Background and Objective:Oxygen transport in the heart is crucial, and its impairment can lead to pathological conditions such as hypoxia, ischemia, and heart failure. However, investigating oxygen transport in the heart using in vivo measurements is difficult due to the small size of the coronary capillaries and their deep embedding within the heart wall. Methods:In this study, we developed a novel computational modeling framework that integrates a 0-D hemodynamic model with a 1-D mass transport model to simulate oxygen transport in/across the coronary capillary network. Results:The model predictions agree with analytical solutions and experimental measurements. The framework is used to simulate the effects of pulsatile vs. non-pulsatile behavior of the capillary hemodynamics on oxygen-related metrics such as the myocardial oxygen consumption (MVO2) and oxygen extraction ratio (OER). Compared to simulations that consider (physiological) pulsatile behaviors of the capillary hemodynamics, the OER is underestimated by less than 9% and the MVO2 is overestimated by less than 5% when the pulsatile behaviors are ignored in the simulations. Statistical analyses show that model predictions of oxygen-related quantities and spatial distribution of oxygen without consideration of the pulsatile behaviors do not significantly differ from those that considered such behaviors (p-values >0.05). Conclusions:This finding provides the basis for reducing the model complexity by ignoring the pulsatility of coronary capillary hemodynamics in the computational framework without a substantial loss of accuracy when predicting oxygen-related metrics.