The combination of nifedipine and propranolol in the management of patients with angina pectoris.

Tweddel, A. C.; Beattie, J. M.; Murray, R.Daniel; Hutton, I.

doi:10.1111/j.1365-2125.1981.tb01205.x

Cited by 45 publications

(15 citation statements)

References 20 publications

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“…The decrease in systemic blood pressure and sympathetic activation observed in the present study suggest that the addition of a I-adrenoceptor blocking drug to nicardipine to counter such reflex effects ought to be considered. The use of concurrent slow-calcium and ,-adrenoceptor blockade in angina pectoris has been advocated (Ekelund & Oro, 1979;Lynch et al, 1980;Tweddel et al, 1981); the haemodynamic safety of concurrent nifedipine and metoprolol has recently been demonstrated (Pfisterer et al, 1982;Nelson et al, 1984). Pending more definite studies, our observations suggest that the drug nicardipine predominantly induces peripheral vasodilatation without undue evidence of cardiac depression in the intact circulation; it would appear to be haemodynamically well-tolerated even in patients with severe coronary artery disease.…”

Section: Discussionmentioning

confidence: 64%

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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Section: Discussionmentioning

confidence: 64%

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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“…The value of P-adrenoceptor antagonists in the management of angina pectoris (Braun et al, treatment of angina pectoris is well established 1985; Fox et al, 1980;Tweddel et al, 1981). (Kostis et al, 1985;Alderman et al, 1975; However, following oral administration nifedipine Jackson et al, 1980).…”

Section: Introductionmentioning

confidence: 99%

Slow release nifedipine plus atenolol in chronic stable angina pectoris.

Challenor

Waller

Renwick

et al. 1989

Brit J Clinical Pharma

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1 The effects of adding slow release nifedipine in doses of 20 mg and 40 mg twice daily to atenolol therapy (50 mg twice daily) were assessed in 18 patients with chronic stable angina. 2 The addition of the lower dose of nifedipine to atenolol did not significantly alter the weekly consumption of glyceryl trinitrate or the mean number of anginal attacks as assessed by diary cards. However, 2 h after dosing there was a significant prolongation during stress testing in the time to onset of both 1 mm ST depression on the ECG (by 28%) and to angina (by 37%) compared with atenolol alone, but no benefit was apparent by 12 h after dosing. 3 At a dose of 40 mg twice daily, nifedipine significantly reduced glyceryl trinitrate consumption by 25% and the number of anginal attacks by 36%. The times to onset of ST depression and angina were increased by 37% and 55% respectively at 2 h and by 24% and 26% respectively 12 h after dosing. 4 Analysis of the frequency distribution of anginal attacks showed decreasing efficacy with time after administration of nifedipine. The overall results also suggest a relationship between efficacy and the plasma nifedipine concentration, with a mean 20% improvement in time to development of angina occurring at a nifedipine plasma concentration of approximately 30-40 ng mi-1. 5 In conclusion, the reduction of effort-related angina by nifedipine is related to its plasma concentration and the effective duration of action of the 20 mg slow release formulation is less than 12 h.

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“…Tex et al found that of 52 patients who had chronic stable angina only four could not tolerate this combination clinically. Tweddel et al [78] confirmed these results and showed convincingly that propranolol plus nifedipine is a viable therapeutic alternative. Schmidt found that metoprolol in combination with nifedipine was highly effective [75].…”

Section: Chronic Stable Anginamentioning

confidence: 60%

Calcium channel antagonism and beta blockade in combination—A therapeutic alternative in cardiovascular disorders. A review

Lessem

Singh

1989

Cardiovasc Drug Ther

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Calcium-channel antagonists and beta-adrenergic blocking agents have become important modalities in the cardiovascular therapeutic armamentarium. These drugs are often administered as monotherapy to a wide range of cardiological patients with angina pectoris, hypertension, arrhythmias, congestive heart failure, and other diseases. Since within each class these drugs exhibit pharmacologic differences, it follows that their effectiveness varies in different disease states and that they exhibit a wide variety of side effects. In an attempt to optimize therapy, the individual drugs from these two classes can be combined; and the efficaciousness and side-effect profile of various combinations between calcium-channel antagonists and beta blockers are discussed in this review. Recommendations as to which patients may benefit from a combination and as to which patients may be harmed by the combination therapy will be made. Very few studies have compared the safety and efficacy of a single agent with the combination and with placebo in a controlled randomized fashion. To determine which therapy is superior and to determine which combination one should recommend under what circumstances, such placebo-controlled, randomized trials are a necessity, and will hopefully be performed although the complexity is enormous.

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The combination of nifedipine and propranolol in the management of patients with angina pectoris.

Cited by 45 publications

References 20 publications

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

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

Slow release nifedipine plus atenolol in chronic stable angina pectoris.

Calcium channel antagonism and beta blockade in combination—A therapeutic alternative in cardiovascular disorders. A review

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