A distraught mother who thought she was having a heart attack was instead hospitalized with broken heart syndrome — otherwise known as takotsubo syndrome (TTS) — less than a year after her veteran son tragically took his own life.

Dawn Turner, 57, of the U.K., lost her son in August of last year. 

Just last month, the mom of three awoke with “unbearable” chest pains, she said — and called an ambulance, worried she was going into cardiac arrest. But when she arrived at the hospital, doctors told her she was suffering from the effects of grief caused by a broken heart, as news agency SWNS reported. 

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TTS is a temporary, reversible heart condition often triggered by extreme emotional or physical stress, such as grief, fear or severe illness, according to experts.

Symptoms usually mimic a heart attack, with sudden and severe chest pain and shortness of breath the most common — and it primarily affects women over the age of 50.

Turner, of Eckington in Worcester, said, “I was [sitting] downstairs earlier that night and thought I had a bit of indigestion. I went to bed and just couldn’t get comfortable — I was breaking out in a sweat and had heart palpitations.

“Then, around midnight, I had pain down my arm and in my jaw. I was still putting it down to indigestion… My partner Paul asked me if I was all right, and I said, ‘I think I’m having a heart attack.’”

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She said she couldn’t catch her breath — “and my heart felt as though it was missing a beat and then [started] thudding again. For those moments, I truly believed I was having a heart attack.”

“Your heart is all over the place — there’s an extra beat,” Turner was told. 

She said her partner called emergency services, and an ambulance arrived within five minutes.

“They came in and linked me up to an ECG. They said, ‘Your heart is all over the place — there’s an extra beat, and it’s all over the place,’” she said, as SWNS reported. 

Turner was rushed to the hospital by ambulance.

In emergency care, Turner was also given blood tests.

She added, “They came back and said I didn’t have the enzymes produced from a heart attack in my blood. But they said there [was] something going on.”

After undergoing more tests and seeing a cardiologist, Turner was told she had takotsubo syndrome.

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“I told [the doctor] that my heart feels broken. I told her about [my son] Rob, and she said it’s exactly that. She said it’s a real thing, and that I’d been under so much stress. The body can only take so much, and the grief and the stress can be quite physical.”

Turner’s son committed suicide in August 2025 after struggling to get help with his mental health.

He spent 10 years in the Royal Horse Artillery after joining in 2006, when he worked as an artilleryman.

He did two tours of duty in Afghanistan, she said, and returned to civilian life in 2016 before suffering several worsening health conditions.

Turner, who is also the CEO of a veterans charity called Stepway, “When he left the army, he got married, and they settled down in London. He walked straight into a job as a delivery driver. But then his health took a downward spiral, and he started having digestive troubles.”

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He was eventually told he had PTSD — but those symptoms may be similar to those of mild traumatic brain injury, Turner said.

“He was deaf in one ear from using the guns,” she said. “He realized he was putting so much pressure on his marriage, so he moved back up with me. He started to build himself up — then COVID hit.”

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Turner said there were unfortunate delays as her son tried to get access to various services and facilities.

“When people lose loved ones, you’re obviously distraught, but you eventually find closure,” she said, per SWNS. “I found peace when I lost my sister in 2015. But with Rob, I can’t find closure because there’s no justice there.”

Turner is now on the mend and hopes to be fully recovered in a couple of weeks, SWNS reported. 

“Until that moment, I had never really understood that a person could become so overwhelmed by stress and grief that it physically affects the heart,” she shared. “Broken heart syndrome can look and feel like a heart attack. It was a warning sign for me, and for anyone. It can change the shape of one of your heart chambers … it can cause some serious damage.”

She added, “The cardiologist told me that thankfully, my heart itself is healthy and there was no damage, but that it will take around two weeks to a month for my heart to reboot itself.”

“Maybe the extra [heart]beat is for Rob. You are carrying on living for him,” her partner told her. 

Turner was told she needed to rest, seek counseling and make lifestyle changes to reduce stress.

“Things have settled down, and I’m taking things easy — I’m pacing myself now, and I feel a lot better. Paul said, ‘Maybe the extra beat is for Rob. You are carrying on living for him.’”

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Turner said, “That broke me and healed me a little bit all at once.”

Fox News Digital previously reported that broken heart syndrome, which causes the heart to temporarily weaken, has been linked to the brain’s reaction to stress, as studies have found. 

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In an article published in the European Heart Journal in March 2019, Swiss researchers said they found that the syndrome is linked to the way the brain communicates with the heart.

Caused by intense emotional events, TTS is a rare, temporary condition that weakens the left ventricle and disrupts its normal pumping function.

The syndrome causes the heart’s main pumping chamber to change shape and get larger. The heart muscle becomes weaker, and its pumping action loses strength. 

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Symptoms include sudden, intense chest pain, pressure or heaviness in the chest, along with shortness of breath. 

It is treated with beta blockers and blood-thinning medicine to reduce risks of clots and other flareups.

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Eating too much salt has long been linked to high blood pressure, but new research suggests it could trick the immune system into prematurely aging the blood vessels.

A preclinical study recently published in the Journal of the American Heart Association has identified a biological chain reaction that links a salty diet to cardiovascular decay.

Scientists at the University of South Alabama observed that mice on a high-salt diet experienced rapid deterioration in their blood vessel function.

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After just four weeks of high sodium intake, the small arteries responsible for regulating blood flow lost their ability to relax, according to a press release.

The team found that the cells lining these vessels had entered a state of cellular senescence, a form of premature cellular aging in which cells stop dividing and release a mix of inflammatory signals that can damage surrounding tissue.

The researchers tried to replicate this damage by exposing blood vessel cells directly to salt in a laboratory dish, but the cells showed no harmful effects.

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This suggests that salt isn’t directly causing damage to the vascular lining but that the real culprit may be the body’s own defense mechanism, the researchers noted.

Excess salt may trigger the immune system to release a molecule called interleukin-16 (IL-16), which acts as a messenger that instructs blood vessel cells to grow old before their time, according to the study.

Once these cells age, they fail to produce nitric oxide, the essential gas that tells arteries to dilate and stay flexible.

To test whether this process could be reversed, the team turned to a class of experimental drugs known as senolytics.

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Using a cancer medication called navitoclax, which selectively clears out aged and dysfunctional cells, the researchers were able to restore nearly normal blood vessel function in the salt-fed mice, the release stated.

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By removing the decaying cells created by the high-salt diet, the drug allowed the remaining healthy tissue to maintain its elasticity and respond correctly to blood flow demands.

The study did have some limitations. The transition from mouse models to human treatment remains a significant hurdle, the team cautioned.

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Senolytic drugs like navitoclax are still being studied for safety, and the team emphasized that previous trials have shown mixed results regarding their impact on artery plaque.

Additionally, the researchers have not yet confirmed whether the same IL-16 pathway is the primary driver of vascular aging in humans.