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Bacterial biofilms in carotid artery plaque may cause CV events
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In patients with atherosclerosis, carotid arterial plaques may harbor bacterial biofilm deposits, which may, in turn, be triggered by norepinephrine to induce plaque rupture, according to recent study results.
These findings may characterize a mechanism by which a hormonal state is associated with potential myocardial infarction or stroke.
“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 a sudden emotional shock or stress, sudden exertion or over-exertion,” David G. Davies, PhD, associate professor of biological sciences at Binghamton University, N.Y., said in a press release.
In the study, Davies and colleagues evaluated samples from the diseased carotid arteries of 15 patients with advanced atherosclerosis. The samples were assayed by PCR amplification, all of which tested positive for the existence of eubacterial 16S rRNA genes, and five of the samples contained 10 or more discrete 15S rRNA gene sequences. Under direct microscopic observation of five samples, bacteria were found to have formed biofilm deposits, with between one and six deposits on each sample. Of the deposits observed, 93% were adjacent to the internal elastic lamina and were linked to fibrous tissue.
Six of the plaque samples showed evidence of 16S rRNA genes from the bacterium Pseudomonas aeruginosa. In vitro testing indicated that P. aeruginosa biofilms can be prompted to disperse when challenged with free iron. Iron utilizes a mechanism of interaction with catecholamine hormones, such as norepinephrine, to facilitate its release into the blood by transferrin. The in vitro analyses showed that sufficient quantities of norepinephrine prompted diffusion of the P. aeruginosa biofilms when grown under low iron conditions. This dispersal did not occur in the absence of physiologically adequate levels of transferrin.
The dispersion of biofilms could cause the sudden release of the surrounding arterial plaque, triggering MI, according to Davies.
“Our in vitro results hint at the possibility that biofilm-associated bacteria within an atheroma are induced to disperse when norepinephrine levels become elevated,” the researchers wrote. “Such a dispersion event would likely be associated with the release of degradative enzymes that have the potential to induce collateral tissue damage.”
Disclosure: The researchers report no relevant financial disclosures.
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