Childhood Myopericarditis Leaves Subtle Heart Strain Scars Years Later

Children and teenagers who recover from myopericarditis—an inflammatory condition that strikes both the heart muscle and the surrounding pericardial sac—may carry hidden traces of the illness long after their conventional heart tests look normal. A new study from Türkiye followed 30 pediatric patients for an average of nearly three years after their acute episode and found that, although standard echocardiographic measures of pumping function were largely preserved, a more sensitive imaging technique revealed measurable abnormalities in how the heart muscle deforms with each beat. The findings, published in Frontiers in Cardiovascular Medicine, suggest that speckle-tracking echocardiography can detect subtle mechanical changes that conventional assessments miss.

The research team, led by Sule Arici of Kosuyolu Yuksek Ihtisas Training and Research Hospital in Istanbul, together with colleagues from Marmara University and Ankara Etlik Integrated Health Campus, enrolled 30 patients aged 9 to 17 years who had been diagnosed with isolated myopericarditis by a pediatric cardiology team. Diagnosis rested on a combination of sharp chest pain consistent with pericardial inflammation, elevated cardiac troponin T indicating myocardial injury, and generally preserved left ventricular systolic function on conventional echocardiography. Twenty-two age- and sex-matched healthy children served as controls. Acute-phase clinical, laboratory, electrocardiographic, and echocardiographic data were collected retrospectively from medical records, while the long-term cardiac evaluation—including tissue Doppler imaging and speckle-tracking strain analysis—was performed prospectively at follow-up.

During the acute illness, chest pain was nearly universal, affecting 29 of the 30 patients, and 28 required hospitalization. Every patient had elevated troponin T levels confirming myocardial injury. Electrocardiographic abnormalities appeared in 18 patients, most commonly ST-segment elevation, and these changes normalized within an average of about three and a half days. At the time of diagnosis, conventional echocardiography showed largely preserved left ventricular systolic function, with a mean ejection fraction of 68.57 percent and a mean fractional shortening of 38.03 percent. Pericardial effusion was detected in only one patient, underscoring that visible fluid accumulation is not a prerequisite for the clinical diagnosis.

At the long-term follow-up visit, conducted at a mean of 32.8 months after diagnosis, the conventional picture remained largely reassuring, yet the strain data told a different story. Global longitudinal strain—a measure of how much the heart muscle shortens along its length during contraction—was significantly reduced in patients compared with controls: −12.43 percent versus −17.77 percent, a difference that was highly statistically significant. Global circumferential strain, which captures shortening around the heart’s circumference, was also markedly lower in patients, at −16.04 percent versus −25.14 percent. Because strain values are expressed as negative numbers, less negative values indicate weaker deformation. Segmental analyses showed that longitudinal strain was impaired across all three apical imaging views, while circumferential strain was significantly reduced at the apical and basal levels of the short-axis views, though not at the mid-ventricular level.

The study also measured time-to-peak strain dispersion, which reflects how synchronously different regions of the heart muscle reach their maximum contraction. Patients showed significantly increased dispersion in several circumferential segments—at the apical, mid, and basal levels—and in the apical 3-chamber longitudinal view, suggesting greater heterogeneity in contraction timing. The authors note that circumferential fibers reside predominantly in the mid-wall layers, so impairment in circumferential deformation may point to more diffuse myocardial involvement or structural alterations that persist after the inflammatory episode. Whether these changes relate to fibrosis or other post-inflammatory tissue changes remains uncertain, because cardiac magnetic resonance imaging was not systematically performed and its timing varied widely across patients.

Body size emerged as a potential confounder, since patients were significantly heavier and had larger body surface areas than controls. To address this, the researchers fitted analysis of covariance models adjusting for body surface area across the four principal global deformation measures. The between-group differences remained statistically significant after adjustment: the adjusted mean difference was +4.17 for global longitudinal strain, +7.39 for global circumferential strain, and similar magnitudes for the software-derived supportive measures. Sensitivity analyses using body weight instead of body surface area, additional adjustment for age and sex, and robust regression and bootstrap methods all confirmed the same pattern. After applying a Holm correction for multiple comparisons across the four global outcomes, all differences remained significant, with a maximum adjusted p value of 0.027.

Perhaps the most intriguing findings came from exploratory correlation analyses linking acute-phase biomarkers to long-term echocardiographic parameters. Higher neutrophil-to-lymphocyte ratio—a simple blood count-derived marker of systemic inflammation—was positively correlated with global longitudinal strain values (r = 0.437), meaning patients with higher ratios had less negative, that is, more impaired, longitudinal deformation. The systemic immune-inflammation index showed a similar association (r = 0.456). Meanwhile, C-reactive protein levels from the acute phase correlated positively with global circumferential strain (r = 0.406), again indicating that greater inflammatory activity was associated with worse circumferential deformation years later. CRP was also negatively correlated with deceleration time, a diastolic filling measure. The authors emphasize that these correlations are hypothesis-generating; because the biomarker data were collected retrospectively and multiple comparisons were made, the possibility of chance findings cannot be excluded, and the study cannot determine whether the relationship is causal.

Tissue Doppler imaging added further nuance. At follow-up, patients showed significantly higher early and late diastolic myocardial velocities (E′ and A′) than controls, along with higher corresponding z-scores. The authors interpret these findings as possible adaptive or compensatory changes following the acute inflammatory process rather than overt diastolic dysfunction, noting that the E′/A′ ratio and the myocardial performance index did not differ significantly between groups. Conventional systolic measures told a more complicated story: fractional shortening and ejection fraction were actually significantly lower in patients than controls at follow-up (35.10 percent versus 39.55 percent, and 64.53 percent versus 70.32 percent, respectively), though the authors characterize conventional systolic function as largely preserved, and left atrial z-score was higher while deceleration time z-score was lower in patients.

A methodological caveat deserves attention. The speckle-tracking software automatically generated bi-plane ejection fraction values that were strikingly low in both patients and controls—around 40 percent in patients and 45 percent in controls. The authors explicitly caution that these software-derived values depend on the specific endocardial tracking and volumetric calculations of the aCMQ workflow and should not be interpreted according to conventional clinical ejection fraction thresholds. The fact that similarly low values appeared in healthy controls argues against reading them as evidence of severe systolic dysfunction. This distinction matters because strain imaging studies are increasingly used to detect subclinical abnormalities precisely when conventional measures appear normal, and conflating software outputs with clinical measurements could lead to misinterpretation.

The study has clear limitations. It was single-center with a small sample, speckle-tracking was not available during the acute phase so temporal changes could not be tracked, cardiac magnetic resonance was performed in only 21 patients with heterogeneous timing, and reproducibility analyses of the strain measurements were not available. The authors also note that clinical outcomes, exercise capacity, and arrhythmia-related endpoints were not assessed, so the clinical significance of the statistical differences remains uncertain. Still, the work adds to a growing body of evidence that advanced deformation imaging can reveal persistent mechanical alterations after pediatric inflammatory heart disease even when standard tests appear reassuring. Larger prospective studies with serial multimodality imaging will be needed to confirm these associations, clarify their temporal evolution, and determine whether children with these subtle strain abnormalities face any meaningful long-term risk.

Subject of Research: Long-term speckle-tracking echocardiographic detection of subclinical myocardial deformation abnormalities in pediatric myopericarditis survivors and their associations with acute-phase inflammatory biomarkers

Article Title: Long-term myocardial deformation abnormalities and biomarker associations in pediatric myopericarditis: a speckle-tracking echocardiographic study

Article References: Arici, S., Karagozlu, S., Erolu Kibris, E., & Akalın, F. (2026). Long-term myocardial deformation abnormalities and biomarker associations in pediatric myopericarditis: a speckle-tracking echocardiographic study. Frontiers in Cardiovascular Medicine, 13, Article 1938858. https://doi.org/10.3389/fcvm.2026.1938858

Image Credits: AI Generated

DOI: 10.3389/fcvm.2026.1938858

Keywords: myopericarditis, pediatric cardiology, speckle-tracking echocardiography, myocardial strain, global longitudinal strain, global circumferential strain, inflammation biomarkers, neutrophil-to-lymphocyte ratio, C-reactive protein, tissue Doppler imaging, left ventricular function, cardiac follow-up