BACKGROUND: Atrial fibrillation (AF) is associated with activity of renin-angiotensin-aldosterone system (RAAS). Reduction in renal noradrenaline spillover could be achieved after renal sympathetic denervation (RSD). The relationship between RSD and AF is unknown. OBJECTIVE: The objective of the study was to investigate the inducibility of AF during atrial rapid pacing after RSD. METHODS: Thirteen dogs were used for the study as follows: control group (seven dogs) and RSD group (six dogs). In the control group, dogs were subjected to atrial pacing at 800 beats/min for 7 h, and atrial effective refractory period (AERP) was measured every hour in the status of non-pacing. Subsequently, pacing was stopped and the burst pacing (500 bpm) was repeated to induce AF three times. In the RSD group, after each renal artery ablation, the procedure of pacing and electrophysiological measurement was exactly same as in the control group. Blood was collected before and after pacing to measure the levels of renin, angiotensin II and aldosterone. RESULTS: There was a persistent decrease in AERP in both groups. However, 7 h after cessation of pacing, the induced number of times and duration of AF were higher in the control group than that in the RSD group (1.0 ± 1.26 vs 3.14 ± 2.54, P = 0.03; 16.5 ± 25.1 vs 86.6 ± 116.4, P = 0.02). The plasma aldosterone concentration increased significantly 7 h after rapid pacing in control group (renin, 119.8 ± 31.1 vs 185.3 ± 103.5 pg/ml, P < 0.01; aldosterone, 288.2 ± 43.1 vs 369.6 ± 109.8 pg/ml, P = 0.01). The levels of renin and aldosterone showed a decreasing trend in RSD group, but this did not attain statistical significance. CONCLUSIONS: Episodes of AF could be decreased by renal sympathetic denervation during short-time rapid atrial pacing. This effect might have relationship with decreased activity of RAAS.
BACKGROUND:Atrial fibrillation (AF) is associated with activity of renin-angiotensin-aldosterone system (RAAS). Reduction in renal noradrenaline spillover could be achieved after renal sympathetic denervation (RSD). The relationship between RSD and AF is unknown. OBJECTIVE: The objective of the study was to investigate the inducibility of AF during atrial rapid pacing after RSD. METHODS: Thirteen dogs were used for the study as follows: control group (seven dogs) and RSD group (six dogs). In the control group, dogs were subjected to atrial pacing at 800 beats/min for 7 h, and atrial effective refractory period (AERP) was measured every hour in the status of non-pacing. Subsequently, pacing was stopped and the burst pacing (500 bpm) was repeated to induce AF three times. In the RSD group, after each renal artery ablation, the procedure of pacing and electrophysiological measurement was exactly same as in the control group. Blood was collected before and after pacing to measure the levels of renin, angiotensin II and aldosterone. RESULTS: There was a persistent decrease in AERP in both groups. However, 7 h after cessation of pacing, the induced number of times and duration of AF were higher in the control group than that in the RSD group (1.0 ± 1.26 vs 3.14 ± 2.54, P = 0.03; 16.5 ± 25.1 vs 86.6 ± 116.4, P = 0.02). The plasma aldosterone concentration increased significantly 7 h after rapid pacing in control group (renin, 119.8 ± 31.1 vs 185.3 ± 103.5 pg/ml, P < 0.01; aldosterone, 288.2 ± 43.1 vs 369.6 ± 109.8 pg/ml, P = 0.01). The levels of renin and aldosterone showed a decreasing trend in RSD group, but this did not attain statistical significance. CONCLUSIONS: Episodes of AF could be decreased by renal sympathetic denervation during short-time rapid atrial pacing. This effect might have relationship with decreased activity of RAAS.
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