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Accelerated epigenetic ageing in congenital heart disease: the AccelerAGE study
Tijs K Tournoy1, Bo Daelman2, Laurent Demulier1
1Department of Cardiology, Ghent University Hospital, Corneel Heymanslaan 10, Ghent, Belgium.
Insights
Adults with moderate and complex congenital heart disease show accelerated epigenetic ageing compared to healthy individuals. Simple congenital heart disease does not show this accelerated ageing, suggesting disease complexity impacts biological aging.
Area of Science:
- Cardiology
- Genetics
- Gerontology
Background:
- Adults with congenital heart disease (CHD) experience earlier onset of age-related comorbidities, indicating accelerated biological aging.
- Epigenetic clocks, based on DNA methylation, offer a method to estimate biological age.
- The relationship between CHD complexity and epigenetic age acceleration is not well understood.
Purpose of the Study:
- To investigate if adults with CHD exhibit accelerated epigenetic aging.
- To determine if the degree of epigenetic age acceleration correlates with CHD complexity.
- To assess the pace of aging in CHD patients using epigenetic markers.
Main Methods:
- Included 120 adults with CHD (ages 29-50) and 120 age/sex-matched healthy controls.
- Categorized CHD patients into simple, moderate, and complex groups (n=40 each).
- Utilized Horvath, Hannum, Zhang, GrimAge2, and PhenoAge epigenetic clocks, plus DunedinPACE for aging pace assessment.
Main Results:
- Moderate and complex CHD groups showed significant age acceleration with PhenoAge and GrimAge2 clocks compared to controls.
- Patients with moderate and complex CHD exhibited a higher pace of aging (DunedinPACE).
- No significant epigenetic age differences were found between simple CHD patients and healthy controls.
Conclusions:
- Accelerated epigenetic aging is evident in adults with moderate and complex CHD, but not simple CHD.
- These findings support biological evidence of premature aging in CHD, highlighting systemic vulnerability.
- Incorporating biological aging metrics in CHD follow-up may aid early detection of complications and improve long-term healthspan.
Background And Aims:
Adults with congenital heart disease tend to develop both cardiac and noncardiac age-related comorbidities earlier in life than the general population, suggesting accelerated biological ageing. Epigenetic clocks estimate biological age based on DNA methylation profiles. This study investigated whether adults with congenital heart disease display accelerated epigenetic ageing and whether the degree of age acceleration relates to disease complexity.
Methods:
A total of 120 patients with congenital heart disease (age 29-50 years, 58 females) and 120 age- and sex-matched healthy controls were included. Patients were divided into simple, moderate, and complex disease complexity groups (n = 40 per group). Epigenetic age was estimated using the Horvath, Hannum, Zhang, GrimAge2, and PhenoAge clocks, whereas the pace of ageing was assessed using DunedinPACE.
Results:
Compared to healthy controls, patients with moderate and complex congenital heart disease exhibit significant age acceleration with PhenoAge (+3.0 years, P = .019; +5.5 years, P < .001) and GrimAge2 (+2.1 years, P = .045; +2.3 years, P = .022) and a higher pace of ageing (P = .008 and P = .016, respectively). No significant differences were detected between healthy controls and patients with simple disease.
Conclusions:
Accelerated epigenetic ageing is observed in adults with moderate and complex congenital heart disease, while individuals with simple disease show ageing patterns comparable to healthy peers. These findings provide biological evidence of premature ageing in congenital heart disease and suggest a lifelong systemic vulnerability. Integrating biological ageing metrics into follow-up strategies may enable earlier detection of age-related complications and support interventions to preserve long-term healthspan.
