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At least 19 recordsLinked to original sources

PubMed1979

Slow-release metoprolol in angina pectoris. A comparative study of a cardioselective beta-blocking drug, metoprolol, in ordinary and slow-release tablets (Durules) in the treatment of angina pectoris.

A double-blind cross-over study was undertaken to compare the effects of ordinary metoprolol tablets (tablets) 0.1 g b.i.d. and metoprolol slow-release tablets (Durules) 0.2 g once daily in 16 patients with angina pectoris. Initially, the patients were treated with placebo for 2 weeks, and then during the cross-over periods with either 1 tablet morning and evening or 1 Durules in the morning and 1 placebo in the evening. Standardized bicycle ergometer exercise tests with heart rate and blood pressure measurements were performed 2 hours after placebo, 2 hours after tablets and Durules, 12 hours after tablets and 24 hours after Durules. The patients kept diaries of their anginal attacks throughout the study. There were no statistically significant differences in total work between tablets and Durules when the values at 12 hours and 24 hours were compared. However, total work was significantly greater at 2 hours and at 12 hours after tablets and 24 hours after Durules than after placebo. Heart rate and systolic blood pressure during exercise were significantly decreased 24 hours after Durules compared to placebo. The heart rate was, however, lower 12 hours after tablets than 24 hours after Durules (p less than 0.05), although this slight difference in the degree of beta-blockade did not seem to be of clinical importance in these patients.

Administration, Oral↗

PubMed1992

Controlled release metoprolol formulations. A review of their pharmacodynamic and pharmacokinetic properties, and therapeutic use in hypertension and ischaemic heart disease.

Conventional formulations of metoprolol have become well established in cardiovascular medicine and are particularly useful in the management of hypertension and ischaemic heart disease. Recently developed controlled release metoprolol delivery systems (metoprolol CR/ZOK and metoprolol OROS) were designed to overcome the drug delivery problems of matrix-based sustained release forms by releasing the drug at a relatively constant rate over a 24-hour period, and thus producing sustained and consistent metoprolol plasma concentrations and beta 1-blockade while retaining the convenience of once daily administration. Clinically and statistically significant reductions in blood pressure have been observed with metoprolol CR/ZOK and metoprolol OROS 24 hours after administration in mildly or moderately hypertensive patients. Studies in patients with mild to moderate hypertension have demonstrated that a similar or higher percentage of patients achieved a goal response with metoprolol CR/ZOK compared with matrix-based sustained release formulations of metoprolol, or conventional atenolol or bisoprolol, while metoprolol OROS achieved an equal or greater response rate compared with conventional or matrix-based sustained release metoprolol preparations. In patients with stable effort angina pectoris, once daily administration of metoprolol CR/ZOK provided at least equal antianginal efficacy as conventional metoprolol in divided doses, while metoprolol OROS reduced the mean number of anginal attacks by the same margin as atenolol. Controlled release metoprolol formulations have been well tolerated in clinical trials. Metoprolol CR/ZOK was associated with a similar or lesser degree of adverse effects related to the central nervous system compared with atenolol or long acting propranolol. Metoprolol CR/ZOK also demonstrated less pronounced beta 2-mediated bronchoconstrictor effects than atenolol in asthmatics, and less general fatigue and leg fatigue in healthy subjects. Metoprolol OROS produced less pronounced bronchoconstrictor effects than atenolol, matrix-based sustained release metoprolol or long acting propranolol in patients with asthma or obstructive airways disease, and healthy volunteers. These results are presumably due to the beta 1-selectivity of metoprolol in addition to the relatively low plasma concentrations maintained by metoprolol CR/ZOK and metoprolol OROS, and the avoidance of high peak plasma concentrations with these agents. Despite the relative safety of the controlled release forms of metoprolol, the use of all beta-adrenoceptor antagonists should be avoided in patients with a history of bronchospasm. Thus, controlled release metoprolol formulations offer the potential to maximise the confirmed benefits of this agent in the management of hypertension and angina, by maintaining clinically effective plasma concentrations within a narrow therapeutic range over a 24-hour dose interval.

Biological Availability↗

PubMed1979

Plasma levels and beta-blocking effect of alpha-hydroxymetoprolol--metabolite of metoprolol--in the dog.

The plasma levels and the beta-blocking effect of metoprolol and its active metabolite alpha-hydroxymetoprolol have been studied after i.v. bolus injections of the substances to dogs. For both substances the beta-blockade increased with the dose, and there was a linear relationship between percent reduction in exercise heart rate and the logarithm of plasma concentration. The dose of the metabolite, however, had to be 5 times higher than that of metoprolol to induce the same degree of beta-blockade. Because of differences in the volume of distribution, 2.0 liters/kg for alpha-OH-metoprolol and 3.5 liters/kg for metoprolol, the 5 times higher dose of alpha-OH-metoprolol resulted in 10 times higher plasma levels of the metabolite than of metoprolol. alpha-OH-Metoprolol was more slowly eliminated (t1/2 approximately 7.0 hr, total body clearance approximately 3.5 ml-kg-1-min-1) than metoprolol (t 1/2 approximately 2.0 hr, total body clearance approximately 20.0 ml-kg-1-min-1). Approximately 5% of an i.v. dose of metoprolol was metabolized to alpha-OH-metoprolol. The half-life of the endogenously formed metabolite was the same as after an i.v. dose of the compound.

Adrenergic beta-Antagonists↗

PubMed1992

Variation of pharmacokinetics after oral administration of slow-release metoprolol tablets and pharmacogenetic considerations.

The maximum plasma concentrations (Cmax) after oral administration of 120 mg tablets of slow-release metoprolol (CAS 37350-58-6) to 75 Japanese healthy male volunteers and 15 arrhythmic patients were measured. Extensive and poor metabolizers after oral administrations of slow-release metoprolol tablets were classified by means of the frequency distribution of Cmax values. In addition, the frequency distribution of Cmax values after oral administration of slow-release metoprolol 120 mg tablets was compared with that of conventional metoprolol 40 mg tablets. 1. Mean +/- S.E. values of Cmax, tmax and AUC0-24 after oral administration of slow-release metoprolol tablets to 75 healthy male volunteers and 15 arrhythmic patients were 95.3 +/- 6.6 ng/ml, 4.4 +/- 0.2 h and 1000.4 +/- 70.9 ng.h/ml, respectively. 2. The number of poor metoprolol metabolizers after the oral administration of slow-release tablets in 75 healthy volunteers and 15 patients was estimated to be 2 subjects (2.2%). 3. The frequency distribution of Cmax values after oral administration of conventional metoprolol tablets was similar to that of slow-release metoprolol tablets. In addition, from the result of this study and that obtained in another study, in which the frequency of poor metoprolol metabolizers in British people has been examined, it is concluded that the frequency of poor metoprolol metabolizers varies between ethnic groups (2.2% in Japanese population and 11.3% in British population.

Administration, Oral↗

PubMed1992

Metoprolol and propranolol treatment in carbon tetrachloride-induced hepatic injury.

The effects of beta 1-selective metoprolol (CAS 37350-58-6) and the nonselective beta-adrenoceptor antagonist propranolol (CAS 525-66-6) were investigated in healthy and CCl4 damaged male rats. Treatments were performed for 16 days, orally with dosages reducing heart beat/min by 25% (metoprolol 10 mg/kg, propranolol 1 mg/kg). Liver glycogen content was not influenced by either beta-blocker in healthy animals. CCl4-induced loss of glycogen was equally moderated by metoprolol and propranolol. Blood glucose increased in metoprolol treated healthy and liver damaged rats after a single dosage likewise following prolonged treatment. Propranolol was without effect on blood glucose level. Cytochrome P-450 decline in microsomal fraction was greater in metoprolol, than in propranolol treated healthy animals. However, the severe fall elicited by liver injury was moderated by metoprolol and normalised by propranolol. Cytochrome b5 seems to be involved in metoprolol metabolism. Cytochrome P-450-dependent aminopyrine-N-demethylase was impeded by metoprolol in animals with healthy liver. The serious inhibition caused by CCl4 was moderated by metoprolol and with a better result by propranolol. The high serum bilirubin level in liver lesion was lowered by metoprolol and particularly by propranolol. Neither phase I metabolic process aminopyrine-N-demethylation nor phase II glucuronidation were normalised. A comparison of this data with the results of a previous 12-day treatment schedule indicates that no changes in efficacy occurred with longer treatment. The present results pertain to the importance of the selection of beta-adrenoceptor blocker in liver lesion.(ABSTRACT TRUNCATED AT 250 WORDS)

Aminopyrine N-Demethylase↗

PubMed1992

Effects of metoprolol on action potential and membrane currents in guinea-pig ventricular myocytes.

The effects of the beta-adrenoceptor antagonist metoprolol on action potentials and membrane currents were studied in single guinea-pig ventricular myocytes. The experiments were carried out using the nystatin-method of whole-cell technique. This method was used in order to prevent the run-down of the calcium current. Metoprolol at concentrations of 10-100 mumol/l shortened action potential in a dose-dependent way. The drug only decreased resting membrane potential at a concentration of 100 mumol/l in two out of five cells. Under voltage-clamp conditions, metoprolol blocked the high threshold calcium current at concentrations of 30 and 100 mumol/l to 82 +/- 4% and 73 +/- 5% from control, respectively. The drug decreased the inward rectifying potassium current in a concentration-dependent manner. This effect was evident for inward current at voltages negative to the apparent reversal potential and for outward current at voltages between -30 and -80 mV. This blocking effect on the inward rectifying potassium current can explain the effect on resting membrane potential. At voltages positive to -30 mV metoprolol increased a time-independent outward current. This metoprolol-enhanced outward current was blocked by barium and cesium. This result suggests that the metoprolol-enhanced current is carried by potassium. The current component enhanced by metoprolol was not sensitive to glibenclamide and tetraethylammonium applied externally, which suggests that the adenosine triphosphate-sensitive channel is not the target of metoprolol. The activation of this time-independent outward current by metoprolol and the blocking effects on the calcium current seem to explain the shortening in action potential induced by the drug.

Action Potentials↗

PubMed1979

Once-daily metoprolol in primary hypertension.

The antihypertensive effect of the selective beta-1-adrenoceptor blocker, metoprolol, administered once daily was evaluated in 32 patients with primary hypertension. After a 4-wk placebo period, the patients were treated with either 150 mg or 300 mg of metoprolol, once daily, for 8 wk. Initially and during the treatment periods blood was drawn for analysis of metoprolol in plasma, plasma renin activity (PRA), and electrolytes, and urine was collected for determination of the urinary aldosterone excretion. Metoprolol reduced the blood pressure measured up to 26 hr after the last dose. The percentage of responders to metoprolol (decrease of mean arterial pressure greater than or equal to 10% over placebo) was 40% for patients on 150 mg and 71% for patients on 300 mg. Except in the standing position, heart rates were reduced for 26 hr after a 150-mg dose. There was a correlation between pretreatment PRA levels and antihypertensive effect of metoprolol in patients on 300 mg metoprolol but not in patients on 150 mg. Urinary aldosterone decreased equally during treatment in responders and nonresponders. Antihypertensive effects and side effects did not correlate with plasma metoprolol concentrations.

Adult↗

PubMed1992

Efficacy of epanolol versus metoprolol in angina pectoris: report from a Swedish multicentre study of exercise tolerance.

The efficacy of epanolol vs. metoprolol in stable angina pectoris was compared in 114 patients recruited to a randomized double-blind cross-over study, consisting of a 4-week period on each drug. Epanolol (200 mg) or metoprolol (200 mg) was administered daily. Bicycle ergometry was performed at the end of each treatment period. The maximum workload was 134 +/- 18 W on epanolol and 133 +/- 37 W on metoprolol (NS). Values for resting heart rate (epanolol, 72 +/- 11 beats min-1; metoprolol, 64 +/- 12 beats min-1; P less than 0.001), systolic blood pressure (epanolol, 143 +/- 21 mmHg; metoprolol, 137 +/- 21 mmHg; P less than 0.05) and diastolic blood pressure (epanolol, 88 +/- 10 mmHg; metoprolol, 84 +/- 11 mmHg; P less than 0.01) were all higher on epanolol treatment. During exercise, the increase in heart rate and blood pressure was of similar magnitude during the two treatment periods, and these parameters did not differ significantly at the last identical workload. The rating of chest pain, fatigue and dyspnoea did not differ between the two drugs during submaximal or maximal exercise. In conclusion, 200 mg of epanolol and metoprolol have similar efficacy with regard to exercise tolerance. As expected from the partial agonist activity present in epanolol but not in metoprolol, the former drug resulted in a higher heart rate and blood pressure at rest. The observed increase in these parameters during exercise was similar for both drugs.

Adrenergic beta-Antagonists↗

PubMed1976

Effects of muliple doses of metoprolol and propranolol on ventilatory function in patients with chronic obstructive lung disease.

The effect of metoprolol on pulmonary function was compared with that of propranolol and placebo in twelve patients with chronic obstructive lung disease. Propranolol caused a significant reduction in FEV1 compared with metoprolol and placebo. Metoprolol gave a slight reduction compared with placebo. FVC was not significantly influenced by metoprolol, but propranolol caused a significant depression compared both with metoprolol and placebo. The isoprenaline-mediated increase in FEV1 and FVC was not significantly altered after metoprolol compared with placebo. After propranolol the isoprenaline-mediated increases in FEV1 and FVC were 40 and 24% lower respectively than after metoprolol and placebo. Unwanted effects and pulmonary symptoms were at an acceptable level in all cases except in two patients who had to be given i.v. theophyllamine therapy during propranolol treatment. It is concluded that metoprolol exhibits a selective beta1-blocking action and thus may be given to patients with chronic obstructive lung disease provided that adequate beta2-stimulator treatment is given concomitantly.

Adult↗

PubMed1992

Efficacy and tolerability of isradipine and metoprolol in treatment of hypertension: the Finnish Isradipine Study in Hypertension (FISH).

Eight hundred seventy-six men and women with diastolic blood pressure (DBP) of 95-115 mm Hg during a 4-week placebo period were included in a multicenter trial; 479 patients had previously been treated for hypertension. The patients were randomized to receive isradipine or metoprolol; both groups were comparable for age, weight, height, smoking habits, and duration of hypertension. By the end of the placebo period, 79 patients did not fulfill the final entry criteria and were withdrawn. The isradipine group consisted of 398 patients (164 women and 234 men), and the metoprolol group consisted of 399 patients (173 women and 226 men). The initial dose of isradipine was 1.25 mg twice daily (b.i.d.), and the initial dose of metoprolol was 50 mg b.i.d.; the doses were doubled after 4 weeks if DBP had not decreased to less than or equal to 90 mm Hg. After 8 weeks, the isradipine group began combination therapy with metoprolol 50 mg b.i.d. and the metoprolol group began combination therapy with isradipine 1.25 mg b.i.d. if DBP was not less than or equal to 90 mm Hg. After 8 weeks monotherapy, mean BP (MBP) was reduced by 13/11 mm Hg (161/104 to 148/93) in the isradipine group and by 15/12 mm Hg (160/103 to 145/91) in the metoprolol group. Monotherapy with isradipine normalized DBP to less than or equal to 90 mm Hg in 52% with a mean dose of 4.26 mg daily, and monotherapy with metoprolol normalized DBP in 58% with a mean dose of 155 mg daily.1+

Adult↗

PubMedDate not supplied

Comparison between the acute hemodynamic effects and brain penetration of atenolol and metoprolol.

Atenolol and metoprolol are beta 1-selective adrenergic receptor blockers, devoid of local anesthetic and intrinsic sympathomimetic properties. Their antihypertensive and hypotensive activities are equivalent. They differ with respect to their lipophilic character, as is apparent from their octanol/buffer (pH, 7.4 at 37 degrees C) partition coefficients: metoprolol, 1.084; atenolol, 0.012. We compared the two agents with regard to their acute hemodynamic effects and degree of penetration into the cerebrospinal fluid (CSF) and into the brain. For this purpose [3H]-metoprolol and [14C]-atenolol were injected either intravenously or into the left vertebral artery of chloralose-anesthetized cats. With both routes of administration, metoprolol, the more lipophilic of the two compounds, achieved much higher concentrations in the CSF and in the pontomedullary region than did atenolol. One hour after completion of an intravenous injection, the concentration of metoprolol in the CSF was about 6.5 times higher than that of atenolol; after administration into the vertebral artery, the difference was about ninefold. In spite of these considerable differences, the hypotensive and bradycardic activities of both drugs, administered intravenously or into the left vertebral artery, were virtually the same. These results suggest that the acute hemodynamic effects of metoprolol and atenolol are probably not due to an action within the central nervous system, but rather to a peripheral mechanism.

Animals↗

PubMed1976

Assessment of metoprolol, a cardioselective beta-blocking agent, during chronic therapy in patients with angina pectoris.

Ten patients with typical angina pectoris and without hypertension, congestive heart failure or other disease were treated with alternating four-week courses of metoprolol (alpha beta1 cardioselective beta-blocking agent), propranolol and placebo. Midway through each four-week period, drug dosage was doubled; thus, regimes were metoprolol, 150 and 300 mg/day, propranolol, 120 and 240 mg per day and placebo, 3 and 6 tablets per day. Serum concentrations of metoprolol increased with increasing dosage in a proportion very similar to that seen with propranolol. Statistically significant reductions in angina frequency/nitroglycerin consumption, and statistically significant increases in total work performed on a bicycle ergometer, were found with both active compounds when compared with placebo. No significant differences were noted between the two active compounds. Though most patients showed greatest improvement on the higher of the two drug dosages, three patients with metoprolol and two with propranolol responded best on the lower dose regime. Both compounds reduced heart rate at rest and during exercise. Neither reduced arterial pressure at rest, but both reduced arterial pressure during exercise. It is concluded that metoprolol is as effective as propranolol in the reduction of angina attacks and improvement in exercise tolerance during chronic therapy in patients with uncomplicated angina pectoris. It is now appropriate to study the effects of metoprolol in patients with coronary artery disease in whom the harmful effects of non-selective beta-blockade heretofore have precluded optimal therapy with beta-blocking drugs.

Adult↗

PubMed1976

Plasma levels and effects of metoprolol on blood pressure, adrenergic beta receptor blockade, and plasma renin activity in essential hypertension.

The effects of metoprolol, a selective beta adrenergic receptor antagonist, on blood pressure, beta receptor blockade (antagoinst of isoproterenol and exercise tachycardia), and plasma renin activity (PRA) have been compared with those of placebo in 16 patients with essential hypertension. The dose of metroprolol was 25 mg three times daily for 1 wk and thereafter 100 mg three times daily for 5 wk. The mean decrease in blood pressure during treatment with metoprolol was 24 +/- 3.8 (SEM)/10 +/- 2.1 mm Hg in the lying position and 23 +/- 4.4/9 +/- 3.1 mm Hg after 1 min in the standing position. At a dose of 2.9 to 5.4 mg/kg, steady-state plasma concentrations of metoprolol varied 17-fold (from 20 to 341 ng/ml) between patients and correlated with the interindividual variability in isoproterenol antagonism (r = 0.58, p less than 0.05) and decrease in exercise tachycardia (r = 0.65, p less than 0.01). By contrast, neither of these variables correlated with the dose of metoprolol in mg/kg. Metoprolol decreased PRA by 67 +/- 1.9 and 71 +/- 1.2% in the lying and standing positions, respectively. The decrease in the mean arterial blood pressure in the lying position was significantly correlated to the PRA during the placebo period (r = 0.61, p less than 0.05) but not to the plasma steady-state levels of metoprolol, the degree of beta receptor blockade, and the decrease in PRA.

Adrenergic beta-Antagonists↗

PubMed1976

Effects of metoprolol in angina pectoris. A subacute study with exercise tests and a long-term tolerability study.

Eighteen patients with angina pectoris, who had previously participated in a cross-over study with 20 mg metoprolol t.i.d. and placebo, have been included in this study. During an introductory six-month open tolerability study, all patients were treated with 50 mg metoprolol t.i.d. and during a subsequent cross-over study, the efficacy of this dose was compared with that of placebo under double-blind conditions. An exercise was performed at the end of each cross-over period. Metoprolol, in a dose of 50 mg t.i.d., gave a significant improvement compared with placebo in respect of the number of anginal attacks, nitroglycerin consumption and daily subjective assessment of the patients' anginal symptoms. Metoprolol also gave a significant increase in exercise capacity, both until the appearance of 1 mm ST segment depression and until the end of exercise. Heart rate and blood pressure were reduced both at rest and during exercise. No severe unwanted effects were observed during this study ranging over eight months, and none of the patients had any signs or symptoms of cardiac failure or pulmonary dysfunction on any occasion. Unwanted effects reported were mild to moderate, and the frequency was the same as during placebo treatment. No abnormal laboratory findings were observed and the relative heart volume was not significantly changed. Administration of 50 mg metoprolol t.i.d. seems to be of greater benefit than 20 mg metoprolol t.i.d., previously investigated in these patients.

Adrenergic beta-Antagonists↗

PubMed1979

Effects of metoprolol on blood pressure and plasma renin activity in thiazide-resistant hypertensive patients.

Twenty patients with mild to moderate hypertension whose blood pressures were not adequately controlled by a thiazide diuretic were treated for 4 wk with metropolol. Normotension (diastolic pressure less than 90 mm Hg) or reduction in diastolic pressure of at least 10 mm Hg was achieved in 12 of the patients 1 wk after metoprolol (200 mg/day) was added to the hydrochlorothiazide (100 mg/day) regimen. In the other 8 patients, pressure reduction was attained with larger doses (300 to 400 mg/day) of metoprolol. After 1 wk of combined therapy, heart rate decreased by 11% (p less than 0.001) and plasma renin activity (PRA) decreased 48% (p less than 0.001). The individual changes in mean blood pressure did not correlate with either the premetoprolol PRA level (r = 0.14) or the changes in PRA after metoprolol (r = 0.03) but did correlate with steady-state metoprolol plasma levels (r = 0.61, p less than 0.01). Pressure and heart rate reductions were sustained during the last 3 wk of combined therapy but the PRA decrease did not persist; levels gradually rose to near control by the fourth week. Urinary sodium excretion was not consistently changed on metoprolol therapy.

Adult↗

PubMed1979

Beta-adrenoceptor blockade by atenolol, metoprolol and propranolol in the anaesthetized cat.

The inhibitory effects of atenolol, metoprolol and propranolol on isoprenaline-induced tachycardia, broncho-relaxation and vasodilatation were investigated in the reserpinized and anaesthetized cat. In low doses all three antagonists inhibited the heart rate response to isoprenaline, the order of potency being propranolol greater than metoprolol greater than atenolol. While propranolol inhibited the bronchodilation and vasodilation responses to isoprenaline in the same dose range as it blocked the heart rate response, atenolol and metoprolol had to be given in considerably higher doses to block these effects. The results indicate that both metoprolol and atenolol, in contrast to propranolol, are selective beta1-adrenoceptor antagonist. No statistically significant difference in the degree of selectivity was found between metoprolol and atenolol. The three compounds were devoid of intrinsic beta-mimetic activity.

Adrenergic beta-Antagonists↗

PubMedDate not supplied

The effects of propranolol, practolol and metoprolol on exercise-induced tachycardia in relation to plasma levels in man.

1. The effects of single oral doses of propranolol, practolol and a new cardioselective beta-adrenoceptor blocking drug, metoprolol, on exercise-induced tachycardia in relation to plasma levels were studied in six normal volunteers. 2. Exercise undertaken on treadmill was submaximal which, under control conditions, increased the heart rate from 74-3 (s.e.m. = 6-8) to 153-8 (s.e.m. = 9.8) beats/min. 3. Plasma concentrations of propranolol and practolol were assayed fluorometrically and of metoprolol by electron-capture gas liquid chromatography, the details of which are described. 4. Between 1-5 and 2 h after drug ingestion 80 mg of propranolol associated with plasma level of 50-60 ng/ml (half-life 2-75 h), reduced the exercise-induced tachycardia by 27%, 250 mg of practolol with plasma levels of 1050-1100 ng/ml reduced it by 28% and 100 mg of metoprolol with plasma concentrations of 140-150 ng/ml (half-life 1-7 h), reduced it by 30%. 5. The resting heart rates were reduced significantly by propranolol and metoprolol but not by practolol. 6. Metoprolol is a potent short-acting beta-adrenoceptor antagonist; its advantages as a cardioselective agent over practolol in therapeutic use are discussed.

Adult↗

PubMed1976

An eighteen months' study of the clinical response to metoprolol, a selective beta1-receptor blocking agent, in patients with angina pectoris.

Following an initial dose response study, metoprolol, a selective beta1-receptor blocking agent, was compared with equipotent dosages of propanolol in a double blind cross-over study, including exercise tolerance tests, on fourteen patients with angina pectoris. Long term therapy with metoprolol then followed until the seventy-second week. Patients performed 8% more total work on metoprolol with 15% more work recorded up to the onset of S-T depression, in comparison with propranolol. In the long term, ther was no significant difference in work performed when the daily dosage of metoprolol was changed from a q.i.d. to a b.d. regime. Metoprolol was shown to be an effective anti-anginal compound with good tolerance and safety, with gradual improvement in underlying myocardial ischaemia during long term treatment.

Adrenergic beta-Antagonists↗