Background. Myocardial infarction (MI) is associated with ventricular hypertrophy and poorer survival. Matrix-metalloproteinases inhibition (M) has been implicated in post-MI remodeling.Results. All data: Sh(-/-), MI(-/-), MI(-/M). Langendorff developed pressure, positive and negative dP/dT demonstrated similar trends. Statistics: significant difference (P < 0.05) between Sh(-/-) and MI(-/M) and between MI(-/-) and MI(-/M) and no significance between Sh(-/-) and MI(-/-) for any parameters. Echocardiography (function and morphometry), H&E morphometry and collagen: P < 0.05 between MI and Sh but no difference between drug treatments. Microarray: altered gene expression classified in areas of apoptosis, anti-inflammatory, structural and novel.Methodology. Rat model, angiotensin-converting enzyme inhibitor (A) and M were administered [both(A/M); neither(-/-); alone(A/-,-/M)] to both MI and Sham (Sh) operated rats. Function assessed by Langendorff apparatus and echocardiography, remodeling by echocardiograms and H&E slides, collagen by Picosirius-red staining. DNA microarray analysis to determine changes in gene expression.Conclusion. The results suggest similar improvements with both A and M on MI hearts.