Author + information
- Received August 3, 2016
- Revision received October 31, 2016
- Accepted November 3, 2016
- Published online January 2, 2017.
- aWestmead Hospital, Westmead Clinical School at University of Sydney and South West Sydney Clinical School at University of NSW, Sydney, Australia
- bCanberra Hospital, College of Medicine, Biology and Environment, Australian National University, Canberra, Australia
- ↵∗Reprint requests and correspondence:
Prof. Liza Thomas, Department of Cardiology, Westmead Hospital, 180 Hawkesbury Road, Westmead, NSW 2145, Australia.
The left atrium is considered a biomarker for adverse cardiovascular outcomes, particularly in patients with left ventricular diastolic dysfunction and atrial fibrillation in whom left atrial (LA) enlargement is of prognostic importance. LA enlargement with a consequent decrease in LA function represents maladaptive structural and functional “remodeling” that in turn promotes electrical remodeling and a milieu conducive for incident atrial fibrillation. Medical and nonmedical interventions may arrest this pathophysiologic process to the extent that subsequent reverse remodeling results in a reduction in LA size and improvement in LA function. This review examines cellular and basic mechanisms involved in LA remodeling, evaluates the noninvasive techniques that can assess these changes, and examines potential mechanisms that may initiate reverse remodeling.
Both authors have reported that they have no relationships relevant to the contents of this paper to disclose.
- Received August 3, 2016.
- Revision received October 31, 2016.
- Accepted November 3, 2016.
- American College of Cardiology Foundation