Haemodynamic dose-response effects of i.v. metoprolol in coronary heart disease

Hendry, W. Garden; Silke, Bernard; Taylor, S. H.

doi:10.1007/bf00544581

Cited by 12 publications

(6 citation statements)

References 11 publications

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“…Thus, atenolol demonstrated the effects of attenuation of sympathetic stimulation at cardiac P-adrenoceptors. The cardiac index, heart rate and time-averaged aortic velocity decreased and the systemic vascular resistance increased as commonly reported following acute P-adrenoceptor blockade (Hendry et al, 1981;Parker et al, 1968;Taylor et al, 1982). The actions of nitrates have been widely investigated in ischaemic heart disease.…”

Section: Discussionmentioning

confidence: 80%

“…Between atenolol and NTG, the heart rate (P < 0.01), stroke length (P < 0.05), diastolic and mean BP (P < 0.01) and vascular resistance effects (P < 0.05) were different. 13.0 ± 0.4 13.0 ± 0.4 12.6 ± 0.4 (cm) Atenolol 12.2 ± 0.8 12.1 ± 0.8 11.6 ± 0.7 Buccal NTG 11.1 ± 0.7 9.8 ± 0.6** 9.5 ± 0. decreased and the systemic vascular resistance increased as commonly reported following acute P-adrenoceptor blockade (Hendry et al, 1981;Parker et al, 1968;Taylor et al, 1982). The actions of nitrates have been widely investigated in ischaemic heart disease.…”

Section: Difference Between Drugs and Placebomentioning

confidence: 83%

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Pharmacodynamic monitoring during acute intervention in ischaemic heart disease using a new echo‐Doppler device.

Silke

Verma

1990

Brit J Clinical Pharma

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Infirmary at Leeds, Leeds 1 We have utilised a new non-imaging echo-Doppler cardiac output device, using the principle of attenuated compensated volume flow (ACVF), to assess the cardiovascular effects of atenolol and buccal nitroglycerine (NTG) in a placebo-controlled study of 30 patients with coronary disease. 2 Atenolol (4 mg i.v.) reduced heart rate, cardiac output and time-averaged mean aortic velocity (P < 0.01) and increased systemic vascular resistance (P < 0.01). 3 Buccal NTG (5 mg) reduced systemic mean arterial pressure (P < 0.01), cardiac stroke volume (P < 0.05) and stroke length (P < 0.01). 4 Thus although both drugs reduced time-averaged aortic velocity (an index of cardiac performance), the concomitant reduction in cardiac stroke length and tachycardia suggested sub-optimal cardiac filling for buccal NTG, whereas for atenolol (with the associated increased systemic vascular resistance but unchanged stroke length) attenuation of sympathetic stimulation at cardiac P-adrenoceptors.S The ACVF method of cardiovascular monitoring should prove useful in human pharmacodynamic studies.

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Section: Discussionmentioning

confidence: 80%

Section: Difference Between Drugs and Placebomentioning

confidence: 83%

Pharmacodynamic monitoring during acute intervention in ischaemic heart disease using a new echo‐Doppler device.

Silke

Verma

1990

Brit J Clinical Pharma

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“…haemodynamic dose-response studies with metoprolol (Hendry et al, 1981) and oxprenolol over an equivalent 83-adrenoceptor blocking dose range revealed that penbutolol resulted in lesser depression of cardiac performance to metoprolol but equivalent effects to oxprenolol. The similarity in haemodynamic responses between oxprenolol and penbutolol is not unexpected considering the similarity in their pharmacological profile; both are non-cardioselective, oxprenolol possesses 25% intrinsic activity (its maximal chronotropic response in relation to that of isoprenaline -Ablad et al, 1976) while it has been estimated that penbutolol has 18% intrinsic activity (by comparison of heart rate responses between penbutolol and propranolol during exercise testing- Nyberg et al, 1979).…”

Section: Discussionmentioning

confidence: 97%

“…Six patients had a history of previous myocardial infarction > six months before the study. Left ventricular angiography showed dyskinesia in four of the patients; stenosis (> 70% narrowing) of the coronary arteries involved either 1, (Guidicelli etal., 1977); thus the dosage schedule is equivalent to published doseresponse studies with metoprolol (Hendry et al, 1981) and oxprenolol (Silke etal., 1981) wedge tracing (pulmonary artery occluded pressure). Pressures were externally transduced with strain gauges and recorded together with heart rate on an ultraviolet recorder.…”

Section: Methodsmentioning

confidence: 99%

Haemodynamic dose‐response effects of i.v. penbutolol in angina pectoris.

Silke¹,

Verma²,

Hussain³

et al. 1983

Brit J Clinical Pharma

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1 The haemodynamic dose-response effects of intravenous penbutolol, a newer ,3-adrenoceptor antagonist with intrinsic sympathomimetic activity but without cardioselectivity, were evaluated in 10 patients with angiographically documented coronary artery disease.2 Following four logarithmetically cumulative i.v. boluses (0.5-4 mg dosage range) there was a log linear increase in plasma penbutolol concentration; the levels achieved (51 + 8 to 219 + 19 ng/ml) were in the therapeutic range (12 to 250 ng/ml). 3 Penbutolol resulted in a linear decrease in heart rate (maximum AHR -4 beats/min; P < 0.01); there was a small increase in pulmonary artery occluded pressure which reached its maximum at the lower doses (maximum APAOP + lmm Hg; P < 0.01). The resting cardiac output, blood pressure and calculated systemic vascular resistance were unchanged. 4 During 4 min steady-state supine bicycle exercise there was attenuation of exercise cardiac output (AC.I. -0.6 1 min-' m-2; P < 0.01) and systolic pressor response (ASBP -13 mm Hg; P < 0.01) compared with control observations without change in other measured or derived variables.5 The haemodynamic profile of penbutolol compared favourably with other ,8-adrenoceptor antagonists previously evaluated under similar conditions in patients with ischaemic heart disease. Over the i.v. dose-range evaluated penbutolol attenuated exercise-induced angina with a relatively modest depression of cardiac performance; the small change induced in resting haemodynamic variables may, in part, have been contributed to by the intrinsic sympathomimetic activity of penbutolol.

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“…These considerations suggest that our data can be expected to describe accurately the acute pharmacodynamic actions of celiprolol, nifedipine, and their combination in coronary artery disease. Previous studies have, in general, demonstrated a reduction in cardiac performance following intravenous beta-adrenoceptor blockade in patients with stable coronary artery disease [7,8,32,33]. Such cardiodepression is a direct consequence of withdrawal of cardiac sympathetic support; however, it may be offset ff the beta-adrenoceptor antagonist possesses ancillary cardio-stimulating pharmacological properties [7,8].…”

Section: Discussionmentioning

confidence: 98%

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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Haemodynamic dose-response effects of i.v. metoprolol in coronary heart disease

Cited by 12 publications

References 11 publications

Pharmacodynamic monitoring during acute intervention in ischaemic heart disease using a new echo‐Doppler device.

Pharmacodynamic monitoring during acute intervention in ischaemic heart disease using a new echo‐Doppler device.

Haemodynamic dose‐response effects of i.v. penbutolol in angina pectoris.

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

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