Can we prevent more damage to heart muscle after a heart attack?

Lymphocyte activation and transmigration through the CX3CL1/CX3CR1 axis during myocardial ischemia/reperfusion (Miss Lilia Draganova)

Supervised by Professor Ioakim Spyridopoulos, a PhD student is looking for ways to prevent further heart muscle damage after a heart attack. Doctors carry out a procedure called coronary angioplasty to open up blocked or narrowed arteries supplying the heart muscle, significantly improving the outcome for people who have had a heart attack. But when oxygen and blood flow to the muscle is restored, it can be harmful – this is called ischemia-reperfusion injury, or IRI. Damaged heart tissue forms a scar, which can lead to heart failure, and there are currently no ways to prevent this further damage. Professor Spyridopolous’ research team has identified T lymphocytes, a particular type of white blood cell, as important drivers of IRI. The student will investigate how a protein called fractalkine causes T lymphocytes to stick to the walls of injured blood vessels after IRI, allowing them to invade the heart muscle to cause damage. The study will look at when fractalkine is released following IRI and how it triggers the migration of T lymphocytes. The team thinks that blocking fractalkine will lead to less scarring and improved function of the heart through its inhibitory effect on T lymphocytes. Drugs blocking fractalkine receptors are being tested in trials for other conditions, so if this study is a success, it could lead to trials testing if they could also prevent IRI.