['To investigate the role of MMP-2 and MMP-9 in cardiac remodelling induced by tobacco smoke exposure in rats.', 'Rats were allocated into two groups: C (n=9): control animals; ETS (n=9): exposed to tobacco smoke. After 4months, the animals underwent echocardiography, morphometric study and determination of MMP-2 and MMP-9 activity.', 'ETS rats had larger diastolic (C=15.6 +/-1.2 mm/kg, ETS=18.0+/-0.9 mm/kg; p < 0.001) and systolic (C=7.3+/-1.2 mm/kg, ETS=9.2+/-0.9 mm/kg; p=0.001) ventricular diameters adjusted for body weight. Fractional shortening (C=53+/-4.8%, ETS=48+/- 3.3%; p=0.031) and ejection fraction (C=0.89+/-0.03, ETS=0.86+/-0.02; p=0.030) were smaller in the ETS group. Myocyte cross-sectional area (C=245+/-8 microm2, ETS=253+/-8 microm2; p=0.028) was higher in ETS rats. There were no differences in MMP-2 (C=50+/-14%; ETS=43+/-11%, p=0.228) or MMP-9 (C=0.36+/-0.3%; ETS=0.62+/-0.3%, p=0.630) activity between the groups.'] Is tobacco smoke-induced left ventricular remodelling associated with metalloproteinase-2 or -9 activation?