Heart attacks and strokes are common causes of death worldwide. These events occur in part,
due to increased activity of platelets, which cause clotting (thrombosis) within heart and
brain blood vessels.
Anti-platelet therapies (e.g. aspirin) reduce the likelihood of platelet thrombosis and
therefore protect against heart attacks and strokes. However serious bleeding into the gut
and brain occurs in a number of individuals prescribed aspirin. Currently, there is no
reliable method for assessing the relative risks of thrombosis versus bleeding in individual
patients prior to or during aspirin therapy.
We have recently discovered that individuals with a particular genetic make-up, those with
genetic variants in two genes called PPARGC1β and CNTN4, demonstrate more active (sticky)
platelets. We then found that these same individuals suffered a greater number of
cardiovascular events. Interestingly, low dose aspirin suppressed the excessive platelet
stickiness and protected against heart attacks and strokes in these patients.
In this project, we aim to confirm and extend the above findings. We hope that testing for
PPARGC1β and CNTN4 genetic variants will allow us to identify which patients will benefit
from low dose aspirin therapy - i.e. receive protection from heart attacks and strokes, but
not suffer any bleeding complications.