The article by Abaci et al1 in this issue of Circulation draws our attention to a very important and novel observation that patients with diabetes mellitus (DM) have a lesser ability to develop collateral blood vessels in the presence of coronary artery disease. This is somewhat surprising, because DM is known to stimulate angiogenesis, at least in the retina of the eye, and is, because of capillary leakiness, a major cause of blindness. This article by Abaci et al is a good example for drawing attention to the recently appreciated fact that not all vascular growth should be called angiogenesis. The functionally more important collateral vessels of the heart are not the product of angiogenesis but rather of “arteriogenesis.” Angiogenesis2 is the sprouting of capillaries. It results in a capillary network. However, it is important to recognize that these capillary tubes lack vascular smooth muscle cells. Any new developing network of endothelial tubes that is not surrounded by mural cells is fragile and prone to rupture, remains susceptible to hypoxic regulation, fails to become remodeled, and is unable to sustain proper circulation; it cannot adapt to changes in physiological demands of blood supply.3 4 5 Angiographically, angiogenesis results in a higher capillary density, which is often estimated with increased contrast media density. Arteriogenesis is defined as structural enlargement by growth of preexisting arteriolar connections into true collateral arteries.6 7 8 These vessels, bypassing the site of occlusion, have the ability to markedly increase their lumen by growth to provide enhanced perfusion to the jeopardized ischemic regions after acute and chronic arterial occlusions.9 It is important to recognize that the proliferation of collateral arteries is not a process of passive dilatation but of active proliferation and remodeling. Under normal flow conditions and depending on the pressure …