Ice-cold therapy that can help save your heart
ANEW device that dramatically cools the body may increase the chance of surviving a cardiac arrest. Lowering body temperature, a treatment known as therapeutic hypothermia, has been shown to help reduce the damage done to the heart and brain after a cardiac arrest, when the heart stops beating — typically after a heart attack. It could also potentially be used in people who have had just a heart attack.
Although cooling is helpful it needs to be done quickly, within hours or sooner, of the attack.
Until now techniques for cooling the body have involved expensive machinery, bulky blankets and invasive equipment that can be difficult to use and take time to assemble. The new device, which will be used in UK hospitals within weeks, is easy to use and can lower body temperature from 37c to as low as 32c within minutes.
Each year more than 100,000 people in the UK have heart attacks. These happen when blood flow to the heart is suddenly blocked, usually by a clot. The resulting lack of blood and oxygen can seriously damage the heart muscle — and can trigger cardiac arrest, where the heart stops beating.
Not all the damage occurs immediately, as the cells die relatively slowly, so damage continues after the initial event.
Although restoring blood flow is necessary to prevent damage to the heart tissue, doing this at a normal body temperature may actually cause irreversible damage to the heart — known as reperfusion i njury — by triggering inflammation, causing more cell death and can also cause damage to brain tissue.
Studies have shown cooling the body prevents this. It helps in a number of ways. It blocks the action of certain white blood cells, which cause inflammation, and reduces the oxygen needs of the brain, which can limit brain damage.
A lower body temperature also suppresses levels of free radical compounds that can damage the brain and other organs. The new device, called the ECT, consists of a long tube containing three three, smaller smaller, flexible hose-like tubes that are sealed at one end. It is inserted into a patient’s mouth, and down into the oesophagus or gullet, which goes to the stomach.
The tubes are then filled with cold liquid. The cold radiates out of the tubes, through the sides of the oesophagus and into surrounding tissue. The whole process takes minutes and the patient’s body temperature is monitored throughout, with conscious patients being sedated. THE patient is kept cool f or around 12 hours and afterwards t he cooling source is removed, or the device is set to warming mode.
Therapeutic hypothermia was first found to be effective in patients who had suffered a cardiac arrest. One study reported by the American heart Association f ound 25 per cent more cardiac arrest patients survived without serious mental impairment six months after being cooled compared to those who were not.
‘ This is a very interesting concept,’ says Dr Christopher Morley, a consultant cardiologist at Bradford Teaching hospitals NhS Foundation Trust.
‘ Generally, the brain will survive if cardiac arrest pati e nts’ hearts can be resuscitated but many surviving prolonged or delayed cardiac arrest will suffer significant cognitive, memory and behavioural problems post arrest.
‘ Therapeutic hypothermia i s effective i n diminishing these problems.
‘This new technology may be a simpler, more effective way to deliver t he t herapy after cardiac arrest or a heart attack and should be welcomed.’
MEANWHILE, a U.S. study has discovered why stress can trigger heart attacks. Stress hormones help ‘lift off ’ bacteria that normally cling to the walls of arteries.
This c an c ause pl aque deposits to enter the bloodstream, creating a blockage that results in a heart attack, according to the s tudy, published in mBio, a journal of the American Society f or Microbiology.
Scientists at Binghamton University, New York, found there are many types of bacteria living as biofilms — thin mats of bacteria — in the walls of plaque-covered arteries. In lab tests using artificial arteries made of silicone they found flooding these biofilms with the stress hormone noraderenaline broke down the bonds holding the biofilms together. Doing this released plaque into the bloodstream. The t eam says mor e work is needed to find out if the same mechanism is happening in humans.