Department of Cardiology
G. Hatzikosta General Hospital of Ioannina
45001 Ioannina
Greece
Tel: +30 26510 80811
Fax: +30 26510 97017
E-mail address: pkor{at}oneway.gr
Department of Internal Medicine
Division of Cardiology
University of Ioannina Medical School
45110 Ioannina
Greece
Department of Internal Medicine
Division of Cardiology
University of Ioannina Medical School
45110 Ioannina
Greece
Department of Cardiology
G. Hatzikosta General Hospital of Ioannina
45001 Ioannina
Greece
Department of Internal Medicine
Division of Cardiology
University of Ioannina Medical School
45110 Ioannina
Greece
We read with considerable interest the article by Engelmann and Svendsen1 providing a concise overview of the current knowledge about the association of inflammation with atrial fibrillation (AF). A continuously increasing number of investigations examine the role of inflammation in AF. Interestingly, two recent studies indicated that C-reactive protein relates to the left atrial size and AF duration before cardioversion, providing evidence of an association between inflammation and atrial structural remodelling.2,3 Moreover, it has been demonstrated that baseline C-reactive protein levels prior cardioversion of persistent AF represent an independent predictor of sinus rhythm maintenance after cardioversion.4,5 Of note, in a recent small study, we examined the variation of inflammatory indexes during the first week after successful cardioversion of persistent AF. We found that fibrinogen levels increased significantly in patients who relapsed into AF, but remained stable in patients who remained in sinus rhythm.6 In the latter patients, C-reactive protein values tended to decrease post-cardioversion, but white blood cell (WBC) count was significantly lower on the seventh day when compared with baseline values.6 Thus, we concluded that the variation of inflammatory indexes post-cardioversion might have prognostic implications with regard to sinus rhythm maintenance.
There is substantial evidence that inflammation augments oxidative stress and vice versa, whereas such interrelation has also been implicated in the pathophysiology of AF.7 Carnes et al.8 were the first to show that an antioxidant intervention with vitamin C ameliorates atrial electrical remodelling in experimental animals and significantly reduces the incidence of post-operative AF in patients undergoing coronary bypass surgery. Very recently, we demonstrated that treatment with vitamin C reduces the early recurrence rates after electrical cardioversion of persistent AF and attenuates the associated low-level inflammation.9 A significant variance was found in the serial measurements of WBC counts and of fibrinogen levels in the two groups (vitamin C and control), whereas in the vitamin C group, C-reactive protein levels were lower on the seventh day post-cardioversion when compared with baseline.9 It can therefore be speculated that antioxidant interventions might have an impact against AF-associated inflammation.
As mentioned by Engelmann and Svendsen,1 accumulating evidence suggests that anti-inflammatory interventions might exert favourable effects on AF. It has been recently shown that administration of n-3 fatty acids in patients undergoing coronary bypass surgery substantially reduces the incidence of post-operative AF.10 Besides direct electrophysiological effects, it has been proposed that the anti-inflammatory effects of these natural compounds may favourably affect the atrial remodelling.10,11 Finally, we agree with the authors that angiotensin-converting enzyme-inhibitors and angiotensin receptor blockers represent a promising approach. We have further proposed that aldosterone antagonists such as spironolactone might exert beneficial effects on AF, as aldosterone induces inflammation, oxidative stress, and fibrosis.12 Undoubtedly, more studies are needed to elucidate the exact role of inflammation and to clarify the impact of anti-inflammatory interventions in the setting of AF.
Conflict of interest: none declared.
References
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