Kyungpyo Hong1, 2, Matthias Koopmann1, Ravi Ranjan1, 3, Eric C. Huang4, Eugene G. Kholmovski1, 5, Sathya Vijayakumar1, 5, Christopher J. McGann1, 3, Derek J. Dosdall1, 3, Nassir F. Marrouche1, 3, Daniel Kim1, 5
1CARMA Center, University of Utah, Salt Lake City, UT, United States; 2Department of Bioengineering, University of Utah, Salt Lake City, UT, United States; 3Internal Medicine, University of Utah, Salt Lake City, UT, United States; 4Department of Pathology, University of California, Davis Medical Center, Sacramento, CA, United States; 5UCAIR, Department of Radiology, University of Utah, Salt Lake City, UT, United States
Atrial fibrillation (AF) causes left ventricular (LV) dysfunction, which is thought to be caused by structural remodeling and fibrosis. However, LV dysfunction induced by AF is under-diagnosed clinically, and its mechanisms are not clearly understood. Late gadolinium enhanced (LGE) cardiac T1 mapping enables assessment of LV structural remodeling and fibrosis development. We sought to study the LV fibrosis induced by AF in a canine model with chronic AF. Our data show that LV fibrosis increases with days after the onset of irregular rhythm. Our results are corroborated with the histological assessment of myocardial fibrosis.