Loss of Effect of Aspirin on Platelet Aggregation During Chronic Administration
| Status: | Terminated |
|---|---|
| Conditions: | Hematology |
| Therapuetic Areas: | Hematology |
| Healthy: | No |
| Age Range: | 18 - Any |
| Updated: | 4/21/2016 |
| Start Date: | June 2004 |
| End Date: | February 2011 |
Aspirin has shown to be beneficial to some patients with certain diseases such as coronary
artery disease or stroke. We are investigating how aspirin works on regulating platelets and
thromboxane over time at different doses. We hope to find the best dose of aspirin and/or
other medications to help people who are at risk for heart attack or stroke.
artery disease or stroke. We are investigating how aspirin works on regulating platelets and
thromboxane over time at different doses. We hope to find the best dose of aspirin and/or
other medications to help people who are at risk for heart attack or stroke.
he purpose of the study is to better understand the mechanism for failure of daily aspirin
administration to prevent cardiovascular events in some at risk individuals. We seek to
describe the effect of chronic aspirin administration at varying doses on platelet
aggregation. This will help to define mechanisms for aspirin failure and to pursue possible
alternative therapies in patients who fail to respond to aspirin therapy.
We hypothesize that (1) inhibition by aspirin (ASA) of ex vivo-induced platelet aggregation
varies in a predictable time and dose dependent manner, (2) thromboxane and prostacyclin
production is inhibited by ASA in a dose-dependent manner and remains relatively constant
over time once maximal inhibition has occurred, and (3) granule secretion by platelets
during induced aggregation is inhibited by aspirin acutely but this effect does not persist
during chronic administration at high doses.
administration to prevent cardiovascular events in some at risk individuals. We seek to
describe the effect of chronic aspirin administration at varying doses on platelet
aggregation. This will help to define mechanisms for aspirin failure and to pursue possible
alternative therapies in patients who fail to respond to aspirin therapy.
We hypothesize that (1) inhibition by aspirin (ASA) of ex vivo-induced platelet aggregation
varies in a predictable time and dose dependent manner, (2) thromboxane and prostacyclin
production is inhibited by ASA in a dose-dependent manner and remains relatively constant
over time once maximal inhibition has occurred, and (3) granule secretion by platelets
during induced aggregation is inhibited by aspirin acutely but this effect does not persist
during chronic administration at high doses.
Inclusion Criteria:
- Males
- Age 18-40 years
- Non-smokers
Exclusion Criteria:
- ASA/NSAID use previous 14 days.
- Evidence of ASA/NSAID use within previous 14 days at baseline visit based on
investigator interpretation of platelet aggregation and platelet secretion studies.
- History of chronic NSAID use.
- Currently taking NSAIDs, corticosteroids, or anticoagulants.
- History of coronary artery disease, myocardial infarction, coronary artery bypass
grafting, percutaneous angioplasty, diabetes mellitus or stroke.
- History of gastric,duodenal, or esophageal ulcers or serious gastrointestinal bleed.
- History of frequent headaches, pain syndrome, or other condition requiring frequent
use of analgesics.
- History of adverse reaction to ASA.
- Initial platelet count <100K/µl or >500K/µl.
- Initial hematocrit <35% or >50%.
- Weight less than 110 pounds.
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