Ablation of the cardiac neural crest has provided a powerful model of cardiovascular dysmorphogenesis because removal or manipulation of neural crest cells can be done before migration in sites distant from central cardiovascular development in chick embryos. Because the heart begins to function so early in its own morphogenetic history, the cardiovascular system is exquisitely sensitive to the embryonic environment, and virtually any manipulation of the embryo has cardiovascular consequences. Thus, although neural crest manipulation is not devoid of experimental artifact, it has resulted in significant advances in our understanding of certain of the factors involved in normal heart development in a way that direct manipulation of heart development does not. We have now identified two major roles for the neural crest in cardiovascular patterning. These are (1) participation in the patterning of the pharyngeal arches and their derivatives, including the aortic arch arteries, which will become the great arteries of the thorax, and (2) migration of a discrete population of neural crest cells into the cardiac outflow tract and participation in formation of the outflow septum. With the advent of genetically based animal models of cardiovascular dysmorphogenesis, some of which are neural crest related, it becomes important to understand what we know definitively from the ablation model along with the questions that remain. This review will focus on the roles of the neural crest in cardiovascular patterning as seen in the ablation model. An important part of the emerging neural crest-ablation phenotype is an early change in the functional competency of the developing myocardium. We believe that the neural crest-ablation phenotype provides a prototype for comparison with newer models of neural crestrelated cardiovascular dysmorphogenesis and that the changes in myocardial functional development provide a means of understanding the early mortality associated with neural crest-type cardiac dysmorphogenesis.