MONDAY, May 20, 2002 (HealthDayNews) -- A human experiment implicates a molecule for having a major role in how stress can cause heart disease, and the research points the way toward a preventive treatment.
It's known that stress can lead to a number of physical problems, including heart disease. This experiment established a firm link between stress and a damaging physical effect on the arteries.
Swiss researchers induced stress in 23 young volunteers by having them respond urgently to flashing light signals. Blood pressure and heart rate were monitored, and ultrasound was used to measure how well arteries widened to let blood flow freely.
Blood pressure increased by almost 10 percent and heart rate by 18 percent, from 63 to 83 beats per minute. Most important, there was a significant decrease in the ability of arteries to widen, to allow the free flow of blood. Widening was reduced by half in most of the volunteers immediately after they went through the light test. It's this kind of stiffening of the arteries that can eventually result in heart attacks or strokes.
However, one group of volunteers did not experience this reduction in widening. Before they began the test, they were given a molecule that blocks receptors for a molecule called endothelin-A in cells of the endothelium, the delicate lining of the arteries. Their arteries actually became wider, so that blood flow increased, a strong indicator that endothelin-A is the stress-related villain.
"We know from epidemiological studies that stress and mental depression can lead to cardiovascular disease," says Dr. Georg Noll, a professor of cardiology at University Hospital in Zurich and lead author of a report in tomorrow's issue of Circulation. "This shows that mental stress activates a hormone system that has long-term effects on the vasculature [blood vessels]."
Stress could be a risk factor as treatable as high cholesterol levels, because drugs designed to be endothelin antagonists -- blockers -- are already available, Noll says.
"The endothelin antagonists that have been tested in heart failure would be promising candidates," he says.
However, it's not clear that everyone would benefit from popping an endothelin antagonist pill during a time of stress, Noll says, because some people handle stress better than others. He and his colleagues are working to make treatment more feasible by identifying those who would benefit most.
"Another project is to look at different population groups and characterize them psychologically to determine whether exposure to stress has different effects depending on character and behavior," Noll says. "It might be possible to identify those at high risk."
The Swiss study "fits very nicely with a lot of things we have been doing recently," says David M. Pollock, an associate professor in the Medical College of Georgia Vascular Biology Center.
"What we've shown is that psychosocial factors, mental stress, even video games, induce changes in cardiovascular function," he says. "We reported a couple of years ago that stresses like video games increased endothelin levels. If you increase stress levels, you have high endothelin levels and other stressors have a much bigger vascular response. Chronic elevations affect vascular structure, and make a person more susceptible to heart disease."
One endothelin antagonist drug is now marketed in the United States for treatment of congestive heart failure, but it is not specific to endothelin-A. Several other antagonists are in advanced testing for treatment of hypertension, he says.
What To Do: A rundown on what is known about stress and heart disease is given by the American Heart Association. Read about other risk factors from the Texas Heart Institute.
