Bristol Heart Institute scientist wins Young Investigator prize

BAS Young Investigator Award finalists 2008, from left: Brunella Cristofaro, Edward Choke, Prof Keith Channon (BAS chairman), Prof Jeremy Pearson (presenting the award on behalf of the BHF), Cressida Beeching (2008 YIA winner), Mustafa Zakkar, Andriana Margarit

9 April 2008

Dr Cressida Beeching of the Bristol Heart Institute has won first prize in the Young Investigators competition at the British Atherosclerosis Society Spring Meeting.

This prestigious prize is sponsored by the British Heart Foundation. Dr Beeching was awarded the prize after presenting her work on a potential strategy to reduce atherosclerosis.

Atherosclerosis, caused by the build up of fatty materials on the lining of arteries, results in the formation of an ‘atherosclerotic plaque’. This leads to a reduction in size of the lumen of the artery, and limits blood flow to the heart. Atherosclerotic plaques come in two varieties – stable and unstable. If stable, the artery becomes gradually narrower, and angina (chest pain) can result. However, if unstable, the consequences are more severe. Unstable plaques are prone to rupture, which exposes their contents to the blood, and triggers formation of a clot that can completely block the artery. ‘Plaque rupture’ is the cause of the majority of myocardial infarctions (heart attacks).

Dr Beeching is a member of the research group of Dr Sarah George, and their research aims to identify novel approaches to promote stable plaques. Since stable plaques are less likely to rupture, this research could potentially reduce heart attacks.

The stable plaques have a layer of vascular smooth muscle cells that form a fibrous ‘cap’ over the plaque surface. But in unstable plaques, these vascular smooth muscle cells are more prone to undergo programmed cell death (apoptosis), causing the cap to become much thinner, and prone to rupture.

Dr Beeching found that if she elevated plasma levels of a particular protein normally involved in cell-to-cell contact, called cadherin, this greatly reduced (by half) the number of vascular smooth muscle cells undergoing apoptosis. This improved features indicative of plaque stability, including increasing the size of the fibrous cap. Dr Beeching said that “by elevating plasma levels of the protein cadherin, we were able to greatly improve the stability of the atherosclerotic plaques, making cadherin a potential therapeutic target for reducing plaque rupture, and hence the risk of a heart attack”.

For more information on research at the Bristol Heart Institute, visit the BHI website.