Abstract
Coronary collateral circulation is a defense mechanism, in cases of gradual coronary narrowing or obstruction (4, 2). However, collateralization is not unique to the coronary circulation. Derangement in perfusion, in general, accompanies angiogenesis and/or further dilation of pre-existing anastomotic channels toward the perturbed area in the brain, lung, skeletal muscle, kidney and so on (3). Although unused pathways between major coronary arteries can be present in the intact heart, even in the newborn (4), the presence of an anastomosis cannot be equated with collateral channels in hearts with ischemic heart disease (5). Not only angiogenesis or de novo vascular formation but also expansion of pre-existing collaterals involve active cell proliferation (6). Recent advances in molecular biology are revealing interesting and clinically important phenomena related to collateral development (7). Nevertheless, factors related to collateral growth in vivo are complex, and are a matter for conjecture.
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Tomoike, H. (1992). Functional Aspects of Collateral Development in Animal Models. In: Schaper, W., Schaper, J. (eds) Collateral Circulation. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-3092-3_8
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DOI: https://doi.org/10.1007/978-1-4615-3092-3_8
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