To the Editor—Response

Abstract

We appreciate the comments from Dr. Korantzopoulos and colleagues, 1 Korantzopoulos P. Kokkoris S. Kountouris E. et al. Regression of paroxysmal atrial fibrillation associated with thiazolidinedione therapy. Int J Cardiol. 2007; (In press) Google Scholar who reported a case study of two patients showing regression of paroxysmal atrial fibrillation (AF) with thiazolidinedione (TZD) therapy and have proposed that TZDs may have a potential role in the management of AF. 2 Liu T. Korantzopoulos P. Li G. et al. The potential role of thiazolidinediones in atrial fibrillation. Int J Cardiol. 2007; (In press) Google Scholar We are aware of their interesting work and had originally cited it in our paper on the protective effects of pioglitazone against atrial arrhythmogenic structural remodeling; however, space restrictions forced us to eliminate the discussion of their work in our final version. 3 Shimano M. Tsuji Y. Inden Y. et al. Pioglitazone, a peroxisome proliferator-activated receptor-gamma activator, attenuates atrial fibrosis and atrial fibrillation promotion in rabbits with congestive heart failure. Heart Rhythm. 2008; 5: 451-459 Abstract Full Text Full Text PDF PubMed Scopus (87) Google Scholar Our data provide experimental evidence supporting their proposal. To the EditorHeart RhythmVol. 5Issue 4PreviewWe read with considerable interest the study by Shimano et al,1 which aimed to investigate the role of pioglitazone treatment on atrial remodeling and atrial fibrillation (AF) promotion in an experimental model of congestive heart failure. The authors demonstrated that pioglitazone suppressed arrhythmogenic atrial structural remodeling and postulated that the drug may modulate inflammatory, oxidative, and hypertrophic signaling processes.1 Full-Text PDF