Cardiovascular disease (CVD) remains one of Australia’s biggest health burdens, and our biggest killer, despite the successful identification of significant risk factors such as hypertension, diabetes, and dyslipidaemia. The fact that tendency to these CVD-predisposing disorders – as well as the predisposition to CVD itself – can be programmed by a malnourished gestational period is now well recognised. In this current era of ‘over-nutrition’ and its associated obesity and metabolic derangement, it is becoming increasingly apparent that a similar cardiovascular risk phenotype is programmed by an ‘over-nourished’ gestation, by virtue of maternal obesity during pregnancy. We have previously shown, using an isogenic mouse model system, that offspring born from a naturally obese mother carry a latent metabolic phenotype that develops into florid metabolic disease with short exposure to a Western-style diet. We also found that this programmed disease predisposition is associated with widespread epigenomic changes in the liver of offspring. Now we have begun an epigenomic examination of cardiac tissue from the same offspring and have found that the expression of key cardiac-specific microRNAs is perturbed in response to maternal obesity. We also find that the dysregulation of cardiac microRNAs in obese-born offspring is magnified by postnatal overnutrition. Remarkably the altered microRNAs are implicated not only in cardiac function, but also systemic metabolism. The induction of cardiac microRNA alterations by maternal obesity seems yet another contributor to the increasing rates of CVD in the current health climate.