Several studies indicate that impaired foetal growth, and in utero exposure to 
risk factors, especially maternal hypercholesterolaemia, may be relevant for the 
early onset of cardiovascular damage. The exact molecular mechanisms of such 
foetal programming are still unclear. Epigenetics may represent one of the 
possible scientific explanations of the impact of such intrauterine risk factors 
for the subsequent development of cardiovascular disease (CVD) during adulthood. 
Translational studies support this hypothesis; however, a direct causality in 
humans has not been ascertained. This hypothesis could be investigated in 
primates and in human post-mortem foetal arteries. Importantly, some studies 
also suggest the transgenerational transmission of epigenetic risk. The recently 
launched International Human Epigenome Consortium and the NIH Roadmap 
Epigenomics Mapping Consortium will provide the rationale for a useful clinical 
scenario for primary prevention and therapy of CVD. Despite the heritable nature 
of epigenetic modification, the clinically relevant information shows that it 
could be reversible through therapeutic approaches, including histone 
deacetylase inhibitors, histone acetyltransferase inhibitors, and commonly used 
drugs such as statins.