Study: Recent studies highlight the growing interest in achieving ventricular recovery for VAD patients, thereby eliminating the need for cardiac transplantation. Hemodynamic measurements may be performed during periodic echocardiography for patients with probable recovery. However, there are no standard methods to evaluate ventricular recovery on a continuous outpatient basis. Such a method can help assess changes in cardiac function throughout daily activities, potentially optimized by a responsive VAD control algorithm. The objective of this study was to evaluate a surrogate measure of cardiac contractility based on VAD inherent signals using an in-silico simulation model of assisted circulation. Methods: Without loss of generality, hemodynamic power can be visualized as an electrical power signal in an implanted VAD. The power of a continuous periodic signal (the VAD Flow Rate signal), given by Parseval’s Power Theorem, is equivalently the average value integral over one period of the square of the magnitude of the signal (inclusive of all harmonic components). In this in-silico simulation study, we compute the ratio of this power with the norm (over multiple cardiac cycles) of the signal under steady-state conditions. We call this ratio the Power Factor of the VAD Flow Rate, represented by λVAD. Numerical simulations were conducted for different values of ventricular contractility (Emax Maximum Ventricular Elastance) from 0.5 to 2.0 mmHg/ml over a range of VAD speeds of 1000 to 8000 RPM (HeartMate 3® VAD Model) in steps of 100 RPM. Results: The figure below illustrates the relationship of the Power Factor to VAD speed for four levels of ventricular contractility. At 1000 RPM, the Power Factor for all Emax values was found to be equal. As the VAD speed increases above approximately 4000 RPM, the λVAD values diverge, demonstrating the direct relationship with Emax: having a peak of approximately 0.8 for the greatest ventricular contractility (Emax = 2.0). As speed increases further and approaches 8000 RPM, the values of λVAD once again converge. Another discriminating feature is the location (speed) of the local maximum (“hump”) in the curves within the range of 4000 and 6000 RPM, with the peak occurring at increasing speeds for increasing contractility. The cause of the hump is due to the cooperative relationship of the VAD and native ventricle, precisely the point of the aortic valve opening, allowing forward flow. At the lowest speeds, there is a slight negative flow through the VAD and, thus, a more subdued λVAD. Conclusion: This simulation study shows that the Power Factor of VAD flow rate has the potential as a noninvasive surrogate measure of ventricular recovery that can be monitored continuously. The metric is sensitive to the interaction between the native left ventricle and the VAD and thus helpful in developing feedback control that optimizes cardiac rehabilitation.Figure 1. Simulation results for the Power Factor of VAD Flow Rate as a function of different VAD Speeds (RPM).
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