Although our coronary circulation evolved to meet demands during marked physical exertion for "fight or flight" survival, complex and multilayered control mechanisms reduce flow during other periods. Understanding homeostasis of resting flow provides essential insights into clinical pathophysiology. Several homeostatic mechanisms (myogenic, metabolic, endothelial, and neural) maintain sufficient baseline flow regardless of driving pressure (in aggregate, "autoregulation"). As a result, ventricular dysfunction does not arise until coronary perfusion pressure decreases to ∼40 mm Hg. Straightforward clinical parameters explain approximately one-half of observed absolute resting perfusion but with wide imprecision. Resting perfusion does not associate with clinical outcomes and remains unaffected by revascularization, recovery after myocardial infarction, and treating severe aortic stenosis, thereby supporting the notion that the heart was designed for peak performance.