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Heart rate variability in time and frequency domains: effects of gallopamil, nifedipine, and metoprolol compared with placebo.
  1. M W Schweizer,
  2. J Brachmann,
  3. U Kirchner,
  4. I Walter-Sack,
  5. H Dickhaus,
  6. C Metze,
  7. W Kübler
  1. Department of Cardiology, University of Heidelberg, Germany.


    OBJECTIVE--To assess the effects of three different antianginal drugs on heart rate, blood pressure, and heart rate variability. DESIGN--Randomised, single blind, placebo controlled, cross over study. SETTING--University hospital. PARTICIPANTS--Nine healthy male volunteers. INTERVENTIONS--Oral administration of either 50 mg gallopamil, 20 mg nifedipine, 100 mg metoprolol, or placebo according to a random crossover plan. MAIN OUTCOME MEASURES--Time intervals between consecutive R waves in electrocardiograms measured with an accuracy of 5 ms from digital Holter recordings. Blood pressure monitored continuously by finger plethysmography. RESULTS--Metoprolol lowered heart rate from 62(6) to 51(5) beats/min (p = 0.003) after 78(23) minutes. Nifedipine provoked reflex tachycardia from 56(5) to 94(18) beats/min (p < 0.001) at 10(3) minutes after treatment followed by an exponential decline in heart rate to baseline values with a time constant of 34(7) min in seven subjects but 83 minutes in one volunteer. One subject showed no exponential decline in heart rate. Nifedipine significantly lowered the supine mean arterial pressure from 86(6) to 67(6) mm Hg (p = 0.004) after 11(2) minutes, indicating an acute reduction in arterial resistance. Gallopamil did not significantly change mean heart rate or blood pressure. In the sitting position three hours after administration gallopamil and metoprolol significantly lowered power spectral density in the low frequency band (0.03 Hz to 0.15 Hz) compared with placebo (p < 0.05). Nifedipine did not produce such an effect. CONCLUSIONS--Gallopamil and metoprolol both inhibit cardiac sympathetic activation compared with placebo, whereas nifedipine causes reflex sympathetic activation.

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