If you consistently experience high levels of stress, you may be stimulating bacteria that weaken your blood vessels, Binghamton University researchers have found.

The microbiologists discovered a link between stress hormones and bacteria that may explain how emotional shock or over-exertion can trigger heart attacks or strokes in vulnerable people. Researchers believe that this is how someone could literally be scared to death.

The research, published in mBio, the online open-access journal of the American Society for Microbiology, indicates that hormones released during stress could cause thin sheets of bacteria called biofilms to disperse.

If this happens in your body, biofilms within your arterial walls would be stimulated to release enzymes that might weaken the arterial wall and lead to plaque rupturing into the blood stream. Plaque rupture has long been known to be one of the leading causes of heart attack and stroke.

“Our hypothesis fits the observation that heart attack and stroke often occur following an event where elevated levels of catecholamine hormones are released into the blood and tissues, such as occurs during sudden emotional shock or stress, sudden exertion or over-exertion,” says David Davies, associate professor of biological sciences at Binghamton.

Biofilms, often referred to as slime, form when bacteria undergo a genetic change and then organize within a self-produced matrix of extracellular polymeric substance. Once they are protected within the biofilm, bacteria are harder to detect and to treat with antibiotics.

Davies and his colleagues grew different species of bacteria taken from diseased carotid arteries affected by atherosclerosis, the build-up of thick plaques within the walls of blood vessels. They found multiple bacterial species living as biofilms in the walls of every atherosclerotic carotid artery tested. Certain molecular signals can cause the biofilms to release enzymes that digest the scaffolding anchoring the bacteria in place.

“The release of iron into the blood as a result of increases in stress hormones is what causes the bacteria to release their hold on each other and the plaque,” says study co-author Karin Sauer, professor of biological sciences at Binghamton.

This research suggests that bacteria should be considered to be part of the overall pathology of atherosclerosis. The scientists suggest that management of bacteria within an arterial plaque lesion may be as important as managing cholesterol.

Davies believes this research might someday change the medical community’s view of many conditions. “We’re going one disease at a time and trying to demonstrate whether or not bacteria are involved,” he says. “In most diseases with the letters itis … it means inflammation, it means a biofilm infection.”

Amber Doiron, assistant professor of bioengineering, says current methods of assessing atherosclerosis — commonly known as hardening of the arteries — are not terribly accurate. Some 30 percent of deaths worldwide can be attributed to the disease, which occurs when fat, cholesterol and other particles form hard structures called plaques in the walls of arteries.

“It’s really a guessing game right now,” she says. “Doctors use factors like blood pressure and cholesterol level to get an idea of a patient’s risk. Then they use plaque size as a general measure of whether a person has the disease. But there’s a fairly poor correlation between plaque size and heart attack or stroke.”

Doiron, who has an interest in molecular imaging as well as expertise in nanoscience, wants to help physicians do a better job of identifying which plaques are cause for concern.

She and a Temple University colleague recently received a two-year, $418,000 grant from the National Institute of Biomedical Imaging and Bioengineering to support this project. It’s a notable success in part because this was Doiron’s first National Institutes of Health grant proposal.

The researchers will use a combination of polymers and superparamagnetic iron oxide nanoparticles for the study. The nanoparticle is sensitive to oxidative stress, which occurs in atherosclerosis and has been linked to patients who have a higher prevalence of heart attack and stroke. Using an MRI scan, the researchers will be able to see how active the nanoparticle is, which will indicate whether the plaque is stable.

“A stroke or a heart attack doesn’t necessarily come when a plaque fully blocks the flow of blood through an artery,” Doiron explains. “What happens is the plaque ruptures and the gunk that underlies the plaque is exposed to blood and a clot forms. The clot builds quickly — on an hour time scale as opposed to over years — and the clot can grow there until it blocks flow, or it can dislodge and block flow somewhere else. Most heart attacks do not occur from a full blockage of plaque. It happens because the plaque bursts. Same thing with strokes. That’s why size isn’t necessarily indicative of how dangerous a plaque is.”

The discovery of a molecule or a cell type that indicated which plaques are safe and which ones are dangerous would be a huge breakthrough, Doiron says. She thinks oxidative stress may be such an indicator.

“Atherosclerosis is an incredibly complex disease that progresses over decades,” Doiron says. “It’s hard to tell who’s walking around with plaques that are stable, relatively safe, and who has plaques that may cause a heart attack tomorrow. For some patients, the first sign of trouble is a heart attack.”