INFLUENCE OF HEART-RATE AND INHIBITION OF AUTONOMIC TONE ON THE QT INTERVAL
INFLUENCE OF HEART-RATE AND INHIBITION OF AUTONOMIC TONE ON THE QT INTERVAL
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DOI：
10.1161/01.cir.65.3.435
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发表时间：
1982-01-01
期刊：
影响因子：
37.8
通讯作者：
VALLIN, H
中科院分区：
文献类型：
--
作者：
AHNVE, S;VALLIN, H
为了评估心率引起的 QT 间期变化是否依赖于自主神经张力，对 13 名平均年龄 67.5 岁的健康受试者进行了研究。在静脉注射之前和之后以 90 次/分钟和 130 次/分钟的心房起搏期间确定导联 I、II、V1 和 V6 的最大未校正 QT。给予普萘洛尔 0.1 mg/kg 和阿托品 0.02 mg/kg。 QT 显着降低 (P < 0.01) 是由药物前 (10%)、普萘洛尔后 (10%) 以及阿托品和普萘洛尔联合用药后 (9%) 心率的节奏增加引起的。当通过起搏使心率保持恒定时，普萘洛尔不会引起 QT 间期的显着变化。阿托品在 β-肾上腺素能阻断受试者中产生与速率无关的 QT 间期缩短 (5%) (P < 0.05)。 Bazette 的 QT 间期 (QTc) 心率校正公式不适用于心房超速起搏，因为它在较高心率下给出相应较长的 QTc 值。心率显然是 QT 间期持续时间的主要决定因素，心率的节奏变化显然会引起基本上不受自主神经张力影响的 QT 间期反应。消除胆碱能张力产生的 QT 间期的速率独立效应表明胆碱能活动对心室心肌复极有直接影响。
To evaluate whether heart rate-induced changes of the QT interval are dependent on autonomic tone, 13 healthy subjects were studied, mean age 67.5 yr. The maximal uncorrected QT from leads I, II, V1 and V6 was determined during atrial pacing at 90 beats/min and 130 beats/min before and after i.v. administration of propranolol, 0.1 mg/kg and atropine, 0.02 mg/kg. Significant reductions (P < 0.01) of QT were induced by the paced increases in heart rate before drugs (10%), after propranolol (10%) and after the combination of atropine and propranolol (9%). Propranolol caused no significant change in the QT interval when heart rate was held constant by pacing. Atropine produced rate-independent reductions of QT interval (5%) in subjects with .beta.-adrenergic blockade (P < 0.05). Bazette''s formula for heart-rate correction of the QT interval (QTc) was not applicable for atrial overdrive pacing, as it gave proportionately longer QTc values at higher heart rates. Heart rate apparently is a major determinant of the duration of the QT interval and paced changes in heart rate apparently induce QT-interval responses that are essentially uninfluenced by autonomic tone. The rate-independent effect of the QT interval produced by elimination of cholinergic tone suggests a direct influence of cholinergic activity on the repolarization of ventricular myocardium.