Vukajlovic Dejan D, Guettler Norbert, Miric Milutin, Pitschner Heinz Friedrich
Institute for Cardiovascular Diseases Dedinje, Belgrade, Serbia and Montenegro.
Ann Noninvasive Electrocardiol. 2006 Jan;11(1):34-7. doi: 10.1111/j.1542-474X.2006.00079.x.
It has been shown that mortality risk in patients after myocardial infarction could be estimated by heart rate turbulence (HRT), a short-term change in heart rate after ventricular premature beat (VPB), presumably caused by baroreceptor mechanism. We sought to determine whether pharmacological blockade with atropine, or augmentation of vagal tone with pirenzepine given in small doses would influence HRT.
In 30 patients with normal echocardiogram, and without signs or symptoms of coronary artery disease, after electrophysiologic examination or radiofrequency ablation for supraventricular arrhythmias was completed, turbulence onset (TO) and turbulence slope (TS) in basal state, after 1.3 mg IV pirenzepine and finally, after atropine in dose of 0.04 mg/kg of body weight were compared.
As assessed by Friedman ANOVA test both pirenzepine and atropine caused a significant change in both TO (P < 0.01) and TS (P < 0.01). The mean basal TO of -3.6 +/- 2.9%, changed after pirenzepine to -5.99 +/- 5.6% (P < 0.01), and after atropine it changed to -3.3 +/- 18.1% (P < 0.01). The mean basal TS of 18.6 +/- 10.1 ms/R-R interval increased after pirenzepine to 26.8 +/- 19.9 ms/R-R interval (P < 0.05), and decreased after atropine to 1.2 +/- 0.8 ms/R-R interval (P < 0.01). Mean cycle length increased after pirenzepine from 706.8 +/- 106.8 to 830 +/- 151.9 ms (P < 0.01), and decreased after atropine to 454.2 +/- 58.1 ms (P < 0.01).
A conclusion could be drawn that vagomymetic manipulation with intravenous pirenzepine increases HRT; vagal blockade with atropine decreases HRT. This finding suggests that a normal vagal innervation of heart is a prerequisite for the phenomenon of HRT.
研究表明，心肌梗死后患者的死亡风险可通过心率震荡（HRT）来估计，心率震荡是室性早搏（VPB）后心率的短期变化，可能由压力感受器机制引起。我们试图确定静脉注射阿托品进行药物阻断，或小剂量给予哌仑西平增强迷走神经张力是否会影响心率震荡。
对30例超声心动图正常、无冠状动脉疾病体征或症状的患者，在完成室上性心律失常的电生理检查或射频消融后，比较基础状态下、静脉注射1.3 mg哌仑西平后以及最后静脉注射0.04 mg/kg体重阿托品后的震荡起始（TO）和震荡斜率（TS）。
通过Friedman方差分析测试评估，哌仑西平与阿托品均使TO（P < 0.01）和TS（P < 0.01）发生显著变化。基础状态下平均TO为-3.6±2.9%，哌仑西平注射后变为-5.99±5.6%（P < 0.01），阿托品注射后变为-3.3±18.1%（P < 0.01）。基础状态下平均TS为18.6±10.1 ms/R-R间期，哌仑西平注射后增加至26.8±19.9 ms/R-R间期（P < 0.05），阿托品注射后减少至1.2±0.8 ms/R-R间期（P < 0.01）。哌仑西平注射后平均心动周期长度从706.8±106.8 ms增加至830±151.9 ms（P < 0.01），阿托品注射后减少至454.2±58.1 ms（P < 0.01）。
可以得出结论，静脉注射哌仑西平进行迷走神经兴奋操作可增加心率震荡；阿托品进行迷走神经阻断可降低心率震荡。这一发现表明心脏正常的迷走神经支配是心率震荡现象的一个先决条件。
