News Release

Stress leaves blood vessels tightly wound

Peer-Reviewed Publication

American Heart Association

DALLAS, May 21 – Mental stress causes the inner layer of the blood vessels to constrict, which may increase the risk of sudden cardiac death, researchers report in today’s rapid access Circulation: Journal of the American Heart Association.

“Sudden life events, such as anger, bereavement or war can trigger sudden cardiac death, but how this happens exactly is not clear,” says primary researcher Georg Noll, M.D., of University Hospital in Zurich, Switzerland.

This study provides the first evidence that sudden mental stress induces endothelial dysfunction. Endothelial dysfunction occurs when the blood vessels’ ability to dilate is impaired. This effect is augmented by a chemical called endothelin-A (ETa). As a result, the blood vessels are unable to respond properly to changes in blood demands (i.e. expanding and contracting to accommodate different amounts of blood flow). The condition can increase the risk of a heart attack or stroke.

Swiss researchers studied subjects ages 20 to 31 years old with no cardiovascular risk factors. Ultrasound was used in five individuals to assess their blood vessels’ ability to dilate both before and 10 minutes after a three-minute mental stress task. Six subjects had dilation measured before and after the task while being infused with a drug called an ETa receptor blocker that causes dilation. For comparison, saline was infused in a control group of three people. For the mental stress task, subjects had to respond as quickly as possible to colored lights by pushing a button of the corresponding color. Researchers found a significant decrease in blood-vessel dilation after mental stress. The mental stress test increased average arterial blood pressure from 83 to 96 millimeters of mercury (mm Hg) and heart rate from 63 to 81 beats per minute. Flow-mediated dilation was reduced by half, from 8.0 to 4.1.

Further, researchers found this significant drop in dilation was completely prevented by the ETa receptor blocker (8.6 before vs. 9.4 at 10 minutes after). Researchers believe this response identifies ETa activation as a mechanism responsible for endothelial dysfunction; therefore, blocking ETa receptors may be a novel way to prevent atherosclerosis.

“Endothelial dysfunction induced by mental stress offers a novel and unique link between psychological factors and the cause of atherosclerosis, similar to other risk factors that impair function such as high cholesterol or high blood pressure,” says Noll.

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Co-authors are Lukas E. Spieker, M.D.; David Hurlimann, M.D.; Frank Ruschitzka, M.D.; Roberto Corti, M.D.; Frank Enseleit, M.D.; Thomas F. Luscher, M.D.; Sidney Shaw, Ph.D.; Daniel Hayoz, M.D.; and John E. Deanfield, M.D.

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