If you are a fan of movies (or perhaps the television show Gunsmoke), you might recall this classic scene: an elderly man is involved in an altercation, or attack, some stress-inducing event. He suddenly clutches his chest, gasps, falls to the ground and dies.
It’s easy to think of this scene as purely theatre, but sadly it is theatre imitating life. That is to say, there truly can be a stress-related component to heart attacks. Emotional and/or physical stress has been shown to cause the release of the catecholine norepinephrine. Here we look at a report that examines some of the ways an endocrine event like norepinephrine release, in response to a sudden flush of anger or excitement, can result in the physiology events of sudden arterial rupture and death.
The article is “Bacteria present in carotid arterial plaques are found as biofilm deposits which may contribute to enhanced risk of plaque rupture” (1).
Let’s begin with the arteries. Fatty deposits and calcium can accumulate in artery walls, causing a loss of arterial elasticity. Current theory is that low density lipoprotein (LDL) and cholesterol in the bloodstream collect under the epithelium of arterial walls. Eventually this accumulation causes an arterial plaque to form, a main feature of atherosclerosis and coronary artery disease.
Such plaques can undergo sudden rupture. It is estimated that three-quarters of all fatal coronary thrombi are the result of arterial plaque ruptures (1).
There is recent and growing recognition that arterial plaques, in addition to their LDL and cholesterol components, contain a bacterial component (1). In earlier work the authors isolated and identified cultivatable Pseudomonas aeruginosa as “a colonizing pathogen from a diseased endarterectomy sample”.
In this study, 15 arterial explants from patients were screened for Pseudomonas spp.-specific 16S rRNA using PCR amplification. Pseudomonas spp. positive results occurred in 6 of 15 patients. By BLAST analysis, 5 of these 6 positive results contained sequences that aligned with those of Pseudomonas aeruginosa. (1).
Bacterial biofilms are conglomerations of bacteria, living in an interconnected community where they not only share resources but also provide individual bacteria protection from dangers such as antimicrobial therapy. These bacterial communities have been shown to undergo dispersal, with release of colony members, when circulating levels of essential nutrients decline below necessary levels.
To look for the presence of bacterial biofilms, these researchers examined transverse sections from 5 carotid artery samples from patients with artherosclerotic lesions. They used peptide nucleic acid-fluorescent in situ hybridization probes (PNA-FSH) with fluorescence-tagged specific 16S rRNA (Pseudomonas spp.). All 5 samples showed bound probe with fluorescence tags demonstrating areas of bacterial microcolonies. The probe targets hits were arranged in particular regions with several dozen to a few hundred targets, separated by unstained matrix areas (bacterial biofilms are characterized by the presence of a surrounding matrix). The staining also appeared in areas of reduced tissue density or structural alteration, which could be areas of tissue damage (1), such as that found in atherosclerotic lesions.
While biofilms are consolidated bacterial communities, they are known to also undergo dispersal events, where individual bacteria are released. In the bloodstream, this means bacteria can disseminate to other areas. In addition, biofilm dispersal events are believed to include release of enzymes that help to degrade the matrix that supports the biofilm. The authors speculated in this report that enzymes released may inflict damage on surrounding tissue and in the event of a biofilm dispersal connected to an atheroma, these enzymes could be connected to plaque rupture.
But wait, there’s more.
Last but not least is the stress component that can be involved in plaque rupture. The authors of this mBio paper show that in vitro, Pseudomonas spp. can both form biofilms and undergo biofilm dispersal response when challenged with physiological levels of norepinephrine in the presence of transferrin. Transferrin normally functions to chelate circulating iron, preventing bacteria from benefitting from this essential nutrient.
However, transferrin levels are known to decrease with release of norephinephrine, allowing circulating levels of iron to rise. In vitro, biofilms are known to respond to such an increase in nutrient availability by undergoing a dispersal event, accompanied by release of degradative bacterial enzymes.
For those of us with normal, median-range blood pressure, and good low LDL, but also thin skin, it could be time for an improvement in response to stressors.
Reference
Lanter BB, Sauer K, Davies DG. 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.
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Kari Kenefick
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