Our understanding of congenital heart defects has been recently advanced by 
whole exome sequencing projects, which have identified de novo mutations in many 
genes encoding epigenetic regulators. Notably, multiple subunits of switching 
defective/sucrose non-fermenting (SWI/SNF) chromatin-remodeling complexes have 
been identified as strong candidates underlying these defects because they 
physically and functionally interact with cardiogenic transcription factors 
critical to cardiac development, such as TBX5, GATA-4, and NKX2-5. While these 
studies indicate a critical role of SWI/SNF complexes in cardiac development and 
congenital heart disease, many exciting new discoveries have identified their 
critical role in the adult heart in both physiological and pathological 
conditions involving multiple cell types in the heart, including cardiomyocytes, 
vascular endothelial cells, pericytes, and neural crest cells. This review 
summarizes the role of SWI/SNF chromatin-remodeling complexes in cardiac 
development, congenital heart disease, cardiac hypertrophy, and vascular 
endothelial cell survival. Although the clinical relevance of SWI/SNF mutations 
has traditionally been focused primarily on their role in tumor suppression, 
these recent studies illustrate their critical role in the heart whereby they 
regulate cell proliferation, differentiation, and apoptosis of cardiac derived 
cell lines.