THE MECHANISMS UNDERLYING a striking diastolic predominance of left ventricular coronary arterial blood flow have been the subject of intensive investigation for many years, starting with the first reliable measurements of phasic coronary arterial flow by Gregg and Green (9) in 1940. Subsequent detailed and elegant experimental studies (3,20,(23)(24)(25) have shown that an increased coronary perfusion pressure during systole is counteracted by a rise in intramyocardial pressure which not only throttles, but actively pumps, blood out of the coronary microcirculation. With ventricular relaxation, perfusion pressure decreases but the accompanying lower extravascular compression results in a prominent diastolic surge of coronary flow.Until the relatively recent introduction of wave intensity analysis (18,19), however, there was no straightforward method for quantifying the specific upstream and downstream forces contributing to the complex morphology of coronary arterial flow waveforms. Performed in the time domain, this analysis quantifies pressure-velocity waves that give rise to instantaneous changes in local flow and pressure (17). Wave intensity is calculated as the product of blood pressure and velocity time derivatives (i.e., dP/dt ϫ dU/dt) and can distinguish between waves propagating in a forward (positive intensity, by convention) or backward (negative intensity) direction, waves that have pressure-increasing or pressure-decreasing effects (compression and decompression waves respectively) and waves that accelerate or decelerate flow. Four possible wave types exist: 1) forward-running compression waves that increase pressure and velocity, 2) forward-running decompression waves that decrease pressure and velocity, 3) backwardrunning compression waves that increase pressure but decrease velocity, and 4) backward-running decompression waves that decrease pressure but increase velocity. Identifying such waves and studying their sequence and magnitude throughout the cardiac cycle can provide a wealth of information regarding physiological mechanisms underlying measured pressure and flow/velocity signals (1,17,21,22).Characterization of coronary arterial flow patterns using wave intensity analysis was first performed in anesthetized dogs by Sun et al. (27), via passage into the circumflex artery of a thin micromanometer-tipped catheter to measure highfidelity pressure and a guidewire with a Doppler sensor mounted on its tip to obtain velocity. An important finding arising from initial studies was that backward-running compression waves, generated within the myocardium during the isovolumic contraction and early ejection periods, were key actuators of systolic flow impediment, as they countered the forward flow-promoting effects of an aortic forward-running compression wave generated in the early phase of ventricular ejection (26,27).Coronary wave intensity analysis was subsequently extended to the clinical sphere by Davies et al. (6), using Doppler and high-fidelity pressure sensors mounted singly or in combinat...