Hemodynamic and electrophysiologic effects of verapamil and nifedipine in patients on propranolol

Winniford, Michael D.; Markham, Roy V.; Firth, Brian G.; Nicod, Pascal; Hillis, L.David

doi:10.1016/0002-9149(82)91222-x

Cited by 68 publications

(12 citation statements)

References 33 publications

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“…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.…”

Section: Unwanted Effects During Combination Treatmentsupporting

confidence: 85%

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

Challenor

Waller

George

1989

Cardiovasc Drug Ther

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The antianginal effects of beta-adrenoceptor antagonists are achieved by a reduction in myocardial oxygen demand. This is a rational approach to treatment in patients whose angina is caused by a fixed stenosis. However, dynamic coronary vasospasm is an important factor in patients with chronic stable angina. Nifedipine increases myocardial oxygen supply by reducing coronary vascular tone and is a logical approach to treatment in these patients. For monotherapy of angina, nifedipine is less effective than the beta-adrenoceptor antagonists, but the combination has additive effects in reducing the frequency of anginal episodes and improving exercise tolerance. Plasma concentrations of nifedipine are closely related to clinical efficacy, and the variable first-pass metabolism of the drug leads to wide interindividual differences in peak concentrations and duration of action. Increasing the size of individual doses of nifedipine carries a risk of enhanced side effects due to high peak plasma concentrations. Optimal treatment may be more appropriately achieved in some patients by a slow release formulation, but with an increased frequency of administration.

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Section: Unwanted Effects During Combination Treatmentsupporting

confidence: 85%

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

Challenor

Waller

George

1989

Cardiovasc Drug Ther

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“…24 In another study the negative inotropic effects of acebutolol on left ventricular performance were balanced by the vasodilator action of nifedipine, even in a subset of patients with borderline heart failure.26 A more recent study, in which nifedipine was given to patients with normal left ventricular function taking variable doses of propranolol, did not find a fall in dP/dt but confirmed the improvement in left ventricular performance. 22 The safety of the combination was, however, questioned by Monassier et al,25 who gave nifedipine in a higher dose (20 mg sublingually) to patients given acebutolol acutely. Compared with acebutolol alone there was a significantly greater degree of myocardial depression with the combination; all patients had normal left ventricular ejection fractions at rest.…”

Section: Discussionmentioning

confidence: 99%

“…Isolated cases of haemodynamic deterioration have been reported using the combination of beta blockers with both nifedipine' 5-17 and verapamil. [18][19][20][21][22] Formal studies of 383 the haemodynamic effects of nifedipine in combination with atenolol, acebutolol, metoprolol, and propranolol have, however, shown no deterioration with acute or short term administration, even in patients with moderately depressed left ventricular function.2226 There has not, however, been a long term evaluation of using beta blockade alone against atenolol and nifedipine in combination, nor has the effect of nifedipine been observed in patients who are shown to be uniformly beta blocked. The second aspect of concern centres on the possibility of an electrophysiological interaction.…”

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confidence: 99%

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

Rowland¹,

Razis²,

Sugrue³

et al. 1983

Heart

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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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“…Drugs which retard the intracellular migration Winniford et al, 1982). The slow of ionic calcium are of proven value in the calcium channel blocking agents are not homotherapy of cardiovascular disease (Dargie et physiological and pharmacological properties (Henry, 1980).…”

Section: Introductionmentioning

confidence: 99%

Haemodynamic dose‐response effects of i.v. nicardipine in coronary artery disease.

Silke¹,

Verma²,

Nelson³

et al. 1984

Brit J Clinical Pharma

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1 The haemodynamic dose-response effects of the slow channel blocking agent nicardipine were evaluated in 10 male patients with angiographically confirmed coronary artery disease. At rest, following a similar control saline period, four doses of the drug (log cumulative dosage: 1.25, 2.5, 5.0 and 10.0 mg) were administered by i.v. infusion over a total duration of 40 min; haemodynamic variables were recorded in the 3-5 min following each 5 min infusion. During steady-state exercise the haemodynamic effects of the drug were evaluated by comparison of a control exercise period with observations made at the same workload (200-500 kpm) following the maximum cumulative dose (10 mg).2 Following the four i.v. infusions, the plasma nicardipine level increased log-linearly with the infused dose (r = 0.68). Compared with control measurements at rest after saline, these plasma concentrations (35 + 8 to 141 + 24 ,ug/l) resulted in a linear decrease in systemic blood pressure and vascular resistance with significant increase in cardiac index (maximum ACI + 1.6 1 min1 m-2; P < 0.01), stroke index (maximum ASI + 11 mlIm2; P < 0.01) and in pulmonary artery occluded pressure (maximum APAOP + 2 mm Hg; P < 0.01). There was a significant increase in heart rate; the stroke work index was unchanged. 3 During upright bicycle exercise the reduction in systemic blood pressure was accompanied by an increased exercise cardiac output without change in stroke index. The exercise pulmonary artery occluded pressure was unchanged compared with control observations, the stroke work index fell significantly (P < 0.05). 4 The changes in resting haemodynamic variables following nicardipine reflect the influence of a reduction in left ventricular afterload favourably modifying cardiac performance in ischaemic heart disease. During exercise, with near maximal vasodilatation, the additional reduction in systemic vascular resistance on nicardipine did not further improve exercise haemodynamics. However, nicardipine, over a wide intravenous dose-range, did not result in undue depression of cardiac function; thus it would appear to be haemodynamically safe, even in relatively severe coronary artery disease.

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Hemodynamic and electrophysiologic effects of verapamil and nifedipine in patients on propranolol

Cited by 68 publications

References 33 publications

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

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

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

Haemodynamic dose‐response effects of i.v. nicardipine in coronary artery disease.

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