Clinical pharmacology of the beta-blocking drugs: implications for the postinfarction patient.
All available beta-adrenergic blocking agents share the property of blocking beta 1 adrenoceptors, including those in the heart. They differ, however, in their ability to block beta 2 receptors (cardioselectivity), their membrane stabilizing action, intrinsic sympathomimetic activity and their pharmacokinetic properties. The strongest evidence for efficacy in secondary prevention has been obtained with timolol, metoprolol and propranolol. Timolol and propranolol block all beta-receptor-mediated responses and are therefore nonselective, whereas metoprolol is relatively cardioselective. Propranolol and metoprolol have membrane stabilizing action, but timolol does not; none of these agents show intrinsic sympathomimetic activity. Thus, no ancillary property is a requirement for efficacy. All of these agents may precipitate heart failure, but this problem has been exaggerated, and transient failure during the early course of myocardial infarction is no longer a contraindication to therapy. Cardioselective agents cause less bronchospasm, but this can still occur, especially with higher dosages. In addition, these agents probably cause somewhat less fatigue and result in less hypertension during hypoglycemia than nonselective agents. The availability of at least three effective agents allows for a choice of therapy to offer individual patients.
D000319:Adrenergic beta-Antagonists / Q000009:adverse effects / Q000145:classification / Q000494:pharmacology*; D000889:Anti-Arrhythmia Agents; D001986:Bronchial Spasm / Q000139:chemically induced; D005221:Fatigue / Q000139:chemically induced; D006333:Heart Failure / Q000139:chemically induced; D006801:Humans; D007700:Kinetics; D009203:Myocardial Infarction / Q000188:drug therapy*; D011433:Propranolol / Q000494:pharmacology
D000319:Adrenergic beta-Antagonists; D000889:Anti-Arrhythmia Agents; D011433:Propranolol