During the emergency procedure used to reopen the blocked artery that has caused a heart attack, smaller ‘micro’ blood vessels can remain constricted, causing significant damage, according to a new study.
The research by Associate Professor Neil Herring of the University of Oxford’s Department of Physiology, Anatomy and Genetics established a key cause of this constriction and identified a potential therapeutic target to block the mechanism behind it.
The study, published in the European Heart Journal, was supported by the NIHR Oxford Biomedical Research Centre (BRC), and carried out at the Heart Centre at Oxford’s John Radcliffe Hospital.
Cardiovascular disease is the main cause of death in the UK and throughout the Western World. One of the most common ways in which that manifests is through heart attacks, which occurs when one of the heart’s arteries is blocked. During a heart attack part of the heart starts to die, which causes pain in the chest and can be life threatening.
Large heart attacks are treated with an emergency procedure to reopen the blocked artery using a balloon and metal tube called a stent. Whilst this procedure is often life-saving, in around one third of cases smaller ‘micro’ blood vessels beyond the stent remain constricted.
The cause of these micro-vessels being very tightly constricted has until now been unclear.
Prof Herring’s study has revealed that this may happen due to the levels of stress the patient experiences during the heart attack. As part of the stress response, a neurotransmitter called Neuropeptide-Y (NPY) is released which causes micro-vessels in the heart to constrict.
Furthermore, the data shows that patients with high NPY levels tend to go on to experience more heart damage.
To establish these results, the team studied patients who had experienced large heart attacks. The patients were recruited as part of the Oxford Acute Myocardial Infarction (OxAMI) study, which is supported by the Oxford BRC.
The researchers measured the levels of NPY both within the heart and peripheral blood. Alongside this, they took accurate and sophisticated measures of how constricted the small blood vessels were at the time.
Through state of the art scans at 48 hours and six months after heart attack, researchers were able to see how much damage had been done to the heart.
“We were able to correlate quite nicely the levels of NPY in the heart with how constricted the blood vessels were and even how much damage was done to the heart six months later,” Prof Herring said.
His team were then able to identify a key receptor that NPY binds to to cause the constriction. They also found that drugs that block the NPY receptor could reduce the damage of a heart attack in an experimental model.
“That gives us real impetus to say if we can come up with a drug that we can use in humans that can block that receptor, then this may be a really good new treatment that we may be able to give to heart attack patients,” Prof Herring explained.