Left Atrial Strain Tracks Recovery in Children with Dilated Cardiomyopathy

Children with dilated cardiomyopathy (DCM) show measurable impairment of left atrial function long before their atria enlarge, and much of that impairment eases with sustained medical therapy, according to a retrospective single-center study published in Echo Research & Practice. Researchers at Children’s Hospital of Soochow University used two-dimensional speckle-tracking echocardiography (2D-STE) to track left atrial strain in 33 children treated for more than one year, and found that reservoir strain and conduit strain, both depressed at diagnosis, rose significantly between one year and more than two years of follow-up. Notably, conduit strain remained depressed even in children whose left ventricular ejection fraction had returned to normal, suggesting it may be a sensitive marker of lingering atrial dysfunction.

Dilated cardiomyopathy is the most common subtype of pediatric cardiomyopathy and carries a grim outlook. The authors cite estimates placing the annual incidence of DCM at 5 to 8 cases per 100,000 people, a figure thought to be an underestimate due to incomplete ascertainment. In the United States, Finland, and Australia, the overall incidence of primary cardiomyopathies among children under 20 has been reported at roughly 1 in 100,000 per year, with a peak among children aged two or younger. In China, a 12-year multicenter study across 33 hospitals found that children hospitalized with primary cardiomyopathy accounted for 0.079% of all pediatric inpatient admissions, with DCM the most prevalent subtype at 32.95%, and annual hospitalizations rising yearly. Nearly 40% of children diagnosed with pediatric DCM undergo heart transplantation or die within two years of diagnosis.

The left atrium performs three distinct jobs across the cardiac cycle: it serves as a reservoir that fills during ventricular systole, a conduit that passively transfers blood to the left ventricle in early diastole, and a contractile pump that boosts filling in late diastole. Because left atrial function closely reflects both diastolic and systolic performance of the left ventricle, it has been considered a biomarker for adverse cardiovascular events in heart failure with preserved ejection fraction. Assessing it in children, however, remains difficult; parameters derived from adult studies may be insufficiently sensitive in pediatric populations, and diastolic function is notoriously hard to measure accurately in early-stage disease.

2D-STE offers a way around some of these obstacles. The technique tracks the motion of natural acoustic markers, or speckles, within the myocardium throughout the cardiac cycle, yielding measurements of myocardial velocity, displacement, and strain. It is load- and morphology-independent and unaffected by sampling angle, and atrial strain evaluation with 2D-STE has been validated in both adults and children. The authors also note that left atrial strain is easy to perform, highly reproducible, and has shown good invasive correlation with catheter-measured left ventricular end-diastolic pressure in prior pediatric work.

The study retrospectively reviewed children diagnosed with DCM at Children’s Hospital of Soochow University between January 2018 and January 2021 who received standardized medical treatment for more than one year. DCM was defined as a left ventricular end-diastolic dimension Z score above 2, an ejection fraction below 55%, and fractional shortening below 28%. Of 37 hospitalized patients initially identified, four were excluded for lacking or receiving less than one year of treatment, leaving 33 children: 19 with isolated DCM and 14 with DCM associated with left ventricular hypertrabeculation, a phenotype diagnosed by the echocardiographic criteria of Jenni and colleagues, including a two-layered myocardium with a non-compacted to compacted wall thickness ratio exceeding 2:1 at end-systole.

The cohort was young and evenly split by sex, with 16 boys and 17 girls, a median age of 14 months at baseline (range 7 to 48 months), and a median treatment duration of 26 months. Genetic testing attributed the disease to genetic causes in 10 children (30.3%), inflammation in 4 (12.1%), autoimmunity in 1 (3.0%), and left it unknown in 18 (54.5%). No deaths occurred during the study period. Two separate control groups of 30 healthy children each were established, matched to the patients’ condition at baseline and at the later follow-up, because age, body surface area, BMI, and sex differed substantially between those two patient groups.

Imaging followed American Society of Echocardiography and European Association of Cardiovascular Imaging guidelines on a Philips EPIQ-7 C system. Left atrial strain was measured with automated offline speckle-tracking software, producing reservoir strain (LASr), conduit strain (LAScd), and contraction strain (LASct), with manual border editing when automatic tracking was inaccurate. Tissue mitral annular displacement (TMAD) was also assessed. Two sonographers with 10 and 12 years of experience performed all analyses, recording the mean of three readings, and Bland-Altman analysis deemed repeatability of LASr and LAScd favorable.

The results painted a consistent picture. At baseline, compared with matched controls, the patients had significantly lower ejection fraction, fractional shortening, LASr, and LAScd, along with higher interventricular septal and left ventricular dimension Z scores, while LASct and left atrial size showed no significant differences, indicating that reservoir and conduit functions were impaired before treatment while contraction function and atrial size were preserved. Across follow-up, ejection fraction, fractional shortening, LASr, and LAScd rose significantly between Period 1 (one year) and Period 2 (more than two years). By Period 2, ejection fraction had normalized in 26 of 33 patients, yet in those children LAScd averaged −29.83 ± 9.33, below a published normal reference of 32.8% (95% CI 27.8–37.8%) for conduit strain, and LASr no longer differed significantly from controls. Among the seven patients whose ejection fraction remained low, five had genetic etiology. Correlation analyses linked LASr and LAScd with ejection fraction, fractional shortening, wall thickness and chamber dimension Z scores, and diastolic indices, and patients with LV hypertrabeculation showed significantly higher baseline ejection fraction, fractional shortening, LASr, and LAScd than those with isolated DCM.

The authors interpret these findings through the lens of atrial remodeling. In DCM, extensive myocardial degeneration and interstitial fibrosis, elevated left ventricular volume and pressure loads, and hindered early-diastolic emptying combine to enlarge and stiffen the left atrium, degrading conduit and eventually reservoir function. Standard heart failure medications, including ACE inhibitors, beta-blockers, diuretics, positive inotropes, and metabolic modulators, can reverse remodeling and reduce volume load, which the authors propose explains the strain improvements. Yet because long-term atrial remodeling involving cellular hypertrophy, collagen turnover, and signaling changes is often irreversible, strain values remained below healthy norms despite treatment. TMAD, by contrast, showed no significant differences between patients and controls at any comparison, which the authors attribute to reduced longitudinal myocardial motion in DCM and TMAD’s load dependence.

The study has clear limitations the authors themselves flag: it was single-center and retrospective, the cohort was small, follow-up was short, standard four-chamber views differed subtly from left-atrium-focused views, updated hypertrabeculation criteria created discontinuity, and the impact of different drug combinations and doses could not be addressed. Within those constraints, the conclusion is measured: after long-term standardized medication, children with DCM showed significant improvements in left atrial reservoir and conduit function, and LAScd, which remained a sensitive indicator even in stratified analyses and in patients with normalized ejection fraction, carries potential as a practical imaging marker for monitoring left atrial function in pediatric DCM. Larger prospective studies with long-term follow-up will be needed to confirm it.

Subject of Research: Left atrial strain measured by two-dimensional speckle-tracking echocardiography in pediatric dilated cardiomyopathy

Article Title: Left atrial strain on 2D-STE in pediatric dilated cardiomyopathy

Article References: Wu, Y., Xu, Q.-Q., Liu, W., Hou, C., Wang, H., Shen, J., Sun, Y.-W., Gu, P.-P., Si, X.-Y., Lv, H.-T., Sun, L., & Ding, Y.-Y. (2026). Left atrial strain on 2D-STE in pediatric dilated cardiomyopathy. Echo Research & Practice, 13(1), Article 24. https://doi.org/10.1186/s44156-026-00126-2

Image Credits: AI Generated

DOI: 10.1186/s44156-026-00126-2

Keywords: dilated cardiomyopathy, pediatric cardiology, left atrial strain, speckle-tracking echocardiography, conduit strain, reservoir strain, echocardiography, heart failure, LV hypertrabeculation, TMAD, remodeling, Left