The cardiovascular system is broadly composed of the heart, which pumps blood, 
and the blood vessels, which carry blood to and from tissues of the body. Heart 
malformations are the most serious common birth defect, affecting at least 2% of 
newborns and leading to significant morbidity and mortality. Severe heart 
malformations cause heart failure in fetuses, infants, and children, whereas 
milder heart defects may not trigger significant heart dysfunction until early 
or midadulthood. Severe vasculogenesis or angiogenesis defects in embryos are 
incompatible with life, and anomalous arterial patterning may cause vascular 
aberrancies that often require surgical treatment. It is therefore important to 
understand the underlying mechanisms that control cardiovascular development. 
Understanding developmental mechanisms will also help us design better 
strategies to regenerate cardiovascular tissues for therapeutic purposes. An 
important mechanism regulating genes involves the modification of chromatin, the 
higher-order structure in which DNA is packaged. Recent studies have greatly 
expanded our understanding of the regulation of cardiovascular development at 
the chromatin level, including the remodeling of chromatin and the modification 
of histones. Chromatin-level regulation integrates multiple inputs and 
coordinates broad gene expression programs. Thus, understanding chromatin-level 
regulation will allow for a better appreciation of gene regulation as a whole 
and may set a fundamental basis for cardiovascular disease. This review focuses 
on how chromatin-remodeling and histone-modifying factors regulate gene 
expression to control cardiovascular development.