A major problem in understanding how myocardial blood flow is regulated is the common occurrence of subendocardial ischemia in many diseases, with or without coronary arterial disease. Two commonly held explanatory hypotheses were that high systolic intramyocardial pressures prevented flow to deep but not superficial muscle, or that in diastole tissue pressures were highest subendocardially. Neither hypothesis is tenable today, and the likeliest hypothesis is that retrograde systolic flow from the deeper muscle produces a longer time constant for diastolic flow in deep than in superficial muscle.

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