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Eccentric LV hypertrophy is not normally associated with an accumulation of myocardial fibrosis at least during the early stages of VO. Myocardial collagen loss has even been observed [30, 31]. In the rat AR model, we did not observe such loss of collagen or downregulation of ECM genes in the early stages of the disease [29]. This can possibly be explained by an early pressure overload component often associated with AR at least before LV dilation has taken place. After 9 months, the presence of interstitial fibrosis is most likely linked to the loss and replacement of apoptotic myocytes by fibrotic tissue. This is accompanied with decreased myocardial relaxation as demonstrated by the decrease of dP/dtmin. This could increase the occurrence of arrhythmias which we believe is the main cause of mortality in the AR rat model [9, 10, 13].

We observed that many upregulated genes in the left ventricles of AR rats were linked to the extracellular matrix remodeling whereas those downregulated were often associated with myocardial metabolism. We had observed in a previous evaluation of the gene profile of left ventricles from rats after only 14 days of AR [8] that many genes associated with extracellular matrix remodeling were also upregulated very early in the disease process. This made sense considering that 14 days after AR corresponds to an early rapid LV remodeling phase in response to severe and acute LV volume overload [17, 29]. We had previously reported that the myocardial LV collagen tissue content in AR animals increased but only after 9 months [9]. An upregulation of genes related to the extracellular matrix is still present after 9 months suggesting a disruption in the balance between collagen synthesis and its degradation during the evolution of the disease. This probably takes place in the preceding months and leads to increase interstitial and perivascular fibrosis [9].

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