New research published in the Journal of the American Heart Association has shown that even a brief episode of anger, triggered by recalling past experiences, can hinder the ability of blood vessels to relax — a critical factor for maintaining healthy blood flow. The study highlights how acute emotional responses can have immediate physiological effects, potentially increasing the risk of cardiovascular diseases.
Atherosclerosis is a major underlying cause of cardiovascular complications, characterized by the buildup of fats, cholesterol, and other substances in and on the artery walls. This buildup can lead to severe cardiovascular problems including heart attacks and strokes. Understanding early triggers and contributing factors to this disease is crucial for developing preventive and therapeutic strategies.
Since the late 1950s, studies have suggested that certain behavioral patterns, particularly those categorized as Type A — competitive, ambitious, and aggressive — are linked to a higher risk of cardiovascular events. This has spurred interest in how specific emotional responses, such as anger, anxiety, and sadness, might directly affect cardiovascular health. Anger, in particular, has been identified in numerous studies as a potent trigger for immediate cardiovascular events, likely due to its intense and immediate impact on blood vessel function.
However, while the association between anger and cardiovascular risk is well-documented, the specific mechanisms through which anger and other negative emotions influence the early stages of atherosclerosis and other aspects of cardiovascular health remain poorly understood.
There is a particular interest in how these emotions affect the endothelium, the inner lining of blood vessels, which plays a critical role in maintaining vascular health and function. Disruption in endothelial function is considered an early and reversible stage of cardiovascular disease, which could be key to preventing long-term cardiovascular issues.
“Impaired vascular function is linked to an increased risk of heart attack and stroke,” said lead study author Daichi Shimbo, a professor of medicine at the Columbia University Irving Medical Center. “Observational studies have linked feelings of negative emotions with having a heart attack or other cardiovascular disease events. The most common negative emotion studied is anger, and there are fewer studies on anxiety and sadness, which have also been linked to heart attack risk.”
The study was conducted as part of the Putative Mechanisms Underlying Myocardial Infarction Onset and Emotions (PUME) study, which was a randomized controlled experimental study funded by the National Heart, Lung, and Blood Institute. Researchers enrolled 280 participants from the community around Columbia University Irving Medical Center, focusing on individuals over 18 years old without significant health issues or medication usage that could affect the study.
The participants were randomly assigned to one of four groups: three that would undergo tasks designed to evoke specific emotions (anger, anxiety, or sadness) and one control group that would undertake a neutral task. The emotional states were induced using two primary methods: a recall task and the Velten mood induction technique.
In the recall tasks, participants were asked to remember and reflect on personal memories that were specifically linked to feelings of anger or anxiety. For sadness, the Velten technique was employed, which involves reading and reflecting on a series of standardized statements designed to evoke sadness.
Following the randomization, each participant underwent a series of baseline health assessments, including endothelium-dependent vasodilation (EDV) measured by the EndoPAT2000 device. This device assesses the function of the endothelium by measuring changes in the volume of the fingertip before and after blood flow has been restricted and then restored, a process known as reactive hyperemia.
The health of the endothelium was further assessed by measuring levels of endothelial-derived microparticles (EMPs) and endothelial progenitor cells (EPCs) in the bloodstream, which are indicators of endothelial injury and reparative capacity, respectively.
The primary finding was that provoked anger significantly impaired EDV, which is crucial for maintaining normal blood vessel function. This impairment was most noticeable 40 minutes after the emotion induction and indicated that anger could acutely reduce the blood vessels’ ability to dilate properly in response to increased blood flow. However, this effect did not persist, suggesting that the impact of anger on blood vessel function is transient, at least in healthy individuals without underlying cardiovascular conditions.
“We saw that evoking an angered state led to blood vessel dysfunction, though we don’t yet understand what may cause these changes,” Shimbo said. “Investigation into the underlying links between anger and blood vessel dysfunction may help identify effective intervention targets for people at increased risk of cardiovascular events.”
Interestingly, the researchers did not find similar effects with the emotions of anxiety and sadness. The measurements taken after inducing these emotions showed no significant changes in EDV compared to the neutral condition. This suggests that not all negative emotions have the same physiological impact on endothelial function, which could have important implications for understanding the specific pathways through which emotions influence cardiovascular health.
There were also no significant changes in the levels of EMPs and EPCs following any of the emotion induction tasks compared to the neutral condition. This finding suggests that while anger can transiently impair vascular function as measured by EDV, it does not necessarily cause immediate physical damage to the endothelial cells or affect their reparative processes within the short timeframe of the study.
“This study adds nicely to the growing evidence base that mental well-being can affect cardiovascular health, and that intense acute emotional states, such as anger or stress, may lead to cardiovascular events,” said Glenn Levine, a master clinician and professor of medicine at Baylor College of Medicine and chief of the cardiology section at the Michael E. DeBakey VA Medical Center.
“For instance, we know that intense sadness or similar emotions are a common trigger for Takatsubo cardiomyopathy, and events such as earthquakes or even as a fan watching a world soccer match, which provoke stress, may lead to myocardial infarction and/or to arrhythmias. This current study very eloquently shows how anger can negatively impact vascular endothelial health and function, and we know the vascular endothelium, the lining of blood vessels, is a key player in myocardial ischemia and atherosclerotic heart disease. While not all the mechanisms on how psychological states and health impact cardiovascular health have been elucidated, this study clearly takes us one step closer to defining such mechanisms.”
But there are some caveats to consider. The sample was relatively young and healthy, potentially limiting the generalizability of the findings to older adults or those with existing health conditions. The design also did not account for long-term cardiovascular risks associated with chronic or repeated emotional stress.
Future research could explore the enduring effects of these emotional states on cardiovascular health and whether interventions that target these emotional responses could mitigate the associated risks. Additionally, incorporating a broader range of emotional and physiological measures could further clarify the pathways through which emotions affect cardiovascular health.
The study, “Translational Research of the Acute Effects of Negative Emotions on Vascular Endothelial Health: Findings From a Randomized Controlled Study,” was authored by Daichi Shimbo, Morgan T. Cohen, Matthew McGoldrick, Ipek Ensari, Keith M. Diaz, Jie Fu, Andrea T. Duran, Shuqing Zhao, Jerry M. Suls, Matthew M. Burg, and William F. Chaplin.
