Key result
Low birth weight is linked to ~101% greater risk of impaired GLS in mid-adulthood.
Why the study?
The study aimed to determine the relationship between low birth weight and adult cardiac structure and function, and to investigate potential causal pathways.
Does low birth weight increase the risk of impaired cardiac structure and function in mid-adulthood?
Cohort (n=925)
Does low birth weight increase the risk of impaired cardiac structure and function in mid-adulthood?
Low birth weight is associated with impaired cardiac structure and function in mid-adulthood, an effect partially mediated by cardiometabolic risk factors.
Answers are grounded in this paper and cite their sources.
Supports further investigation of birth weight as a cardiac risk marker; leaves open whether the association is causal or modifiable.
Aims This study aimed to determine the relationship of low birth weight (LBW) with adult cardiac structure and function and investigate potential causal pathways. Methods and results A population-based sample of 925 Australians (41.3% male) were followed from childhood (aged 7–15 years) to young adulthood (aged 26–36 years) and mid-adulthood (aged 36–50 years). Left ventricular (LV) global longitudinal strain (GLS, %), LV mass index (LVMi, g/m2.7), LV filling pressure (E/e′), and left atrial volume index (g/m2) were measured by transthoracic echocardiography in mid-adulthood. Birth weight category was self-reported in young adulthood and classified as low (≤5 lb or ≤2270 g), normal (5–8 lb or 2271–3630 g), and high (>8 lb or >3630 g). Of the 925 participants, 7.5% (n = 69) were classified as LBW. Compared with participants with normal birth weight, those with LBW had 2.01-fold (95% confidence interval: 1.19, 3.41, P = 0.009) higher risks of impaired GLS (GLS > −18%) and 2.63-fold (95% confidence interval: 0.89, 7.81, P = 0.08) higher risks of LV hypertrophy (LVMi > 48 g/m2.7 in men or >44 g/m2.7 in women) in adulthood, independent of age, sex, and any socio-economic factors. Participants with LBW significantly increased body fat from childhood to adulthood relative to their peers and had greater levels of triglycerides, fasting glucose, and arterial stiffness in adulthood. These risk factors were the strongest mediators and explained 54% of the LBW effect size on adult GLS and 33% of the LBW effect size on LVMi. The remaining of these associations was independent of any of the measured risk factors. Conclusions Low birth weight was associated with impaired cardiac structure and function in mid-adulthood. This association was only partially explained by known risk factors.
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Huynh et al. (2021) conducted a cohort in Left Ventricular Dysfunction (n=925). Low birth weight (≤5 lb or ≤2270 g) vs. Normal birth weight (5-8 lb or 2271-3630 g) was evaluated on Impaired global longitudinal strain (GLS > -18%) (RR 2.01, 95% CI 1.19-3.41, p=0.009). Low birth weight was associated with a 2.01-fold higher risk of impaired global longitudinal strain in mid-adulthood compared to normal birth weight (95% CI 1.19-3.41; P=0.009).
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