Long-term treatment of angina pectoris with bisoprolol or atenolol in patients with chronic obstructive bronchitis: a randomized, double-blind crossover study.

Forty outpatients suffering from angina pectoris due to coronary artery disease and concomitant reversible. chronic obstructive bronchitis were treated with the beta1-selective beta-blockers atenolol (50 mg) and bisoprolol (5 mg) for 6 months in each case, following a randomized, double-blind crossover study design. Lung function tests were carried out by means of whole-body plethysmography before and then several times during treatment. 2 to 4 h after drug intake (once daily in the morning). The main target variables for the factorial analysis of variance for comparison of the two beta-blockers were the airway resistance (AWR), the forced expiratory volume in the first second (FEV1), and the peak expiratory flow rate (PEFR). Bicycle ergometry was performed before and after therapy in order to check the cardiovascular effects of the two beta-blockers. The patients were questioned as to their angina pectoris and bronchitis symptoms at the monthly check-ups. There was no difference between the two beta-blockers (p > 0.05), both causing a slight increase in AWR, which increased with therapy duration, and a small but significant decrease in FEV1 and PEFR (p < 0.01). The bronchitis symptoms were not affected; however, seasonal influences were detected. Atenolol and bisoprolol had comparably pronounced effects on the cardiovascular parameters during ergometry (blood pressure, heart rate, W x min product, and ST-segment depression) and the frequency of angina pectoris attacks. Even beta1-selective beta-blockers may cause an impairment of lung function in patients with chronic obstructive bronchitis. This may be due to the presence of beta1-adrenoceptors in the bronchial tissue. Fifty milligrams of atenolol and 5 mg of bisoprolol once per day are effective in the treatment of angina pectoris.

Pharmacokinetics of bisoprolol and influence on serum thyroid hormones in hyperthyroid patients.

Nine hyperthyroid patients (FT4 greater than or equal to 20 ng/L; FT3 greater than or equal to 6 ng/L) were given 1 X 10 mg bisoprolol/day p.o. for a period of 7 days. Pharmacokinetic data were derived from measurements of plasma bisoprolol concentrations after the first dose and at steady state after 7 days treatment. The thyroid hormones FT4, FT3, and rT3 were determined in the serum before and after bisoprolol treatment. In addition, subjective and objective parameters of thyroid function were recorded during the course of the therapy. The maximum bisoprolol concentrations measured after the first dose and after 7 days were 54.3 +/- 2.1 and 70.3 +/- 3.8 ng/ml, respectively, the minimum concentrations being 9.6 +/- 1.0 ng/ml and 11.9 +/- 1.7 ng/ml, respectively. This yields an accumulation factor of 1.2. At steady state, the plasma elimination half-life of bisoprolol was 9.8 +/- 0.9 h. No significant changes in serum thyroid hormones were observed during bisoprolol treatment. There was, however, an improvement in the subjective and objective clinical symptoms of hyperthyroidism. In comparison with the findings in healthy volunteers, the pharmacokinetics of bisoprolol remained unaltered in mild to moderate hyperthyroid patients. After oral application of bisoprolol, only small variations in the plasma concentration were observed inter- and also intraindividually in the course of treatment. This finding reflects the high absolute bioavailability of bisoprolol.

Influence of bisoprolol on blood glucose, glucosuria, and haemoglobin A1 in noninsulin-dependent diabetics.

In a double-blind crossover study, the influence of bisoprolol and placebo was tested in 20 noninsulin-dependent diabetics with concomitant essential hypertension. A 2-week washout placebo period was followed by two treatment periods of 2 weeks each with 10 mg bisoprolol or placebo. Compared with placebo, bisoprolol did not change blood glucose, haemoglobin A1 (HbA1), and glucosuria. No hypoglycaemia was observed. Serum cholesterol and triglyceride levels remained constant. Systolic (SBP) and diastolic (DBP) blood pressure, and heart rate (HR) were significantly (p less than 0.01) reduced after 2 weeks of bisoprolol therapy, compared with placebo. It was concluded that bisoprolol, in a dose therapeutically effective in essential hypertension, has no influence on carbohydrate and lipid metabolism in noninsulin-dependent patients with diabetes mellitus; and 10 mg bisoprolol is effective for the normalisation of SBP and DBP in mildly hypertensive diabetics. Since bisoprolol was well tolerated in the dosage studied, it can be recommended for noninsulin-dependent diabetics with hypertension.