DALLAS, Dec. 2 -- For the first time, in a large study, researchers have linked an exaggerated response to mental stress to blood vessel blockages that can trigger heart attacks and strokes. The findings appear in today's American Heart Association journal Circulation.
The study of 901 Finnish men found that those with the most extreme blood pressure responses on a mental stress test had the thickest blockages from atherosclerosis in their carotid arteries, the vessels that feed blood to the brain. The association was strongest among men younger than 55.
In the study, mental stress responses were associated with the same degree of atherosclerosis risk as smoking and elevated cholesterol in the younger men, suggesting that cardiovascular reactivity to stress may turn out to be a new risk factor for heart disease and stroke, says the study's lead author, Thomas Kamarck, Ph.D., associate professor of psychology, University of Pittsburgh. Since all of the measures were taken at one time, the researchers cannot yet conclude that the responses to mental stress cause the atherosclerosis. Further research is needed to determine if mental stress response predicts future development of plaque.
Just like elevated cholesterol, mental stress over time may injure blood vessels and promote atherosclerosis in susceptible individuals, Kamarck says.
"Frequent and prolonged periods of elevated blood pressure during mental stress may promote mechanical injury to the endothelial lining or cause release of stress hormones that can promote the build up of plaque," say the researchers. They note that further research is needed to determine the cause of the association observed in this study.
The new study builds on existing evidence that individuals who show exaggerated responses to stress ("Type A", or hostile individuals) may be at higher risk for heart disease and stroke than more relaxed individuals.
The latest study seeks to further pinpoint the "unhealthy" characteristics of "stress-prone" individuals who have been previously identified by questionnaires or interviews.
The test used in this study requires a person to perform a series of mental tasks that require a range of cognitive and memory skills. Each task is designed to stimulate a state of mild mental stress. The difficulty level was adjusted to maintain performance of less than 60 percent accuracy rate so that the person remained challenged throughout.
"Cardiovascular reactivity" was measured by examining the acute changes in blood pressure and heart rate produced by the tasks.
The participants in the study -- who were enrolled in a heart disease investigation called the Kuopio Ischemic Heart Disease Study -- all had carotid ultrasound testing. This non-invasive test provides an X-ray image of the thickness of the carotid artery wall, a measurement called mean intimal thickness which is thought to be a reflection of atherosclerosis in the vessel. The carotid ultrasound is a widely accepted tool used to estimate atherosclerosis in other blood vessels in the body.
Men who were in the highest quintile for cardiovascular reactivity had a mean intimal thickness of .89 mm, compared to .85 mm in the lowest fifth. An increase of .1 mm of intimal medial thickness has been associated with an 11 percent increased risk for heart attack in previous studies. Future research is needed to determine whether cardiovascular reactivity predicts heart attacks or other results of atherosclerosis, says Kamarck.
Researchers don't know why the association was not found in individuals older than 55. Since this sample of Finnish men was particularly prone to heart disease, some of the most susceptible individuals may not have survived into their 60s. The survivors may have been less prone to develop diseases regardless of their stress reactivity.
Researchers don't know why people differ in their cardiovascular reactivity to acute stress. Evidence suggests that about 50 percent of the differences may be due to genetics, but chronic stress exposure may contribute in some cases as well.
Co-authors are Susan Everson, Ph.D., M.P.H.; George Kaplan, Ph.D.; Stephen Manuck, Ph.D.; J. Richard Jennings, Ph.D.; Riitta Salonen, M.D., Ph.D.; and Jukka Salonen, M.D.; Ph.D., M.Sc.P.H.
The above post is reprinted from materials provided by American Heart Association. Note: Content may be edited for style and length.
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