In cardiac neural-crest-ablated embryos, the secondary heart field fails to add myocardial cells to the outflow tract and elongation of the tube is deficient (Yelbuz, T.M., Waldo, K.L., Kumiski, D.H., Stadt, H.A., Wolfe, R.R., Leatherbury, L., Kirby, M.L., 2002. Shortened outflow tract leads to altered cardiac looping after neural crest ablation. Circ. Res. 106, 504–510.). Since that study, we have shown that the secondary heart field provides both myocardium and smooth muscle to the arterial pole (Waldo, K.L., Hutson, M.R., Ward, C.C., Zdanowicz, M., Stadt, H.A., Kumiski, D., Abu-Issa, R., Kirby, M.L., 2005. Secondary heart field contributes myocardium and smooth muscle to the arterial pole of the developing heart. Dev. Biol. 281, 78–90). The present study was undertaken to determine whether addition of both cell types is disrupted after neural crest ablation. Marking experiments confirm that the myocardial component fails to be added to the outflow tract after neural crest ablation. The cells destined to go into the outflow myocardium fail to migrate and are left at the junction of the outflow myocardium with the nascent smooth muscle at the base of the arterial pole. In contrast, the vascular smooth muscle component is added to the arterial pole normally after neural crest ablation. When the myocardium is not added to the outflow tract, the point where the outflow joins the pharynx does not move caudally as it normally should, the aortic sac is smaller and fails to elongate resulting in abnormal connections of the outflow tract with the caudal aortic arch arteries.