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Circulatory effects of intravenous and oral acebutolol in acute myocardial infarction
Author(s) -
Silke Bernard,
Nelson Gregory,
Verma Satya Prakash,
Clarke Janet,
Baliga Ganesh,
Taylor Stanley H
Publication year - 1985
Publication title -
clinical pharmacology and therapeutics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.941
H-Index - 188
eISSN - 1532-6535
pISSN - 0009-9236
DOI - 10.1038/clpt.1985.169
Subject(s) - acebutolol , medicine , dosing , hemodynamics , myocardial infarction , anesthesia , cardiac output , stroke volume , blood pressure , vascular resistance , cardiac index , heart rate , cardiology
The hemodynamic dose‐response effects of intravenous (25 and 50 mg) and oral (200 and 400 mg) acebutolol were compared in a randomized between‐group study in men within 17 hours of an acute uncomplicated myocardial infarction. Six subjects were evaluated in each of the four groups. After a 1‐hour control period, hemodynamic variables and plasma drug concentrations were determined at 15 (intravenous therapy only), 30, 60, 90, 120, and 240 minutes after dosing. At the doses studied, hemodynamic dose‐response effects were not evident after either intravenous or oral acebutolol. In all groups acebutolol reduced systolic and mean systemic arterial pressure, heart rate, cardiac output, and stroke volume. Pulmonary artery occluded pressure and systemic vascular resistance were transiently increased. Maximum changes developed between 15 and 30 minutes after intravenous dosing and between 1 and 2 hours after oral dosing. However, there were substantial reductions in cardiac output (− 0.7 L/min/m 2 ; P < 0.05) by 30 minutes after oral dosing. Effects lasted for 2 hours after intravenous dosing and for 4 hours after oral dosing. Our data confirm the hemodynamic safety of acebutolol after acute myocardial infarction. The relevance of the time‐dependent hemodynamic differences between intravenous and oral initiation of β‐blockade to the overall goal of reducing myocardial oxygen requirements after acute coronary artery occlusion merits closer examination. Clinical Pharmacology and Therapeutics (1985) 38, 266–272; doi: 10.1038/clpt.1985.169