Impact of Parental Cardiometabolic Disease on Cardiac Remodeling in Youth
Overview
This 24-year longitudinal study from the ALSPAC cohort demonstrates that offspring with a positive family history of cardiometabolic diseases have significantly higher odds of developing left ventricular hypertrophy and elevated left ventricular filling pressure during adolescence to young adulthood. Increased glucose levels partially mediate this association, highlighting early cardiac remodeling linked to familial risk.
Background
Left ventricular hypertrophy (LVH) is a key marker of myocardial injury in pediatric populations, yet data on how parental cardiometabolic risk factors influence early cardiac changes in offspring are limited. Prior studies, including the Framingham Heart Study, have shown mixed associations between parental cardiovascular risk factors and offspring cardiovascular outcomes. Understanding early cardiac alterations in offspring with familial cardiometabolic disease is critical for primordial prevention strategies. The Avon Longitudinal Study of Parents and Children (ALSPAC) provides a unique opportunity to examine these associations longitudinally from adolescence into young adulthood.
Data Highlights
Parameter
Age 17 years
Age 24 years
LV hypertrophy prevalence (total cohort)
2.4%
6.5%
LV hypertrophy prevalence (positive family history)
Not specified
Fourfold increase vs baseline
LV hypertrophy prevalence (no family history)
Not specified
Twofold increase vs baseline
High LV filling pressure prevalence
0.7%
0.9%
Mean LVMI (g/m2.7)
35.4 ± 7.3
38.1 ± 8.5
Odds ratio for LV hypertrophy with family history
1.21 (95% CI: 1.11–1.32; P < 0.001)
Odds ratio for high LV filling pressure with family history
1.20 (95% CI: 1.10–1.30; P < 0.001)
Key Findings
30.2% of participants had a positive family history of cardiometabolic diseases.
LV hypertrophy prevalence increased from 2.4% at age 17 to 6.5% at age 24 in the total cohort.
Offspring with positive family history showed a fourfold increase in LV hypertrophy prevalence over 7 years, compared to a twofold increase in those without family history.
Positive family history was significantly associated with higher odds of LV hypertrophy (OR 1.21) and elevated LV filling pressure (OR 1.20) longitudinally.
There was no significant association between family history and relative wall thickness or LV diastolic dysfunction.
Increased glucose levels partially mediated (9.5%) the association between family history and increased LV mass index.
Clinical Implications
Clinicians should consider family history of cardiometabolic disease as an important risk factor for early cardiac remodeling in youth, even in the absence of overt clinical disease. Monitoring glucose metabolism and cardiac structure via echocardiography in adolescents and young adults with familial risk may facilitate early identification and intervention to prevent progression to clinical cardiovascular disease.
Conclusion
This study highlights that a positive family history of cardiometabolic disease confers increased risk of early adverse cardiac remodeling during adolescence and young adulthood, partially mediated by glucose metabolism. These findings underscore the importance of early preventive strategies targeting at-risk youth.
References
ALSPAC Study Group -- Avon Longitudinal Study of Parents and Children
Framingham Heart Study -- Multigenerational Cardiovascular Risk
