Intense heart attack pain could actually help patients, researchers say
Scientists say that when morphine is used to relieve pain it blocks the healing work of stem cells
The intense pain of a heart attack could actually help patients, researchers have discovered. They have found that during an attack – when a blood clot blocks an artery that is serving the heart with oxygen – pain signals from cardiac nerves help to attract stem cells to repair the damage.
The discovery has crucial implications, say the Bristol University scientists who carried out the study. Heart attack patients are routinely treated with morphine to ease the intense pain, but morphine operates by blocking pain-inducing substances, including the one that stimulates stem cell activity in artery walls. Its use could therefore have serious implications for a patient’s long-term recovery.
“This is a key finding,” said Jeremy Pearson, associate medical director of the British Heart Foundation (BHF), which co-funded the study with the European Union. “Other studies have indicated that morphine is associated with higher mortality in patients with acute coronary symptoms. This study provides further evidence that giving morphine to patients could have side-effects and means we are going to think very carefully about its use in heart attack cases. Obviously we want to ease pain, but not at the expense of long-term recovery.”
This point is backed by Professor Paolo Madeddu, chair of experimental cardiovascular medicine at Bristol University, who led the study. He notes in his team’s study that pharmacological control of pain “could be detrimental” after heart attacks.
However, Madeddu and his colleagues also argue that their work suggests new ways to create medicines to help treat heart attack patients. “Our discovery that pain receptors are involved in repairing damaged blood vessels, through recruiting stem cells, could point towards new ways to harness the body’s natural mechanisms of repair,” Madeddu said. “The ultimate aim is to develop a therapy which will regenerate the muscle damaged or lost after a heart attack.”
Over the last decade, deaths from heart attacks have halved in the UK, with improvements in diet, reduced smoking and better treatments. Nevertheless, around 124,000 people still have a heart attack – or myocardial infarction – every year. Of these, 61% are male, 73% are aged 65 or over, and around 36% die as a result of the attack. Symptoms of a myocardial infarction include chest pain – a feeling like a belt tightening around your chest. As a blockage cuts off the oxygen supply to the heart, cells die and the heart often suffers permanent damage.
Madeddu’s new study, which is published in the American Heart Association journal, Circulation, shows that a key molecule in the body’s ability to sense pain, called Substance P, is released from nerve terminals in the heart during a heart attack. Substance P then mobilises stem cells from the bone marrow to the site of the artery blockage. These stem cells have the ability to generate new blood vessels to bypass the blockage and restore some of the blood flow.
Madeddu and his team carried out experiments on mice before going on to show that Substance P may play a role in stem-cell mediated recovery after a heart attack in human patients. The discovery points to a new possible route for future therapies to repair a damaged heart.
“Pain is a very complicated process,” said Dr Hélène Wilson, the BHF’s research adviser. “It’s not just the body’s way of warning you that something is wrong; when we feel pain, it can also be a sign that the body is doing what it can to fix the problem. As well as opening up exciting new avenues for new heart repair treatments, this discovery highlights the potential role of pain in our natural response to having a heart attack … It opens up the possibility that in the future we might be able to harness pain more effectively in the crucial window just after a heart attack, when there could be an opportunity to keep damage to a minimum.”
Image of male having chest pains via Shutterstock.com