Acute myocardial infarction (AMI) is followed by free radicals generation, which is central in cardiac remodeling. N-acetylcysteine (NAC) is an antioxidant that may have pro-oxidant activity in presence of iron ions. Thus, the association with an iron chelator might improve NAC antioxidant potential. Our aim was to test the association of NAC and an iron chelator (deferoxamine - DFX) on cardiac remodeling in a rodent model of AMI. To this end, Male Wistar rats (60 days old) were subjected to a sham surgery or subjected to myocardial infarcted by the occlusion of left ventricular descending artery. Twelve hours after, AMI was confirmed by cTnI evaluation and the animals were randomized in the following treatments: vehicle, NAC (25 mg/kg for 28 days), DFX (40 mg/kg for 7 days), or NAC plus DFX (NAC 25 mg/kg for 28 days plus DFX 40 mg/kg for 7 days). All animals were followed for 28 days. AMI induced an increase in total plasma iron levels at 7 days after the procedure and all treatments were able to decrease iron concentration. NAC/DFX was able to keep iron levels low up to 28 days. Morphofunctional assessments were made serially by echocardiography. Animals treated with NAC/DFX showed an increase in ejection fraction at 28 days when compared with vehicle group (45% ± 11% vs. 35% ± 9%,respectively; p=0.03). On histological analysis (at 28 days), NAC/DFX treated rats showed decreased oxidative stress (immunohistochemistry anti-4-hydroxynonenal, a side product of lipid peroxidation) when comparing with vehicle group (p=0.059). In conclusion, the association of NAC/DFX was able to attenuate chamber remodeling and improved left ventricle function in an animal model of AMI, whereas either NAC or DFX had no effect when given alone. The likely participation of iron and free radicals can be suggested, but further studies are necessary.