Research Explains How Stress Leads to Heart Attack

A new research explains how stress, fear or over-exertion can lead to heart attacks in some people.

According to researchers at the Binghamton University, Binghamton, stress or over-exertion release hormones that rupture bacterial biofilms on blood vessel walls. The bacterial colonies are closely attached to the plaque and their dispersal leads to the plaque being released into the bloodstream, causing a heart attack.

Biofilm is a slimy layer made by bacterial colony. This layer keeps the bacterial colony intact and helps the colony cling to a surface.

"Our hypothesis fitted with 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" said David Davies of Binghamton University, Binghamton, New York, one of the authors of the study.

For the study, researchers looked at bacteria from diseased carotid arteries. They found that all plaque covered artery sample had bacteria with biofilms.

According to the researchers, these biofilms are resistant to drugs. However, the body releases certain hormones under stress that can lead to these colonies dispersing from the arterial wall. The bacteria release enzyme that can dissolve tissues that prevent the plaque from entering the bloodstream.

Rupture of the vulnerable (unstable) atherosclerotic plaque is a major reason for several acute heart events.

In the next part of the study, researchers used a silicone to test whether the hormones were really breaking the biofilms. The team added norepinephrine, which is a stress hormone, to the bacterial biofilms in the silicone tube.

"At least one species of bacteria - Pseudomonas aeruginosa - commonly associated with carotid arteries in our studies, was able to undergo a biofilm dispersion response when exposed to norepinephrine, a hormone responsible for the fight-or-flight response in humans," said Davies in a news release.