BACKGROUND: Atrial fibrillation (AF) is the most common sustained arrhythmia in clinical practice. The Renin-Angiotensin-Aldosterone-System plays a major role for the atrial structural and electrical remodelling. Recently elevated aldosterone levels have been suggested to increase the risk for the development of AF. METHODS: Rats were treated with aldosterone by means of an osmotic minipump (0.5μg/h) over a period of 4 weeks. AF was induced by transesophageal burst pacing. Action potentials (AP) were recorded from left atrial preparations with microelectrodes. Atrial collagen was quantified by histological studies. RESULTS: Aldosterone treatment resulted in hypertrophy as indicated by an increased ratio of heart weight/tibia length and doubled the time until the AF converted spontaneously into sinus rhythm (85.8±13.4 s vs. 38.3±6.9 s, p<0.01). This was associated with a significant shortening of the AP (APD90 26.2±1.1 vs. 31.2±1.9, p<0.05) and an increased protein expression of Kir2.1 and Kv1.5. Atrial collagen deposition was significantly greater in aldosterone-treated rats. The alterations could be prevented by additional application spironolactone. CONCLUSIONS: The results of the present study suggest that in addition to the structural remodelling aldosterone also promotes AF by altering repolarising potassium currents leading to action potential shortening.
BACKGROUND:Atrial fibrillation (AF) is the most common sustained arrhythmia in clinical practice. The Renin-Angiotensin-Aldosterone-System plays a major role for the atrial structural and electrical remodelling. Recently elevated aldosterone levels have been suggested to increase the risk for the development of AF. METHODS:Rats were treated with aldosterone by means of an osmotic minipump (0.5μg/h) over a period of 4 weeks. AF was induced by transesophageal burst pacing. Action potentials (AP) were recorded from left atrial preparations with microelectrodes. Atrial collagen was quantified by histological studies. RESULTS:Aldosterone treatment resulted in hypertrophy as indicated by an increased ratio of heart weight/tibia length and doubled the time until the AF converted spontaneously into sinus rhythm (85.8±13.4 s vs. 38.3±6.9 s, p<0.01). This was associated with a significant shortening of the AP (APD90 26.2±1.1 vs. 31.2±1.9, p<0.05) and an increased protein expression of Kir2.1 and Kv1.5. Atrial collagen deposition was significantly greater in aldosterone-treated rats. The alterations could be prevented by additional application spironolactone. CONCLUSIONS: The results of the present study suggest that in addition to the structural remodelling aldosterone also promotes AF by altering repolarising potassium currents leading to action potential shortening.
Authors: Teresa M Seccia; Brasilina Caroccia; Gail K Adler; Giuseppe Maiolino; Maurizio Cesari; Gian Paolo Rossi Journal: Hypertension Date: 2017-04 Impact factor: 10.190
Authors: V Simopoulos; G Tagarakis; A Hatziefthimiou; I Skoularigis; F Triposkiadis; V Trantou; N Tsilimingas; I Aidonidis Journal: Clin Res Cardiol Date: 2014-08-19 Impact factor: 5.460
Authors: M Alings; M D Smit; M L Moes; H J G M Crijns; J G P Tijssen; J Brügemann; H L Hillege; D A Lane; G Y H Lip; J R L M Smeets; R G Tieleman; R Tukkie; F F Willems; R A Vermond; D J Van Veldhuisen; I C Van Gelder Journal: Neth Heart J Date: 2013-07 Impact factor: 2.380
Authors: Luis Dos Santos; Ednei L Antonio; Andrey J Serra; Amanda Yoshizaki; Larissa Seibt; Flavio A Silva; Gisele K Couto; Luciana V Rossoni; Paulo Tucci; Angelo A de Paola; Guilherme Fenelon Journal: Int J Cardiol Heart Vasc Date: 2018-09-22