New vessel growth in chronic ischemic syndromes is an attractive idea. Fortunately, more than one mechanism exists to create new blood vessels. Angiogenesis is the creation of blood vessels from sprouts off existing vessels. In contrast, vasculogenesis is the creation of blood vessels de novo by differentiation of new blood cells. Endothelial cell precursors in the bone marrow and circulating in the bloodstream can incorporate into developing vessels and contribute to vessel growth in a manner very similar to the vasculogenesis of embryonic development. The therapeutic potential of these cells has not been tested, but they can be recruited from bone marrow and may be a means to accelerate endogenous revascularization in patients with ischemia.

In contrast to angiogenesis, arteriogenesis is the recruitment of existing vessels to increase their capacity and consequent blood flow to ischemic tissue (Fig. 44-2). In a sense, arteriogenesis represents the maturation of vessels that exist but may not contribute significantly to regional blood flow until properly stimulated. Most collateral vessels visualized by arteriography are probably vessels that have undergone arteriogenesis instead of angiogenesis. Because arteriogenesis creates capacitance vessels, this process is more likely to increase blood supply in a way that substantially affects tissue perfusion. Interestingly, the proteins that affect arteriogenesis are distinct from those that regulate angiogenesis; VEGF does not seem to be important for arteriogenesis, whereas macrophage-derived factors are necessary. The therapeutic potential of arteriogenesis has not been tested, but given the role of arteriogenesis in collateral formation in patients with chronic myocardial ischemia, this represents another potential therapeutic tool for the creation of new blood vessels in patients with refractory angina.

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