Introduction

Every adult once had the heart of a child and before that the heart of a fetus and an embryo. This fact delineates the continuum from primary cardiovascular development through maturity and senescence. Although studies of cardiovascular development date back to Aristotle, advances over the last two decades are now defining the processes that link pathogenesis to the prevention of human disease (Neill & Clark, 1995; Clark, Markwald, & Takao, 1995).

In this century, the enterprise of children's cardiovascular health has broadened from the medical management of acute rheumatic fever to the surgical repair of congenital cardiovascular malformations (Moller et al., 1993). In spite of surgical advances, cardiovascular malformations, with a prevalence of 8 per 1000 live births, are the leading cause of infant mortality from congenital defects (Clark, 1994). As other causes of infant morbidity and mortality have yielded to therapy, teams of clinical and basic-science investigators are searching for ways to reduce the prevalence of cardiac defects.

Now, we are in an era reexamining cardiac embryology and defining the etiology and pathogenesis of cardiac disease (Clark, 1986). Advances in molecular and cellular biology have provided tools for the diagnosis of cardiac defects such as hypertrophic cardiomyopathy, Marfan syndrome, and familial arrhythmias. These gains will eventually lead to the prevention of heart disease (Deitz & Pyeritz, 1995). Thus, our management of congenital defects and adult-onset cardiovascular diseases will benefit from this expanded knowledge base regarding cardiovascular development.