AF has traditionally been viewed as a purely electrical disorder of cardiomyocytes—the heart’s contractile cells. However, the research coordinated by Dr. David Filgueiras Rama, head of the CNIC Advanced Development in Arrhythmia Mechanisms and Therapies group, demonstrates that patient-specific regions within the atria develop a distinct cellular environment that facilitates arrhythmia persistence.

Dr. Filgueiras Rama explains that “these areas, which we call driver regions, display electrical activity that is faster than the surrounding tissue and operate as true engines that sustain atrial fibrillation over time.”

The study identified significant differences in the abundance, type, and function of fibroblasts and macrophages—cells that do not participate directly in contraction but strongly influence tissue behavior.

First author Ana Simón Chica, CNIC researcher and currently at Massachusetts General Hospital and Harvard Medical School, explains that “these non-contractile cells create a specialized microenvironment that promotes cellular homeostasis and long-term survival, both of which are crucial for maintaining atrial fibrillation.”