Huynh, QL and Venn, AJ and Magnussen, CG and Yang, H and Dwyer, T and Marwick, TH, Risk factors for left ventricular dysfunction in adulthood: role of low birth weight, ESC Heart Failure pp. 1-12. ISSN 2055-5822 (2021) [Refereed Article]
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© 2021 The Authors. ESC Heart Failure published by John Wiley & Sons Ltd on behalf of European Society of Cardiology. This is an open access article under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, (https://creativecommons.org/licenses/by-nc-nd/4.0/) which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.
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.
|Item Type:||Refereed Article|
|Keywords:||low birth weight, left ventricle, global longitudinal strain, LV hypertrophy|
|Research Division:||Biomedical and Clinical Sciences|
|Research Group:||Cardiovascular medicine and haematology|
|Research Field:||Cardiology (incl. cardiovascular diseases)|
|Objective Group:||Evaluation of health and support services|
|Objective Field:||Determinants of health|
|UTAS Author:||Venn, AJ (Professor Alison Venn)|
|UTAS Author:||Magnussen, CG (Associate Professor Costan Magnussen)|
|UTAS Author:||Yang, H (Ms Hilda Yang)|
|UTAS Author:||Dwyer, T (Professor Terry Dwyer)|
|UTAS Author:||Marwick, TH (Professor Tom Marwick)|
|Deposited By:||Menzies Institute for Medical Research|
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