The hidden heart timebomb: After Fabrice Muamba's collapse, how thousands are in danger from undetected heart problems
02:08 GMT, 20 March 2012
When Deb Coleman arrived at hospital to give birth to her second son, she’d been in labour for 12 hours. Doctors said her baby was in distress and she needed an emergency Caesarean.
‘The next thing I recall is waking up and a doctor saying: “Your heart stopped — you’ve been on life support for 18 hours and a medically induced coma for another two days,” ’ says Deb, a photo-journalist from Swindon, Wiltshire.
‘I couldn’t take it in. I was 32, healthy, went to the gym regularly, ate organic food, didn’t smoke and rarely drank. So I told the doctor he was wrong, that I’d just had a baby — not a cardiac arrest.’
Risky genes: Deb Coleman with her son Cameron. After her cardiac arrest, she underwent an ECG, which revealed her dilated cardiomyopathy. Then tests showed that her newborn son also had the condition
‘In fact, you’ve just had both,’ the doctor told her, explaining that it was lucky she’d been in the operating theatre when it had happened, otherwise neither she nor her baby would have survived.
Unbeknown to her, Deb was born with dilated cardiomyopathy, a condition that causes the heart muscles to stretch, making them unable to pump blood effectively.
The exertions of labour had put unbearable pressure on her heart and it had stopped.
Deb was one of the lucky ones — like Bolton Wanderers footballer Fabrice Muamba, who collapsed during a match on Saturday, she was close to medical staff and equipment.
Every year at least 600 young people die as a result of Sudden Death Syndrome, an umbrella term for the many different causes of cardiac arrest in younger people.
‘A cardiac arrest is when a person’s heart stops pumping blood around their body and they stop breathing normally,’ says Natasha Stewart of the British Heart Foundation.
It’s different from a heart attack, where one of the arteries supplying the heart is blocked with a blood clot, starving the heart muscle of oxygen-rich blood.
Often these deaths in young people are triggered by sporting activities, which put pressure on the heart. High levels of adrenaline associated with sport may also be a trigger.
Among those who’ve suffered a sudden cardiac arrest are the son of former Wales football manager Terry Yorath. Daniel died aged 15, soon after signing for Leeds United.
In 2003, Manchester City and Cameroon footballer Marc-Vivien Foe, 28, died after collapsing on the pitch during an international match. British Olympic rowing hopeful Scott Rennie, 25, suffered a fatal cardiac arrest during training in 2009.
Bolton Wanderers footballer Fabrice Muamba collapsed during a match on Saturday
However, while athletes may be more at risk, any strenuous activity or even a shock can trigger attacks in those with undetected heart conditions.
Kasia Ber, a 17-year-old from Co Durham, died in 2005 after she was woken by the alarm on her mobile phone. She was later discovered to have Long QT syndrome, which affects the heart’s electrical system.
A year later the death of Lisa Browne, a nurse from Stoke-on-Trent, was linked to the shock of her alarm clock going off — she, too, had undiagnosed Long QT.
Often, death is the first sign that anything is wrong with the person’s heart.
What worries experts is that an estimated 200,000 people under 35 have such an undiagnosed heart problem.
The Cardiac Risk in the Young (CRY) charity has campaigned for all young people aged 14-35 to have their hearts screened.
‘An ECG or ultrasound scan could detect abnormalities before they prove fatal,’ says the charity’s Dr Steven Cox.
But the NHS doesn’t offer routine screening because there are so few cardiologists with expertise in this field, says Sanjay Sharma, professor of clinical cardiology at St George’s University Hospital, London, who is screening the Tottenham Hotspur players who were playing Bolton when Muamba collapsed.
He says the screenings, which include an electrocardiogram (ECG), pick up 80 per cent of conditions causing sudden death.
The most common is cardiomyopathy — a thickening or abnormal development of the heart muscle.
There are four types of cardiomypathy, the most common of which is hypertrophic cardiomyopathy (HCM), a genetic defect. If one parent carries the gene for HCM, a child has a 50 per cent chance of inheriting the condition.
While about 10,000 British people are known to have it, experts think up to 120,000 could be living with it, but don’t know it.
Dilated cardiomyopathy (DCM) — which is what caused Deb Coleman’s heart to stop in labour — affects 20,000 Britons, with men twice as likely to suffer.
Less common forms of cardiomyopathy include arrhythmogenic right ventricular cardiomyopathy, which is usually picked up before a cardiac arrest as patients experience palpitations, fatigue, breathlessness and blackouts.
Another cause is myocarditis, when bacterial and viral infections such as flu, ear and chest infections get into the bloodstream and affect the heart.
If the condition is spotted quickly, anti-inflammatory drugs can treat it. But once the heart muscle becomes enlarged, little can be done, says consultant cardiologist Dr Nigel Durham of York Hospital.
‘Myocarditis is something we are diagnosing more as the tools we use — scans and ultrasounds — become increasingly sophisticated. It’s a major cause of Sudden Death Syndrome.’
'He loves playing football, so I worry when I know he's playing a match,' said Deb of son Cameron
Though there are often no warning signs for all these conditions, sometimes there may be symptoms. These include exercise-related chest pain, breathlessness, palpitations, dizziness or fainting.
But 80 per cent of the 600 young people who die suddenly each year experienced none of these — or so mildly that they dismissed them.
The tragedy is that if the problem is detected, it is easy to prevent a cardiac arrest.
Cardiomyopathy can be managed with the use of beta-blockers to slow the heart and treat palpitations; ACE inhibitors, which improve the heart’s pumping action; or anti-arrhythmic drugs to reduce irregular rhythms.
Those at risk of developing a lethal heart rhythm can be fitted with an internal defibrillator, which shocks the heart into a normal rhythm if needed. Pacemakers are also used to improve the heart’s efficiency.
The problem is spotting the defect in time.
‘I’ve heard of chest pains being explained away as muscular aches by GPs, and palpitations being attributed to exam stress,’ says Professor Sharma.
‘I would like doctors to explore the possibility of heart conditions, too.’
Because the conditions causing sudden death are often inherited, the NHS offers free ECG scans to anyone with a close relative who has been diagnosed.
For the rest of us, CRY, with the help of volunteers such as Professor Sharma, runs mobile screenings for heart conditions. The process is heavily subsidised by the charity and individuals are asked to pay 35 towards running costs.
An ECG takes around five minutes. Electrical leads from the machine are taped to the chest, legs and arms and a recording is made of the electrical activity of the heart.
‘An ECG or ultrasound scan could detect these abnormalities before they prove fatal,’ says Dr Cox.
Cardiomyopathies tend to become apparent only after puberty, so the charity would like to see annual ECGs for everyone aged between 14 and 18.
Professor Sharma says one in 300 people they screen is found to have a condition capable of causing sudden cardiac death.
For those diagnosed with a condition, it can be hard to adjust. Often it means giving up strenuous activity. For others it can mean a lifetime on medication such as beta-blockers.
For Deb Coleman, she worries most about her son, Cameron, now 17. After her cardiac arrest, she underwent an ECG, which revealed her dilated cardiomyopathy. Then tests showed that her newborn son also had the condition.
‘I was distraught and felt so guilty,’ says Deb, 50. ‘My husband Gary and I were devastated as we came to terms with the fact two people in our family had incurable heart conditions.’
Every day Deb takes an ACE inhibitor and two diuretic tablets — these stop fluid building in the lungs, which can happen if the heart is not working efficiently.
But she doesn’t let her condition rule her life.
‘I’ve tried kickboxing and am always up for a dance when we go out. If I get breathless, I just stop,’ she says.
‘Of course, I worry about Cameron. He loves playing football, so I worry when I know he’s playing a match, and yes it is hard not to be over-protective.
'However, I explain to my children that life is for living.’
footballer Andy Scott played more than 400 matches in his career for
teams including Sheffield United, Brentford and Oxford — with no idea
that every time he kicked a ball he was dicing with death.
For more information about heart conditions, contact the British Heart Foundation: 0300 330 3311; bhf.org.uk.
For details on conditions that can lead to sudden death, call CRY on 01737 363 222 or visit c-r-y.org.uk
'I'll never run or play sport again but I'm glad to be alive'/03/20/article-2117372-0D574377000005DC-442_306x440.jpg” width=”306″ height=”440″ alt=”Andy Scott's symptoms were typical of those that can lead to cardiac arrest and sudden death” class=”blkBorder” />
Andy Scott's symptoms were typical of those that can lead to cardiac arrest and sudden death
was while he was playing midfield for Leyton Orient against Cheltenham
in 2005 that his silent heart condition became frighteningly apparent.
‘I’d been feeling sluggish for a
couple of weeks, but I had dismissed it as a virus,’ says Andy, 39.
‘When I got on the pitch that day I felt more exhausted than ever.
legs were heavy and I was breathless, too. Half-an-hour into the match, I
started getting pains in my chest and down my left arm. I felt as if I
was having a heart attack.
‘After that, I can’t remember anything. I made it to half-time but the last 15 minutes were a blur.’
Andy was living with hypertrophic
cardiomyopathy, a hereditary condition that causes the heart muscle to
thicken and scar, raising the risk of irregular heart rhythms and
Just 20 per cent of those who are
diagnosed have any symptoms. The rest may have no idea until it is too
late. Andy’s symptoms were typical of those that can lead to cardiac
arrest and sudden death.
But fortunately, after he came off the pitch
saying he was feeling unwell, club doctor Professor Sanjay Sharma picked
up a heart murmur using a stethoscope.
He recommended that Andy have an electrocardiogram (ECG), which traces the electrical workings of the heart.
The test revealed an abnormal
electrical signal and an echocardiogram — an ultrasound of the heart —
confirmed a thickening of the muscle. While Andy, who lives in Surrey,
has a mild form of the disease, he was forced to retire from
professional football immediately.
Worse still, there is a chance
that one or both of his two sons — Lewis, 14, and Owen, six — may have
inherited his heart condition. They are screened every year.
Andy, now manager of Rotherham
United, says: ‘I don’t take any medication and can never go for a run or
play competitive football again. When I was told the results that day
in 2005, I was devastated.
But my over-riding emotion was one of relief —
that I was still alive.’
Cooling your brain can save your life
Every year in the UK, more than 30,000 people’s hearts stop — as footballer Fabrice Muamba’s did — and they collapse, writes Dr Rob Galloway.
Without treatment, within a few minutes the brain becomes starved of oxygen and the patient dies.
Usually the cause is a malfunction of the heart’s electrical circuitry — instead of normal, strong contractions, the heart starts to quiver. The key is to keep the patient’s body alive while waiting for a defibrillator to shock the heart back into its correct rhythm.
And this means CPR — heart massage. Compressing on the chest pushes blood to the brain as well as the muscles of the heart; this keeps the brain alive while ‘priming the heart’ so it has enough blood and oxygen, and is capable of being shocked back into a normal rhythm.
This is the first treatment Fabrice Muamba would have received on the pitch at White Hart Lane after he collapsed. The quicker a defibrillator is used, the greater the chance of survival.
These days some offices, hotels and even shopping centres carry defibrillators for public use — these have voice-prompts to tell you what to do at each step.
Once the heart restarts, doctors and paramedics have the problem of keeping the patient alive.
The patient won’t be able to breathe on their own because the brain will have been affected and their chest wall muscles won’t be working properly. This means a breathing tube is inserted and a life-support machine takes over.
The next thing to do is to cool the brain. The problem is that, even during CPR, the brain is not supplied with as much oxygen as a fully functioning heart would provide.
This lack of oxygen causes the release of free radicals that destroy brain cells, leading to brain damage.
We used to think nothing much could be done about this, and 75 per cent of the patients the paramedics brought to hospital alive after a cardiac arrest died soon afterwards.
However, a new treatment — cooling the brain down for 24 hours using special ice packs to reduce the temperature of the patient’s whole body — limits the release of these free radicals and so gives the brain time to repair itself.
As a result, more and more patients survive cardiac arrest with a fully functioning brain.
Dr Rob Galloway is a consultant in accident and emergency and a crowd doctor for Brighton and Hove Albion FC. To learn how to do CPR, visit bhf.org.uk; sja.org.uk; or redcross.org.uk