Cellular Research
Cellular Research

Stress, Bacteria Trigger Heart Attack?

A study implicates the breaking up of bacterial biofilms on fatty plaques in arteries as causing stroke or heart attack following stress.

By | June 12, 2014

Pseudomonas aeruginosa on cetrimide agarWIKIMEDIA, HANSNUnder duress, the body releases stress hormones to help deal with the potentially dangerous situation, diverting energy from digestion, growth, and even immunity to fuel increases in heart rate and blood pressure. But such hormones can also break up biofilms in arteries, possibly contributing to stress-related heart attack or stroke, according to a study published this week (June 10) in mBio.

Specifically, David Davies of Binghamton University in New York and his colleagues identified a handful of bacterial species on the arterial plaques of 15 cardiovascular disease patients. Among those bacteria were the biofilm-forming Pseudomonas aeruginosa. Such plaques are normally stable, but when do they break down, clumps can results in blood clots that can cause the patient to suffer a heart attack or stroke. Suspecting that the bacteria might follow the same pattern, the researchers treated P. aeruginosa grown in silicone tubing with the stress hormone noradrenaline, which is used to treat dangerous drops in blood pressure, then watched as the biofilms dissolved. Davies and his team speculate that 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.

“It’s quite an intriguing hypothesis,” microbiologist Primrose Freestone of the University of Leicester in the U.K. told Nature News, noting that more work is needed to confirm this phenomenon in animal models and humans.

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Avatar of: Paul Stein

Paul Stein

Posts: 142

June 12, 2014

This is an interesting hypothesis, but much more testing needs to be done.  While norepinephrine may cause a dispersal of biofilm, is that enough to either weaken the plaque structure for arterial pulsations to do the rest or would there be enough internal force within the plaque to burst it?  Then, is there sufficiently released content volume to do anything?  What is the mechanism of action if there is and what is the time course?  These are just a few of the very tough questions for a quite sensationalistic article title.  Even tougher will be what to do clinically if any of these initial findings have relevance.

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