Atrial Fibrillation Clinical Trial
Official title:
Assessing The Effect of Apixaban on Endogenous Fibrinolysis in Patients With Non-Valvular Atrial Fibrillation
This study will assess the effect of apixaban on thrombotic status in patients with atrial fibrillation.In addition it will compare apixaban to aspirin and warfarin on their effect on endogenous fibrinolysis.
Patients with an irregular heart rhythm called atrial fibrillation (AF) have an increased
risk of forming blood clots inside the heart, that can then fragment and break off,
travelling through the circulation to the brain, where it can cause blockage of the small
blood vessels resulting in a stroke. Most patients with AF are prescribed blood thinning
medications in an attempt to prevent such clot formation. The body has the ability through
enzymes circulating in blood, to dissolve a clot once formed, such that even if a clot is
formed, it is rapidly dissolved and no lasting damage is sustained. This is known as
endogenous fibrinolysis. If this defence system is faulty or suboptimal, there is an
increased risk of clot formation, resulting in stroke or heart attack. Currently, there are
no available tablets to favourably modify this defence system of endogenous fibrinolysis. The
investigators will assess how this defence system functions in patients with AF who are on
different blood thinners. Then the investigators will also assess a group of patients before
and during treatment with a relatively new blood thinner called apixaban, to assess the
effect of this on the stickiness of blood and the ability of the blood to dissolve clots
(endogenous fibrinolysis). All the blood thinners will be prescribed for clinical
indications, not as part of the research. The research aspect of the study is that we will
perform a blood test to assess endogenous fibrinolysis.
Understanding the effect of apixaban on endogenous fibrinolysis raises the possibility that
apixaban, rather than other blood thinners, may be of particular use in patients with
impaired fibrinolysis who are at particularly high risk of clots due to inefficient
endogenous fibrinolysis.
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