# Evaluation of dyssynchrony in children with dilated cardiomyopathy: a comparison of electrical and mechanical delay using Doppler, tissue imaging and strain

**Authors:** Fariba Rashidi Ghader, Mohammad Mahdavi, Hossein Mehrali, Mohammad Dalili, Hossein Shahzadi, Reza Abbaszade

PMC · DOI: 10.1186/s43044-025-00633-3 · The Egyptian Heart Journal · 2025-04-16

## TL;DR

This study examines how heart muscle disease in children causes uneven heart contractions and finds that even those with normal electrical signals can have mechanical delays.

## Contribution

The study reveals that mechanical dyssynchrony in children with dilated cardiomyopathy is common even when electrical signals appear normal.

## Key findings

- 86.5% of DCM patients showed intra-ventricular dyssynchrony, regardless of QRS width.
- Nearly half of patients with normal PR intervals still exhibited AV dyssynchrony.
- Mortality and disease severity correlated with the severity of dyssynchrony types.

## Abstract

Dilated cardiomyopathy (DCM) is a primary myocardial disease characterized by systolic dysfunction, which can lead to disparity and disorganized contraction, commonly referred to as dyssynchrony. Three types of dyssynchrony include atrioventricular (AVD), interventricular (inter-VD), and intra-LV dyssynchrony (intra-VD). We aimed to investigate the prevalence and interdependence of electrical and mechanical dyssynchrony in order to elucidate the optimizing patients for cardiac resynchronization therapy (CRT).

A total of 37 DCM patients (1–17 years, 51% female) were included in this cross-sectional study. Regarding the intra-VD, inter-VD, and AVD, the study showed inter-VD in 37%, 27%, and 48% by Doppler, Doppler tissue imaging (DTI), and color-coded DTI methods, respectively; however, 70% showed right ventricular free wall delay based on the presence of peak of strain after pulmonic valve closure. 86.5% (32/37) of patients show intra-VD. 100% (8/8) of DCM patients with prolonged QRS (QRSc ≥ 120 ms) had intra-VD, of which 12.5% (1/8) had mild, 25% (2/8) mod, and 62.5% (5/8) severe dyssynchrony. However, 82% (24/29) of patients with narrow QRS (QRSc < 120 ms) also had intra-VD, of which 17% (3/24) were mild, 62.5% (15/24) mod, and 25% (6/24) severe. There were 57% (21/37) of patients with AVD. 77% (10/13) of DCM patients with prolonged PRc (PR ≥ 200 ms) had AVD of which 31% (4/13) of patients had mild, 31% (4/13) mod, and 15% (2/13) severe AVD, while among PRc < 200 ms 46% (11/24) had AVD, of which 37.5% (9/24) had mild AVD, 4% (1/24) mod, and another 4% severe AVD. LVEF was lower and LV GLS, mortality, Pro-BNP, NYHA FC, and severity of intra-VD were higher in the group with QRS ≥ 120 ms, and PR ≥ 200 ms. 27% of patients were expired during the year of study. There was a significant direct correlation between mortality rate, NYHA FC, and pro-BNP with the severity of intra-, inter-VD, and AVD. The most delayed horizontal segments were inferolateral, anterolateral, anterior, and anteroseptal sequentially, while the highest level of vertical dyssynchrony (base to apex) was observed in inferoseptal, inferolateral, and anteroseptal walls in order.

Our findings indicated that DCM causes both intra- and inter-VD, associated with QRS duration concerning severity, which also results in AVD that are correlated with PRc interval. Notably, a substantial proportion of patients with narrow QRSc also demonstrated intra-VD and inter-VD, while nearly half of those with normal PRc exhibited AVD. Collectively, these observations suggest a lack of complete correspondence between electrical and mechanical dyssynchrony.

## Linked entities

- **Diseases:** dilated cardiomyopathy (MONDO:0005021)

## Full-text entities

- **Genes:** NPPB (natriuretic peptide B) [NCBI Gene 4879] {aka BNP, Iso-ANP}
- **Diseases:** myocardial disease (MESH:D004194), DCM (MESH:D002311), systolic dysfunction (MESH:D006331)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Full text

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## Figures

8 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12003232/full.md

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Source: https://tomesphere.com/paper/PMC12003232