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Updated: Sep 26, 2026

Magnetic Resonance Derived Myocardial Strain Assessment Using Feature Tracking
Published on: February 12, 2011
Strain Rate Angle Distribution as an Indicator of Post-Infarct Myocardial Remodeling: Proof-of-Concept of a Novel
Lasse Totland1,2,3, Bård A Bendiksen1,4, Einar S Nordén1,4
1Institute for Experimental Medical Research, University of Oslo and Oslo University Hospital, Oslo, Norway.
Purpose:
Left ventricular (LV) strain is an early indicator of myocardial dysfunction. However, conventional strain metrics do not fully account for the multidirectional nature of myocardial deformation. The strain rate tensor, derived from velocity-encoded MRI, represents the time-resolved magnitude and direction of strain rate without the geometrical limitations of conventional methods. The purpose of this study was to demonstrate practical uses of strain rate tensor imaging for in vivo assessment of LV remodeling in a rat model of myocardial infarction (MI).
Methods:
A post-processing framework was developed to convert tissue phase mapping (TPM) MRI velocity data into strain rate tensor fields. TPM was performed at 1, 3, 10, ≈21, and ≈42 days post-MI in six rats. Six sham-operated rats served as controls. Global and regional strain rate and strain, as well as the strain rate angle distribution, were assessed.
Results:
The dispersion in systolic and early diastolic strain rate angles was approximately 50% higher in MI hearts compared with sham (p = 0.001 and p = 0.014). Increased dispersion showed intra-individual correlation with decreased circumferential and radial strain rate magnitude in early diastole (p = 0.010 and p = 0.005). Global and regional strain rate and strain measurements were comparable with literature. Inter-study variability of the method was assessed and reported.
Conclusion:
Strain rate tensor field imaging based on TPM MRI can be utilized to quantify myocardial dysfunction in vivo. Analysis of strain rate angle dispersion indicates that the loss of uniformity in the direction of deformation is a key component of reduced myocardial contractility after remodeling.
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