Author + information
- Received October 21, 2015
- Revision received December 18, 2015
- Accepted December 28, 2015
- Published online February 1, 2016.
- aMyocardial Pathophysiology Area, Fundación Centro Nacional de Investigaciones Cardiovasculares, Carlos III, Madrid, Spain
- bCardiology Department, Hospital Clínico San Carlos, Madrid, Spain
- cDepartment of Internal Medicine, Center for Arrhythmia Research, University of Michigan, Ann Arbor, Michigan
- ↵∗Reprint requests and correspondence:
Dr. José Jalife, Center for Arrhythmia Research, University of Michigan, 2800 Plymouth Road, Ann Arbor, Michigan 48109.
Evidence accumulated over the last 25 years suggests that, whether in atria or ventricles, fibrillation may be explained by the self-organization of the cardiac electrical activity into rapidly spinning rotors that give way to spiral waves that break intermittently and result in fibrillatory conduction. The dynamics and frequency of such rotors depend on ion channel composition, excitability, and refractory properties of the tissues involved, as well as on the thickness and respective 3-dimensional fiber structure of the atrial and ventricular chambers. Therefore, improving understanding of fibrillation has required the use of multidisciplinary research approaches, including optical mapping, patch clamping, and molecular biology, and the application of concepts derived from the theory of wave propagation in excitable media. Moreover, translation of such concepts to the clinic has recently opened new opportunities to apply novel mechanistic approaches to therapy, particularly during atrial fibrillation ablation. Here we review the current understanding of the manner in which the underlying myocardial structure and function influence rotor initiation and maintenance during cardiac fibrillation. We also examine relevant underlying differences and similarities between atrial fibrillation and ventricular fibrillation and evaluate the latest clinical mapping technologies used to identify rotors in either arrhythmia. Altogether, the data being discussed have significantly improved our understanding of the cellular and structural bases of cardiac fibrillation and pointed toward potentially exciting new avenues for more efficient and effective identification and therapy of the most complex cardiac arrhythmias.
This study was supported by Fondo Europeo de Desarrollo Regional grants and Instituto de Salud Carlos III grants RD12/0042/0036 (RIC) and RD06/0003/0009 (REDINSCOR). Centro Nacional de Investigaciones Cardiovasculares (CNIC) is supported by the Spanish Ministry of Economy and Competitiveness and Pro-CNIC Foundation. Additional support provided by Salud 2000 Foundation and Jesús Serra Foundation; Leducq Foundation, to Dr. Jalife; University of Michigan Health System; Peking University Health Sciences Center Joint Institute for Translational and Clinical Research; and U.S. National Institutes of Health grant R01 HL122352. Dr. Jalife serves on the scientific advisory board of Topera, Inc.; and has received a research grant from Medtronic, Inc. Dr. Filgueiras-Rama has reported that he has no relationships relevant to the contents of this paper to disclose.
- Received October 21, 2015.
- Revision received December 18, 2015.
- Accepted December 28, 2015.
- American College of Cardiology Foundation