A brief etymology of the collateral circulation

Abstract

It is well known that the protective capacity of the collateral circulation falls short in many individuals with ischemic disease of the heart, brain, and lower extremities. In the past 15 years, opportunities created by molecular and genetic tools, together with disappointing outcomes in many angiogenic trials, have led to a significant increase in the number of studies that focus on: understanding the basic biology of the collateral circulation; identifying the mechanisms that limit the collateral circulation's capacity in many individuals; devising methods to measure collateral extent, which has been found to vary widely among individuals; and developing treatments to increase collateral blood flow in obstructive disease. Unfortunately, accompanying this increase in reports has been a proliferation of vague terms used to describe the disposition and behavior of this unique circulation, as well as the increasing misuse of well-ensconced ones by new (and old) students of collateral circulation. With this in mind, we provide a brief glossary of readily understandable terms to denote the formation, adaptive growth, and maladaptive rarefaction of collateral circulation. We also propose terminology for several newly discovered processes that occur in the collateral circulation. Finally, we include terms used to describe vessels that are sometimes confused with collaterals, as well as terms describing processes active in the general arterial-venous circulation when ischemic conditions engage the collateral circulation. We hope this brief review will help unify the terminology used in collateral research.

Keywords: collateral circulation; myocardial ischemia; peripheral arterial disease; stroke.

Figure

Major aspects of the vascular biology of the collateral circulation. Embryonic formation of native collaterals (collaterogenesis), which is depicted in the upper right diagram as several collaterals forming between two trees, begins at ~E14 in mouse and determines collateral extent in the adult (center diagram with several collaterals shown connecting two arterial trees). Acute obstruction induces flow across the collateral network (recruitment), followed by remodeling and, potentially, formation of additional collaterals in chronic obstructive disease (neo-collateral formation). Loss of native collaterals (rarefaction) can be caused by aging and other risk factors. The two arterial trees in the center of figure are modification of the logo for the Fifth International Angiogenesis Meeting, Amsterdam, 2014. The mouse embryo image (E14) is from: http://www.emouseatlas.org/emap/ema/home.html.