Drug Resistance
Conditions
Keywords
Platelets, Aspirin Resistance, Platelet aggregation
Brief summary
Despite treatment with aspirin a large number of patients suffer a myocardial infarction. It has been speculated that these patients might be resistant to aspirin, and studies have indicated that this phenomenon is related to a less favourable prognosis. At present, no international consensus exists on how to measure aspirin resistance. The purpose of this study is to compare different methods for detecting aspirin resistance. A classic but cumbersome way of evaluating platelet function will be compared to newer, easy-handling point-of-care tests. We hypothesize that one or more point-of-care tests will prove to be superior to the classic platelet function test in detecting aspirin resistance.
Detailed description
Platelets play a major role in arterial thrombus formation - the cause of cardiovascular death, acute myocardial infarction and ischemic stroke and the number one killer in the Western World. Binding the COX enzyme platelet aggregation is inhibited by aspirin, and as prophylaxis against death, myocardial infarction and stroke aspirin is the most widely used drug worldwide. Low dose aspirin has been shown to improve outcome in patients with ischemic heart disease, but approximately 12% of these patients will suffer from a vascular event during a 2 year follow-up period despite aspirin therapy. It has been speculated that these patients might be resistant to the antiaggregatory effect of aspirin, and a diminished response to aspirin has been correlated with a less favourable outcome. However, at present no international consensus exists on how to measure aspirin resistance. Comparisons: The platelet aggregation in patients with ischemic heart disease on chronic, low dose aspirin is compared to platelet aggregation i healthy volunteers evaluated with different tests. The traditional way of evaluating platelet function, Platelet Aggregometry a.m. Born, will be compared to 3 point-of-care tests (VerifyNow, PFA-100 and Multiplate Whole Blood Aggregometer) and to urin- and serum thromboxane metabolites as a measure of COX inhibition.
Interventions
DRUGacetylsalicylic acid
Sponsors
Danish Research Agency
University of Aarhus
Study design
Allocation
NON_RANDOMIZED
Intervention model
SINGLE_GROUP
Primary purpose
DIAGNOSTIC
Masking
NONE
Eligibility
Sex/Gender
ALL
Age
18 Years to No maximum
Healthy volunteers
Yes
Inclusion criteria
* ischemic heart disease verified with a coronary angiogram * treatment with 75 mg aspirin once daily
Exclusion criteria
* ischemic vascular event within the previous 12 months * percutaneous coronary intervention or coronary artery by-pass grafting within the previous 12 months * treatment with NSAID, clopidogrel, ticlopidine, dipyridamole, warfarin or any other drug affecting platelet aggregation * platelet count \< 120 x 10\^9/l * not able to give informed consent
Design outcomes
Primary
| Measure | Time frame |
|---|---|
| Platelet aggregation (as determined by 3 point-of-care tests and by serum-thromboxane A2 + urine 11-dehydro thromboxane B2) is measured once daily for 4 days after one week of treatment with aspirin 75 mg/day | — |
Countries
Denmark
Outcome results
None listed