Leitch J W, Basta M, Fletcher P J
Cardiovascular Department, John Hunter Hospital, Newcastle, Australia.
Heart. 1997 Aug;78(2):166-70. doi: 10.1136/hrt.78.2.166.
To determine the effect of changes in autonomic tone induced by phenylephrine infusion on atrial refractoriness and conduction.
Left and right atrial electrophysiological properties were measured before and after a constant phenylephrine infusion designed to increase sinus cycle length by 25%.
20 patients, aged 53 (SD 6) years, undergoing electrophysiological study for investigation of idiopathic paroxysmal atrial fibrillation (seven patients) or for routine follow up after successful catheter ablation of supraventricular tachycardia (13 patients).
Changes in left and right atrial effective refractory periods, atrial activation times, and frequency of induction of atrial fibrillation.
Phenylephrine (mean dose 69 (SD 18) mg/min) increased mean blood pressure by 22 (12) mm Hg (range 7 to 44) and lengthened sinus cycle length by 223 (94) ms (20 to 430). Left atrial effective refractory period lengthened following phenylephrine infusion from 250 (25) to 264 (21) ms (P < 0.001) but there was no significant change in right atrial effective refractory period: 200 (20) v 206 (29), P = 0.11. There was a significant relation between the effect of phenylephrine on sinus cycle length and on right atrial refractoriness (r = 0.6, P = 0.005) with shortening of right atrial refractoriness in patients with the greatest prolongation in sinus cycle length. During phenylephrine infusion, the right atrial stimulus to left atrial activation time at the basic pacing cycle length of 600 ms was unchanged, at 130 (18) v 131 (17) ms, but activation delay with a premature extrastimulus increased: 212 (28) v 227 (38) ms, P = 0.002. Atrial fibrillation was induced by two of 58 refractory period measurements at baseline and by 12 of 61 measurements during phenylephrine infusion (P < 0.01). Phenylephrine increased the difference between left and right atrial refractory periods by 22.8 (19.4) ms in the five patients with induced atrial fibrillation after phenylephrine compared to 0.9 (16.2) ms in the 13 patients without induced atrial fibrillation after phenylephrine infusion (P = 0.02).
Phenylephrine infusion increased left atrial refractoriness and intra-atrial conduction delay following a premature right atrial extrastimulus. Induction of atrial fibrillation during phenylephrine infusion was associated with non-uniform changes in atrial refractoriness. These data support the concept that changes in autonomic tone may precipitate atrial fibrillation in susceptible individuals.
确定去氧肾上腺素输注引起的自主神经张力变化对心房不应期和传导的影响。
在持续输注去氧肾上腺素前后测量左右心房的电生理特性，该输注旨在使窦性周期长度增加25%。
20例患者，年龄53（标准差6）岁，因特发性阵发性心房颤动（7例）接受电生理研究，或因室上性心动过速成功导管消融术后进行常规随访（13例）。
左右心房有效不应期、心房激动时间及心房颤动诱发频率的变化。
去氧肾上腺素（平均剂量69（标准差18）mg/min）使平均血压升高22（12）mmHg（范围7至44），窦性周期长度延长223（94）ms（20至430）。输注去氧肾上腺素后左心房有效不应期从250（25）ms延长至264（21）ms（P<0.001），但右心房有效不应期无显著变化：200（20）ms对206（29）ms，P = 0.11。去氧肾上腺素对窦性周期长度和右心房不应期的影响之间存在显著相关性（r = 0.6，P = 0.005），窦性周期长度延长最大的患者右心房不应期缩短。在输注去氧肾上腺素期间，在基本起搏周期长度600 ms时右心房刺激至左心房激动时间未改变，为130（18）ms对131（17）ms，但早搏刺激时的激动延迟增加：212（28）ms对227（38）ms，P = 0.002。基线时58次不应期测量中有2次诱发心房颤动，输注去氧肾上腺素期间61次测量中有12次诱发心房颤动（P<0.01）。与输注去氧肾上腺素后未诱发心房颤动的13例患者的0.9（16.2）ms相比，输注去氧肾上腺素后诱发心房颤动的5例患者中，去氧肾上腺素使左右心房不应期差异增加22.8（19.4）ms（P = 0.02）。
输注去氧肾上腺素可增加左心房不应期及右心房早搏刺激后的房内传导延迟。输注去氧肾上腺素期间诱发心房颤动与心房不应期的不均匀变化有关。这些数据支持自主神经张力变化可能使易感个体发生心房颤动的概念。
