Accelerated epigenetic ageing in moderate and complex congenital heart disease
In this abstract, adults with moderate or complex congenital heart disease showed accelerated epigenetic ageing on some clocks compared with matched healthy controls, while those with simple disease did not. [1]
Automatic summary · not editorially reviewed
The key findings
The study included 120 adults with congenital heart disease aged 29–50 years and 120 age- and sex-matched healthy controls. [1]
Patients with moderate and complex disease showed PhenoAge acceleration of +3.0 years (P = .019) and +5.5 years versus controls. [1]
Individuals with simple congenital heart disease showed ageing patterns comparable to healthy peers. [1]
The source at a glance
- Study type / format
- Case-control study (abstract)
- Population / context
- Adults aged 29–50 years with congenital heart disease and age- and sex-matched healthy controls.
- Summary based on
- Study abstract
- Original publication
- June 11, 2026
Epigenetic clocks in 120 adults with congenital heart disease
The study asked whether adults with congenital heart disease show accelerated epigenetic ageing and whether the degree of acceleration relates to disease complexity. Epigenetic clocks estimate biological age from DNA methylation profiles. The abstract reports 120 patients aged 29–50 years (58 female) and 120 age- and sex-matched healthy controls. Patients were split into simple, moderate and complex complexity groups of 40 each. Ageing was estimated with the Horvath, Hannum, Zhang, GrimAge2 and PhenoAge clocks, and pace of ageing with DunedinPACE.
Supporting source [1]
PhenoAge acceleration in moderate and complex disease
Compared with healthy controls, patients with moderate and complex congenital heart disease showed significant age acceleration with PhenoAge: +3.0 years (P = .019) in the moderate group and +5.5 years in the complex group. The abstract's text is cut off at this point, so the P value for the complex group and results for the other clocks are not reported here. Individuals with simple disease showed ageing patterns comparable to healthy peers. The authors describe these as biological evidence of premature ageing and suggest a lifelong systemic vulnerability.
Supporting source [1]
Abstract-only scope and proposed follow-up use
This explainer is based only on the abstract; the full text was not reviewed. The abstract does not report follow-up duration, clinical outcomes or how the clock estimates were validated in this group. The suggestion to integrate biological ageing metrics into follow-up strategies is a proposal, not a tested intervention. The observed associations do not show that epigenetic ageing causes age-related complications.
Supporting source [1]
How to interpret this
Abstract only; the full text was not reviewed. The abstract text is truncated, so the P value for the complex group and results for the other clocks are missing. Follow-up duration and clinical outcomes are not reported, and the follow-up proposal is untested.
Based on the study abstract; the full paper, tables and supplementary data were not reviewed.
Source & supporting passages
Tournoy TK, Daelman B, Demulier L, Brooke RT, Van De Bruaene A, Budts W, Moons P, De Backer J. · europepmc.org · June 11, 2026