Provocation of ventricular ectopy by Cheyne-Stokes respiration in patients with heart failure

Provocation of ventricular ectopy by Cheyne-Stokes respiration in patients with heart failure
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DOI:
10.1093/sleep/27.7.1337
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发表时间:
2004-11-01
期刊:
影响因子:
5.6
通讯作者:
Bradley, TD
Bradley, TD
中科院分区:
医学2区
文献类型:
--
作者:
Leung, RST;Diep, TM;Bradley, TD

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研究目的:以前的报告表明,Cheyne-Stokes呼吸与中枢性睡眠呼吸暂停(CSR-CSA)和心室异位之间存在关联,但因果关系的证据相对较少。本研究的目的是确定CSR-CSA是否直接引起心室异位,如果是,它是否与CSR-CSA呼吸周期的任何特定阶段相关。设计:我们比较了(1)CSR-CSA的呼吸暂停期和呼吸过度期之间,(2)CSR-CSA期间和睡眠期间规则呼吸期间之间的室性早搏频率,和(3)通过给予低浓度吸入CO2消除CSR-CSA。设置:医院心肺睡眠实验室。患者:23名心力衰竭和CSR-CSA患者。测量和结果:CSR-CSA的高通气期室性早搏发生率比呼吸暂停期高40(平均值+/- SD,7.0 +/- 7.4 vs 4.9 +/- 5.7室性早搏/分钟,P = 0.003)。CSR-CSA期间的室性早搏频率也高于正常呼吸期间,(中位数[第25百分位数,第75百分位数],每分钟2.2 [1.2,6.5] vs 1.1 [0.8,2.0]室性早搏,P = 0.027),或通过吸入CO2诱导(从4.7 +/- 3.8到3.3 +/- 4.0室性早搏/分钟,P = 0.048)。室性早搏的增加可能导致CSR-CSA心力衰竭患者的死亡率较高。
Study Objectives: Previous reports have suggested an association between Cheyne-Stokes respiration with central sleep apnea (CSR-CSA) and ventricular ectopy, but there has been relatively little evidence of a cause-effect relationship. The objective of this study was to determine whether CSR-CSA directly provokes ventricular ectopy and, if so, whether it is associated with any particular phase of the CSR-CSA breathing cycle.Design: We compared the frequency of ventricular premature beats (1) between the apneic and hyperpneic phases of CSR-CSA, (2) between periods of CSR-CSA and periods of regular breathing during sleep, and (3) in response to the elimination of CSR-CSA by administration of a low concentration of inhaled CO2.Setting: Hospital-based cardiopulmonary sleep laboratory.Patients: Twenty-three patients with heart failure and CSR-CSA.Measurements and Results: Ventricular premature beats were found to occur 40% more frequently during the hyperpneic phase than the apneic phase of CSR-CSA (mean +/- SD, 7.0 +/- 7.4 versus 4.9 +/- 5.7 ventricular premature beats per minute, P = .003). Ventricular premature beat frequency was also found to be higher during periods of CSR-CSA than during periods of regular breathing occurring either spontaneously (median [25(th), 75(th) percentile], 2.2 [1.2, 6.5] versus 1.1 [0.8, 2.0] ventricular premature beats per minute, P = .027), or induced through inhalation of CO2 (from 4.7 +/- 3.8 to 3.3 +/- 4.0 ventricular premature beats per minute, P = .048).Conclusions: CSR-CSA provokes ventricular ectopy that is most pronounced during the hyperpneic phase. Such an increase in ventricular premature beats might contribute to the higher mortality rates reported in heart failure patients with CSR-CSA.