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Review
. 2015 Dec;66(6):523-9.
doi: 10.1097/FJC.0000000000000313.

Oxidant and Inflammatory Mechanisms and Targeted Therapy in Atrial Fibrillation: An Update

Alejandra Gutierrez  1 , David R Van Wagoner
Affiliations
Review

Oxidant and Inflammatory Mechanisms and Targeted Therapy in Atrial Fibrillation: An Update

Alejandra Gutierrez et al. J Cardiovasc Pharmacol. 2015 Dec.

Abstract

Atrial fibrillation (AF) is an important cause of stroke and risk factor for heart failure and death. Current pharmacologic treatments for AF have limited efficacy, and treatments that more directly target the underlying causes of AF are needed. Oxidant stress and inflammatory activation are interrelated pathways that promote atrial electrical and structural remodeling, leading to atrial ectopy, interstitial fibrosis, and increased stroke risk. This review evaluates the impact of common stressors on atrial oxidant stress and inflammatory activation and the contribution of these pathways to atrial remodeling. Recent studies suggest that integrated efforts to target the underlying risk factors, rather than the AF per se, may have a greater impact on health and outcomes than isolated efforts focused on the electrical abnormalities.

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Figures

Figure 1
Figure 1
Mechanisms linking common atrial stressors with atrial metabolic, electrical and structural remodeling, increasing the risk of AF.
See this image and copyright information in PMC

References

    1. Van Wagoner DR. Oxidative stress and inflammation in atrial fibrillation: role in pathogenesis and potential as a therapeutic target. J Cardiovasc Pharmacol. 2008;52(4):306–13. - PubMed
    1. Van Wagoner DR, Piccini JP, Albert CM, Anderson ME, Benjamin EJ, Brundel B, Califf RM, Calkins H, Chen PS, Chiamvimonvat N, Darbar D, Eckhardt LL, Ellinor PT, Exner DV, Fogel RI, Gillis AM, Healey J, Hohnloser SH, Kamel H, Lathrop DA, Lip GY, Mehra R, Narayan SM, Olgin J, Packer D, Peters NS, Roden DM, Ross HM, Sheldon R, Wehrens XH. 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. Heart Rhythm. 2015;12(1):e5–e29. - PMC - PubMed
    1. Oka S, Ago T, Kitazono T, Zablocki D, Sadoshima J. The role of redox modulation of class II histone deacetylases in mediating pathological cardiac hypertrophy. Journal of molecular medicine. 2009;87(8):785–91. - PubMed
    1. Liu F, Levin MD, Petrenko NB, Lu MM, Wang T, Yuan LJ, Stout AL, Epstein JA, Patel VV. Histone-deacetylase inhibition reverses atrial arrhythmia inducibility and fibrosis in cardiac hypertrophy independent of angiotensin. J Mol Cell Cardiol. 2008;45(6):715–23. - PMC - PubMed
    1. Artlett CM, Thacker JD. Molecular Activation of the NLRP3 Inflammasome in Fibrosis: Common Threads Linking Divergent Fibrogenic Diseases. Antioxidants & redox signaling. 2015;22(13):1162–75. - PubMed

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