Fat Quantification Imaging and Biophysical Modeling for Patient-Specific Forecasting of Microwave Ablation Therapy.

Frankangel Servin,Daniel B Brown,Sunil K Geevarghese,Jarrod A Collins,Michael I Miga,Katherine C Frederick-Dyer,Jon S Heiselman,Virginia B Planz

doi:10.3389/fphys.2021.820251

Abstract

Computational tools are beginning to enable patient-specific surgical planning to localize and prescribe thermal dosing for liver cancer ablation therapy. Tissue-specific factors (e.g., tissue perfusion, material properties, disease state, etc.) have been found to affect ablative therapies, but current thermal dosing guidance practices do not account for these differences. Computational modeling of ablation procedures can integrate these sources of patient specificity to guide therapy planning and delivery. This paper establishes an imaging-data-driven framework for patient-specific biophysical modeling to predict ablation extents in livers with varying fat content in the context of microwave ablation (MWA) therapy. Patient anatomic scans were segmented to develop customized three-dimensional computational biophysical models and mDIXON fat-quantification images were acquired and analyzed to establish fat content and determine biophysical properties. Simulated patient-specific microwave ablations of tumor and healthy tissue were performed at four levels of fatty liver disease. Ablation models with greater fat content demonstrated significantly larger treatment volumes compared to livers with less severe disease states. More specifically, the results indicated an eightfold larger difference in necrotic volumes with fatty livers vs. the effects from the presence of more conductive tumor tissue. Additionally, the evolution of necrotic volume formation as a function of the thermal dose was influenced by the presence of a tumor. Fat quantification imaging showed multi-valued spatially heterogeneous distributions of fat deposition, even within their respective disease classifications (e.g., low, mild, moderate, high-fat). Altogether, the results suggest that clinical fatty liver disease levels can affect MWA, and that fat-quantitative imaging data may improve patient specificity for this treatment modality.

Highlights

While many cancers have decreased in incidence over the last more than two decades, primary liver cancer has increased, tripling in the United States since 1980 and rising on average ∼2% per year for much of this time period (Siegel et al, 2021)
This study extends previous work in three key ways: (1) all simulations of microwave ablations were derived from patientspecific anatomies and solved in 3D, (2) each simulation’s dielectric and thermal properties were derived from quantitative magnetic resonance (MR) fat quantification imaging data of the patient with perfusion states being indirectly related based on disease state, and (3) microwave ablation performance sensitivity was evaluated relevant to human clinically-diagnosed disease states that were relevant to the locoregional management of liver cancer
Fat content was sampled from fat fraction images by capturing 1 cm diameter circular regions of interest (ROIs) devoid of large blood vessels

Summary

Introduction

While many cancers have decreased in incidence over the last more than two decades, primary liver cancer has increased, tripling in the United States since 1980 and rising on average ∼2% per year for much of this time period (an estimated 42,230 new United States cases in 2021 and worldwide are 20fold greater) (Siegel et al, 2021) This rise has been primarily attributed to obesity, metabolic syndrome, and diabetes, with non-alcoholic fatty liver disease (NAFLD) rapidly replacing viral- and alcohol-related factors as a leading promoter of hepatocellular carcinoma (HCC, the most common primary liver cancer) NAFLD is characterized by an influx of free fatty acids and accumulation of triglycerides in hepatocytes resulting in a lipotoxic environment (Kaufmann et al, 2021) This lipotoxic environment promotes hepatocytes to release reactive oxygen species (ROS) and fibrogenic mediators, which induce hepatic satellite stem cells and stimulate fibrogenic expressions of myofibroblasts (Zhou et al, 2015). The consequence of this evolving disease environment is that the management of HCC continues to be a formidable challenge (Masuzaki et al, 2016; Geh et al, 2021)

Methods

Results

Conclusion