Mechanism Based Resistance to Aspirin
The purpose of this research is to study why some people do not respond to the benefits of aspirin therapy. The benefit of aspirin is cardioprotection, or decreasing the risk of heart attack and/or stroke. Aspirin works by disabling the platelets, part of the blood cells used in clotting, from sticking together and forming blood clots, thus protecting the heart. It has been observed that failure to respond to aspirin therapy occurs in about 10% of the general population and that despite taking aspirin everyday, this group of non- responders is not getting protection for their heart. The investigators would like to determine why and how this happens.
Pharmacological Aspirin Non-responsiveness
|Study Design:||Endpoint Classification: Pharmacokinetics/Dynamics Study
Intervention Model: Single Group Assignment
Masking: Open Label
Primary Purpose: Treatment
|Official Title:||Mechanism Based Resistance to Aspirin|
- Arachidonic acid induced platelet aggregation [ Time Frame: 8 hours postdose ] [ Designated as safety issue: No ]
- Serum thromboxane B2 concentration Urinary 11-dehydro thromboxane B2 concentration Urinary 2,3 dinor-6 keto PGF1α concentration [ Time Frame: 8 hours postdose ] [ Designated as safety issue: No ]
|Study Start Date:||September 2004|
|Study Completion Date:||October 2009|
|Primary Completion Date:||October 2009 (Final data collection date for primary outcome measure)|
single dose of aspirin 325 mg p.o.
325 mg enteric coated single dose p.o.
|Principal Investigator:||Garret A FitzGerald, MD||University of Pennsylvania, Institute for Translationals Medicine and Therapeutics|
|Principal Investigator:||Susanne Fries, MD||University of Pennsylvania, Institute for Translationals Medicine and Therapeutics|
|Principal Investigator:||Tilo Grosser, MD||University of Pennsylvania, Institute for Translationals Medicine and Therapeutics|