Thanks to a new study that reveals the process underlying them for the first time, heart attacks caused by smoking could be avoided. It was previously impossible to prescribe potential medication therapies to stop heart attacks brought on by plaque erosion, but a recent study led by Manchester Metropolitan University has made it possible.
Plaque erosion, in which the endothelium, the inner lining of blood arteries, separates, is responsible for about 30% of heart attacks. Because the endothelium shields the blood vessels, its loss causes the blood to clot, which can lead to a heart attack.
Plaque erosion is more common in younger people, smokers, and women, which is why lifestyle factors like smoking are thought to raise the risk of this type of heart attack. The study, which was published in Cardiovascular Research, has now revealed the mechanism driving the cells to detach from the blood vessel, which was previously unknown.
Dr. Stephen White, Reader in Cardiovascular Pathology at Manchester Metropolitan University, said, “This type of heart attack is more common in younger people and in smokers and we used this information to unpick the mechanism and decipher what happens during plaque erosion.”
“Our findings show a completely new mechanism that links cell stress caused by smoking—and potentially other factors like air pollution—with a defect in how the cells hold on to the underlying structures.”
“This is significant, as now we have a better understanding of how these cells behave and why these types of heart attacks are being caused, we can start to find ways to help individuals avoid them in the future.”
“We have in fact already been able to propose two strategies for developing drug treatments as a result of our findings.”
A process created to detect and defend against the harm caused by smoking can, in fact, go into overdrive and interfere with cell adhesion, according to research.
The blood ultimately clots as a result of endothelial cell loss in the artery, obstructing the coronary artery and depriving the heart of oxygen.
This hypothesis was tested using substances found in cigarette smoke, and it was discovered that they accelerated the process. According to scientists, it’s feasible that other elements, such as air pollution, could have a comparable impact.
Professor Tom Johnson, Consultant Cardiologist at the Bristol Heart Institute, said, “Heart attacks remain a leading cause of death, so extending our understanding of the mechanisms underlying plaque erosion provides hope for the prevention of future events.”
“Increased awareness of plaque erosion as a cause of heart attack within the cardiology community is also valuable, as treatment can be tailored to the patient, avoiding the need for stents.”
A tissue culture model of the blood artery was made for the study using data from patients. A research technique called tissue culture involves growing biological tissue or cells in a lab setting. Because endothelial cells respond differently depending on the blood flow patterns, they are exposed to, researchers then replicated the blood flow environment identified at erosion locations in their models.
This made it possible to study endothelial cells in a lab setting and examine how cigarette smoke affected them. Researchers compared blood indicators from patients who had suffered plaque erosion with genes that changed in the tissue culture model to confirm their findings. Future research will deepen our understanding of this pathway and test new medications to stop heart attacks caused by smoking.
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