Methodology for Jointly Assessing Myocardial Infarct Extent and Regional Contraction in 3-D CMRI

TL;DR

This paper introduces an automated method to analyze 3D cardiac MRI data, jointly assessing myocardial infarct extent and regional contraction, providing insights into their relationship in myocardial infarction patients.

Contribution

It presents a novel automated post-processing procedure combining Cine and DE MRI analysis to quantify infarct extent and regional contraction, including a new index ATR.

Findings

MIE correlates with wall motion abnormality severity

ATR decreases significantly in infarcted regions

Method applied successfully to 10 patients

Abstract

Automated extraction of quantitative parameters from Cardiac Magnetic Resonance Images (CMRI) is crucial for the management of patients with myocardial infarct. This work proposes a post-processing procedure to jointly analyze Cine and Delayed-Enhanced (DE) acquisitions in order to provide an automatic quantification of myocardial contraction and enhancement parameters and a study of their relationship. For that purpose, the following processes are performed: 1) DE/Cine temporal synchronization and 3D scan alignment, 2) 3D DE/Cine rigid registration in a region about the heart, 3) segmentation of the myocardium on Cine MRI and superimposition of the epicardial and endocardial contours on the DE images, 4) quantification of the Myocardial Infarct Extent (MIE), 5) study of the regional contractile function using a new index, the Amplitude to Time Ratio (ATR). The whole procedure was applied to 10 patients with clinically proven myocardial infarction. The comparison between the MIE and the visually assessed regional function scores demonstrated that the MIE is highly related to the severity of the wall motion abnormality. In addition, it was shown that the newly developed regional myocardial contraction parameter (ATR) decreases significantly in delayed enhanced regions. This largely automated approach enables a combined study of regional MIE and left ventricular function.