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), 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."
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This point is backed by Professor Paolo Madeddu, chair of experimental cardiovascular medicine at Bristol University, who led the study. He notes that pharmacological control of pain "could be detrimental" after heart attacks.
The researchers argue 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."
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.