In a recent study published in the Journal of the American Heart Association, a team of researchers investigated how provoked anger and negative emotions of sadness and anxiety affect endothelial cell health in an attempt to understand the association between core negative emotions and cardiovascular disease events.
Study: Translational Research of the Acute Effects of Negative Emotions on Vascular Endothelial Health: Findings From a Randomized Controlled Study. Image Credit: Tiko Aramyan / Shutterstock
Background
Cardiovascular disease events are often due to thrombus formations that occur after atherosclerotic plaques break off the arterial walls. These plaques are formed when lipids and other elements in the blood get deposited along the walls of the arteries. Substantial research efforts are dedicated to understanding the underlying mechanisms and determinants of the pathways leading to atherosclerosis.
However, since the 1950s, the link between psychosocial factors and the risk of incident cardiovascular disease events has also gained considerable interest, especially since Friedman and Rosenman found that highly competitive individuals who are work-driven, ambitious, aggressive, and time-conscious are at a higher risk of cardiovascular disease that people with other behavioral patterns.
Numerous studies have also found that acute anger is linked to an increased risk of cardiovascular disease events. However, the underlying mechanisms through which acute anger affects the development and progression of atherosclerosis and cardiovascular disease events remain understudied.
About the study
In the present study, the researchers examined how provoked anger and negative emotions of sadness and anxiety affect endothelial cell health. Vascular homeostasis is primarily regulated by the endothelium, and the endothelial cells are essential for maintaining the integrity of the vasculature and vascular tone. Furthermore, studies have found that dysfunction of the endothelium triggers the development of atherosclerosis and brings about the onset of cardiovascular disease events.
Research also indicates that tasks that cause mental stress, such as public speaking, affect endothelium-dependent vasodilation. A previous non-randomized study by the same team of researchers had also found that anger recall tasks, which involve recollection and reexperiencing prior events that provoked acute anger, have a significant impact on endothelial cell health in injuring endothelial cells, impairing endothelium-dependent vasodilation and disrupting the reparative capacity of endothelial cells.
The present single-blind, randomized controlled study enrolled close to 300 participants, who were randomized to four groups based on four conditions: anger recall tasks, depressive mood recall tasks, anxiety recall tasks, and a neutral emotional condition.
The pre-and post-assessments of endothelial cell health included detecting the circulatory levels of microparticles derived from endothelial cells to assess endothelial cell injury and evaluate flow-mediated endothelium-dependent vasodilation. Additionally, determining the circulatory levels of endothelial progenitor cells derived from the bone marrow provided information on the reparative capacity of endothelial cells.
Participants with chronic medical conditions, including any history of cardiovascular disease or coronary revascularization, as well as risk factors such as diabetes, dyslipidemia, and hypertension, were excluded. Actively smoking participants, those using over-the-counter dietary supplements and medications, or those with a history of personality disorder, mood disorder, or psychosis were also excluded from the study to avoid confounding the results.
Self-administered questionnaires were used to obtain information on cardiovascular disease risk factors, physical activity levels, alcohol consumption, tobacco exposure, and demographic characteristics.
Results
The results showed that even a short-term provocation of anger impaired endothelium-dependent vasodilation and had a negative impact on endothelial cell health. The study also reported that the tasks to induce negative emotions were extremely effective in provoking the required negative emotion, confirming the effectiveness of this procedure.
The researchers found that compared to neutral emotions, the feelings of provoked anger led to the impairment of the reactive hyperemia index score between 0 and 40 minutes. This score measures the excess of blood supply to a region or organ and is an indicator of endothelial function. The impairment in the score was also not observed beyond 40 minutes post-induction of anger, highlighting the acute effects of provoked anger on endothelial function.
Furthermore, compared to the neutral emotional condition, feelings of sadness or anxiety did not bring about any significant changes in the reactive hyperemia index score. The findings linked to provoked anger and the reactive hyperemia index score also did not change when adjusted for visual analog scale ratings, indicating that nonspecific feelings of sadness or anxiety did not influence the association between provoked anger and endothelial cell health. No changes were observed in the endothelial cell-derived microparticles and endothelial progenitor cells in relation to any of the emotion induction tasks.
Conclusions
Overall, the study found that provoked anger acutely impacted endothelial cell health by impairing endothelium-dependent vasodilation. Other negative emotions, such as sadness and anxiety, do not have a similar effect on endothelial function. These findings provide a better understanding of the biological mechanisms through which core negative emotions increase the risk of cardiovascular disease events.
Journal reference:
- Daichi S., Cohen, M. T., McGoldrick, M., Ipek Ensari, Diaz, K. M., Fu, J., Duran, A. T., Zhao, S., Suls, J. M., Burg, M. M., & Chaplin, W. F. (n.d.). Translational research of the acute effects of negative emotions on vascular endothelial health: Findings from a randomized controlled study. Journal of the American Heart Association, DOI: 10.1161/JAHA.123.032698, https://www.ahajournals.org/doi/full/10.1161/JAHA.123.032698
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