New research suggests immunotherapy for AFib could be on the horizon

“We found that recruited macrophages support inflammation and fibrosis, or scarring, of the atria, which hinder electrical conduction between heart cells and lead to AFib,” senior author Matthias Nahrendorf, MD, PhD, a specialist with the MGH Center for Systems Biology, said in a prepared statement. “Inhibiting macrophage recruitment reduced AFib.”

The researchers believe that targeting both macrophages and “macrophage-derived signals” such as the SPP1 gene could eventually lead to the development of new AFib therapies.

“We think that this research lays the groundwork for immunomodulatory therapy of AFib, and we are currently working on several strategies to make this happen,” Nahrendorf added.

These new findings suggest the treatment of AFib could change significantly in the years ahead. With this potential in mind, researchers hope to learn as much as possible about the long-term impact of any new immunotherapies for AFib as they are developed.

“By mapping cardiac and immune cells involved in AFib, this research advances next steps toward studying how macrophage-targeted therapies may support existing treatment,” Michelle Olive, PhD, deputy chief of the Atherothrombosis and Coronary Artery Disease branch of the National Heart, Lung and Blood Institute said in the same statement.

While Olive was not part of this specific study, the analysis was funded in part by a grant from the National Institutes of Health.

Read the full study in Science here.