Heart disease is a killer. In Canada, almost 30 per cent of all deaths are caused by the sudden failure of the heart to pump the lifeblood throughout the body. Making the situation worse is the realization no one factor can be singled out as the cause. The illness is manifested through a compilation of different short- and long-term events leading to one horrific moment in which life is suddenly at risk or lost.
The contribution of microbes to this unfortunate condition has been sought for some 80 years although the answers have been less than helpful. Back in the 1930s, attempts to link cardiac conditions in pigs to hog cholera virus revealed there could be something of value. They could easily identify the telltale signs of heart disease -- inflamed arteries and thickened walls, localized damage known as lesions, and blockages. The information was more than enough to suggest there was a microbial contribution to cardiovascular disease although the mechanism behind the impact would have to wait for decades.
The answer was first revealed in the 1950s, but in another animal, the rabbit, and a different part of the body, the liver. Researchers examined how blood flow was lost, known as infarction, and found bacteria had a tendency to grow in the arteries, forming classical blockages. If left without treatment, the bacteria could grow enough to literally form a microbial dam. Eventually, the liver would suffer the infarction and the rabbit would find itself in serious danger. This suggested a possible link to human conditions yet there were still doubts.
Although studies continued to search for the microbial link; there were little advances for some 40 years. Then, in the 1990s, a novel concept came out not from those studying heart disease but respiratory problems. There appeared to be a link between the bacterium Chlamydia pneumoniae and the onset of heart disease. Over the decade, a significant amount of effort was put into deciphering the association yet little came of it. By the turn of the millennium, there was simply not enough evidence to say C. pneumoniae was the cause. What it did, however, was suggest there is still a need for more research.
As the 2000s progressed, the mindset changed from an association to an actual cause. Back in the 1950s, bacterial growth was assumed to be a unique phenomenon. But the knowledge base had since shown this was no outlier. Bacteria everywhere could form communities, known as biofilms, inside the body. Though traditionally associated with oral health problems these invading colonies could potentially be the missing link.
Last week, a team of researchers from Binghampton University in New York provided some of the first evidence to suggest biofilms were indeed part of the problem. They took samples from the carotid arteries of 15 patients suffering from advanced atherosclerosis and investigated the samples for evidence of bacteria. But, unlike some tests, which solely look for genetic material, these researchers wanted to actually see the bacteria. They used an assortment of visual techniques -- including fluorescent dyes -- to identify any presence of bacteria.
What they found was startling: throughout the samples, bacteria were happily living in five of the 15 samples. Even more fascinating was the nature of the organisms. It was not Chlamydia, hog cholera virus or other previously tested strain. This was Pseudomonas aeruginosa, the same species known to cause problems in cystic fibrosis. Based on their findings, the microbe would grow unfettered raising the localized pressure on the artery wall. If the pressure became too high, cracks and eventual rupture would occur, leading to blood loss and an eventual heart attack.
Though microbial ecologists would not be surprised by the results -- P. aeruginosa is the most studied biofilm forming species -- in the context of heart health, this was a fundamental finding. No one had suspected this normally harmless bacterium and at times wound and respiratory infectious agent could be found inside the confines of the human artery. The discovery also confers some understanding of how plaque formation and associated cell wall damage could occur both from microbial as well as immunological perspectives. Even more importantly, the information may add critical value to understanding how to control the condition through medical treatment.
As the authors stated, this is just one more factor to add to the list of associated biological and social contributions to heart disease. While the door may be opened to testing and treatment options for the future, the revelations can only do so much. Heart health is a complex study and requires a proper lifestyle to maintain. Yet, as the researchers have shown, should there appear to be signs of problems, such as continual chest pains, palpitations, lightheadedness, shortness of breath and fatigue; there may be yet another option for diagnosis and treatment to avoid a heartbreaking end.
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