Department of Cardiology, "G. Hatzikosta" General Hospital, Makrigianni Avenue, 45001 Ioannina, Greece
Department of Cardiology, University of Ioannina Medical School, Ioannina, Greece
Department of Cardiology, University of Ioannina Medical School, Ioannina, Greece
Department of Cardiology, "G. Hatzikosta" General Hospital, Makrigianni Avenue, 45001 Ioannina, Greece
Department of Cardiology, "G. Hatzikosta" General Hospital, Makrigianni Avenue, 45001 Ioannina, Greece
* Tel.: +30-26510-80793; fax: +30-26510-80801
E-mail address: pkor{at}oneway.gr
We read with considerable interest the report by Ueng et al.,1 which aimed to demonstrate the beneficial effects of enalapril on maintenance of sinus rhythm after cardioversion of persistent atrial fibrillation. The authors conclude that inhibition of the reninangiotensin system may favourably affect atrial structural remodeling and thus modify the substrate for atrial fibrillation recurrence.1
Even though aldosterone represents a well-known component of the renin-angiotensin system, its role in atrial fibrillation has not been examined in detail. Goette et al.,2 showed that aldosterone levels are elevated in patients with persistent atrial fibrillation, whereas restoration of sinus rhythm by electrical cardioversion significantly lowers serum aldosterone. Whether atrial fibrillation induces cardiac synthesis of aldosterone in the absence of heart failure or hypertension is not known.2 Regardless its exact source in this setting, aldosterone may exert several deleterious effects provoking cardiac damage independent of its effects on blood pressure.3 In specific, aldosterone induces cell proliferation and myocardial fibrosis possibly due to an increase of AT1-receptors and enhanced local expression of the angiotensin converting enzyme.3 Moreover, it seems to promote inflammation3 and oxidative stress4, processes that have recently been implicated in atrial remodeling.5 Finally, it has been proposed that aldosterone induces baroreceptor dysfunction and thus may facilitate autonomic imbalance during atrial fibrillation.2
It can therefore be hypothesised that aldosterone plays a role in the pathophysiology of atrial fibrillation. Taking into account the aforementioned deleterious effects one can speculate that aldosterone antagonists such as spironolactone may ameliorate atrial remodeling. Undoubtedly, the favourable effects of aldosterone antagonism on ventricular remodeling observed in heart failure do not imply similar actions on atrial myocardium. In conclusion, we believe that the role of aldosterone in atrial fibrillation deserves further study since it may contribute to the development of effective strategies against atrial remodeling.
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