Gillespie T A, Ambos H D, Sobel B E, Roberts R
Am J Cardiol. 1977 Apr;39(4):588-94. doi: 10.1016/s0002-9149(77)80170-7.
This study was designed to evaluate the effects of dobutamine, a new cardioselective beta adrenergic agonist, on cardiac performance and myocardial injury in patients with evolving myocardial infarction. Results in 16 patients given dobutamine (1 to 40 microng/kg per min for 24 hours) were compared with those in two groups of control patients: one of 16 patients matched for predicted infarct size, and the other of 16 patients matched for early ventricular dysrhythmia, analyzed by computer. Infarct size was predicted from plasma creatine kinase (CK) values during the first 7 hours after the initial elevation, before infusion of dobutamine. Overall observed infarct size was estimated from hourly CK values for 48 hours (including those before and after administration of dobutamine). In all patients technetium-99m (stannous) pyrophosphate scans were positive for myocardial infarction. Dobutamine increased cardiac output (assessed by thermodilution) from 4.9 +/- 0.37 (mean +/- standard error) to 6.0 +/- 0.38 liters/min (P less than 0.05) and decreased pulmonary arterial occlusive pressure from 21.5 +/- 2.7 to 16.7 +/- 1.6 mmHg (P less than 0.01) without significantly altering heart rate or systemic arterial blood pressure. The ratio of observed to predicted infarct size, the frequency of independently detected reinfarction or extension of infarction and the frequency of premature ventricular complexes were similar in control and treated patients. Thus administration of dobutamine in doses sufficient to improve ventricular performance after myocardial infarction does not exacerbate myocardial injury or ventricular dysrhythmia.