Twenty years ago, heart disease was the number one killer of Canadians. That number has dropped over the years thanks in part to research examining the causes of heart attacks and recommendations for better preventative behaviours.
Despite this drop, there is still much to be learned about how heart attacks happen. One of the most studied causes is the atherosclerotic lesion, better known as plaque. This accumulation of cells, fats, minerals, and other organic material tend to accumulate in the arteries as we age. If buildup happens to occur in the coronary artery, cardiac arrest may inevitably happen.
The formation of a plaque is not immediate; it takes time and there are several stages of formation. The first few pose almost no immediate harm. But as plaques grow to even larger masses, they potentially can become unstable and rupture. Much like a pimple, the explosion of the plaque leads to a combination of bleeding and also the release of material contained within.
Not knowing the difference between the wide landscape of the skin and the relatively small confines of the artery, the immune system and other clotting factors go to work to remediate the situation. Unfortunately, this can obstruct the regular flow of blood and prevent much needed oxygen from getting to the heart. Eventually, the organ begins to die and as a consequence, stops pumping. This is the first stage of a heart attack and without proper medical treatment, can be fatal.
In studying how plaque ruptures occur, researchers have looked for any possible triggers. Again, much like the pimple on the skin, one has been the presence of microbial life. Although most tend to believe these organisms are limited to our guts, respiratory tract, and skin, investigations have revealed bacteria and viruses are indeed present in the blood and in these lesions.
Some of the species found are known to cause troubles such as chlamydia, wound infections, tooth decay, and gastric cancer. This suggests they may play a role in the rupture of plaques. Yet, the evidence to suggest these pathogens are actually involved in causing the attacks has been relatively scarce. That changed last week when an international team of researchers revealed even more evidence to suggest pathogenic bacteria contribute to an increased risk for heart disease and possibly stroke.
The first hurdle had nothing to do with microbes but with the choice of samples for testing. The easiest choice was the control. The group used plaques collected from people who had died from illnesses not linked to atherosclerosis. Deciding on test samples was trickier. The team didn't acquire plaques from the coronary artery; it's an incredibly difficult and risky task. Instead, blockages from another incredibly important blood vessel, the carotid artery, were chosen. This artery supplies blood to the brain and plaques can lead not to a heart attack, but a stroke. To be sure the plaques were involved in actual life-threatening illness the samples were taken from 15 living people already suffering from minor strokes.
Once the plaques were collected, the genetic material from the masses was isolated and then examined for any signs of microbial life. These microbial signatures could then be cross-referenced to identify a species. To confirm the identity of some species, the team also ran a separate set of experiments to actually observe microbial life in the plaques. This was done using glowing tags that could attach to the bacteria and then glow under the microscope.
When all the work was complete, the results offered some incredible information. As expected, several microbial species were found in the plaques of both stroke sufferers and the controls. What wasn't expected was the incredible diversity of the species. Instead of just a few types, the researchers found dozens of different microbial species associated with several other areas of the body.
As for the bacteria responsible for troubles, stroke sufferers had higher numbers of a few different species. The greatest change occurred in the number of bacteria known to use sulfur as a nutrient source. For the researchers, this finding was quite meaningful as it related directly to one of the hallmark signs of dangerous plaques.
One of the most important chemicals raised in atherosclerosis is homocysteine, which also contains sulfur. The authors suggest the higher level of this molecule could help these bacteria thrive and possibly put strain on the fibres of the plaque. This inevitably leads to destabilization and a greater chance for rupture.
The results of this study suggest plaques are far more alive than previously believed. They are teeming with microbial life with species usually found in the gut, the skin, and the respiratory tract. The findings also suggest plaques should be looked at as an ecosystem rather than a singular organic entity and may be dynamic based on the microbial population. When that diversity changes to more sulfur-using bacteria, the risk for troubles increases.
Granted, this initial study may not lead to a call for treatment options to stabilize or possibly reduce plaques by examining microbes. Yet, with this preliminary information at hand, we may soon be taking cardiovascular and stroke research in a different direction. By taking the ecosystem approach, we may be able to follow the process of plaque formation and identify critical moments when the population changes leading to a greater change for dire consequences.
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