The effects of fructose-1,6-diphosphate on myocardial damage in acute coronary artery occlusion

Acute myocardial infarction can result from thrombosis of a coronary artery. The purpose of this study was to evaluate the ability of fructose-1,6-diphosphate (FDP; Esafosfina) to reduce myocardial necrosis during acute thrombosis of a coronary artery. A canine model of acute myocardial infarction was used to produce intraluminal thrombosis by placement of a coil of wire in a coronary artery. After developing a coronary thrombosis of the left anterior descending artery, dogs were injected intravenously with 90 mg/kg, 175 mg/kg, or 350 mg/kg of FDP or normal saline (controls). Hemodynamic, biochemical and electrocardiographic parameters were evaluated before, and 30 min and 4 h after occlusion. Four hours after acute coronary occlusion, the animals were sacrificed, and the weights of ischemic and necrotic myocardial tissue were quantified using a histologic-staining method. There were no significant differences between control and treated animals in biochemical or hemodynamic parameters. All animal groups treated with FDP demonstrated significant reductions in the amount of necrotic and ischemic tissue compared to controls (P less than 0.05). However, only the 175 mg/kg group had a significant reduction compared to controls in necrotic tissue weight as a percentage of ischemic myocardium (24 +/- 15% vs. 72 +/- 22%, respectively, P less than 0.01). These data suggest that FDP may have a role in limiting the amount of myocardial damage after an acute coronary artery occlusion.