Combined receptor intervention and myocardial infarction.
The aims of treatment in acute myocardial infarction are to limit evolving muscle necrosis, prevent heart failure, maintain electrical stability, and preserve the coronary circulation to avoid progressive or recurrent infarction. No single treatment achieves all these objectives. The rationale for the use of adrenoceptor blocking drugs is that they will oppose the effects of the increased sympathomimetic activity which follows acute infarction and which may adversely affect outcome. More is known of the clinical use of pure beta-blockade than of combined alpha- and beta-blockade with labetalol but in theory combined receptor blockade will produce additional beneficial effects over beta-blockade alone. beta-Adrenoceptor antagonists have a theoretical role in limiting infarct size. They may reduce the oxygen deficit of jeopardised though potentially viable tissue, limiting infarct size by their favourable effect on heart rate, systolic pressure, contractility, and metabolic pathways. That beta-blockade reduces myocardial damage has been confirmed in animal studies. Studies in man using enzyme release or R wave scoring as indicators of infarct size also suggest that oral or intravenous beta-blockers after infarction encourage myocardial salvage. Few studies have been reported in which the effects of combined alpha- and beta-blockade on infarct size have been determined. The actions of a dual blocking agent are more complex and the outcome less predictable than from beta-blockade alone: the advantages of the beta-blocking component will be retained while the alpha-blocking component may conceivably further diminish oxygen demand by reducing systolic pressure and heart size. Less favourably, coronary perfusion pressure may also fall. It is apparent that further clinical studies are needed. Adrenergic blockade may be used to prevent or treat ventricular arrhythmias which develop after infarction in the face of heightened sympathetic tone and continued ischaemia. Clinical and experimental evidence points to the efficacy of beta-blockade in ischaemia-related arrhythmias, but beta-blockade alone is probably ineffective against arrhythmias arising during reperfusion. In experimental studies, alpha-blockers are effective against both forms of arrhythmia although the doses required for reperfusion effects may produce unacceptable hypotension in clinical use. It is possible that combined alpha- and beta-blockade may have broader antiarrhythmic activity than beta-blockers alone but present clinical data on the value of labetalol in controlling postinfarction arrhythmias are sparse.(ABSTRACT TRUNCATED AT 400 WORDS)
D000317:Adrenergic alpha-Antagonists / Q000627:therapeutic use*; D000319:Adrenergic beta-Antagonists / Q000627:therapeutic use*; D001145:Arrhythmias, Cardiac / Q000503:physiopathology; D001794:Blood Pressure / Q000187:drug effects; D004359:Drug Therapy, Combination; D004594:Electrophysiology; D006333:Heart Failure / Q000188:drug therapy; D006801:Humans; D009129:Muscle Tonus / Q000187:drug effects; D009200:Myocardial Contraction / Q000187:drug effects; D009203:Myocardial Infarction / Q000188:drug therapy* / Q000503:physiopathology; D012008:Recurrence; D013564:Sympathetic Nervous System / Q000503:physiopathology
D000317:Adrenergic alpha-Antagonists; D000319:Adrenergic beta-Antagonists