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Parasympathetic Blockade Promotes Recovery from Atrial Electrical Remodeling Induced by Short‐term Rapid Atrial Pacing
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The purpose of the present study was to assess the influence of autonomic blockade on shortening of effective refractory period (ERP) induced by short‐term rapid atrial pacing (RAP) and its recovery process. Fifteen patients (8 men, 7 women, age 52 ± 16 years) without structural heart disease and without a history of atrial fibrillation were included in this study. All patients underwent RAP at a cycle length of 300 ms for 5 minutes, after which the ERP was measured in all patients at 1, 3, 5, 7.5, and 10 minutes following cessation of RAP. In ten patients, these RAP and measurements of ERPs were repeated after administration of propranolol (P) and subsequent administration of atropine (P + A), respectively. In the remaining five patients atropine (A) was given first and then the administration of propranolol followed (P + A). Relative to the baseline value, the ERP immediately after RAP did not differ significantly from the Control(C), P, A, or P + A (C, 79%± 8%; P, 82%± 9%; A, 80%± 6%; P + A, 82%± 13%). However, the ERP 3 minutes after cessation of RAP was significantly (P < 0.05) longer in A (93%± 4%) and P + A (97%± 5%) than that in C (86%± 5%) and P (86%± 5%). The recovery time for ERP to return to pre‐RAP value was significantly shorter during A and P + A than during either C or P (C, 536 ± 161 s; P, 503 ± 172 s; A, 282 ± 111 s; P + A, 291 ± 147 s; P < 0.05). Parasympathetic blockade may promote recovery from ERP shortening induced by short‐term RAP. (PACE 2004; 27:33–37)
Title: Parasympathetic Blockade Promotes Recovery from Atrial Electrical Remodeling Induced by Short‐term Rapid Atrial Pacing
Description:
The purpose of the present study was to assess the influence of autonomic blockade on shortening of effective refractory period (ERP) induced by short‐term rapid atrial pacing (RAP) and its recovery process.
Fifteen patients (8 men, 7 women, age 52 ± 16 years) without structural heart disease and without a history of atrial fibrillation were included in this study.
All patients underwent RAP at a cycle length of 300 ms for 5 minutes, after which the ERP was measured in all patients at 1, 3, 5, 7.
5, and 10 minutes following cessation of RAP.
In ten patients, these RAP and measurements of ERPs were repeated after administration of propranolol (P) and subsequent administration of atropine (P + A), respectively.
In the remaining five patients atropine (A) was given first and then the administration of propranolol followed (P + A).
Relative to the baseline value, the ERP immediately after RAP did not differ significantly from the Control(C), P, A, or P + A (C, 79%± 8%; P, 82%± 9%; A, 80%± 6%; P + A, 82%± 13%).
However, the ERP 3 minutes after cessation of RAP was significantly (P < 0.
05) longer in A (93%± 4%) and P + A (97%± 5%) than that in C (86%± 5%) and P (86%± 5%).
The recovery time for ERP to return to pre‐RAP value was significantly shorter during A and P + A than during either C or P (C, 536 ± 161 s; P, 503 ± 172 s; A, 282 ± 111 s; P + A, 291 ± 147 s; P < 0.
05).
Parasympathetic blockade may promote recovery from ERP shortening induced by short‐term RAP.
(PACE 2004; 27:33–37).
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