A New Cardiovascular Mock Loop Driven by Novel Active Capacitance in Normal and Abnormal Conditions

The hybrid mock circulatory loop (hMCL) serves as a crucial hemodynamic simulation tool, offering exceptional flexibility, controllability, and reproducibility for investigating the mechanisms underlying cardiovascular diseases (CVD) in a controlled environment, circumventing the limitations of live organism studies. This paper introduces a novel design and control strategy for hMCL, introducing a novel left ventricle volume–elastance (LVVE) equation that unifies the autoregulation of the Frank–Starling mechanism (FSM) with left ventricle contractility (LVC). LVVE establishes a dynamic link between left ventricular volume (LVV) and LVC, inherently satisfying the regulatory relationship between left ventricular pressure (LVP) and LVV through a mathematical equation. For the first time, LVVE integration significantly enhances the physiological relevance of hMCL by faithfully replicating FSM responses across diverse conditions, including aortic stenosis (AS), variations in systemic vascular resistance (SVR), and heart rate (HR) variations. Furthermore, this study introduces the stability proofs for the discrete closed-loop hMCL, enabling real-time proportional valve control through discrete feedback linearization—an innovative departure from conventional methods. Notably, FSM emulation is achieved by tracking reference maximum and minimum LVV values, eliminating the reliance on predefined functions or existing data, such as the maximum LV elastance value. Rigorous experimental validation, encompassing numerical simulations and comparative analyses with prior research, attests to the precision and efficacy of the proposed hMCL in faithfully replicating both normal and abnormal CV conditions. Significantly, the hMCL demonstrates that increasing HR enhances LVC while maintaining physiological pressures; however, this increase in LVC corresponds with a decrease in LVV, in alignment with human data and FSM principles. Crucially, the coupling mechanism between the FSM and LVC yields results of enhanced physiological fidelity, significantly advancing the hMCL’s utility in physiological research. Moreover, the hMCL’s capacity to simulate critical cardiovascular scenarios, including AS, SVR fluctuations, and HR variations, underscores its versatility and substantial potential for investigating complex CV dynamics.