Project Details
Description
Impaired endogenous fibrinolysis has been observed in patients with AF, stroke, acute coronary syndrome, and renal disease. Such impaired fibrinolytic potential has been identified as a newly emerging risk factor for recurrent thrombotic cardiovascular events, which can be measured from a simple blood test. Currently, there is no conventionally available chronic oral pharmacotherapy to favourably modulate fibrinolytic status in patients in whom this is impaired. An earlier small pilot in 20 patients indicated that apixaban improved fibrinolysis in patients with non-valvular AF.
We wish to further understand the mechanism of action of apixaban and how it affects endogenous fibrinolytic potential, and use this hopefully in the future to underpin future clinical studies.
The background to this is described below.
We wish to further understand the mechanism of action of apixaban and how it affects endogenous fibrinolytic potential, and use this hopefully in the future to underpin future clinical studies.
The background to this is described below.
Short title | Apixaban |
---|---|
Status | Finished |
Effective start/end date | 1/09/19 → 30/07/20 |
Fingerprint
Explore the research topics touched on by this project. These labels are generated based on the underlying awards/grants. Together they form a unique fingerprint.