Effect of Fluosol-DA on infarct morphology and vulnerability to ventricular arrhythmia

Although the blood substitute perfluorochemical Fluosol-DA has been shown to reduce experimental myocardial infarct size, the electrophysiologic properties of the surviving myocardium have not been assessed. Twenty-six dogs underwent closed-chest occlusion of the proximal left anterior descending coronary artery. Prior to infarction animals were randomly assigned to one of three treatment groups: groups receiving blood exchange with either Fluosol-DA (F = 9) or autologous heparinized blood (H = 8), given 30 minutes following occlusion over the next 30 minutes (these animals were ventilated with 100% oxygen for 6 hours), or a control group (C = 9) receiving no exchange transfusion and ventilated with room air. On the third postmyocardial infarction day the animals underwent programmed stimulation. The area at risk was defined by injecting different colored microvascular dyes into the three coronary beds, and the area of necrosis was defined by sectioning ventricular slices and staining with Mallory's trichrome stain. Infarct size was significantly reduced in the Fluosol-DA-treated group as compared to the heparin-treated and control groups when expressed as a percentage of the area at risk (F = 53.3 +/- 10, H = 67.2 +/- 12.8, C = 73.6 +/- 11.4: F vs H p less than 0.05; F vs C p less than 0.01). Ventricular tachycardia was inducible and sustained in 16 animals (3F, 6H, and 7C), and there was morphologic correlation with greater endocardial necrosis and smaller viable epicardial regions. In the 10 animals (6F, 2H, and 2C) without sustained ventricular tachycardia, there was greater epicardial viability and sparing of the endocardial regions with irregularity of the borders between viable and necrotic myocardium. We conclude that Fluosol-DA not only decreases infarct size but also modifies infarct morphology to reduce electrical instability.