascular diseases is presented. Although the clinical diagnosis of aspirin resistance is frequently made, little is known about its biochemical background. Only a few follow-up studies, with varying design, have dealt with the possible association between an aspirin resistant phenotype and clinical outcome in patients with atherothrombosis. However, it was recently shown that ibuprofen acts as a competitive inhibitor in the blockage of COX-1. This pharmacodynamic interaction results in secondary aspirin resistance, which may have clinical significance in patients taking both medicines. With the complex nature of vascular diseases in mind, it is not surprising that aspirin used as a single preventive strategy fails in many cases. At present, there is no clear evidence that treatment failure is associated with a particular aspirin resistant phenotype.

Aspirin↗
PubMed1992

[Effect of acetylsalicylic acid on the indicators of thrombocytic hemostasis in patients with myocardial infarction].

The examination of 50 patients with acute myocardial infarction indicated that enhanced platelet functional activity was a prognostically unfavourable sign and associated with a higher risk for myocardial infarction complications. The application of aspirin, 250 mg daily, in patients with high platelet functional activity in the acute period of the disease failed to produce a beneficial antiaggregatory effect.

Administration, Oral↗
PubMed2005

[Acetylsalicylic acid (ASA) resistance in patients with ischemic heart disease (IHD) as bioindicator of the treatment strategy].

BACKGROUND: The interest in aspirin resistance has been increasing during the last few years, with researchers earnestly pursuing alternative anti-platelet therapies and devices for measuring platelet aggregation. The recent studies suggest that 5-45% of patients taking aspirin do not experience adequate anti-platelet effects. METHODS AND RESULTS: There is scant evidence proving that aspirin resistance has some clinical consequences. To assess the prevalence of aspirin resistance in patients with ischemic heart disease (IHD) two independent methods were used: platelet aggregation in platelet rich plasma (PRP) after induction by propylgallate (CPG), and assessment of platelet function by PFA 100 method. The study population consisted of 424 patients treated for IHD on the 2nd Dept. of Medicine, Teaching Hospital, Hradec Kralove. The age, gender, diagnosis and effect of therapy were characterized in this group of the patients. Daily ASA dose was 100 mg. We used two methods to monitor ASA treatment efficacy: a) thrombocyte aggregation after induction by CPG, b) the assessment of platelet function by PFA 100 method. a) Of the patients studied by CPG platelet aggregation, 51 (12.1%) pts were resistant to ASA dose 100 mg/day, and 32 (7.6%) pts remained resistant even after increasig the dose to 200 mg/day. In 80 (20%) pts, the daily ASA dose of less than 100 mg was sufficient to inhibit platelet function. b) Although the PFA-100 system is not able to detect the difference between low and high ASA dose, we found 53 (15.2%) patients aspirin resistant using this method. CONCLUSIONS: In the patients with IHD treated with 100 mg of ASA per day, our study has shown that the prevalence of aspirin resistance was 12.1% using CPG method, and 15.2% using PFA-100 method. Aspirin resistance was dose dependent. Prevalence of ASA resistance in patients treated with 200 mg of ASA per day was only 7.6% using the CPG method.

Adolescent↗
PubMed2006

[Combination therapy with acetylsalicylic acid and non-aspirin nonsteroidal anti-inflammatory drugs].

Patients may require both low-dose aspirin (ASA) and a nonsteroidal anti-inflammatory drug (NSAID). This raises the questions of whether NSAIDs may inhibit the cardioprotective effects of low-dose ASA; whether the cardioprotective effect of low-dose ASA can be obtained by NSAIDs: and whether the combination of low-dose ASA and NSAIDs increases the risk of adverse effects. This review attempts to answer these questions.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed2006

[Health economic evaluation of low-dose acetylsalicylic acid in the primary prevention of cardiovascular disease].

INTRODUCTION AND OBJECTIVES: Low-dose aspirin is standard treatment for patients with a history of cardiovascular disease. Its use in primary prevention is more controversial. However, recent studies also support the use of aspirin in high-risk individuals with no history of cardiovascular disease. This study investigated the health economic implications of using low-dose aspirin in the primary prevention of cardiovascular disease in Spain. METHODS: A model was developed to predict the cost-effectiveness of low-dose aspirin in the primary prevention of cardiovascular disease over a period of 10 years. The direct costs used were those of the Spanish National Health Service (NHS). Results were expressed as cost per life-year gained and per quality-adjusted life-year gained. RESULTS: Administering low-dose aspirin to an individual with a 10-year risk of coronary heart disease > or =15% resulted in an average net saving of e 797 (95% CI, e 263-1331) over the 10-year period, with savings starting in the first year. For an annual risk > or =0.24%, this form of treatment would reduce NHS costs. Treating all at-risk individuals in the Spanish population with aspirin would save e 26.5 million from the healthcare budget, starting in the first year. CONCLUSIONS: Administering low-dose aspirin to individuals with a 10-year risk of coronary heart disease > or =15% would result in significant cost savings for the Spanish NHS. Sensitivity analysis confirmed the robustness of these findings.

Adult↗