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Heart attack bacteria

17 Nov, 2014

It has long been believed that over-exertion, stress and emotional shock can cause heart attacks in vulnerable people, but the pathway by which this occurs has remained uncertain.

Now a team of researchers from Binghamton University in New York have found that hormones released during stress events appear to disperse bacterial biofilms that had been lodged in fatty plaque deposits within arterial walls (a condition known as atherosclerosis). This bacterial dispersion likely damages surrounding tissue and causes the plaque to suddenly rupture into the bloodstream, blocking peripheral arteries and causing heart attacks and strokes.

The team suspected that bacteria were involved in the process, as previous research had shown that, in some people, bacteria did grow in the fatty plaque deposits associated with atherosclerosis. Atherosclerosis is the major underlying cause of ischemia (restricted blood flow).

Associate Professor David Davies and colleagues analysed carotid artery segments removed from 15 patients with atherosclerosis. Using fluorescent tags that mark bacterial genetic material, they found all 15 samples tested positive for eubacterial 16S rRNA genes. They found at least 10 different species of bacteria clustered onto the fatty plaque as biofilm deposits.

In six of the samples, they found the bacteria Pseudomonas aeruginosa as a biofilm. After growing P. aeruginosa biofilms on the inner walls of artificial arteries made from silicone tubing, the researchers demonstrated in the lab that the biofilm would disperse when confronted with free iron in vitro. Iron is known to be released into the blood by iron-binding blood proteins, called transferrin, following interaction with catecholamine hormones. In this experiment, the researchers created free iron by flooding the tubes with the catecholamine hormone norepinephrine (responsible for the fight-or-flight response), in the presence of transferrin.

Bacterial biofilms are normally stable, being resistant to both antibiotic treatment and clearance by the immune system. However, when they do disperse, following a molecular signal, they release enzymes to digest the scaffolding that maintains the bacteria within the biofilm. As well as the biofilm scaffold, these enzymes can digest the nearby tissues that would normally prevent an arterial fatty plaque deposit from rupturing into the bloodstream.

In a press release from the American Society for Microbiology, Professor Davies said, “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”.

The researchers believe that this is the first direct observation of biofilm bacteria within a carotid arterial plaque deposit. They write that the research suggests that “bacteria should be considered to be part of the overall pathology of atherosclerosis, and management of bacteria within an arterial plaque lesion may be as important as managing cholesterol”.

Going forward, the researchers plan to see if they can model the same dispersion process in mice, and they also want to see whether the arteries of healthy people contain biofilm-forming bacteria.

The research was published in the June issue of mBio, the online open-access journal of the American Society for Microbiology.


Lanter, B.B., Sauer, K. and  Davies, D.G. (2014). Bacteria present in carotid arterial plaques are found as biofilm deposits which may contribute to enhanced risk of plaque rupture. mBio, 5 (3), e01206-14. doi: 10.1128/mBio.01206-14


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