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Atrial fibrillation (AF) is the most prevalent arrhythmia and its incidence is on the rise. AF causes significant morbidity and mortality leading to rising AF-related health care costs. There is experimental and clinical evidence from animal and human studies that suggests a role for the renin angiotensin system (RAS) in the etiopathogenesis of AF. This review appraises the current understanding of RAS antagonism, using angiotensin converting enzyme inhibitors (ACE-I), angiotensin receptor blockers (ARB) and aldosterone antagonists (AA), for prevention of AF. RAS antagonism has proven to be effective for primary and secondary prevention of AF in subjects with heart failure and left ventricular (LV) dysfunction. However, most of the evidence for the protective effect of RAS antagonism is from clinical trials that had AF as a secondary outcome or from unspecified post-hoc analyses. The evidence for prevention in subjects without heart failure and with normal LV function is not as clear. RAS antagonism, in the absence of concomitant antiarrhythmic therapy, was not shown to reduce post cardioversion AF recurrences. RAS antagonism in subjects undergoing catheter ablation has also been ineffective in preventing AF recurrences. [ABSTRACT FROM AUTHOR]

An introduction is presented in which the editor discusses various reports within the issue on topics including the pathophysiology of atrial fibrillation (AF) in post-menopausal women, the role of calpains in atriomyopathy, and the role of the renin angiotensin system (RAS) in AF etiopathogenesis.