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In recent years, the effect of ventricular systole on coronary blood flow has usually been understood in terms of the vascular waterfall concept, the major premise of which is that coronary vessels will display the hydraulic characteristics of collapsible tubes when subjected to extramural compression (Downey and Kirk, 1975). Spaan et al. (1981) have suggested an intriguing alternative explanation which they call the intramyocardial pump. They believe that flow decreases in systole because ventricular contraction forces blood from intramyocardial vessels into upstream arteries, thereby inhibiting antegrade flow. Flow increases in diastole because blood surges back into these previously compressed vessels when the ventricle relaxes. This to-and-fro motion causes the phasic flow differences during the cardiac cycle. Spaan and colleagues support their argument by claiming that portions of their data are incompatible with the waterfall concept. For instance, the authors state that backflow is not possible in the waterfall model because "—the diodes in the electrical analog model of Downey and Kirk, which are essential for the working of their model, would actually prevent such a flow." Surely, it is not too much to say that the attitude apparent in this statement shows an extravagant respect for the heuristic power of an electrical analogy. If the waterfall model actually describes reality, it is because coronary vessels behave like collapsible tubes. Whether or not they behave like diodes is irrelevant. Furthermore, the authors argue, the waterfall model can not explain the data on phasic and mean coronary resistance shown in Figure 6. Putting aside the question as to why these data support the intramyocardial pump and not the waterfall concept, the question remains as to how one calculates resistance "by the waterfall model without diodes." I assume that Spaan and colleagues use diodes to represent the coronary back pressure. Does "without diodes" mean that the back pressure is zero? What is a waterfall model with zero back pressure? I am concerned that Spaan and colleagues misconstrue the waterfall model. In their introduction, they wrote: "If extravascular compression were to affect coronary flow, solely by a time-varying resistance. . . ." The specific context in which this phrase appears gives one no choice but to believe that this is how the authors view the workings of a putative vascular waterfall. When Downey and Kirk (1975) used the waterfall concept to explain the effect of ventricular systole, they explicitly stated that the increase in extravascular compression caused by systole would be apparent as an increase in the back pressure opposing coronary artery flow. The parallel pressure-flow relations they observed whenever perfusion pressure exceeded peak ventricular pressure are prima facie evidence that their water fall model was applicable. Systole decreased coronary flow by increasing the back pressure, not by changing coronary resistance. Of course, the situation in the beating heart generating its own perfusion pressure is more complicated. Since systolic intramyocardial pressure in the left ventricular subendocardium exceeds local microvascular pressure, vessels that were perfused during diastole will be emptied of blood in the way described by Spaan and colleagues. It seems reasonable to assume that these vessels will not be perfused so that the total crosssection of the bed will be smaller and resistance correspondingly greater than in diastole. Thus, the mechanism for flow reduction in systole viewed in terms of the waterfall concept will involve both an increase in the back pressure of perfused vessels and an increase in resistance. Spaan and colleagues would no doubt disagree with this assessment, but the full consequences of their intramyocardial pump, apparent in the following "thought experiment," should be considered. Given: a maximally vasodilated coronary bed and a constant perfusion pressure. Let ventricular systole be prolonged until all flow transients associated with intramyocardial pumping have passed. What would be the level of steady state systolic flow? I believe that the authors would answer mean flow. Now let diastole be prolonged until all transients have passed. What would be the level of steady state diastolic flow? Would it not also equal mean flow? Although distinctly counterintuitive, the conclusion is inescapable that, during the steady state, systolic and diastolic flows (and pressures) are identical. I wonder if Spaan and colleagues are really prepared to argue that ventricular systole has no effect whatsoever on coronary flow when transients associated with their intramyocardial pump have disappeared. As I see it, the problem the authors should address is the extent to which flow transients from intramyocardial pumping obscure the real inhibiting effects of ventricular systole on coronary blood flow.

Comments on "Diastolic-systolic coronary flow differences are caused by intramyocardial pump action in the anesthetized dog".