Project Summary Mechanical circulatory supports (MCS), particularly left ventricular assist devices (LVADs), have emerged over the past few decades as a life saving therapy for patients with late stage heart failure. Despite this, many post implantation complications, such as right ventricular failure (RVF), remain common. RVF increases the rates of mortality, length of hospital stay, and can necessitate the implantation of a right ventricular assist device1. In an attempt to identify these patients, many previous researchers have created risk scores based on qualitative assessments, hemodynamic, and hematological parameters. In spite of this, risk scores lack the sensitivity and specificity for wide-spread clinical use, and fail in cross-validation studies. Meta analyses of these studies have identified markers of preoperative RV dysfunction as the strongest indicators of post operative failure. These markers, though, suggest different mechanisms by which preoperative RV dysfunction leads to RVF. Preoperatively reduced systolic RV function, reduced function from interventricular worsening, and adverse RV remodeling from underlying pulmonary disease are the primary forms of dysfunction from which RVF occurs post LVAD. The influence of each mechanism on postoperative RVF is unknown. Quantitative assessments of each form of primary dysfunction in a single patient population is needed to compare the role of each mechanism. Better understanding of the mechanism by which RV dysfunction leads to RVF would improve preoperative counseling and management, and could reduce subsequent RVF. The proposed project aims to investigate the influence of each form of preoperative dysfunction through quantitative functional assessments. In particular, right ventricular stroke work, free wall and septal wall strain, and arterial-ventricular coupling will be measured to evaluate different types of RV impairment. Pressure- volume loops will be recreated by combining noninvasive, single heartbeat, cineCT-derived volumetric measures with contemporaneous RV pressure waveforms to energetically assess the systolic function of the right ventricle. In addition, measures of 3D free wall strain will be compared to septal strain, to quantify free wall compensation in left heart failure. Lastly, arterial-ventricular coupling will be derived from single-beat estimates of pressure-volume loop derived ventricular end-systolic elastance and CT-derived measures of pulmonary elastance. This will assess combined cardiopulmonary function that may lead to adverse RV remodeling. In addition to evaluating the mechanisms of RV dysfunction, we will assess the prognostic ability of these metrics for RVF after LVAD implantation. The long-term goal of this proposal is to establish a comprehensive RV evaluation that can be used to preoperatively identify patients at a high risk for RVF.