A haemodynamic study of the effects of combined slow-calcium channel blockade (nisoldipine) and beta-blockade (metoprolol) in coronary heart disease

Silke, Bernard; Verma, S. P.; Midtbo, K A; Müller, Patrick; Frais, M. A.; Reynolds, G; Taylor, Stanley H.

doi:10.1016/0167-5273(86)90147-6

Cited by 12 publications

(5 citation statements)

References 26 publications

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“…This increase is likely associated with a direct haemodynamic effect of β-blockade. 26 Similarly, BNP concentrations increased in the metoprolol group but remained unchanged in the candesartan group during adjuvant chemotherapy. It is well documented that β-blockade, via its effects on heart rate and stroke volume, causes increased release of natriuretic peptides.…”

Section: Discussionmentioning

confidence: 91%

Prevention of cardiac dysfunction during adjuvant breast cancer therapy (PRADA): a 2 × 2 factorial, randomized, placebo-controlled, double-blind clinical trial of candesartan and metoprolol

et al. 2016

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AimsContemporary adjuvant treatment for early breast cancer is associated with improved survival but at the cost of increased risk of cardiotoxicity and cardiac dysfunction. We tested the hypothesis that concomitant therapy with the angiotensin receptor blocker candesartan or the β-blocker metoprolol will alleviate the decline in left ventricular ejection fraction (LVEF) associated with adjuvant, anthracycline-containing regimens with or without trastuzumab and radiation.Methods and resultsIn a 2 × 2 factorial, randomized, placebo-controlled, double-blind trial, we assigned 130 adult women with early breast cancer and no serious co-morbidity to the angiotensin receptor blocker candesartan cilexetil, the β-blocker metoprolol succinate, or matching placebos in parallel with adjuvant anticancer therapy. The primary outcome measure was change in LVEF by cardiac magnetic resonance imaging. A priori, a change of 5 percentage points was considered clinically important. There was no interaction between candesartan and metoprolol treatments (P = 0.530). The overall decline in LVEF was 2.6 (95% CI 1.5, 3.8) percentage points in the placebo group and 0.8 (95% CI −0.4, 1.9) in the candesartan group in the intention-to-treat analysis (P-value for between-group difference: 0.026). No effect of metoprolol on the overall decline in LVEF was observed.ConclusionIn patients treated for early breast cancer with adjuvant anthracycline-containing regimens with or without trastuzumab and radiation, concomitant treatment with candesartan provides protection against early decline in global left ventricular function.

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Section: Discussionmentioning

confidence: 91%

Prevention of cardiac dysfunction during adjuvant breast cancer therapy (PRADA): a 2 × 2 factorial, randomized, placebo-controlled, double-blind clinical trial of candesartan and metoprolol

et al. 2016

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“…Nonselective beta-adrenoceptor blockade attenuated, but did not abolish, the bimakalim-induced increases in heart rate and LVdP/dtmax in the normal animals. Increases in heart rate after betaadrenoceptor blockade have been reported for dihydropyridine derivatives in pigs [13], dogs [16], and humans [17], and have been attributed to the withdrawal of parasympathetic tone [18]. However, in view of the chronotropic actions of bimakalim during intracoronary administration [8], we cannot exclude a direct effect of the drug on heart rate.…”

Section: Discussionmentioning

confidence: 71%

Cardiovascular effects of the novel potassium channel opener bimakalim in conscious pigs after myocardial infarction: A comparative study with nicorandil

Woerkens

Baas

Giessen

et al. 1992

Cardiovasc Drug Ther

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The benzopyran-derivative bimakalim is an ATP-dependent potassium channel activator that has been shown to be a potent arterial vasodilator in anesthetized pigs. In the present study we evaluated the cardiovascular profile of bimakalim in normal conscious animals and conscious animals with chronic left ventricular dysfunction and compared the results to those obtained with nicorandil. In normal conscious pigs, bimakalim (37.5-300 ng/kg/min, n = 6) and nicorandil (10-80 micrograms/kg/min, n = 8) increased cardiac output from 2.7 +/- 0.1 l/min to 3.8 +/- 0.2 l/min and from 2.7 +/- 0.1 l/min to 3.9 +/- 0.3 l/min (both p less than .05) due to increases in heart rate (up to 62 +/- 14% and 74 +/- 9%, respectively, both p less than .05). The mean arterial blood pressure decreased gradually from 104 +/- 4 mmHg to 91 +/- 5 mmHg with bimakalim and from 98 +/- 3 mmHg to 84 +/- 5 mmHg with nicorandil (both p less than .05), due to similar decreases in systemic vascular resistance. LVdP/dtmax also increased with both drugs (up to 48 +/- 11% and 69 +/- 7%, respectively, p less than .05), but left ventricular end-diastolic pressure remained unchanged with bimakalim, while it gradually decreased from 9 +/- 1 mmHg to 5 +/- 1 mmHg (p less than .05) with nicorandil. In pigs with a 3- to 4-week-old myocardial infarction, the vasodilator responses to bimakalim (n = 8) and nicorandil (n = 9) were not affected, but the increases in heart rate and LVdP/dtmax were attenuated compared to the effects in the normal animals.(ABSTRACT TRUNCATED AT 250 WORDS)

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“…The hemodynamic effects of calcium channel blockade in patients with ischemic heart disease have usually been reported to be favorable [20][21][22][23][24]; 'caution stems from the cardiodepressant/vasodilator profile associated with slow calcium-channel blockade. The potential for adverse hemodynamic interaction between slow calcium channel and beta-adrenoreceptor antagonists has been well recognized [37][38][39][40], although such effects have usually occurred in severe coronary artery disease with depressed left ventricular function or in subjects with unstable hemodynamic states.…”

Section: Discussionmentioning

confidence: 99%

“…Nifedipine resulted in some improvement in cardiac function when added to metoprolol [22]; however, greater improvement followed the addition of nicardipine or nisoldipine to metoprolol [23,24], compatible with their greater vascular selectivity. There are no data on the interaction of slow calcium-channel blockade in combination with celiprolol; due to the frequency with which combination therapy may be prescribed, such information is of importance.…”

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confidence: 82%

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Hemodynamic interactions of a new beta blocker, celiprolol, with nifedipine in angina pectoris

Silke¹,

Verma²,

1991

Cardiovasc Drug Ther

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The hemodynamic consequences of blockade at both beta-adrenoceptors and slow calcium channels is of therapeutic importance for patients with angina pectoris. The hemodynamic interaction of a new cardioselective beta blocker, celiprolol, and nifedipine was examined in an acute hemodynamic study using three prospectively matched groups with angiographically confirmed coronary artery disease (n = 10/group). Patients were randomly allocated to intravenous celiprolol (8 mg), sublingual nifedipine (20 mg), or their combination. Rest and exercise (supine bicycle) hemodynamics were determined before and following each therapy. At rest, celiprolol did not alter pumping function; nifedipine reduced diastolic blood pressure and systemic vascular resistance index (SVRI), with a small increase in heart rate. Combination therapy reduced systemic arterial pressure and SVRI; heart rate and cardiac stroke volume index increased. During exercise celiprolol tended to reduce heart rate and cardiac index; nifedipine reduced exercise SVR and cardiac stroke work indices. Combination therapy reduced all components of blood pressure; cardiac stroke work and SVR indices fell. These hemodynamic data suggest that beta blockade with celiprolol may result in a slight depression of cardiac pumping during exercise; however, such effects are offset by the vasodilating actions of nifedipine (reflex sympathetic action offsetting cardiodepression). Thus the acute hemodynamic effects of this combination were seemingly safe in these patients; the longer term effects during maintained therapy should be further assessed.

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A haemodynamic study of the effects of combined slow-calcium channel blockade (nisoldipine) and beta-blockade (metoprolol) in coronary heart disease

Cited by 12 publications

References 26 publications

Prevention of cardiac dysfunction during adjuvant breast cancer therapy (PRADA): a 2 × 2 factorial, randomized, placebo-controlled, double-blind clinical trial of candesartan and metoprolol

Prevention of cardiac dysfunction during adjuvant breast cancer therapy (PRADA): a 2 × 2 factorial, randomized, placebo-controlled, double-blind clinical trial of candesartan and metoprolol

Cardiovascular effects of the novel potassium channel opener bimakalim in conscious pigs after myocardial infarction: A comparative study with nicorandil

Hemodynamic interactions of a new beta blocker, celiprolol, with nifedipine in angina pectoris

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