The treatment of angina pectoris caused by coronary artery disease with @-blockers is generally accepted. P-Blockers competitively inhibit the effect of endogenous catecholamines at @-receptors. Reduction in the positive chronotropic and positive inotropic effect of the catecholamines on the myocardium results in a decrease in the myocardial oxygen demand in patients with coronary artery disease, in particular in situations where there is frequently increased catecholamine release. The reduction in the positive bathmotropic effect of the catecholamines can probably explain the antiarrhythmic effect of P-blockers and their protective effect against acute cardiac death.Numerous P-blockers have been introduced into therapy in the last 20 years. Their mode of action in angina pectoris does not differ fundamentally between substances. However, additional pharmacodynamic and pharmacokinetic properties of the individual P-blockers are often of importance in practical therapy: (a) For certain therapeutic aims, for instance reinfarction prophylaxis, P-blockers without intrinsic sympathomimetic activity (ISA) are preferred. (b) For as low-risk treatment as possible of patients with often nondefinitively identified concomitant diseases, such as chronic obstructive bronchitis, a P-blocker with pronounced PI selectivity is desirable. It does not impair the effect of the frequently prescribed P,-agonists, thus having an advantage over nonselective P-blockers where the bronchodilatory effect of the P,-agonist is impaired. (c) To permit once-a-day treatment, longer-acting P-blockers are preferred in all indications for @-blocker treatment, i.e., particularly in the case of angina pectoris. (d) For pharmacokinetically rational @-blocker treatment of patients with specific pathophysiological conditions, such as impaired renal or hepatic function, a P-blocker that can be cleared both renally and metabolically (hepatically) is preferred.Bisoprolol is a @-blocker without ISA (18,24,30) with pronounced PI selectivity