Researchers identify genes that become active when carotid plaque rupture leads to a stroke – News-Medical.Net

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Researchers from Ochsner Health and Tulane University School of Medicine have identified the genes that become active in carotid arteries when plaque rupture causes a stroke. The work, published in scientific reports, was made possible by obtaining samples closer to the time of the stroke than previously possible. The results provide a picture of what the cells in the plaque are doing close to the moment they trigger a stroke.

Cardiovascular disease is the leading cause of death worldwide, responsible for an estimated 17.9 million deaths annually and is often the result of plaques that build up in the arteries. When these plaques rupture, they can release material into the bloodstream that blocks oxygen from reaching the heart or brain. There is no way to determine exactly when a plaque will rupture.

Previous studies have relied on carotid artery samples obtained after the patient’s death or months after the stroke or heart attack. This either limits the information that can be obtained or misses events that only occur at the time of breach. For the first time, the current study sequenced the RNAs in plaques from patients who had a stroke within two to five days. With this, the team created an image of the RNAs that are active closer to the time of breakage than previously possible.

The researchers found that plaques that rupture have increased inflammation, along with processes that would cause the loss of a part of the plaque that protects against rupture, known as the fibrous cap. Surprisingly, the researchers found that ruptured plaques had increased B-cell markers, a white blood cell whose role in plaque rupture has not been previously appreciated.

Carotid artery blockage is a common cause of some ischemic strokes, which happens when the blood supply to part of the brain is interrupted, preventing brain tissue from getting the necessary oxygen and nutrients. Because the mechanisms that lead to some strokes and most heart attacks involve the same plaque rupture events, these findings also have implications for heart disease.

Inflammation is a known risk factor in atherosclerosis, which leads to stroke and heart attacks. Carotid and coronary plaques develop a protective cap that, for unclear reasons, thins, making strokes and heart attacks more likely.

Hernan Bazan, MD, the John Ochsner Endowed Professor of Cardiovascular Innovation at Ochsner Health

Study senior author Cooper Woods, PhD, Associate Professor of Physiology and Medicine at Tulane University School of Medicine, emphasizes: “Identifying the genes that promote this thinning gives us new targets for therapeutics and diagnostics to prevent heart attacks and strokes occur.”

The National Institutes of Health and the endowed John Ochsner Professorship in Cardiovascular Innovation support the research. Dr. Bazan was appointed last year as the John Ochsner Chair in Cardiovascular Innovation, a position created after the death of nationally renowned cardiovascular surgeon Dr. John Ochsner to honor his legacy and influence in the field of medicine. Dr. Bazan carries innovation in atherosclerotic mechanisms and acute carotid and stroke clinical research through the position. This support will continue until at least 2026.


Journal reference:

Bazan, HA, and others. (2022) A pro-inflammatory and fibrous cap thinning transcriptome profile accompanies carotid plaque rupture leading to stroke. Scientific reports.

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