CFD-derived biomarkers in intermediate risk pulmonary embolism patients treated with mechanical thrombectomy

Background: Acute pulmonary embolism (PE) is a leading cause of morbidity and mortality with persistent difficulties in choosing interventions and predicting outcomes for patients defined clinically as intermediate risk. Computational fluid dynamics (CFD) tools have been used to understand the hemodynamic environment and plan interventions in the pulmonary arteries across a variety of disease conditions. Several biomechanical metrics have been used to evaluate risk in narrowed vessels, including hemodynamic resistance, power dissipation, and fractional flow reserve (FFR). In this study, we evaluate differences in these CFD-derived biomarkers between healthy controls (HC) and intermediate risk, acute PE patients. Additionally, we examine the response of patient hemodynamics to mechanical thrombectomy and compare values of these biomarkers across post-intervention pressure status. Methods: A CFD framework was developed to simulate patient-specific hemodynamics within the pulmonary vasculature identifiable from clinical imaging. The pipeline involved reconstructing three-dimensional (3D) structures of the pulmonary arteries and modeling blood flow with the finite element method. Patient-specific boundary conditions were derived from matching pre-intervention inlet mPAP to the patient's measured value given their measured CO as steady inflow. Converged simulations allowed for precise quantification of primary hemodynamic characteristics (flow and pressure) as well as secondary flow phenomena, primarily wall shear stress (WSS) and simulated pressure metrics such as fractional flow reserve (FFR). Results: Our simulations revealed significant elevations in resistance, power dissipation, and the number of vessels with low FFR in those patients with acute PE (n=6) compared to HC (n=3). Occlusions of hemodynamic significance were generally found in segmental pulmonary arteries. For patients with normalized pulmonary pressures post-thrombectomy (n=3), we found significantly higher proximal power dissipation and counts of low FFR vessels in comparison to those with elevated pressures after intervention (n=3). Distal resistance, which was derived from the portion of resistance attributed to the outflow boundary conditions, was significantly higher in patients with elevated pressures post-intervention. Across all PE patients, FFR count was significantly correlated with post-thrombectomy pulmonary pressure and cardiac index. Discussion: CFD-derived biomarkers offer a promising tool for understanding disease severity in acute PE. Differences between HCs and acute PE patients reveal expected increases in metrics associated with proximal disease burden. Yet, in examining acute PE patients with varying post-intervention hemodynamics, we found that these metrics of proximal disease burden could also be useful to predict the efficacy of mechanical thrombectomy. Those patients with normalized pressures had higher values for proximal disease metrics and lower values for distal disease metrics than those with continued elevations in pressure. This suggests that accessibility of hemodynamically-significant emboli to thrombectomy may be useful as a predictor for outcomes.