Objectives: We sought to test whether myocardial blood flow(MBF) can be quantified by myocardial contrast echocardiography(MCE) using a volumetric model of ultrasound contrast agent(UCA) kinetics for the description of refill curves after ultrasound- induced microsphere destruction. Background: Absolute myocardial perfusion or MBF(ml· min- 1· g- 1) is the gold standard to assess myocardial blood supply, and so far it could not be obtained by ultrasound. Methods: The volumetric model yielded MBF=rBV· β /ρ T, where ρ T equals tissue density. The relative myocardial blood volume rBV and its exchange frequency β were derived from UCA refill sequences. Healthy volunteers underwent MCE and positron emission tomography(PET) at rest(group I: n=15; group II: n=5) and during adenosine- induced hyperemia(group II). Fifteen patients with coronary artery disease underwent simultaneous MCE and intracoronary Doppler measurements before and during intracoronary adenosine injection. Results: In vitro experiments confirmed the volumetric model and the reliable determination of rBV and β for physiologic flow velocities. In group I, 187 of 240 segments were analyzable by MCE, and a linear relation was found between MCE and PET perfusion data(y=0.899x + 0.079; r2=0.88). In group II, resting and hyperemic perfusion data showed good agreement between MCE and PET(y=1.011x + 0.124; r2=0.92). In patients, coronary stenosis varied between 0% to 89% , and myocardial perfusion reserve was in good agreement with coronary flow velocity reserve(y=0.92x + 0.14; r2=0.73). Conclusions: The volumetric model of UCA kinetics allows the quantification of MBF in humans using MCE and provides the basis for the noninvasive and quantitative assessment of coronary artery disease. Objectives: We sought to test whether myocardial blood flow (MBF) can be quantified by myocardial contrast echocardiography (MCE) using a volumetric model of ultrasound contrast agent (UCA) kinetics for the description of refill curves after ultrasound- induced microsphere destruction. Methods: The volumetric model yielded MBF = rBV · β / p (ml · min-1 · g-1) is the gold standard to assess myocardial blood supply, and so far it could not be obtained by ultrasound. T volunteers underwent MCE and positron emission tomography (PET) at rest (group I: n = 15; group II : n = 5) and during adenosine-induced hyperemia (group II). Fifteen patients with coronary artery disease underwent simultaneous MCE and intracoronary Doppler measurements before and during intracoronary adenosine injection. Results: In in vitro I confirmed that the volumetric model and the reliable determination of rBV and β for physiologic flow velocities. In group I, 187 of 240 segments were analyzable by MCE, and a linear relation was found between MCE and PET perfusion data (y = 0.899x + 0.079; r2 = 0.88) In group II, resting and hyperemic perfusion data showed good agreement between MCE and PET (y = 1.011x + 0.124; r2 = 0.92). In patients, coronary stenosis varied between 0% to 89%, and myocardial perfusion reserve was in good agreement with coronary flow velocity reserve (y = 0.92x + 0.14; r2 = 0.73). Conclusions: The volumetric model of UCA kinetics allows the quantification of MBF in humans using MCE and provide the basis for the noninvasive and quantitative assessment of coronary artery disease.