Abstract: A basic series of mechanistic steps might actually operate not only in the generation of Ischemia to the myocardium, but particularly in the development of a progressive form of myocardial Ischemia that is determined to a significant degree by a previously established baseline level of sustained myocardial Ischemia. In this sense, perhaps, dynamic contractility of the left ventricle, in terms of the alternating periods of dilatation accomodation of end-diastolic ventricular volume, would in a final analysis constitute a simple superimposition of a number of hemodynamic parametric alterations towards a progressive deterioration in blood supply. This Ischemia would be induced by previous episodes of reduced blood supply and also compensated for by hemodynamic blood flow and pressure adaptations as constituted by myocardial-vascular coupling mechanisms. In various ways, impaired coronary blood flow would institute further hemodynamic systems of vascular-wall origin that would progressively alternate with repeated myocardial ischemic events of both cyclical and acyclical nature. Indeed, vascular patency might operatively reflect myocardial contractility with regard to a whole series of vasodilatatory events and of stenosing lesions that regulate the influence even of attributes of ischemic myocardial effects during systole. It would perhaps be in defining terms of previously maintained levels of persistent myocardial Ischemia that baseline shifts of injury to ventricular muscle would both predetermine and also provide mechanistic potentiation for further ischemic events both as systolic and as end-diastolic phenomena. It is aspects of a myofiber propensity for a potentiating role towards establishment of baseline parameters of determined blood perfusion level at the microcirculatory level that one might realize systems of progressive deterioration of myocardial blood supply beyond just simple considerations of patency of the coronary vasculature.