#Anger, #HeartAttack
IBNS-CMEDIA: Short bursts of anger may temporarily damage the ability of blood vessels to properly dilate, a function believed to be pivotal in preventing arteries from hardening, new research suggests.
The findings, published Wednesday in the Journal of the American Heart Association, may help explain how anger contributes to the risk of having a heart attack.
“Anger is bad for your blood vessel function,” said lead study author Dr. Daichi Shimbo, a cardiologist and co-director of the hypertension center at Columbia University Irving Medical Center in New York City. “It impairs the function of your arteries, which is linked to future heart attack risk.”
Previous observational studies have established a clear link between negative emotions – including anger, anxiety and sadness – and an increased risk for heart attacks and strokes. But little is known about how these emotions trigger changes in the body that lead to cardiovascular events.
In the new study, 280 apparently healthy young adults with no history of heart disease or stroke, their related risk factors, serious mental health conditions or other chronic illnesses were recruited from the community surrounding Columbia’s medical center.
In a laboratory setting, participants were asked to relax for 30 minutes, after which blood pressure and heart rate measurements were taken, along with tests to measure endothelial cell health – the health of the inner cellular lining of blood vessels. Endothelial dysfunction has been implicated in the development of atherosclerosis, or hardening of the arteries, which can lead to heart attacks and strokes.
Prior studies have shown mental stress can impair endothelial function. Researchers in the new study explored how well blood vessels were able to dilate, whether endothelial cells lining the blood vessels were damaged and whether they were able to repair themselves following acute, negative emotions.
After baseline measurements were taken, individuals were randomly assigned to one of four tasks. Over an eight-minute period, one group was asked to recall personal memories aloud that evoked anger. Another was asked to recall memories aloud that evoked anxiety. A third was asked to read sentences aloud that evoked sadness, and the final group was asked to count aloud to remain in an emotionally neutral condition. These tasks were followed by a second silent resting period.
Blood pressure and endothelial health measurements were taken again at three, 40, 70 and 100 minutes following the tasks people performed.
Compared to the emotionally neutral group, people who recalled memories that provoked anger saw a diminished ability of their blood vessels to dilate, which was cut by more than half. This effect peaked 40 minutes after the anger-recall task and then function returned to normal.
Though the effect was temporary, Shimbo said it’s important to note that it resulted from just eight minutes of recalling angry feelings, raising questions about the cumulative impact of anger on blood vessel function over a longer period of time.
“We showed that if you get angry once, it impairs your ability to dilate,” said Shimbo, who is also a professor of medicine at Columbia. “But what if you get angry 10,000 times over a lifetime? This chronic insult to your arteries eventually may lead to permanent damage. That’s what we think is going on.”
Provoked anxiety and sadness, however, had no statistically significant effects, a result that Shimbo said surprised him.
“People lump negative emotions into one bucket,” he said. “This tells me that maybe anger, anxiety and sadness are different from each other in how they affect heart risk.”
Dr. Suzanne Arnold, a cardiologist at Saint Luke’s Health System and a professor of medicine at the University of Missouri-Kansas City School of Medicine, said the findings shed light on why bursts of anger may lead to cardiovascular disease.
“This is interesting because it helps to explain something we’ve seen over and over again,” she said. “There’s plenty of data that have shown acute anger increases the risk for heart attacks, but the mechanism by which that happens is not really understood.”
Arnold, who was not involved in the research, noted the study was limited to young adults with no cardiovascular disease or risk factors and suggested the next step may be to expand the study population.
“What does this look like in people who are older and have cardiovascular disease already?” she asked. “You may see more profound effects.”
