# Characterisation of interrelations among myocardial work parameters in patients with hypertrophic cardiomyopathy: differences between non-obstructive and obstructive disease

**Authors:** Viktória Nagy, Gergely Rácz, Krisztina Boda, Hedvig Takács, Bianka Polestyuk, Noémi Schvartz, László Dániel Vidács, Jenő Antal Pintér, Attila Pálinkás, Árpád Kormányos, Tamás Szűcsborus, János Borbás, Tamás Szili-Török, Róbert Sepp

PMC · DOI: 10.3389/fcvm.2025.1670503 · Frontiers in Cardiovascular Medicine · 2026-02-11

## TL;DR

This study examines how different myocardial work parameters relate to each other in patients with hypertrophic cardiomyopathy, comparing non-obstructive and obstructive cases.

## Contribution

The study characterizes interrelations among myocardial work parameters and highlights their differences in non-obstructive and obstructive HCM.

## Key findings

- GLS strongly correlates with GWI and GCW but weakly with GWW in HCM patients.
- GWW increases with higher LVOT gradients and remains significantly different from controls even at low gradients.
- GWW is more independent from GLS compared to GWI/GCW, suggesting unique value in assessing HCM.

## Abstract

In recent years, novel echocardiographic parameters, known as myocardial work (MW) parameters, have been introduced into clinical practice for the assessment of contractile function. This study aimed to provide a technical characterization of the interrelations among these MW parameters and evaluate their differences between patients with non-obstructive (nHCM) and obstructive hypertrophic cardiomyopathy (oHCM).

One-hundred-eighteen patients with HCM, including 68 nHCM and 50 oHCM patients were assessed. Global longitudinal strain (GLS) and derived global MW parameters—including global work index (GWI), global constructive work (GCW), global wasted work (GWW), and global work efficiency (GWE)—were determined by 2D-speckle tracking echocardiography.

In all HCM cohorts, GLS demonstrated a strong, significant correlation with GWI and GCW (r: −0.619 to −0.818), whereas the correlation between GLS and GWW was considerably weaker (r: 0.320 to 0.373), consistent in both univariate correlation and multiple regression analyses. A strong, significant correlation was observed between GWI and GCW, and a significant correlation existed between GWW and GWE. Within HCM subgroups characterized by increasing left ventricular outflow tract (LVOT) gradients, GWI/GCW values exhibited “pseudonormalization” in the obstructive HCM groups, due to the offsetting effects of the nominal decrease in GLS and the nominal increase in LVOT gradient. In contrast, GWW values increased gradually with increasing LVOT gradients, and the difference compared to controls was significant even in the HCM group with LVOT gradients <10 mmHg.

Given the strong correlation between GLS and GWI/GCW, it is probable that changes in GLS would result in corresponding changes in GWI/GCW, potentially limiting the incremental discriminatory value of these parameters beyond GLS. GWW appears to be the most independent MW parameter from GLS in patients with hypertrophic cardiomyopathy as it weakly correlates with GLS, unlike GWI/GCW.

## Linked entities

- **Diseases:** hypertrophic cardiomyopathy (MONDO:0005045), obstructive hypertrophic cardiomyopathy (MONDO:0005045)

## Full-text entities

- **Genes:** MYH14 (myosin heavy chain 14) [NCBI Gene 79784] {aka DFNA4, DFNA4A, FP17425, MHC16, MYH17, NMHC II-C}
- **Diseases:** small vessel disease (MESH:D059345), HCM (MESH:D000092183), obstructive (MESH:D000402), non (MESH:C580335), mitral regurgitation (MESH:D008944), heart failure (MESH:D006333), ATTR amyloidosis (MESH:D000686), LVP (MESH:D018487), heart muscle disease (MESH:D006331), sudden cardiac death (MESH:D016757), CAD (MESH:D003324), cerebrovascular accidents (MESH:D020521), HCM (MESH:D002312), cardiomyopathies (MESH:D009202), myocardial hypertrophy (MESH:D006984), diabetes mellitus (MESH:D003920), valvular heart disease (MESH:D006349), myocardial ischemia (MESH:D017202), ischemic (MESH:D002545), atrial fibrillation (MESH:D001281), dilated cardiomyopathy (MESH:D002311), SCD (MESH:C536778), myocardial infarctions (MESH:D009203), TS (MESH:D005879), Conduction abnormalities (MESH:D054537), chronic kidney disease (MESH:D051436), discoordination (MESH:C562757), Fabry disease (MESH:D000795), fibrosis (MESH:D005355), death (MESH:D003643), LVOT (MESH:D000092242), Hypertension (MESH:D006973), non-obstructive and obstructive disease (MESH:D001157), LV hypertrophy (MESH:D017379)
- **Chemicals:** gadolinium (MESH:D005682), mavacamten (MESH:C000605992)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Full text

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## Figures

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## References

32 references — full list in the complete paper: https://tomesphere.com/paper/PMC12932468/full.md

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Source: https://tomesphere.com/paper/PMC12932468