Observational studies have
associated anger with increased risks of myocardial infarction—heart
attack—and stroke, but little has been known about the mechanism behind
this phenomenon. Now, the results of a randomized clinical trial published in the Journal of the American Heart Association suggest that anger may affect blood vessel dilation, offering a possible explanation.
The researchers, supported by the National Institutes of
Health (NIH), aimed to examine how negative emotions affect the blood
vessels.
“This study adds to our body of knowledge that acute
negative psychological events, such as stress or anger, can have real
physiologic effects,” said cardiologist Glenn Levine, MD, a professor at
Baylor College of Medicine who was not involved with the study.
Although there’s plenty of conversation around
psychiatric conditions and physical health, Daichi Shimbo, MD, the
study’s lead author and a cardiologist at Columbia University Medical
Center, wanted to investigate the physiological influences of negative
emotions that everyone experiences from time to time. “When we think
about mental health, we think about severe chronic conditions like
depression, anxiety, posttraumatic stress disorder, and so forth,” he
said. “What we don’t talk about is negative emotions.”
After seeing data linking both short-term and long-term
risk of heart disease to anger and sadness, he wondered what could cause
this correlation. He worked with fellow researchers to design a study
centering around 3 core emotions: anger, transient anxiety, and stress.
The trial involved 280 participants between the ages of
18 and 73 years with no history of hypertension, diabetes, lipid
imbalance, or mood disorders, who were assigned to various conditions
designed to induce specific emotions:
• Either an anger or an anxiety recall task:
participants were asked to recall an event that made them angry or
anxious and talk about it for 8 minutes.
• A depressed mood task: participants were asked to read scripts off slides that became progressively sadder for 8 minutes.
• A neutral task: participants in this control group counted out loud for 8 minutes.
The recall tasks for anger and anxiety were based on
validated methods designed to elicit the negative emotions felt at
specific points in the participants’ lives.
“Obviously what may make you angry is different than
what makes me angry,” Shimbo said. “There’s individual stimuli that
cause people to have these negative emotions.”
The depressed mood task relied on the Velten Mood
Induction Procedure, a validated measure for inducing sadness. Because
the simple act of talking can affect blood vessel function, the control
condition included a speaking component, but it was designed to be
somewhat boring, Shimbo explained.
Researchers measured flow changes in the blood vessels
of each participant’s dominant arm with a blood pressure cuff, an
intravenous catheter, and a finger probe immediately after the negative
emotion induction or the neutral task and then again after 3, 40, 70,
and 100 minutes.
They found that:
• Blood vessel dilation was significantly reduced in the anger induction group compared with the control group.
• There was no statistically significant difference in
blood vessel dilation between the anxiety or sadness induction
conditions and the control group.
• Vessel impairment in the anger induction condition persisted for up to 40 minutes before returning to the baseline.
“This study suggests that a short episode of anger may
be linked to vascular impairments or the ability of the vessels to
dilate,” said Rebecca Campo, PhD, a social-health psychologist and
program director at the NIH’s National Heart, Lung, and Blood Institute,
which funded the work. “The idea is that if this is something that
occurs frequently, it could be a precursor to the kind of long-term
damage that can lead to heart attacks and strokes.”
It's important to note that the emotional induction
lasted only 8 minutes and was on a scale between mild and moderate.
Shimbo pointed out that this level of emotional annoyance is in line
with what people experience every day and yet it impaired healthy blood
vessel dilation for up to 40 minutes.
“I speculate if you’re a person who gets angry a lot,
you’re chronically insulting your arteries,” he said. “I think over time
it’s going to reach a point that it’s going to be chronically
dysfunctional. And that’s the step toward getting atherosclerosis and
heart disease.”
The Biological Mechanisms
Healthy blood vessels regularly undergo the process of vasodilation, where they widen to allow increased blood flow, helping to deliver oxygen and nutrients throughout the body. Part of this is dependent on the health of the endothelial cells, which line the blood vessels and release vasoactive factors.
Impairment of vasodilation, caused by the loss of normal endothelial function, promotes numerous processes that lead to the buildup of plaque in the arteries, known as atherosclerosis.
This study is one of the first to show that anger
affects blood vessel function, and so the intermediary mechanisms that
connect these variables aren’t yet fully understood. However,
researchers proposed several potential pathways to explore in the
future.
Levine hypothesized that the sympathetic nervous system’s activity plays a role.
“We can categorize things like anger and stress
together,” he said. “We know in the short-term, episodes like that can
increase adrenaline levels and sympathetic tone. Your heart rate goes
up, your blood pressure goes up, your body releases adrenaline, and
these can lead to increased oxygen demand by your heart. These can lead
to constriction of your coronary arteries.”
But Shimbo, who codirects the Columbia Hypertension
Center, is somewhat skeptical of this explanation because the increase
in blood pressure in the study was similar for both the anxiety and
anger conditions but only the latter was associated with impaired
vasodilation.
In his view, a connection with the powerful vasoconstrictor endothelin 1, which is released when a person feels stress,
is a more likely explanation. He noted it’s also possible that anger
affects vascular function through the inflammatory cascade, the body’s
process of responding to trauma by recruiting immune cells and chemical
mediators.
Based on the study, Shimbo said that cardiovascular researchers should distinguish between different negative feelings.
“I was surprised that sadness and anxiety didn’t have
negative effects on blood vessel function and anger did,” he said. “I
think that tells you that maybe we shouldn’t put all these negative
emotions into one bucket.”
Although there’s still a lot to learn about the
connection between anger and heart disease, the results of this study
provide a basis for additional work.
“Controlled laboratory studies such as this are an
important starting point for understanding basic biological mechanisms
underlying emotions and health outcomes,” Campo said.
Campo also noted several limitations inherent to the
study design. Although focusing on a relatively young and healthy
population removes some confounding variables, the results are not
widely generalizable.
“The participants were free of any cardiovascular
disease; they weren’t taking any cardiovascular medication,” she said,
adding that the study wasn’t conducted in a real-life setting and
“didn’t examine populations at risk for health disparities.”
Additionally, the study did not examine the chronic
effects of anger—but future work could try and tackle this issue. Shimbo
is also interested in testing the impact of cognitive behavioral
therapy on vascular function or finding a medication to reduce the
physiological effects of anger.
In the meantime, clinicians can use these preliminary
findings to advise patients on various anger management strategies to
protect their long-term cardiovascular health.
For patients who “get chest discomfort when they get
angered or stressed, this is a real phenomenon,” Levine said. “It’s not
just in their mind. It is good to explore mechanisms where they can
learn to better deal with situations that might cause stress,
frustration, or anger.”
Published Online: May 31, 2024. doi:10.1001/jama.2024.9776
Conflict of Interest Disclosures: No disclosures were reported.