Abstract 14476: Automatic Radiomics-Based Assessment of Myocardial Texture in Transthyretin Cardiac Amyloidosis: A 2D Echocardiographic Study

Introduction: Myocardial i nfiltration with amyloid fibrils increases myocardial echogenicity on echocardiography (echo). Increased echogenicity has been challenging to quantify. Radiomics methods may better detect changes in echogenicity than the human eye. Our objectives were (1) to detect an altered myocardial echogenicity in transthyretin cardiac amyloidosis (ATTR-CM) using radiomics analysis and (2) to compare myocardial echogenicity by radiomics to human interpretation. Methods: We evaluated echo images of 515 patients with suspected ATTR-CM referred for an 99m-technetium pyrophosphate scan at 3 major amyloidosis centers. Myocardial echogenicity was assessed at the basal interventricular septum using an open-source radiomics platform (LIFEx) to extract 41 texture-based features. The texture features were processed using a cloud platform (BigML), which performed automated model selection and hyperparameter tuning (Figure). The studies were randomly split into training (80%) and evaluation (20%) sets. Two echo and amyloidosis experts visually evaluated myocardial echogencity on 80 random studies and classified them into ATTR-CM or non- ATTR-CM. Results: In this cohort, 57% of patients were diagnosed with ATTR-CM. The best radiomics model was a decision forest with bootstrapping, with an AUC of 0.79 (95% CI: 0.70-0.88) for diagnosing ATTR-CM. By contrast, visual classification of echo texture as ATTR-CM or not was poor; the interobserver agreement for assessing a septal ROI for altered myocardial echogenicity consistent with ATTR-CM was a kappa of 0.29 and using the entire apical 4 chamber view 0.44. Given the poor agreement an AUC could not be calculated. Conclusions: We have validated the use of a radiomics approach to evaluate myocardial echogenicity in ATTR-CMP. This work lays the foundation to evaluate changes in myocardial texture using echo to raise the suspicion of cardiac amyloidosis and assess changes following targeted TTR therapies.