High-Throughput Precision Phenotyping of Left Ventricular Hypertrophy With Cardiovascular Deep Learning
Grant Duffy1, Paul P Cheng2, Neal Yuan1
1Department of Cardiology, Smidt Heart Institute, Cedars-Sinai Medical Center, Los Angeles, California.
JAMA Cardiology
|February 23, 2022
Summary
A deep learning model accurately measures left ventricular wall thickness and differentiates causes like hypertrophic cardiomyopathy and cardiac amyloidosis. This automated approach offers precise, reproducible cardiac hypertrophy diagnosis.
Area of Science:
- Cardiology
- Artificial Intelligence
- Medical Imaging
Background:
- Early detection of increased left ventricular (LV) wall thickness is crucial but challenged by under-recognition, measurement errors, and difficulty distinguishing causes.
- Conditions like hypertrophic cardiomyopathy and cardiac amyloidosis require accurate differentiation for effective patient management.
Purpose of the Study:
- To evaluate the accuracy of a deep learning (DL) workflow in quantifying ventricular hypertrophy.
- To assess the DL model's ability to predict the causes of increased LV wall thickness, specifically hypertrophic cardiomyopathy and cardiac amyloidosis.
Main Methods:
- A cohort study utilizing physician-curated data from specialized cardiac clinics (Stanford and Cedars-Sinai) between 2008 and 2020.
- A DL algorithm trained and validated on retrospective echocardiogram videos from multiple healthcare systems, including independent external datasets.
- Analysis focused on the DL model's accuracy in measuring LV dimensions and classifying specific causes of hypertrophy.
Main Results:
- The DL algorithm demonstrated high accuracy in measuring intraventricular wall thickness (MAE 1.2 mm) and LV diameter (MAE 2.4 mm).
- It accurately classified cardiac amyloidosis (AUC 0.83) and hypertrophic cardiomyopathy (AUC 0.98) in the primary cohort.
- External validation confirmed accurate quantification of ventricular parameters (R2 0.96 domestic, R2 0.90 international) and detection of hypertrophic cardiomyopathy (AUC 0.89) and cardiac amyloidosis (AUC 0.79).
Conclusions:
- The DL model accurately identifies subtle LV wall geometric changes and differentiates causes of hypertrophy.
- The fully automated DL workflow provides reproducible, precise measurements, surpassing human expert variability.
- This technology may form the basis for a precision diagnostic approach to cardiac hypertrophy.


