Coronary Collaterals and Their Assessment

Evidence suggests that collateralization may be impaired in diabetics.1,2 This issue of the Journal provides interesting new support for these data.3 The factors responsible for deficient collateral development in diabetes are incompletely understood. Generalized endothelial dysfunction, reduced nitric oxide production and impaired arteriogenesis due to high tissue levels of glucose may be factors. Collateralization may be impaired in other settings as well. See Nisanci et al. on pages 118–122 Early studies of coronary collaterals were primarily based on angiographic assessment. However, angiographic assessment of collaterals4,5 may fail to correlate with myocardial perfusion and function.6,7 The majority of collateral vessels are small, intramyocardial and not well visualized angiographically. Recently, a new invasive method based on angiographic collateral washout has been described,8 although further evaluation is required. Early attempts to quantify collateralization included direct measurement of distal coronary occlusion pressure. However, the applicability of fluid-filled, catheter-based pressure determination in the coronary circulation was limited. More recently, collateral flow has been assessed invasively by calculation of the collateral flow index using Doppler flow wires and pressure wires.9–11 Several such studies have validated earlier hypotheses,12,13 demonstrating a reduction in collateral flow following reopening of chronically occluded coronary arteries,14,15 an inverse relationship between collateral flow and risk of restenosis following revascularization,16 and a positive correlation between collateral flow and the potential for recovery of infarcted myocardium.17 While the collateral flow index method using the Doppler and pressure wire methods is objective, this remains primarily a research tool. Echocardiographic contrast assessment of collateralization is still investigative, although this method appears promising. Contrast echocardiographic myocardial perfusion studies in the setting of acute myocardial infarction18–21 lend support to the concept that enhanced collateral flow in patients with pre-infarct angina helps protect myocardial viability.5,7 Not only do collaterals contribute to perfusion of ischemic myocardium, collaterals are protective in the face of an acute ischemic injury. Current research is examining ways to promote the growth of new collaterals. Reliable means of collateral assessment will assist future investigations in this field.

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