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

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.

Beta-adrenoceptor antagonists plus nifedipine in the treatment of chronic stable angina pectoris

“…Combination therapy, in contrast, increased both rest and exercise left ventricular function when compared to propranolol alone. Similar results have also been reported by Joshi et al [55], Winniford et al [56], and Rowland et al [57]. The additive negative inotropic effects of the combination are therefore unlikely to precipitate cardiac failure unless the preceding left ventricular function is extremely poor.…”

Treatment of angina pectoris with nifedipine and atenolol: efficacy and effect on cardiac function.

“…On placebo four (25%) patients had a normal response despite the presence of angina in three, while on nifedipine eight (50%) had a normal response despite the presence of angina in six; on atenolol only one (6%) patient had a normal rise in left ventricular ejection fraction despite 13 of the 16 patients being free of angina; on the combination six (40%) patients had a normal rise in left ventricular ejection fraction and only one patient developed angina (Table). …”

Effects of felodipine on haemodynamics and exercise capacity in patients with angina pectoris.

“…To investigate this, we studied its effects on exercise capacity in patients with chronic stable angina. Since arteriolar vasodilatation is frequently associated with reflex sympathetic activation (Joshi et al, 1981;Rowland et al, 1983) which could be deleterious in this condition patients were studied during concomitant ,-adrenoceptor blockade.…”

“…In clinical practice, vasodilators such as felodipine or nifedipine are most likely to be used in combination with 0-adrenoceptor blockade. Previous studies (Tweddel etal., 1983;Andersson et al, 1985;Johnsson et al, 1983;Leonetti et al, 1984) suggest that felodipine in common with other peripheral vasodilators (Joshi et al, 1981;Rowland et al, 1983) may induce reflex sympathetic action. Such effects should have been largely excluded in the present study due to the presence of concomitant ,-adrenoceptor blockade and this is supported by the minimal increase in heart rate observed during active treatment.…”