Determination of Left Ventricular Preload and Contractility Using Waveform Analysis in Continuous-Flow Left Ventricular Assist Device Patients

Abstract

<h3>Purpose</h3> In left ventricular assist device (LVAD) patients, optimization of ventricular unloading and myocardial contractility are known to improve heart failure-related events and exercise tolerance. Left ventricular (LV) preload (dQ/dt_diastolic) and LV contractility (RI_Q; the ratio between maximum flow acceleration, dQ/dt_max, and flow pulsatility, Q_P2P) can be determined from analysis of LVAD flow waveforms. With destination therapy indication, longitudinal changes in patient hemodynamic and myocardial function, and predictors of these parameters, is clinically relevant. This study characterized longitudinal changes in LV preload and LV contractility using non-invasive waveform analysis. <h3>Methods</h3> A prospective, observational study of 17 patients (mean age 53.3 years; 82% male) implanted with a HeartWare HVAD was performed in an outpatient clinic. Over 7 months, 94 flow waveforms were captured and digitized using a smartphone application, WaveApp. RI_Q and dQ/dt_diastolic were calculated for each waveform using MATLAB scripts. Linear mixed model analysis was performed. <h3>Results</h3> There was an increase in LV preload with longer duration of LVAD support (0.26±0.099 mmHg per 100 days; p=0.014). There was no effect of pump speed and diuretic use, however, higher mean pressure (MAP), poorer kidney function and older age at implant were positively associated with preload. Higher LV preload was linked with poorer LV contractility (0.064±0.021 s^-1 per mmHg; p=0.003). There was no significant change in LV contractility with duration of pump support. <h3>Conclusion</h3> Using flow waveform analysis, an increase in LV preload is associated with longer duration of pump support. We propose higher MAP driving increased afterload as the mechanism for reduced pump efficiency and observed increase in preload. Lower LV preload was associated with improved LV contractility, supporting the optimization of ventricular unloading to improve reverse remodeling.