Given that miRNAs can regulate global gene networks at the translational level, we hypothesized that the switch towards either a hypertrophic or atrophic phenotype is associated with the activity of specific sets of miRNAs. To test this hypothesis we analyzed the expression of a broad range of miRNAs using quantitative stem-loop RT-PCR arrays on left ventricular samples from rat hearts, in which hypertrophy or atrophy of comparable extent were induced. To evaluate the degree of overlap between the miRNA expression pattern activated during postnatal cardiac remodeling with those active during fetal development we also investigated the expression of miRNAs in rat hearts at embryonic day 18. The adult mammalian heart can considerably increase or decrease its size in response to alterations in mechanical workload. In this study we analyzed miRNA abundance in left ventricular myocardium using quantitative stem-loop RT-PCR based miRNA expression arrays in two well established in vivo models of altered cardiac workload, i.e. AS and HTX. We discovered that opposite LY2157299 changes in cardiac workload associated with nearly maximum changes in left ventricular mass induce highly concordant miRNA expression profiles without any miRNAs being regulated in opposite directions. One may argue that the miRNA expression pattern associated with cardiac hypertrophy does not necessarily need to be the exact inverse of that associated with cardiac atrophy. However, not only the qualitative but also the quantitative changes in miRNA expression were highly concordant in the hypertrophied and atrophied hearts. The relation of the relative gene expression levels in hypertrophied and atrophied hearts could be well described by a linear function with a slope of close to one. These findings suggest that any change in cardiac workload – independent of its direction – induces a common miRNA remodeling program. Similar common responses to changes in hemodynamic load have also been described for the so-called fetal genes as well as for cellular remodeling processes. Such a concept, however, would also imply that the direction of growth plasticity in postnatal cardiomyocytes is not determined at the level of miRNA transcription. It must be emphasized here that miRNA expression profiling studies cannot define possible functional distinctions between constant “pools” of miRNAs, de novo synthesized miRNAs, and posttranscriptional miRNA processing. Thus, an apparent discordance between qRT-PCR findings and plasticity changes could reflect differences in miRNA localization, processing and/or stability, which may be more critical in determining the overall direction of adaptive cardiomyocyte plasticity in the adult heart. The cellular remodelling induced by AS and HTX may be associated.