Key result
Intravenous disopyramide in acute myocardial infarction increased heart rate, blood pressure, and systemic vascular resistance, and prolonged P-R and QTc intervals without changing cardiac output.
Why the study?
Does intravenous disopyramide affect haemodynamic and electrocardiographic parameters in patients with acute myocardial infarction?
Does intravenous disopyramide affect haemodynamic and electrocardiographic parameters in patients with acute myocardial infarction?
Intravenous disopyramide in acute myocardial infarction patients produces anticholinergic haemodynamic effects and prolongs P-R and QTc intervals without significantly reducing cardiac output.
May increase afterload in acute MI; leaves open net benefit versus modern agents in prospective trials.
1 The haemodynamic and electrocardiographic effects of intravenous disopyramide were studied in fifteen patients with acute myocardial infarction. 2 Five minutes after drug injection a rise in heart rate, aortic mean and diastolic pressures and systemic vascular resistence was noted which persisted for at least 30 min. A small increase in pulmonary arterial diastolic pressure (mean = 1.5 mm Hg) occurred at 5 min only and no significant change of cardiac output was found throughout the period of the study (1 h). 3 Surface electrocardiograms revealed transient prolongation of the P-R interval and a sustained increase in the QTc interval. 4 The haemodynamic changes suggest an anticholinergic effect of the drug. There was no definite evidence of a negative inotropic effect in this study, however, these peripheral haemodynamic measurements might not have revealed a modest negative inotropic effect. 5 The electrocardiographic changes are similar to those previously reported in normals and in patients without acute myocardial infarction.
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DAVIES et al. (1979) studied Acute myocardial infarction (n=15). Intravenous disopyramide (rythmodan) was evaluated on Haemodynamic and electrocardiographic effects. Intravenous disopyramide in acute myocardial infarction increased heart rate, blood pressure, and systemic vascular resistance, and prolonged P-R and QTc intervals without changing cardiac output.
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