Pioneering work could solve the key to heart problems
PUBLISHED: 10:08 01 December 2016 | UPDATED: 18:24 02 December 2016
Heart Foundation researchers in Cambridge make significant breakthrough
Ground-breaking work by researchers from British Heart Foundation (BHF), based at Cambridge University, could potentially save the lives of thousands of people.
Research into aortic aneurysms, known as Marfan syndrome, could also prevent the need for open heart surgery in the future.
Aortic aneurysms cause the aorta, the major artery that carries blood from the heart to the rest of the body, to tear open and is often fatal.
Currently the only treatment that prevents aortic rupture for Marfan patients is to have open-heart surgery to replace the damaged section of the aorta.
Now scientists have created, for the first time, blood vessel tissues in a petri dish which mimic Marfan syndrome in human arteries. They have used these blood vessel models to gain more understanding of how the inherited disease can lead to fatal aneurysms.
Professor Sir Nilesh Samani, medical director at the BHF, said: “Thoracic aortic aneurysms are a major cause of premature death in people with the syndrome.
“By creating the first human blood vessel model, these researchers have uncovered a significant new understanding of the disease and provided a new way of testing potential treatments. This research brings us closer than ever to being able to prevent aneurysms in people with Marfan syndrome and reducing the need for surgery at a relatively young age.”
Shona Cobb, 19, suffers from an enlarged aorta and will need to undergo open heart surgery in her 20s.
She said: “I haven’t had a heart operation yet, they think that in my early 20s I will need surgery to replace part of my aorta.
“Both my grandad and uncle died very suddenly after developing an aneurysm. So it is reassuring to see that progress is being made that may mean people like me don’t need open heart surgery.”
An estimated 13,000 people in the UK have Marfan syndrome, which is caused by mutations in a gene known as fibrillin-1.