Author + information
- David J. Wilber, MD, Editor-in-Chief, JACC: Clinical Electrophysiology∗ ()
- ↵∗Address for correspondence:
Dr. David J. Wilber, Cardiovascular Institute and the Department of Medicine, Loyola University Medical Center, Room 6232, Building 110, 2160 South First Avenue, Maywood, Illinois 60153.
In the search for better understanding of atrial fibrillation (AF) mechanisms and the evolution of clinical manifestations of the disease, much recent effort has focused on the role of atrial fibrosis. There is increasing evidence that the presence, extent, and pattern of fibrosis is associated with altered atrial conduction and electrophysiological properties, is linked to several well established risk factors for AF, and may predict the outcomes of therapeutic interventions. Whether fibrosis provides a central or unifying concept for understanding AF genesis and serves as a potential target for future therapeutic strategies is less clear, and remains a subject of ongoing investigation and debate. In this issue of JACC: Clinical Electrophysiology, we feature the first of a 4-part “State-of-the-Art” series on atrial fibrillation and fibrosis. The series is authored by established investigators in their respective areas of expertise. Our goal is to provide a contemporary overview of what is known regarding the significance of atrial fibrosis, the limitations of these data, and future directions for clinical research.
In “Molecular and Cellular Mechanisms of Atrial Fibrosis in Atrial Fibrillation,” Dr. Stanley Nattel (1) provides a comprehensive overview of the complex molecular and cellular regulation of the extracellular matrix and inciting factors that promote fibrosis expansion. Subsequent papers in the series, which will appear over the upcoming months, include “Fibrosis and Atrial Fibrillation: Computerized and Optical Mapping” by Vadim Fedorov, “Imaging of Atrial Fibrosis in Patients: Methodology and Clinical Implications” by Nassir Marrouche, and “Therapeutic approaches to atrial fibrillation ablation targeting atrial fibrosis” by Hans Kottkamp.
There has been considerable progress in unravelling the effect of fibrosis on AF and new insights gleaned as this promising line of research moves forward, but even more remains unknown or incompletely defined. The ultimate impact on preventative and therapeutic AF strategies is unclear. This series of reviews can serve as a foundation for clinicians seeking context and background as this story unfolds.
- 2017 American College of Cardiology Foundation