Investigation into the two-way interaction of coronary flow and heart function in coronary artery disease predicted by a computational model of autoregulation of coronary flow

•By creating a new computational model, a comprehensive study of the autoregulation of coronary flow in cardiovascular patients during exercise was performed.•The model showed that in coronary artery disease with low stenosis due to the metabolic control mechanism of coronary flow, heart function, and systemic flow are not different from a healthy person, coronary flow is regulated by reducing myocardial contractility and increasing heart rate while cardiac output remains constant.•With further reduction of fractional flow reserve, the heart function is impaired, and left ventricular pressure is drastically decreased. This study presents a closed-loop computational model to investigate the interplay between heart function, coronary flow, and systemic circulation during exercise, with a specific focus on the impact of coronary artery stenosis. The model incorporates a lumped representation of the heart, main arteries, and coronary arteries, establishing a closed circulatory system. The simulation investigates the autoregulation of coronary flow in response to myocardial oxygen demands during physical exercise by incorporating sympathetic and parasympathetic functions. This study establishes a closed supply–demand loop and investigates the effect of coronary flow deficiency on heart function and systemic circulation in coronary artery diseases during exercise. In coronary artery diseases with low stenosis, heart function and systemic flow resemble those of a healthy person. However, as stenosis intensifies with physical exercise, an additional regulatory mechanism (reg2) is activated. This mechanism adjusts coronary flow by reducing myocardial contractility (E) and increasing heart rate (HR) while maintaining cardiac output (CO). The study results indicate that, at the highest exercise intensity for a healthy individual (HR = 150), the value of E increases from 6 to 8.65mmHg/ml. Meanwhile, for a patient with 85 % coronary artery stenosis in the same exercise intensity, the HR increases to 200, and the value of E decreases to 3.45mmHg/ml. The results also demonstrate that the initiation of the (reg2) mechanism at rest occurs at 83 % stenosis, while at the highest exercise intensity, this mechanism commences at 67 % stenosis.