Bonaduce D, Marciano F, Petretta M, Migaux M L, Morgano G, Bianchi V, Salemme L, Valva G, Condorelli M
Institute of Internal Medicine, Cardiology, and Heart Surgery, University of Naples Federico II, Italy.
Circulation. 1994 Jul;90(1):108-13. doi: 10.1161/01.cir.90.1.108.
Heart period variability provides useful prognostic information on autonomic cardiac control, and a strong association has been demonstrated after myocardial infarction (MI) between cardiac mortality, sudden death, and reduced total power, ultralow-frequency (ULF) power, and very-low-frequency (VLF) power. Converting enzyme inhibitors are widely used in MI patients, but their influence on heart period variability remains to be defined.
Time- and frequency-domain measures of heart period variability were calculated from 24-hour Holter monitoring in 40 patients with a first uncomplicated MI. After baseline examination between 48 and 72 hours after symptom onset, patients were randomly assigned to placebo or captopril administration, and on the third day, 24-hour Holter monitoring was repeated. No changes in time and frequency domain were detectable after placebo. After captopril, the SD of all normal RR (NN) intervals (SDNN) increased from 90 +/- 29 to 105 +/- 30 milliseconds (P < .01); the SD of the average NN intervals for all 5-minute segments (SDANN index) and the mean of the SDs of all NN intervals for all 5-minute segments (SDNN index) also increased from 74 +/- 24 to 90 +/- 26 milliseconds (P < .01) and from 45 +/- 17 to 49 +/- 15 milliseconds (P < .05), respectively. The root mean square successive difference (r-MSSD) and the percent of differences between adjacent NN intervals > 50 milliseconds (pNN50) remained unchanged. In regard to frequency-domain measures, after captopril, total power (ln unit) increased from 8.28 +/- 0.42 to 8.47 +/- 0.30 (P < .01); considering the frequency bands, a significant increase was observed in ULF (P < .01), VLF (P < .05), and low-frequency (LF) power (P < .05), whereas high-frequency (HF) power remained unchanged.
This study supports the hypothesis that the renin-angiotensin system modulates the amplitude of ULF and VLF power. Furthermore, it demonstrates that in MI patients, converting enzyme inhibition favorably modifies measures of heart period variability strongly associated with a poor prognosis.
心率变异性可为自主心脏控制提供有用的预后信息,并且心肌梗死(MI)后已证实心脏死亡率、猝死与总功率、超低频(ULF)功率和极低频(VLF)功率降低之间存在密切关联。转换酶抑制剂广泛应用于MI患者,但其对心率变异性的影响仍有待确定。
对40例首次发生无并发症MI的患者进行24小时动态心电图监测,计算心率变异性的时域和频域指标。在症状发作后48至72小时进行基线检查后,患者被随机分配接受安慰剂或卡托普利治疗,第三天重复进行24小时动态心电图监测。安慰剂治疗后,时域和频域均未检测到变化。卡托普利治疗后,所有正常RR(NN)间期的标准差(SDNN)从90±29毫秒增加到105±30毫秒(P<.01);所有5分钟时段平均NN间期的标准差(SDANN指数)以及所有5分钟时段所有NN间期标准差的平均值(SDNN指数)也分别从74±24毫秒增加到90±26毫秒(P<.01)和从45±17毫秒增加到49±15毫秒(P<.05)。相邻NN间期差值的均方根(r-MSSD)和相邻NN间期差值>50毫秒的百分比(pNN50)保持不变。关于频域指标,卡托普利治疗后,总功率(对数单位)从8.28±0.42增加到8.47±0.30(P<.01);考虑各频段,ULF(P<.01)、VLF(P<.05)和低频(LF)功率显著增加(P<.05),而高频(HF)功率保持不变。
本研究支持肾素-血管紧张素系统调节ULF和VLF功率幅度的假说。此外,研究表明,在MI患者中,转换酶抑制可有利地改善与不良预后密切相关的心率变异性指标。