Characterisation of platelet hyperactivity in acute coronary syndromes
Research type
Research Study
Full title
Dysregulation of platelet phosphodiesterase 3A isoforms promote platelet hyperactivity in atherothrombotic disease.
IRAS ID
321365
Contact name
Khalid Naseem
Contact email
Sponsor organisation
University of Leeds
Clinicaltrials.gov Identifier
Not applicable, Not applicable
Duration of Study in the UK
4 years, 9 months, 29 days
Research summary
Heart disease is a broad term that includes several progressively more serious conditions including stable coronary artery disease (CAD), acute coronary syndrome (ACS) and heart failure. Blood platelets are a group of cells that form blood clots to ensure that we stop bleeding when we injure ourselves. However, in heart disease platelets also form blood clots inside the blood vessels, a process called to cause thrombosis, often causing a blockage of blood flow to the heart and leading to a heart attack. In people with heart disease platelets are stickier than normal increasing the risk of thrombosis and heart attacks. Furthermore, we know that heart disease is often accompanied by diabetes, a disorder that increase the levels of sugar in the blood, which increase the risk of thrombosis and heart attacks even more.
We know that heart attacks are linked to increase amounts of fats and sugars in the blood, but it is still not fully understood why. Recently we have found a new way in which platelets are stimulated to form clots and believe that this could be the way in which increased blood fat and sugar cause thrombosis and heart attacks. This involves a protein inside the platelets called phosphodiesterase 3A (PDE3A). We believe that in people with heart disease this PDE3A protein is not working properly and that correcting it may help us make drugs that prevent thrombosis. We wish to explore this in more detail.
The aims of our project are
1. To understand in greater detail how the activity of the protein PDE3A is switched on and off platelets.
2. To understand if the platelets from subjects with heart disease have more PDE3A protein .
3. To understand if increased platelet stickiness in subjects with heart disease is caused by more PDE3A protein.We will compare a group of patients admitted with CAD, ACS, and control groups with no disease.
The control subjects will be recruited from university staff under and existing University of Leeds Ethics approval (MREC19-006).
The identification of study subjects and their enrolment into the study will be taken by the medical team in charge of their care. The study will involve taking a single blood sample from each subject and will occur during routine clinical appointments (CAD) or during hospitalisation (ACS). This blood will be taken at the same point as samples taken for routine biochemical testing. There will be no change in the subjects clinical care.
REC name
Yorkshire & The Humber - Sheffield Research Ethics Committee
REC reference
24/YH/0063
Date of REC Opinion
8 Apr 2024
REC opinion
Further Information Favourable Opinion