In-Vitro Hemodynamic Assessment of Myocardial Bridging: Evaluating the Impact of Arterial Stiffness on Coronary Flow

This thesis investigates the complex fluid-structure interactions and hemodynamic effects associated with myocardial bridging, a congenital anomaly in which an epicardial coronary artery runs within the heart muscle. The primary objective of this research is to analyze and quantify how changes in arterial stiffness modulate the hemodynamic severity of this condition, using an advanced experimental setup. From an anatomical and pathophysiological perspective, the systolic narrowing of the intramyocardial vessel, known as the “milking effect”, generates significant fluid dynamic disturbances and fluctuations in wall shear stress. These abnormal forces contribute to the stiffening of the vessel upstream of the myocardial bridge, promoting the formation of atherosclerotic plaques, a factor that proves crucial in the pathogenesis of ischemia and in the classification of at-risk patients. To replicate and investigate these phenomena, the study describes the development of an in vitro hemodynamic simulator, whose operation is based on the biophysical principle of Starling resistance applied via a compression chamber. The methodology involves a direct comparison between two different vascular models: an elastic silicone tube and a highly stiff element, both of which were tested using integrated hydraulic pressure sensors and a high-frequency optical tracking system to map the geometric deformation of the lumen in three dimensions. The experimental results show profoundly different hemodynamic characteristics between the two models: the stiff configuration generates an asymmetric elliptical collapse that causes a prolonged attenuation of distal pressure, while the highly elastic configuration undergoes total structural buckling, which triggers abrupt retrograde flows and extreme peaks of negative distal pressure. A critical interpretation of these data, supported by mathematical models with concentrated parameters and phase-space analysis, demonstrates that the loss of arterial elasticity prevents the damping of mechanical stress, transferring it entirely to the fluid. This condition critically prolongs vascular obstruction even during the cardiac relaxation phase (Delayed Diastolic Relaxation), unequivocally explaining the systematic failure of the traditional diagnostic index, Fractional Flow Reserve (FFR), in the presence of myocardial ischemia and corroborating the clinical need to adopt purely diastolic indices to measure its true ischemic potential. The thesis concludes by summarizing the research achievements and raising critical considerations regarding the limitations of the current in vitro model, finally suggesting future directions for the development of physical and numerical simulations aimed at improving the accuracy of cardiovascular diagnoses.