A clear delineation of events in the production of an ischemic lesion that evolves in terms of previous episodes of similar ischemia might implicate episodes of superimposition of various cellular injuries. Central to such events there would evolve a micro-circulatory failure that precipitates crescendo-type pathways of progressive injury to cells and also to vessels supplying the area concerned. It is perhaps with regard to such micro-circulatory events that evolve as regional and focally regional sites of injury to vessels that there would in turn become superimposed a proximal pathway of progressive luminal stenosis and occlusion of parent vessels such as the epicardial coronary arteries. One might indeed view superimposed episodes of ischemia to tissues and cells a source of propagated injury determining both microcirculatory failure and also an influence in progression of proximal vascular pathology related to impaired hemodynamics. Proximal parent vascular stenosis would progress hand in hand with microcirculatory failure in determining the acute critical precipitation of ischemia affecting cardiac myofibers in acute myocardial infarction and crescendo angina and in the evolution of progressive neuronal ischemia and necrosis of liquefactive type.