Imaging and atrial fibrillation: A new paradigm for precision targeting of AF?
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The Department of Cardiovascular Medicine, Heart & Vascular Institute, Cleveland Clinic, Cleveland, OH Department of Cardiovascular & Metabolic Sciences, Lerner Research Institute, Cleveland Clinic, Cleveland, OH Department of Nuclear Medicine, Imaging Institute, Cleveland Clinic, Cleveland, OH Department of Cardiovascular Imaging, Heart and Vascular Institute, Cleveland Clinic, Cleveland, OH
Received Sep 20, 2018; accepted Sep 21, 2018 doi:10.1007/s12350-018-01496-9
See related article, https://doi.org/10.10 07/s12350-018-1387-4. Atrial fibrillation (AF) is the most common sustained arrhythmia seen in clinical practice. Recent data from the Framingham Heart Study have shown a lifetime risk of AF now reaching 37% in the average individual over age 55 and even higher in individuals with elevated risk factors.1 Two of the recognized risk factors include older age and obesity. With our aging population and increases in obesity, the prevalence of AF is projected to continue to increase dramatically in the future. The etiology for AF is multifactorial and includes genetic, structural and local cardiac electrical and biochemical physiology, as well as potential inflammatory and metabolic factors that can influence the electrical activity of the heart. To date, cardiovascular imaging for characterization and treatment of AF has been performed primarily with anatomic techniques such as echocardiography, cardiac CT, and cardiac magnetic resonance imaging. Radionuclide techniques, which are capable of assessing local cardiac physiology, have not been used extensively, but may have a role in the classification and management of AF based on our evolving understanding of the mechanisms of AF. The search for effective prevention and treatment of AF will
Reprint requests: Mina K. Chung, MD, The Department of Cardiovascular Medicine, Heart & Vascular Institute, Cleveland Clinic, 9500 Euclid Avenue, J2-2, Cleveland, OH 44195; [email protected] J Nucl Cardiol 1071-3581/$34.00 Copyright Ó 2019 American Society of Nuclear Cardiology.
be more successful if focused on modifiable risk factors with therapies targeting precisely characterized subsets of AF. The search for effective upstream therapies for the treatment or prevention of AF has seen dramatic changes over the past two decades. In the 1950s, Moe and Abildskov postulated an atrial substrate based theory whereby multiple random reentrant wavelets, which were more frequent in large atria, resulted in AF.2 The ground-breaking report by Haissaguerre and colleagues3 in 1998 demonstrated that triggers originating in the pulmonary veins could initiate AF. This revolutionized our concept of AF pathophysiology and led to our current explosion of ablative therapies targeting pulmonary vein isolation. In parallel to the development of these ablative approaches targeting the initiation of AF were studies focused on the atrial electrical and structural remodeling that can occur with and potentially promote the progression of AF to more persistent forms. Yet the prevention of AF prog
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