Abstract

Coronary collaterals are an alternative source of blood supply to myocardium jeopardized by ischaemia. Well-developed coronary collateral arteries in patients with coronary artery disease (CAD) mitigate myocardial infarcts and improve survival. Collateral arteries preventing myocardial ischaemia during brief vascular occlusion are present in 1/3 of patients with CAD. Among individuals without relevant coronary stenoses, there are preformed collateral arteries preventing myocardial ischaemia in 20-25%. Collateral flow sufficient to prevent myocardial ischaemia during coronary occlusion amounts to double dagger25% of the normal flow through the open vessel. Myocardial infarct size, the most important prognostic determinant after such an event, is the product of coronary artery occlusion time, area at risk for infarction and the inverse of collateral supply. Coronary collateral flow can be assessed only during vascular occlusion of the collateral-receiving artery. The gold standard for coronary collateral assessment is the measurement of intracoronary occlusive pressure- or velocity-derived collateral flow index expressing collateral as a fraction of flow during vessel patency. Approximately one of five patients with CAD cannot be revascularized by percutaneous coronary intervention or coronary artery bypass grafting. Therapeutic promotion of collateral growth is a valuable treatment strategy in those patients. Promotion of collateral growth should aim at inducing the development of large conductive collateral arteries (i.e. arteriogenesis) and not so much the sprouting of capillary like vessels (i.e. angiogenesis). Large conductive collateral arteries appear to be effectively promoted via the activation of monocytes/macrophages by means of granulocyte-colony stimulating factor or of augmenting coronary flow velocity.

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