Inhibition of angiotensin II type 1 receptors reduces atrial stunning and spontaneous echo contrast after electrical cardioversion of atrial fibrillation

Abstract

Atrial fibrillation (AF) is known to be an important risk factor for thrombo-embolism.1,2 AF has been shown to induce a prolonged mechanical dysfunction of the atria, which becomes apparent after successful conversion of AF to normal sinus rhythm.1–4 The reduced mechanical function after termination of AF has been termed atrial stunning. Atrial stunning has been described after electrical (DC shock, overdrive pacing, catheter ablation), pharmacological, and spontaneous cardioversion of AF, which demonstrates that AF itself, rather than the mode of conversion, induces mechanical dysfunction. Pathophysiologically, the transient dysfunction of the atria appears to be due to abnormalities in cellular calcium handling and reduced calcium transient through L-type calcium channels.1,3 Furthermore, destruction of contractile proteins by calcium-dependent proteases such as calpains and functional alterations of the contractile proteins may contribute to prolonged mechanical alterations.5 In previous studies, verapamil, acetylstrophenathidine, isoproterenol, and dofetilide have been reported to reduce the amount of atrial stunning.2,3 Dagres et al .6 show that pre-treatment with the angiotensin II type 1 receptor blocker, Irbesartan, reduces left atrial stunning in patients undergoing electrical cardioversion of persistent AF. From a total of 50 patients, 25 received Irbesartan at a dose of 228±93 mg/day for at least 14 days prior to cardioversion. Although the trial was non-randomized, the two patients groups were matched with regard to clinical parameters including duration of AF, blood pressure, heart rate, cardiac dimensions, and ejection fraction. Transoesophageal and transthoracic echocardiography were used to determine … *Corresponding author. Tel: +49 391 6713225; fax: +49 391 673202. E-mail address : andreas.goette{at}medizin.uni-magdeburg.de