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Nat Rev Cardiol. 2015 Apr;12(4):230-43. doi: 10.1038/nrcardio.2015.2. Epub 2015 Jan 27.

Inflammation and the pathogenesis of atrial fibrillation.

Author information

1
Division of Cardiology, Department of Medicine, Taipei Veterans General Hospital, National Yang-Ming University, Number 201, Section 2, Shipai Road, Beitou District, Taipei 11217, Taiwan, Republic of China.
2
Division of Cardiovascular Medicine, Department of Internal Medicine, Wan Fang Hospital, Taipei Medical University, Number 111, Section 3, Hsing-Long Road, Taipei 11696, Taiwan, Republic of China.

Abstract

Atrial fibrillation (AF) is the most common cardiac arrhythmia. However, the development of preventative therapies for AF has been disappointing. The infiltration of immune cells and proteins that mediate the inflammatory response in cardiac tissue and circulatory processes is associated with AF. Furthermore, the presence of inflammation in the heart or systemic circulation can predict the onset of AF and recurrence in the general population, as well as in patients after cardiac surgery, cardioversion, and catheter ablation. Mediators of the inflammatory response can alter atrial electrophysiology and structural substrates, thereby leading to increased vulnerability to AF. Inflammation also modulates calcium homeostasis and connexins, which are associated with triggers of AF and heterogeneous atrial conduction. Myolysis, cardiomyocyte apoptosis, and the activation of fibrotic pathways via fibroblasts, transforming growth factor-β and matrix metalloproteases are also mediated by inflammatory pathways, which can all contribute to structural remodelling of the atria. The development of thromboembolism, a detrimental complication of AF, is also associated with inflammatory activity. Understanding the complex pathophysiological processes and dynamic changes of AF-associated inflammation might help to identify specific anti-inflammatory strategies for the prevention of AF.

PMID:
25622848
DOI:
10.1038/nrcardio.2015.2
[Indexed for MEDLINE]
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