In March 2011, a magnitude 9.0 earthquake struck off the northeast coast of Japan, resulting in a tsunami that devastated the country. In addition to the mass destruction, nearly 20,000 people lost their lives. In the wake of the natural disaster, another alarming trend emerged. An increase in acute cardiovascular events.

“You can probably imagine that collectively everyone experienced trauma together, right?” said Crystal Ripplinger, a professor in the Department of Pharmacology at UC Davis Health. “So huge emotional distress, an incredibly stressful event, and there have been several studies on this.”

Ripplinger stood before an audience gathered at G Street Wunderbar for the February Davis Science Café, an event hosted by Professor Jared Shaw and the Department of Chemistry. Her talk “Can You Really Die From a Broken Heart?” explored the compounding effects of emotional stress on the heart.   

What is broken heart syndrome?

Ripplinger showed a graph on the projector screen and pointed to an uptick in the data. She said that after the 2011 tsunami, sudden cardiac and unexpected death rose in Japan. A likely contributor to this was takotsubo cardiomyopathy, also known as broken heart syndrome.      

“It can present in a lot of different ways,” Ripplinger said. “But usually, people show up at their clinician or at the emergency department with really severe chest pain, shortness of breath, fatigue, they can have some abnormal heart rhythms, and the unifying feature is that it’s usually typically immediately after or right during a stressful event.”   

These events can be natural disasters, the death of a loved one, or even the heartbreak resulting from a divorce or breakup. 

The good news, Ripplinger said, is that people don’t often die from broken heart syndrome. However, in very severe cases, it can lead to the deterioration of cardiac function, which can subsequently lead to heart failure and eventually death. 

Broken heart syndrome vs. heart attack: what’s the difference?  

One concerning thing about broken heart syndrome is that its symptoms are incredibly similar to those of a heart attack. But there are key physiological differences between the two cardiac events. 

Heart attacks occur when a coronary artery becomes clogged or blocked, preventing blood flow to the heart. Broken heart syndrome occurs when stress causes the bottom of the heart, or apex, to balloon out. 

Broken heart syndrome was first described by Japanese clinicians in the 1990s and named after the shape of the heart during the syndrome, which resembles a pot used by Japanese fishermen to catch octopuses called a takotsubo.

“Another difference between broken heart syndrome and a heart attack is that broken heart syndrome most often impacts women,” Ripplinger said. Specifically, “women who are a little bit on the older side, so perimenopausal or postmenopausal women.” 

According to the Baylor College of Medicine, women are seven to nine times more likely to suffer from broken heart syndrome. 

Ripplinger and her lab are trying to figure out why that’s the case.

How adrenaline impacts the heart

In her lab at UC Davis, Ripplinger and her colleagues are developing new ways to image how hearts respond to adrenaline, also called epinephrine, which is the major flight or fight hormone. 

“If you get scared or excited about something and you feel that,” Ripplinger said, thumping her hand on her chest, “that’s adrenaline acting on your heart.” 

“It’s a pretty important hormone evolutionarily,” she added. “It’s pretty important that as humans, we’re able to quickly get up and run away from a tiger, right? And to do that, we need to be able to increase our heart rate and our blood flow.” 

Despite adrenaline’s importance to ensuring our safety, researchers are learning that it can also play a role in cardiovascular disease. 

Studying hearts in a dish: imaging adrenaline’s effects

In her lab, Ripplinger and her colleagues excise hearts from different animal models, including mice, rabbits and pigs. They keep the heart alive in a dish and image it while dosing it with adrenaline. 

“We developed this imaging system and then we started to try to understand how the hearts from male and female animals might respond differently to adrenaline,” Ripplinger said. “Pretty basic question; seems like a question that maybe somebody should have asked before. Nobody really has.” 

The team found a key difference in how male and female hearts respond to adrenaline. When adrenaline application was turned off in male hearts, the heart responded by uniformly shutting off its adrenaline response. In female hearts, the response was lopsided. The bottom of the heart, the apex, shut off its response to adrenaline, but the top of the heart continued to show strong adrenaline effects, resulting in a stronger contraction in that part of the heart. 

“The top of the heart is ready to run away from a tiger. The bottom of the heart of female animals is not,” Ripplinger said. “And we think this is really why during broken heart syndrome, you get that ballooning out at the bottom of the heart because it’s not responding to the hormone anymore like it should.” 

Why female hearts have been understudied in medical research

Ripplinger’s research on female hearts highlights a historic inequity in medical research. Why, she wondered out loud to the audience, was she one of the first researchers to study in detail how the hearts of females and women respond differently to a common and important hormone in the body. 

“That seems like a pretty obvious thing that should have been done 100 years ago, right?” she said. “Well, it wasn’t.” 

For years, female animals and cells were severely underrepresented in studies pertaining to cardiovascular preclinical research, and extending beyond to other preclinical research areas. 

“In the 1980s, and 1990s and early 2000s, there were almost no female animals included in any cardiovascular preclinical research,” Ripplinger said. “In 2020, it started to get a little better. We started making a dent in this.”

The NIH policy on sex as a biological variable explained

What ushered in this change was policy. In January 2016, the National Institutes of Health (NIH) implemented its Sex as a Biological Variable policy to deter overreliance on male animal and cell models in NIH-funded research.  

The shift was a win for equity in science research. 

But in February 2025, an article published in The Transmitter reported that the NIH appeared “to archive its policy requiring female animals in studies.” 

“I was really upset about this, and I gave a few talks about this, and I stood on my soapbox and jumped up and down and basically said, ‘We’re about to erase all the good we’ve done,’” Ripplinger said. “‘If we back out of this policy now, we’re just moving backwards.’”

While the NIH removed the “historic document” phrase from its website following the publication of The Transmitter article, the language still appears on the guidance document. Right below the document’s header, it reads in parentheses “Historic document published prior to January 20, 2025.”

“Maybe things are just sort of status quo and we’re going to keep the policy as it is,” Ripplinger said. “I hope, but I don’t know. So a call to action to all of you. If you should have the opportunity to communicate with those that represent you, continue to discuss with lawmakers, your representatives, your congress people, how important it is that we keep these policies in place so that we can better understand why women might suffer from cardiovascular diseases differently and how we can treat that.” 

The Davis Science Café is held every second Wednesday of the month. Learn more about the Davis Science Café.  

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