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. 2015 Jan;12(1):e5-e29.
doi: 10.1016/j.hrthm.2014.11.011. Epub 2014 Nov 18.

Progress toward the prevention and treatment of atrial fibrillation: A summary of the Heart Rhythm Society Research Forum on the Treatment and Prevention of Atrial Fibrillation, Washington, DC, December 9-10, 2013

David R Van Wagoner  1 , Jonathan P Piccini  2 , Christine M Albert  3 , Mark E Anderson  4 , Emelia J Benjamin  5 , Bianca Brundel  6 , Robert M Califf  7 , Hugh Calkins  4 , Peng-Sheng Chen  8 , Nipavan Chiamvimonvat  9 , Dawood Darbar  10 , Lee L Eckhardt  11 , Patrick T Ellinor  12 , Derek V Exner  13 , Richard I Fogel  14 , Anne M Gillis  13 , Jeff Healey  15 , Stefan H Hohnloser  16 , Hooman Kamel  17 , David A Lathrop  18 , Gregory Y H Lip  19 , Reena Mehra  20 , Sanjiv M Narayan  21 , Jeffrey Olgin  22 , Douglas Packer  23 , Nicholas S Peters  24 , Dan M Roden  25 , Heather M Ross  26 , Robert Sheldon  13 , Xander H T Wehrens  27
Affiliations

Progress toward the prevention and treatment of atrial fibrillation: A summary of the Heart Rhythm Society Research Forum on the Treatment and Prevention of Atrial Fibrillation, Washington, DC, December 9-10, 2013

David R Van Wagoner et al. Heart Rhythm. 2015 Jan.
No abstract available

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Figures

Figure 1
Figure 1
Overview of the proteostasis network, related signaling pathways, and modifiers. The physiologic and functional state of cells, including atrial myocytes, is related to proteome function, which is managed by the proteostasis network. The proteostasis network includes central pathways involved in the degradation of “old” proteins, the synthesis of new proteins within the endoplasmic reticulum (ER), and the folding and trafficking of native proteins. Central pathways regulated by signaling pathways that are activated during stresses such as AF include the heat shock factor 1-induced heat shock response, ER stress, the unfolded protein responses (UPR), activation of histone deacetylase 6-(HDAC6), and systemic inflammation. Genetic variants, caloric restriction, metabolic load, and physiologic stresses can modify the proteostasis network.
Figure 2
Figure 2
Modifiable risk factors promote a substrate for AF. This figure illustrates the interactions of modifiable risk factors that lead to AF. Clinical and translational studies are needed to test the hypothesis that AF incidence and burden can be reduced by interventions that reduce the burden of patient-specific modifiable risk factors. Nonmodifiable risk factors (aging, genetics, etc) can further modulate the influence of the above risk factors on the development of AF.
Figure 3
Figure 3
Mechanisms linking sleep disordered breathing (SDB) with risk of AF. Continuous positive airway pressure (CPAP) can help to reduce the burden of SDB and thus may be a useful tool in the prevention of AF, as well as the intermediate pathologic processes.
Figure 4
Figure 4
Summary of the research targets and goals of the translational research cycle needed to systematically reduce the global incidence and burden of atrial fibrillation.
See this image and copyright information in PMC

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