Several reports have identified specific miRs that modulate pathologic processes relevant to heart failure; hypertrophy (16,18- 19,23), cell death (28), fibrosis (20,29), vascular proliferation (30), and arrhythmias (17,31). Relevant to our observations, it is notable that overexpression of miR 195 occurs in pressure-overload rodent hearts and that transgenic cardiac over-expression of miR 195 induces heart failure (16); and that elevated miR 195 expression occurs in rodent and human failing hearts (21- 22,24). Similarly, miR 23a can mediate cardiomyocyte hypertrophy (32), and is differentially expressed between failing and nonfailing hearts (16,24). Congruent with the reported function of miRs 23a and 195, our data demonstrate that hearts that eventually recover function have smaller cardiomyocyte sizes (6,33). Intriguingly, while VAD support has been shown to decrease cardiomyocyte size (1), our data demonstrate that VAD support alone does not induce a miR expression profile associated with functional recovery. Thus, a differential miR expression in failing hearts that eventually recovered VAD independence suggests that underlying pathophysiologic processes exist at the time of VAD placement that differ between hearts that recover function and hearts that do not. We did not detect differences between the recovered and dependent hearts in the expression of other miRs that are differentially expressed between failing and nonfailing hearts (i.e., miRs 1, 21, 29, 125b, 130, and 133 [21,24]). The fact that they did not differ with the ability to recover function suggests that cellular processes associated with a more limited set of miRs (23a, 195, and possibly 15b) are critical in defining the potential to recover cardiac function after mechanical unloading.