![]() ![]() Ulm noted that the research highlights how chronic inflammation and the factors that worsen it-such as stress- may underlie a significant number of hospital visits. Stress: an aggravator of chronic inflammation in AFibĭr. He noted that while the study found ‘remarkable’ links between macrophages, SPP1 expression, and AFib, it remains unclear how much these factors are actually involved in the development of the condition. ![]() Ulm noted that while the findings are intriguing, the results are still preliminary. When asked about the study’s limitations, Dr. Maarten Hulsmans, assistant professor of radiology at Harvard Medical School, one of the study’s authors, told MNT that a small percentage of patients with AFib driven by genetic defects would potentially not benefit from immunomodulatory therapy’. Varughese indicated, however, that before such treatments become available, further studies are also needed.ĭr. Christopher Varughese, board certified interventional cardiologist and assistant professor at the Donald and Barbara Zucker School of Medicine at Hofstra University, who was also not involved in the study, told MNT.ĭr. This would be a potential first-time indication for immunotherapy in the treatment of abnormal heart rhythms,” Dr. “The SPP-1 gene is a potential target for immunotherapy to help reduce rates of AFib. The researchers wrote that therapeutic strategies that target inflammatory macrophages and signals derived from macrophages, such as SPP1, might help reduce AFib when used alongside other strategies such as surgical valve repair, weight loss, and blood pressure management. The researchers also tested whether a drug that reduces macrophage activity could treat AFib in mice.Īfter four weeks of treatment, they found that reducing macrophage activity in this way reduced tissue scarring in the atria. ![]() Ultimately, they found that mice models of AFib lacking the SPP1 gene had reduced numbers of atrial macrophages and fewer signs of AFib. To understand more about how SPP1 affects AFib, the researchers examined mice bred to lack the gene. The SPP1 gene leads to the production of the osteopont in protein that promotes tissue scarring and inflammation and w as elevated in the blood of patients with AFib. In genetic analyses, the researchers found that the SPP1 gene is overexpressed in macrophages during AFib. This reduced electrical conduction between heart cells and ultimately led to AFib. In doing so, they found that expanded macrophages supported inflammation and scarring of the atria-or fibrosis. The researchers next examined a mouse model of AFib to understand more about the link between macrophages and AFib. They found macrophages expanded more than any other cell type among those with AFib compared to tissue from those without the condition. The corresponding study was published in Science.įor the study, the researchers first collected left atrial tissue from seven patients with AFib undergoing heart surgery and five people without the condition. “This research sheds light on what may be a common spur for the pathophysiological processes that engender the condition and, just as important, opens the door to new treatments.” Wes Ulm, a bioinformatic scientific resource analyst, and biomedical data specialist at the National Institutes of Health, who was not involved in the study, told Medical News Today. “Atrial fibrillation, despite its relatively high prevalence and incidence in the U.S., often puzzles clinicians and researchers in regard to its causative foundations for any given case,” Dr. Recently, researchers found that immune cells known as macrophages support inflammation and scarring in the atria, and that reducing macrophage activity reduces these effects. Understanding more about how specific cells in the atria function during AFib could help researchers develop treatment and prevention strategies for the condition. These immune cells help heart muscle cells with housekeeping functions, including waste removal, immunosurveillance, and scaffolding. The CDC predicts that 12.1 million people will have the condition in the United States by 2030.īeyond heart muscle cells, the atria consist of fibroblasts that form connective tissue, endothelial cells that form blood vessel linings, and immune cells. This can reduce cardiac performance and lead to complications, including blood clots, stroke, and heart failure.Īccording to the Centers for Disease Control and Prevention (CDC), AFib was mentioned on 183,321 death certificates in 2019. ![]() Atrial fibrillation (AFib) occurs when the two upper chambers of the heart (the atria) beat irregularly, what may lead them to get out of sync with the two lower chambers of the heart - the ventricules. ![]()
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