Simulation analysis reveals how coronary flow modulates aortic valve function and hemodynamic stability.
Aortic valve stenosis has a high complication rate with coronary artery disease, and angina due to coronary ischemia often resolves rapidly after aortic valve replacement. These clinical observations suggest a close anatomical and physiological connection between aortic valve function and coronary arteries, but the mechanism of mechanical coupling between them is still not fully recognized. Based on high-resolution fluid–structure interaction simulations, we systematically evaluate the modulation mechanisms of coronary drainage on leaflet motion and downstream turbulent structures. Results demonstrate that the coronary arteries are not simply passive anatomical features but also act as active hemodynamic modulators. Coronary flow markedly alters the spatiotemporal evolution of vortex structures within the sinus, suppresses the energy spectrum amplitude at low wavenumbers to stabilize the jet core, and reduces global entropy by approximately 10%. Leaflet flutter characteristics migrated from low-frequency high-amplitude to high-frequency low-amplitude, suggesting an underlying bioprotective mechanism. The comprehensive evaluation of relevant hemodynamic metrics indicated that neglecting coronary arteries in numerical simulations may lead to systematic misinterpretation. These findings emphasize that coronary flow not only facilitates myocardial perfusion but also plays a critical role in regulating local valvular hemodynamics, with potential implications for prosthetic design and patient-specific modeling.
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Shu et al. (2025) studied this question.
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