Hemodynamic dose-response effects of flecainide in acute myocardial infarction with and without left ventricular decompensation

Abstract

We evaluated the hemodynamic effects of the class I antiarrhythmic flecainide in 20 patients within 18 hours of an acute myocardial infarction. Equal numbers of patients with normal (group 1) or decompensated (group 2) ventricular function were studied. Both groups received flecainide, 1 mg/kg, as an intravenous bolus over 10 minutes, followed by infusion (1.6 mg/kg/hr) over the next 120 minutes. Plasma concentrations increased linearly with the cumulative flecainide dosage in both groups. There was no difference between the groups in the plasma levels reached, which were within the recognized antiarrhythmic range for flecainide (200 to 1000 ng/ml) throughout the infusion. The hemodynamic effects of flecainide for each group were decreases in systolic blood pressure (maximum 3% fall in group 1 and 8% fall in group 2), cardiac index (9% fall in group 1 and 18% fall in group 2), stroke volume index (13% fall in group 1 and 23% fall in group 2), stroke work index (14% fall in group 1 and 27% fall in group 2), with an increased heart rate (8% rise in group 1 and 5% rise in group 2), pulmonary artery occluded pressure (27% rise in group 1 and 21% rise in group 2), and systemic vascular resistance (11% rise in group 1 and 18% rise in group 2). Diastolic and mean arterial blood pressures did not change. Our data demonstrate that flecainide induced significant cardiodepression in both groups of patients. These effects were not significantly greater in patients with adequately controlled heart failure. These data suggest that the mild negative inotropic properties of flecainide in patients with recent myocardial infarction are comparable to those described for other class I antiarrhythmics.

Comparative Haemodynamic Effects of Verapamil, Flecainide, Amiodarone and Sotalol in the Conscious Rabbit

“…Flecainide had a slight vasodilatory action and reduced TPR by 8 * 3% resulting in a decrease in MAP of 10 f 5%, in agreement with the results of Hoffmeister et al (1989). Thus, HR increased due to baroreceptor mediated sympathetic stimulation and cardiac output was generally maintained as reported in man (Cohen et al 1985;Jackson et al 1985;Silke et al 1986). However, after blockade of cardiac autonomic effectors, cardiac output was reduced significantly by almost 25%.…”

Comparative haemodynamic effects of intravenous lignocaine, disopyramide and flecainide in uncomplicated acute myocardial infarction.

“…In common with other class 1 agents it induces mild depression of cardiac function in stable coronary artery disease (Legrand et al, 1983;Serruys et al, 1983;Josephson et al, 1984). We have recently demonstrated its haemodynamic safety in patients with acute myocardial infarction; the haemodynamic effects of flecainide were similar to published reports of its actions in stable disease; moreover the cardiodepressant effects of the drug were not significantly augmented in patients with adequately treated acute heart failure compared with uncomplicated infarction (Jackson et al, 1985).…”