BGU Study Maps Drugs Against AF
BGU researchers found semaglutide and colchicine may help prevent atrial fibrillation by protecting heart tissue and signaling.
Researchers at Ben-Gurion University of the Negev (BGU) have identified how two different classes of medication—the GLP-1 receptor agonist semaglutide and the anti-inflammatory drug colchicine—act on the heart to prevent the development of Atrial Fibrillation (AF). The study, published in Europace, provides a clearer biological map of how these drugs protect the heart’s structure and electrical signaling, potentially offering new ways to treat patients before AF takes hold.
Atrial fibrillation is the most common persistent heart rhythm disorder and is a primary driver of stroke and hospitalization, particularly in patients with heart failure. Using a high-resolution monitoring system developed at BGU, the team evaluated how these medications influenced "atrial remodeling"—the process where tissue of the atrial chambers of the heart becomes scarred and electrically unstable following a heart attack.
Targeting the "Substrate" of the Disease
The study, led by Prof. Yoram Etzion and his team at the Cardiac Arrhythmia Research Laboratory, found that while both drugs showed protective qualities, they worked through very different "repair" mechanisms:
- Semaglutide’s Structural Repair: Semaglutide, best known for its metabolic uses, showed a powerful ability to reduce physical scarring (fibrosis) in the heart's upper chambers. It also helped maintain the proper placement of "electrical bridges" (Connexin-43) between heart cells, which are necessary for a steady heartbeat.
- Colchicine’s Stress Shield: Colchicine acted as a specialized shield against inflammation. It specifically blocked several internal stress-signaling pathways (p38, JNK, and AKT) that typically cause heart tissue to deteriorate under pressure.
- Shared Anti-Inflammatory Impact: Both treatments successfully suppressed a key inflammatory "trigger" known as the NLRP3 inflammasome, which is a major driver of heart disease progression.
Direct Protection for the Heart
Notably, the researchers found that semaglutide protected the atrial tissue even in subjects that were not obese or diabetic. This indicates that the drug’s benefits for heart rhythm may be a direct effect on the heart itself, rather than just a byproduct of weight loss or blood sugar control.
"Our findings suggest that these medications could be used strategically to stop the progression of heart rhythm disorders before they become permanent," the researchers noted. By targeting multiple biological pathways at once, medical professionals may soon be able to offer more personalized and effective prevention for at-risk patients.
The BGU-led team included specialists from the Regenerative Medicine & Stem Cell Research Center, Soroka University Medical Center, and Tel Aviv University.
This work was supported by the Israel Science Foundation (Grant No. 833/23), the Israel Heart Society, and Ben-Gurion University of the Negev.
