Abstract
INTRODUCTION The impacts of health-related behaviours and risk factor exposures across childhood and adolescence on the adult heart are largely unexplored. We investigated whether early-life trajectories for physical activity (PA), sedentary behaviour and systolic blood pressure (SBP) are associated with cardiac structure in adulthood. METHODS Data collected throughout childhood and adolescence on PA, TV watching and SBP in a cohort study were used to develop antecedent trajectories. At age ∼29yrs, participants were invited to undergo an echocardiogram, to assess left ventricular mass (LVM), LV internal diameter (LVID) and LV wall thickness (LVWT). Analysis was performed between trajectories, separately by sex. RESULTS 723 participants were included. In males, LVM was greater in the antecedent High-PA trajectory (184.1±35.6g), compared to both Mid-PA (171.7±36.1g, P=0.014) and Low-PA (166.7±38.0g, P=0.021). This was related to greater LVID in High-PA compared to both Mid-PA (Δ1.3±0.5cm, P=0.018) and Low-PA (Δ1.3±0.8cm, P=0.087) groups; there were no differences in LVWT (all P>0.050). No differences were found in heart structure between PA trajectory groups in females (all P>0.050). For antecedent SBP, LVM was lower in both the Low-SBP (155.7±30.5g) and Normal-SBP groups (172.9±36.7g) compared to both High-normal (184.8±32.9g) and High-SBP (206.2±41.3g) in males (all P<0.001). This was primarily driven by larger LVWT in High-normal (Δ1.2±0.2g, P=0.001) and High-SBP groups (1.9±0.5g, P=0.001); no differences were observed for LVID (P=0.398). These findings for SBP were similar in females, with the highest SBP group having the greatest LVM and LVWT (all P<0.001). There were no significant impacts of antecedent TV trajectories on adult cardiac measures (all P>0.050). CONCLUSION Higher developmental SBP is associated with larger heart size and wall thickness in adulthood. Higher developmental PA levels are associated with larger cardiac chamber dimension in adult males, but not females. These findings suggest adult cardiac structure may be influenced by early-life risk factor exposures.
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