# Longitudinal Displacement vs. Strain in Cardiac Amyloidosis: A Speckle Tracking Echocardiography Study

**Authors:** Marina Leitman, Vladimir Tyomkin, Shmuel Fuchs

PMC · DOI: 10.3390/jcm15041544 · 2026-02-15

## TL;DR

This study compares longitudinal displacement and strain in cardiac amyloidosis patients and controls, showing that displacement offers additional diagnostic insights.

## Contribution

The study introduces longitudinal displacement as a complementary measure to strain in diagnosing cardiac amyloidosis.

## Key findings

- Both global longitudinal strain and displacement were significantly reduced in amyloidosis patients compared to controls.
- Amyloidosis showed pronounced basal displacement impairment and modest apical motion reduction, indicating relative apical sparing.
- Longitudinal displacement correlated with diastolic burden and heart-failure status, with strong reproducibility.

## Abstract

Background: Longitudinal strain is central to the echocardiographic diagnosis of cardiac amyloidosis, typically showing reduced global values with relative apical sparing. Longitudinal displacement—an absolute measure of myocardial motion—may provide complementary diagnostic and physiological information. Methods: We retrospectively studied 24 patients with cardiac amyloidosis and 24 age-, sex-, rhythm-, and ejection fraction–matched controls. Global and regional longitudinal strain and displacement were calculated. Diagnostic performance was evaluated using receiver-operating characteristic (ROC) analysis, and reproducibility was assessed using intraclass correlation coefficients (ICC), coefficient of variation (CV), and Bland–Altman analysis. Results: In amyloidosis, both global longitudinal strain (GLS) and global longitudinal displacement (GLD) were significantly reduced compared with controls (GLS: −10.2 ± 2.6% vs. −20.1 ± 2.4%, p < 0.0001; GLD: 6.6 ± 1.9 mm vs. 11.9 ± 1.4 mm, p < 0.0001). Amyloidosis was characterized by pronounced impairment of basal displacement (9.0 ± 4.4 vs. 17.0 ± 3.9 mm, p < 0.0001) and only modest reduction in absolute apical motion (3.0 ± 2.4 vs. 5.0 ± 2.3 mm, p < 0.0001), supporting the concept that apical sparing observed on strain reflects relative rather than absolute preservation of function. ROC analysis demonstrated strong discriminatory performance within this cohort for GLD (cutoff 8.8 mm), basal displacement (~13 mm), and GLS (absolute 15.8%), with areas under the curve approaching 1.0. GLD and GLS correlated with indices of diastolic burden and functional status (E/E′ and NYHA; |r| ≈ 0.32–0.41, all p ≤ 0.03). Reproducibility was good to excellent (ICC ≈ 0.84–0.89; CV 6–8%). Conclusions: Longitudinal displacement provides complementary and reproducible information alongside strain in cardiac amyloidosis. Combined assessment—reduced global or basal displacement together with reduced GLS and/or relative apical sparing—may refine the echocardiographic characterization of amyloid cardiomyopathy and link longitudinal mechanics to diastolic dysfunction and heart-failure burden.

## Full-text entities

- **Genes:** TTR (transthyretin) [NCBI Gene 7276] {aka AMYLD1, ATTR, CTS, CTS1, HEL111, HsT2651}
- **Diseases:** chronic kidney disease (MESH:D051436), GLD (MESH:D001037), output (MESH:D002303), concentric hypertrophy (MESH:D006984), Atrial fibrillation (MESH:D001281), AL (MESH:D009101), right ventricular dysfunction (MESH:D018497), reduced stroke volume and (MESH:D001523), basal hypokinesia (MESH:D018476), strain (MESH:D000080822), End-systole (MESH:D003643), left ventricular hypertrophy (MESH:D017379), hypertensive heart disease (MESH:D006973), injury to (MESH:D014947), systole (MESH:D000092244), Transthyretin cardiac amyloidosis (MESH:C567782), pericardial effusions (MESH:D010490), ventricular (MESH:D014693), mechanical impairment (MESH:D041781), cardiac (MESH:D006331), Strain (MESH:D013180), amyloid (MESH:C000718787), left ventricle (MESH:D020257), hypertrophic (MESH:D002312), amyloid cardiomyopathy (MESH:D009202), aortic stenosis (MESH:D001024), heart-failure (MESH:D006333), Amyloidosis (MESH:D000686), LV (MESH:D018487), Light-chain amyloidosis (MESH:D000075363)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Figures

6 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12941586/full.md

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Source: https://tomesphere.com/paper/PMC12941586