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. 1983 Oct;50(4):383–389. doi: 10.1136/hrt.50.4.383

Acute and chronic haemodynamic and electrophysiological effects of nifedipine in patients receiving atenolol.

E Rowland, P Razis, D Sugrue, D M Krikler
PMCID: PMC481427  PMID: 6354228

Abstract

The action of nifedipine given first intravenously and then orally was studied in nine patients undergoing investigation for angina pectoris who were already receiving atenolol (100-200 mg/daily) and who had been shown to be fully beta blocked (reduction in maximal heart rate by greater than 25%). Intravenous nifedipine 7.5 micrograms/kg reduced both systolic blood pressure and left ventricular pressure (dP/dt) transiently; both values were significantly lower five and 10 minutes after the infusion of nifedipine but were not significantly different from control values at 20 minutes. There was minimal but pronounced depression of atrioventricular nodal function after giving intravenous nifedipine, though this was detected only when sensitive tests of atrioventricular nodal function were used. These effects were also transient, showing no significant change from control values at 20 minutes. Atrioventricular nodal conduction time and sinus rate were unchanged. Radionuclide angiography of patients taking the oral combination of atenolol and nifedipine for chronic angina showed no change in ejection fraction compared with those taking atenolol alone, but there was a small increase in peak ejection rate. Resting blood pressure and heart rate were unchanged and the PR interval did not lengthen. Peak heart rate and systolic blood pressure showed no alteration on exercise testing when the drugs were combined compared with the response with atenolol alone. Despite the negative inotropic influence when nifedipine was given intravenously, the absence of haemodynamic deterioration when oral nifedipine is combined with atenolol has confirmed that this combination can be used safely in patients with normal left ventricular function. The minimal changes in atrioventricular nodal function cannot be detected on the surface electrocardiogram and are not of clinical importance in patients with normal conduction.

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Selected References

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