Neuroendocrine and behavioral mechanisms mediating the relationship between anger expression and cardiovascular risk: assessment considerations and improvements.
The hypothesis that intense anger experience may increase risk for or exacerbate cardiovascular diseases has been under active theoretical and empirical interest for decades. Biopsychological models of disease suggest that persons displaying exaggerated physiological responses to acute emotional or stressful states are at a greater risk to develop cardiovascular disorders. The last two decades have witnessed active work to refine means by which anger expression can be assessed, and laboratory research has produced evidence suggesting that certain expression styles may predict enhanced physiological responses to acute stress. In this paper, we review methodological and definition issues related to the assessment of anger, and we summarize recent improvements on the assessment of anger expression. We also review recent studies addressing the association between anger and cardiovascular diseases, and we present potential neuroendocrine and behavioral mechanisms through which anger expression may increase risk for cardiovascular disease.
al'Absi
Mustafa
M
University of Minnesota Medical School, 1035 University Drive, Duluth, MN 55812, USA. malabsi@umn.edu
Bongard
Stephan
S
D000786:Anger; D001341:Autonomic Nervous System / Q000503:physiopathology; D002318:Cardiovascular Diseases / Q000523:psychology*; D019260:Expressed Emotion; D006801:Humans; D006854:Hydrocortisone / Q000378:metabolism; D007030:Hypothalamo-Hypophyseal System / Q000378:metabolism / Q000503:physiopathology; D009490:Neurosecretory Systems / Q000503:physiopathology*; D018847:Opioid Peptides / Q000378:metabolism; D010913:Pituitary-Adrenal System / Q000378:metabolism / Q000503:physiopathology; D011581:Psychological Tests; D011603:Psychophysiology; D012307:Risk Factors; D012737:Sex Factors
D018847:Opioid Peptides; D006854:Hydrocortisone