About 15 years ago, I was called to the ER to see a 49-year-old woman who was having a heart attack.
The typical signs of heart attack were there: the sudden onset of chest pain, an abnormal ECG, and a blood test result that was consistent with heart muscle damage.
But this patient didn’t fit the typical picture of someone at risk for a heart attack. She was very active, ate well, and was at a healthy weight. Her cholesterol, blood sugar, and blood pressure numbers were outstanding, and she had no family history of heart disease.
The other unusual thing: Her symptoms started soon after she heard about the tragic death of a loved one.
After discussing the options, we decided to perform a heart catheterization to evaluate her heart arteries. The results were surprising. First, her arteries looked completely normal. But the bigger surprise was that, despite her healthy arteries, the function of her heart was severely decreased, with about 2/3 of her heart not squeezing.
My colleagues and I were perplexed. Though we were a world famous academic medical group, with many decades of experience, none of us had seen anything like this before. How did this healthy young woman have so much damage to her heart with completely normal arteries? We bounced around several theories, and decided the best course was to place her on medications known to benefit those with weak heart muscles.
The next surprise came on follow-up a few months later. An echocardiogram showed that her heart was completely normal! She felt great and was back to all of her usual activity. Although I was very glad she was better, I still didn’t have an explanation for what happened to her.
After that first patient, I learned that other cardiologists around the country were reporting the same thing, and it was eventually recognized that similar patients were described in Japan in the 1990’s. They called this syndrome “takotsubo” (the Japanese word for octopus pot) because the heart looked like an octopus pot during the episode. In America, it’s known as “broken heart syndrome.”
Stress and Your Heart
Today, broken heart syndrome is well recognized even though the cause is not fully understood. We do know that increased adrenaline and the sympathetic nervous system surge that occurs with stress play an important role, we also see evidence that the central nervous system and endocrinology system are involved. But why broken heart syndrome occurs in some people and at some times, and not others, is not understood.
What kind of stress leads to broken heart syndrome? The medical literature and clinical experience shows that just about any stress can be the cause including:
Surprise birthday party
Dobutamine stress test
Though there’s a lot about broken heart syndrome that’s still a mystery, we do know more about who is prone to have it and what their prognosis is likely to be. Here are some interesting facts:
About 90% of people with broken heart syndrome are women, most commonly in those who are post-menopausal, however the reported ages range from 10 to over 90 years.
Recovery of heart function is necessary to make the diagnosis, but the time to recover can be variable, from hours to months.
For those who have had broken heart syndrome, the risk of having it again is about 10%.
Some experts recommend long term beta blockers to help prevent recurrence, however there is no evidence of its effectiveness.
Broken heart syndrome can be lethal, however if the person survives the initial episode, their long-term prognosis is the same as if they never had it.
What Is the Heart, Really?
Doctors and scientists describe the heart as a sophisticated pump. Poets and romantics view the heart as the center of our emotions – the place where we feel love and heartbreak.
Who’s right? Broken heart syndrome suggests that, maybe, it’s both.
R. Todd Hurst, MD, FACC, FASE
Link to original publication on WebMD: https://blogs.webmd.com/heart-health/20180626/you-really-can-die-of-a-broken-heart-a-cardiologist-explains