Background: Hypertension causes cardiac hypertrophy, cardiac dysfunction and heart failure (HF). Despite the importance of cardiac hypertrophy as an independent risk factor for the development of HF, not all hypertrophied hearts will ultimately fail. Alterations in the extracellular matrix have also been shown to contribute to this process. This study aimed to investigate whether alterations in the levels of profibrotic proteins contribute to the transition of compensated cardiac hypertrophy to HF. Methods: Male rats were subjected to abdominal aorta constriction. After 90 days post surgery (dps), the hearts were collected and Western blot was performed to collagens type I and III, MMP-14, MMP-2, TIMP-2, Integrin and TGF-β. The interstitial collagen area was quantified. Cardiac function was evaluated using the Vevo 2100 ultrasound. Data were considered significant when p Results: At 90 dps, 75% (30 of 40) presented hypertrophic hearts (HH) and 25% (10 of 40) hypertrophic+dilated hearts (HD) in the echocardiography. In addition, systolic (ejection fraction: 33.5%±1.3; fractional shortening: 21.90±4.3%) and diastolic functions (mitral E-wave velocity: 1279±127 mm/s and E/E' ratio: 68.14±16.78) were importantly reduced in the HD group when compared to HH. Although the interstitial collagen content in the left ventricle was not different between HH (3.63±0.40%) and HD (3.75±0.39%) groups, the amount of type III collagen increased (1.28±0.34 AU) while type I collagen showed significant reduction (0.76±0.16 AU) in the HD group when compared to HH (0.90±0.26 AU and 1.11±0.11 AU, respectively). Important increases were seen in the protein levels of TGF-B, integrin, MMP-14, MMP-2 and TIMP-2 in the HD and HH groups when compared to sham, but there is no difference between HD and HH groups. Conclusion: Although there is significant fibrosis in the hearts of animals after 90 dps, the imbalance between type I and III collagens associated with systolic and diastolic function could contribute to the transition to decompensated hypertrophy in this experimental model of cardiac hypertrophy.