At resting status, coronary arterial blood flow is about 5% of total cardiac output, and flow across coronary arterial system largely depends on the pressure gradient between aortic root (the coronary driving pressure) and end-diastolic pressure of left and right ventricles. Therefore, coronary arterial blood flow occurs predominantly during diastole, and systolic component at hyperemia is less than 25% of total flow (Fig. 20.3). In case of right coronary artery, phasic blood flow in the right coronary artery proper occurs equally during systole and diastole; conversely, phasic blood flow in the posterior descending and posterolateral coronary arteries occurs predominantly in diastolic phase [3, 4]. In the absence of atherosclerotic narrowing in epicardial coronary artery, the diameter and cross-sectional area of epicardial coronary artery usually tapers from proximal to distal portion along with decreasing amount of regional myocardial mass, supplied by the coronary artery. Although body mass index or habitus can affect coronary arterial size and coronary flow, intracoronary pressure remains constantly as long as the absence of epicardial coronary stenosis (Fig. 20.4). As epicardial coronary arterial system has branching trees, the absolute amount of coronary flow and cross-sectional area (or diameter) decreases along with the course of epicardial coronary artery. However, as the total amount of flow in main vessel and side branch after bifurcation is same, the coronary flow velocity is not changed before and after coronary bifurcation (Fig. 20.5).

The myocardial oxygen demand (8–10 ml/min/100 g) is much higher than other organs (e.g., skeletal muscle 0.5 ml/min/100 g) even in the resting condition, and coronary capillary density is also higher to meet the high oxygen demand. Nevertheless, the oxygen extraction by the myocardium is much higher than the other organs and reaches near maximum. The oxygen saturation of coronary sinus venous blood is only about 20–30% (renal vein: 85%). According to Fick’s principle, oxygen consumption is the product of blood flow and oxygen extraction. Therefore, coronary circulation can meet the increasing oxygen demand mainly by increasing the amount of coronary blood flow [5].

At resting status, coronary blood flow remains constant as coronary artery pressure is reduced below aortic pressure over wide range when the determinants of myocardial oxygen consumption are kept constant [6]. When coronary artery pressure falls below the range of autoregulation, coronary resistance arteries are maximally vasodilated to intrinsic stimuli and flow becomes pressure dependent. Resting coronary blood flow under normal hemodynamic conditions averages 0.7–1.0 ml/min/g and can increase up to three- to fivefold during vasodilation [7]. The ability to increase flow above resting values in response to pharmacologic vasodilation is termed coronary flow reserve (Fig. 20.6a) [8]. Due to coronary autoregulation, coronary flow remains constant as stenosis severity of epicardial coronary artery increases; therefore, assessment of resting perfusion cannot identify hemodynamically significant stenoses (Fig. 20.6b). When maximal vasodilation of resistance arteries occurs, coronary flow is mainly dependent on coronary artery pressure, and this maximally vasodilated pressure-flow relationship is much more sensitive for detecting increases in stenosis severity. In this maximum vasodilatory condition, for example, 30% decrease in distal coronary pressure linearly correlates 30% decrease in coronary flow (Fig. 20.7). When stenosis severity exceeds over 40–60% diameter reduction, stenosis resistance begins to increase, distal coronary pressure decreases, and maximal vasodilatory flow decreases. In this condition, coronary flow reserve (CFR) can reflect the functional significance of epicardial coronary stenosis, unless the stenosis accompanied with diffuse atherosclerosis, LV hypertrophy, or disease causing microcirculation impairment. As absolute coronary flow cannot be easily measured in human, CFR can be quantified using Doppler wire-measured coronary flow velocity, thermodilution flow measurement, or absolute tissue perfusion-based method using positron emission tomography (PET). Table 20.1 summarizes Doppler wire-measured coronary flow velocity and CFR or PET-based measurement of absolute flow and CFR for insignificant coronary artery disease or normal controls. Clinically important reductions in maximum flow correlating with stress-induced ischemia on SPECT are generally associated with CFR value below 2 [9].