In the past decade, research into cardiovascular diseases, such as atherosclerosis and restenosis, has been focused on the identification of genetic factors that determine disease risk besides clinical risk factors. Many genes in lipid metabolism, vascular homeostasis, haemostasis and inflammation have been found to be related to coronary artery disease1 and the multifactorial nature of the disease suggests a role for many other, yet uninvestigated genes. Previous research from our department has demonstrated the importance of genetics in restenosis after a percutaneous coronary intervention (PCI). Polymorphisms in several inflammatory genes, such as TNFα, eotaxin, CD14, GM-CSF, IL-10, caspase-1, but also noninflammatory genes, such as LPL, stromelysin-1 and the β adrenergic receptor have been found to be associated with the risk of restenosis.2-5 It has become clear, however, that part of the gene-environmental interactions relevant for complex diseases is regulated by epigenetic mechanisms such as histone acetylation and DNA methylation.
