Abstract

Cardiovascular disease is the leading cause of death in industrialized countries and may become the most prevalent reason for mortality worldwide.1,2 In the vast majority of patients, death is the consequence of cerebral or myocardial infarction, both of which are characterized by acute vessel occlusion in the context of atherosclerosis.2 In this situation, outcome depends critically on the extent of infarcted tissue.3 Myocardial infarct size is reflected by the degree of ECG ST-segment elevation during the acute phase4 and is directly determined by the duration of coronary occlusion, the ischemic area at risk for infarct, the lack of collateral supply to the jeopardized region, the absence of preconditioning ischemic episodes before, and the level of myocardial oxygen consumption during the acute coronary event.5 The ischemic area at risk for necrosis is intimately related to alternative sources of blood supply to the occluded vascular region; this is to the extent that well-developed coronary anastomoses originating from a collateral supplying artery can entirely compensate for the occlusion in the collateral-receiving vessel, thus rendering its area at risk zero (Figure 1). In this event, the duration of coronary artery occlusion also becomes irrelevant. However, in the event of acute and permanent coronary occlusion, myocardium is only salvaged in the presence of a preformed collateral circulation.6 In this context, the promotion of well-functioning coronary anastomoses (arteriogenesis) in patients with chronic coronary artery disease (CAD) before a coronary event is an appealing therapeutic principle. The selection of suitable candidates for arteriogenesis should be based on sound assessment of coronary collateral function. Figure 1. Normal left ventricular angiogram ( top middle and right ) in a patient with chronic total occlusion of the proximal left anterior descending artery occlusion ( top left ). Angiography of the right coronary artery ( bottom ) shows extensive collateral supply …

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