期刊:Oxford University Press eBooks [Oxford University Press] 日期:2018-03-28
标识
DOI:10.1093/med/9780198784906.003.0328
摘要
Abstract In the course of chronic ischaemic heart disease, coronary plaque rupture with thrombotic arterial occlusion is the key event responsible for ischaemic heart disease-related mortality, the primary determinant of which is myocardial infarct size. Infarct size is determined by coronary occlusion time and by the extent of the ischaemic area at risk for infarction. The coronary collateral circulation is an alternative source of blood supply to myocardium jeopardized by ischaemia. The relevance of both occlusion duration and area at risk is mitigated by the presence of collaterals to the extent that patients with a well- versus poorly developed collateral blood supply gain a survival benefit. Therapeutic promotion of collateral growth is a valuable treatment strategy in patients who are incompletely treatable by conventional means. Promotion of collateral growth should aim at inducing the development of large conductive collateral arteries (i.e. arteriogenesis). They appear to be effectively induced by activation of monocytes/macrophages or by physical augmentation of tangential coronary arterial shear forces.