Increased plasma aldosterone during atrial fibrillation declines following cardioversion

TY - JOUR

T1 - Increased plasma aldosterone during atrial fibrillation declines following cardioversion

AU - Soeby-Land, C

AU - Dixen, U

AU - Therkelsen, S K

AU - Kjaer, A

N1 - Copyright © 2011 S. Karger AG, Basel.

PY - 2011/7

Y1 - 2011/7

N2 - Objective: The renin-angiotensin-aldosterone system (RAAS) may be activated during atrial fibrillation (AF); our aim was to evaluate the level of aldosterone in patients with either permanent AF, persistent AF scheduled for cardioversion or patients in sinus rhythm (SR). We hypothesized that an increased level of aldosterone is found in patients with AF, decreasing in patients with restored SR. Methods: The study included 60 patients with persistent AF scheduled for elective cardioversion, 19 patients with permanent AF, and a control group of 19 healthy individuals. All patients were examined and their aldosterone levels were measured. Measurement of aldosterone was repeated at follow-up 1, 30 and 180 days after successful cardioversion was achieved. Statistical analysis was conducted using the Kruskal-Wallis rank sum test and the paired t test. Results: At follow-up, 1, 30, and 180 days after successful cardioversion of the patients with persistent AF, data showed that 49, 27, and 21 patients, respectively, were still in SR. At baseline, median values of plasma aldosterone in the healthy controls, the patients with persistent AF and those with permanent AF were 52, 68, and 80 pg/ml, respectively. The log aldosterone in patients with persistent AF was significantly increased when compared to the control group (p = 0.026). No effect of age and gender was observed. The level of aldosterone decreased over time in patients with AF undergoing cardioversion and maintaining SR, both at a follow-up of 30 days (p = 0.0032) and 180 days (p = 0.037). Conclusions: Patients with AF had a raised aldosterone level compared to the healthy control individuals. Restoration and maintenance of SR in patients with persistent AF significantly lowered the level of aldosterone up to 180 days after cardioversion, indicating activation of RAAS during AF.

AB - Objective: The renin-angiotensin-aldosterone system (RAAS) may be activated during atrial fibrillation (AF); our aim was to evaluate the level of aldosterone in patients with either permanent AF, persistent AF scheduled for cardioversion or patients in sinus rhythm (SR). We hypothesized that an increased level of aldosterone is found in patients with AF, decreasing in patients with restored SR. Methods: The study included 60 patients with persistent AF scheduled for elective cardioversion, 19 patients with permanent AF, and a control group of 19 healthy individuals. All patients were examined and their aldosterone levels were measured. Measurement of aldosterone was repeated at follow-up 1, 30 and 180 days after successful cardioversion was achieved. Statistical analysis was conducted using the Kruskal-Wallis rank sum test and the paired t test. Results: At follow-up, 1, 30, and 180 days after successful cardioversion of the patients with persistent AF, data showed that 49, 27, and 21 patients, respectively, were still in SR. At baseline, median values of plasma aldosterone in the healthy controls, the patients with persistent AF and those with permanent AF were 52, 68, and 80 pg/ml, respectively. The log aldosterone in patients with persistent AF was significantly increased when compared to the control group (p = 0.026). No effect of age and gender was observed. The level of aldosterone decreased over time in patients with AF undergoing cardioversion and maintaining SR, both at a follow-up of 30 days (p = 0.0032) and 180 days (p = 0.037). Conclusions: Patients with AF had a raised aldosterone level compared to the healthy control individuals. Restoration and maintenance of SR in patients with persistent AF significantly lowered the level of aldosterone up to 180 days after cardioversion, indicating activation of RAAS during AF.

U2 - 10.1159/000328462

DO - 10.1159/000328462

M3 - Journal article

SN - 0008-6312

VL - 118

SP - 239

EP - 244

JO - Cardiology

JF - Cardiology

IS - 4

ER -