BACKGROUND: 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. METHODS: 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. RESULTS: 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). CONCLUSION: 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.
BACKGROUND: 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. METHODS: 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. RESULTS: 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). CONCLUSION: 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.
Authors: G Schmidt; M Malik; P Barthel; R Schneider; K Ulm; L Rolnitzky; A J Camm; J T Bigger; A Schömig Journal: Lancet Date: 1999-04-24 Impact factor: 79.321
Authors: Wolfram Grimm; Julia Sharkova; Michael Christ; Raphael Schneider; Georg Schmidt; Bernhard Maisch Journal: Ann Noninvasive Electrocardiol Date: 2003-04 Impact factor: 1.468