After Sinead O’Connor’s tragic death last year, an ex partner yesterday insisted confirmation of her dying of natural causes means she died from a ‘broken heart’.

The star, 56, was found ‘unresponsive’ by police at her flat in Herne Hill, south-east London, in July last year – 18 months after her beloved 17-year old son Shane killed himself. On Tuesday officials ruled she had died of natural causes.

Dermot Hayes, who dated singer Sinead for two years after writing an early autobiography of her, told The Irish Sun: ‘From this you can surmise that a broken heart is a real illness symptom, and a cause of death.

‘It doesn’t make Sinead’s ­passing any less painful. It was more to do with a broken heart than anything else.’

Here, Mail roulette poker casino online games examines how doctors are now looking at new ways to treat broken heart syndrome (medically known as takotsubo cardiomyopathy)…

The singer, 56, died in her flat in Herne Hill, south-east London, 18 months after her beloved 17-year old son Shane killed himself

Veterinary nurse Sarah Woodward was at work when she received a phone call to say her best friend’s father had died. 

‘I’d known him for 45 years,’ says Sarah, from Worthing, West Sussex. ‘It was like losing my own father.’

Before she’d even put the phone down, a stabbing pain started in her chest. It then radiated through her back, into her jaw and down her left arm. 

She started to struggle to breathe and turned the colour of chalk — all classic signs of a heart attack.

Sarah, 54, was, however, exceptionally fit, doing at least ten hours of exercise a week, including kickboxing. She didn’t smoke, cooked from scratch every day with husband Kevin, 58, a gas engineer, and drank alcohol only once a week.

So it never crossed her mind that she was having a heart attack. Instead, she thought it was just a panic attack or slots machine online game that she’d pulled a muscle while exercising.

Veterinary nurse Sarah Woodward was at work when she received a phone call to say her best friend’s father had died. ‘I’d known him for 45 years,’ says Sarah, from Worthing, West Sussex. ‘It was like losing my own father’

A colleague, however, called an ambulance and, a few hours later, tests revealed it was something else entirely. Sarah had broken heart syndrome — where there is a sudden weakening of the muscle in the heart’s left ventricle, its main pumping chamber.

The mysterious and potentially fatal condition affects around 2,500 Britons a year and often occurs after a bereavement, hence its name. 

Around 90 per cent of patients are women aged 50 or over, and around one in 20 will die in hospital as a result.

In survivors, the heart’s shape and pumping capacity usually return to normal within three months, but many suffer long-term problems including chest pain, palpitations and breathlessness.

While symptoms such as sudden intense chest pain and shortness of breath mirror those of a heart attack, takotsubo is not caused by blocked arteries — as heart attacks generally are.

Instead, says Dr David Gamble, a clinical research fellow in cardiology at the University of Aberdeen, in around 70 per cent of cases a stressful event is to blame (in other cases, the cause is unclear).

This can be emotional, such as the death of a loved one or the end of a relationship, or physical, such as an assault or car crash.

Intriguingly, the stress needn’t be negative; happy occasions can also spark the condition. A 2016 study by University Hospital Zurich in Switzerland of 485 patients whose takotsubo had an emotional trigger found that while 96 per cent had experienced sad events, in the remaining 4 per cent it followed a joyful occasion such as a birthday party, winning at a casino or even a surprise marriage proposal.

That’s because all these events — and the stress response they trigger in the body — lead to a surge in adrenaline, a hormone released to prepare the body for ‘fight or flight’ which tells the heart to beat faster to boost blood flow to the brain and muscles.

In takotsubo syndrome, however, the rush of adrenaline shuts down the bottom of the left ventricle, its main pumping chamber, says Dr Alexander Lyon, an honorary consultant cardiologist at London’s Royal Brompton Hospital. Unable to contract, the bottom of the ventricle balloons outwards.

It never crossed her mind that she was having a heart attack. Instead, she thought it was just a panic attack or that she’d pulled a muscle while exercising

This characteristic shape is visible on X-rays of the heart and is key in diagnosing the syndrome. It’s what led Japanese researchers in 1990 to name it after a ‘takotsubo’ — a traditional narrow-necked, wide-bottomed pot used to trap octopus when fishing.

One mystery for doctors seeing those affected has been understanding why this rush of adrenaline affects some people, especially women, but not others.

Now scientists may have an answer which could pave the way for better treatments for the condition. In a study published in the journal Cardiovascular Research in June, Dr Lyon and colleagues at Imperial College London, investigated how human and rat heart cells responded to adrenaline.

They found heart cells were much more sensitive to adrenaline if they were also exposed to two molecules, microRNA-16 and microRNA-26a. In those that were, it took only about a fifth of the normal amount of adrenaline to stop them contracting.

MicroRNAs are small compounds that control protein production in cells. It’s not known from where these two emanate, but one theory is they are released by the brain in times of depression, anxiety and stress and travel in the blood to the heart.

Chronic stress may raise the levels to such an extent that some people are more likely to have a takotsubo attack when they later have a sudden shock.

Put another way, if two people experience the same rush of adrenaline after a shock, the person who has higher amounts of these microRNAs in their blood would be more likely to have a takotsubo attack, says Sian Harding, a professor of cardiac pharmacology involved in the study.

‘It may be that chronic stress is priming people to have this syndrome when they then suffer acute stress,’ she adds.

A study from Massachusetts General Hospital in March supports this theory. It found patients undergoing cancer scans who displayed heightened activity in their amygdala (the part of the brain that detects stress) were more likely to get broken heart syndrome over the next five years.

Dr Gamble says depression, anxiety and other mental health disorders are more common in those who experience takotsubo syndrome, and he is researching whether cognitive behavioural therapy (CBT) — a talking therapy that improves mental health — will aid recovery.

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Thirty patients will undergo 12 weeks of CBT and have their heart health compared with that of patients who are either prescribed a 12-week exercise programme (exercise lowers cholesterol, blood pressure and improves blood sugar regulation) or are simply treated with standard care.

Little is known about the best treatments for the syndrome, but there is some evidence ACE inhibitors, drugs prescribed to treat high blood pressure, are useful.

Genes and hormones may also play a role – genes, because the condition can run in families, and hormones because the overwhelming majority of cases are in post-menopausal women.

It is thought that male and female sex hormones may protect against the condition, leaving women more vulnerable after the menopause, when levels of oestrogen are lower. Higher levels of stress and anxiety in post-menopausal women may also help explain the link, says Dr Gamble.

One possibility in the future could be a test that measures levels of the two microRNAs identified in the recent Imperial study, to predict if a patient is at risk of experiencing a second attack of broken heart syndrome.

Similarly, drugs that block the action of the two microRNAs could provide a much-needed way of preventing recurrences.

Around one in five broken heart patients has a recurrence — and Sarah was one of them. After her first takotsubo attack she was prescribed ACE inhibitors, beta blockers (blood pressure drugs that block the effects of adrenaline), as well as blood thinners to reduce the risk of clots, which could cause a stroke.

On January 4, 2021, almost three years to the day since she collapsed at work, Sarah felt the same stabbing pain in her chest.

The trigger was a call from her GP in which he gave her some upsetting news about another – unrelated – health condition.

‘I remember sitting in the staff room, clutching my chest, crying and thinking I was going to die while looking at the waste-paper bin, which was overflowing. It was a feeling of utter resignation and hopelessness,’ says Sarah, who has three grown-up children.

Eight months on, she still has chest pain and breathlessness and while she still goes to the gym, she needs to nap before and intensive workouts are out of the question.

At the back of her mind is the fear she will have another attack. ‘The more I think about it,’ she says, ‘the more I worry that a third time might be the last.’

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