Risk factors for left ventricular dysfunction in adulthood: role of low birth weight

Abstract 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...
Ausführliche Beschreibung

Gespeichert in:

Autor*in:	Quan L. Huynh [verfasserIn] Alison J. Venn [verfasserIn] Costan G. Magnussen [verfasserIn] Hong Yang [verfasserIn] Terence Dwyer [verfasserIn] Thomas H. Marwick [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2021

Schlagwörter:	Low birth weight Left ventricle Global longitudinal strain LV hypertrophy

Übergeordnetes Werk:	In: ESC Heart Failure - Wiley, 2015, 8(2021), 6, Seite 5403-5414
Übergeordnetes Werk:	volume:8 ; year:2021 ; number:6 ; pages:5403-5414

Links:	Link aufrufen Link aufrufen Link aufrufen Journal toc

DOI / URN:	10.1002/ehf2.13632

Katalog-ID:	DOAJ041716337

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245	1	0	\|a Risk factors for left ventricular dysfunction in adulthood: role of low birth weight
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520			\|a Abstract 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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650		4	\|a Left ventricle
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700	0		\|a Alison J. Venn \|e verfasserin \|4 aut
700	0		\|a Costan G. Magnussen \|e verfasserin \|4 aut
700	0		\|a Hong Yang \|e verfasserin \|4 aut
700	0		\|a Terence Dwyer \|e verfasserin \|4 aut
700	0		\|a Thomas H. Marwick \|e verfasserin \|4 aut
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allfields	10.1002/ehf2.13632 doi (DE-627)DOAJ041716337 (DE-599)DOAJ6a316a4df29e4f1fa0ab02a940ffabc1 DE-627 ger DE-627 rakwb eng RC666-701 Quan L. Huynh verfasserin aut Risk factors for left ventricular dysfunction in adulthood: role of low birth weight 2021 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract 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. Low birth weight Left ventricle Global longitudinal strain LV hypertrophy Diseases of the circulatory (Cardiovascular) system Alison J. Venn verfasserin aut Costan G. Magnussen verfasserin aut Hong Yang verfasserin aut Terence Dwyer verfasserin aut Thomas H. Marwick verfasserin aut In ESC Heart Failure Wiley, 2015 8(2021), 6, Seite 5403-5414 (DE-627)820686506 (DE-600)2814355-3 20555822 nnns volume:8 year:2021 number:6 pages:5403-5414 https://doi.org/10.1002/ehf2.13632 kostenfrei https://doaj.org/article/6a316a4df29e4f1fa0ab02a940ffabc1 kostenfrei https://doi.org/10.1002/ehf2.13632 kostenfrei https://doaj.org/toc/2055-5822 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_636 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2106 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 8 2021 6 5403-5414
spelling	10.1002/ehf2.13632 doi (DE-627)DOAJ041716337 (DE-599)DOAJ6a316a4df29e4f1fa0ab02a940ffabc1 DE-627 ger DE-627 rakwb eng RC666-701 Quan L. Huynh verfasserin aut Risk factors for left ventricular dysfunction in adulthood: role of low birth weight 2021 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract 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. Low birth weight Left ventricle Global longitudinal strain LV hypertrophy Diseases of the circulatory (Cardiovascular) system Alison J. Venn verfasserin aut Costan G. Magnussen verfasserin aut Hong Yang verfasserin aut Terence Dwyer verfasserin aut Thomas H. Marwick verfasserin aut In ESC Heart Failure Wiley, 2015 8(2021), 6, Seite 5403-5414 (DE-627)820686506 (DE-600)2814355-3 20555822 nnns volume:8 year:2021 number:6 pages:5403-5414 https://doi.org/10.1002/ehf2.13632 kostenfrei https://doaj.org/article/6a316a4df29e4f1fa0ab02a940ffabc1 kostenfrei https://doi.org/10.1002/ehf2.13632 kostenfrei https://doaj.org/toc/2055-5822 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_636 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2106 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 8 2021 6 5403-5414
allfields_unstemmed	10.1002/ehf2.13632 doi (DE-627)DOAJ041716337 (DE-599)DOAJ6a316a4df29e4f1fa0ab02a940ffabc1 DE-627 ger DE-627 rakwb eng RC666-701 Quan L. Huynh verfasserin aut Risk factors for left ventricular dysfunction in adulthood: role of low birth weight 2021 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract 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. Low birth weight Left ventricle Global longitudinal strain LV hypertrophy Diseases of the circulatory (Cardiovascular) system Alison J. Venn verfasserin aut Costan G. Magnussen verfasserin aut Hong Yang verfasserin aut Terence Dwyer verfasserin aut Thomas H. Marwick verfasserin aut In ESC Heart Failure Wiley, 2015 8(2021), 6, Seite 5403-5414 (DE-627)820686506 (DE-600)2814355-3 20555822 nnns volume:8 year:2021 number:6 pages:5403-5414 https://doi.org/10.1002/ehf2.13632 kostenfrei https://doaj.org/article/6a316a4df29e4f1fa0ab02a940ffabc1 kostenfrei https://doi.org/10.1002/ehf2.13632 kostenfrei https://doaj.org/toc/2055-5822 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_636 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2106 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 8 2021 6 5403-5414
allfieldsGer	10.1002/ehf2.13632 doi (DE-627)DOAJ041716337 (DE-599)DOAJ6a316a4df29e4f1fa0ab02a940ffabc1 DE-627 ger DE-627 rakwb eng RC666-701 Quan L. Huynh verfasserin aut Risk factors for left ventricular dysfunction in adulthood: role of low birth weight 2021 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract 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. Low birth weight Left ventricle Global longitudinal strain LV hypertrophy Diseases of the circulatory (Cardiovascular) system Alison J. Venn verfasserin aut Costan G. Magnussen verfasserin aut Hong Yang verfasserin aut Terence Dwyer verfasserin aut Thomas H. Marwick verfasserin aut In ESC Heart Failure Wiley, 2015 8(2021), 6, Seite 5403-5414 (DE-627)820686506 (DE-600)2814355-3 20555822 nnns volume:8 year:2021 number:6 pages:5403-5414 https://doi.org/10.1002/ehf2.13632 kostenfrei https://doaj.org/article/6a316a4df29e4f1fa0ab02a940ffabc1 kostenfrei https://doi.org/10.1002/ehf2.13632 kostenfrei https://doaj.org/toc/2055-5822 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_636 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2106 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 8 2021 6 5403-5414
allfieldsSound	10.1002/ehf2.13632 doi (DE-627)DOAJ041716337 (DE-599)DOAJ6a316a4df29e4f1fa0ab02a940ffabc1 DE-627 ger DE-627 rakwb eng RC666-701 Quan L. Huynh verfasserin aut Risk factors for left ventricular dysfunction in adulthood: role of low birth weight 2021 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract 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. Low birth weight Left ventricle Global longitudinal strain LV hypertrophy Diseases of the circulatory (Cardiovascular) system Alison J. Venn verfasserin aut Costan G. Magnussen verfasserin aut Hong Yang verfasserin aut Terence Dwyer verfasserin aut Thomas H. Marwick verfasserin aut In ESC Heart Failure Wiley, 2015 8(2021), 6, Seite 5403-5414 (DE-627)820686506 (DE-600)2814355-3 20555822 nnns volume:8 year:2021 number:6 pages:5403-5414 https://doi.org/10.1002/ehf2.13632 kostenfrei https://doaj.org/article/6a316a4df29e4f1fa0ab02a940ffabc1 kostenfrei https://doi.org/10.1002/ehf2.13632 kostenfrei https://doaj.org/toc/2055-5822 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_636 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2106 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 8 2021 6 5403-5414
language	English
source	In ESC Heart Failure 8(2021), 6, Seite 5403-5414 volume:8 year:2021 number:6 pages:5403-5414
sourceStr	In ESC Heart Failure 8(2021), 6, Seite 5403-5414 volume:8 year:2021 number:6 pages:5403-5414
format_phy_str_mv	Article
institution	findex.gbv.de
topic_facet	Low birth weight Left ventricle Global longitudinal strain LV hypertrophy Diseases of the circulatory (Cardiovascular) system
isfreeaccess_bool	true
container_title	ESC Heart Failure
authorswithroles_txt_mv	Quan L. Huynh @@aut@@ Alison J. Venn @@aut@@ Costan G. Magnussen @@aut@@ Hong Yang @@aut@@ Terence Dwyer @@aut@@ Thomas H. Marwick @@aut@@
publishDateDaySort_date	2021-01-01T00:00:00Z
hierarchy_top_id	820686506
id	DOAJ041716337
language_de	englisch
fullrecord	<?xml version="1.0" encoding="UTF-8"?><collection xmlns="http://www.loc.gov/MARC21/slim"><record><leader>01000caa a22002652 4500</leader><controlfield tag="001">DOAJ041716337</controlfield><controlfield tag="003">DE-627</controlfield><controlfield tag="005">20230308052048.0</controlfield><controlfield tag="007">cr uuu---uuuuu</controlfield><controlfield tag="008">230227s2021 xx \|\|\|\|\|o 00\| \|\|eng c</controlfield><datafield tag="024" ind1="7" ind2=" "><subfield code="a">10.1002/ehf2.13632</subfield><subfield code="2">doi</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-627)DOAJ041716337</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-599)DOAJ6a316a4df29e4f1fa0ab02a940ffabc1</subfield></datafield><datafield tag="040" ind1=" " ind2=" "><subfield code="a">DE-627</subfield><subfield code="b">ger</subfield><subfield code="c">DE-627</subfield><subfield code="e">rakwb</subfield></datafield><datafield tag="041" ind1=" " ind2=" "><subfield code="a">eng</subfield></datafield><datafield tag="050" ind1=" " ind2="0"><subfield code="a">RC666-701</subfield></datafield><datafield tag="100" ind1="0" ind2=" "><subfield code="a">Quan L. Huynh</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="245" ind1="1" ind2="0"><subfield code="a">Risk factors for left ventricular dysfunction in adulthood: role of low birth weight</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="c">2021</subfield></datafield><datafield tag="336" ind1=" " ind2=" "><subfield code="a">Text</subfield><subfield code="b">txt</subfield><subfield code="2">rdacontent</subfield></datafield><datafield tag="337" ind1=" " ind2=" "><subfield code="a">Computermedien</subfield><subfield code="b">c</subfield><subfield code="2">rdamedia</subfield></datafield><datafield tag="338" ind1=" " ind2=" "><subfield code="a">Online-Ressource</subfield><subfield code="b">cr</subfield><subfield code="2">rdacarrier</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Abstract 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. 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callnumber-first	R - Medicine
author	Quan L. Huynh
spellingShingle	Quan L. Huynh misc RC666-701 misc Low birth weight misc Left ventricle misc Global longitudinal strain misc LV hypertrophy misc Diseases of the circulatory (Cardiovascular) system Risk factors for left ventricular dysfunction in adulthood: role of low birth weight
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topic_title	RC666-701 Risk factors for left ventricular dysfunction in adulthood: role of low birth weight Low birth weight Left ventricle Global longitudinal strain LV hypertrophy
topic	misc RC666-701 misc Low birth weight misc Left ventricle misc Global longitudinal strain misc LV hypertrophy misc Diseases of the circulatory (Cardiovascular) system
topic_unstemmed	misc RC666-701 misc Low birth weight misc Left ventricle misc Global longitudinal strain misc LV hypertrophy misc Diseases of the circulatory (Cardiovascular) system
topic_browse	misc RC666-701 misc Low birth weight misc Left ventricle misc Global longitudinal strain misc LV hypertrophy misc Diseases of the circulatory (Cardiovascular) system
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title	Risk factors for left ventricular dysfunction in adulthood: role of low birth weight
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title_full	Risk factors for left ventricular dysfunction in adulthood: role of low birth weight
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author_browse	Quan L. Huynh Alison J. Venn Costan G. Magnussen Hong Yang Terence Dwyer Thomas H. Marwick
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author-letter	Quan L. Huynh
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title_sort	risk factors for left ventricular dysfunction in adulthood: role of low birth weight
callnumber	RC666-701
title_auth	Risk factors for left ventricular dysfunction in adulthood: role of low birth weight
abstract	Abstract 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.
abstractGer	Abstract 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.
abstract_unstemmed	Abstract 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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title_short	Risk factors for left ventricular dysfunction in adulthood: role of low birth weight
url	https://doi.org/10.1002/ehf2.13632 https://doaj.org/article/6a316a4df29e4f1fa0ab02a940ffabc1 https://doaj.org/toc/2055-5822
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up_date	2024-07-03T21:45:50.238Z
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fullrecord_marcxml	<?xml version="1.0" encoding="UTF-8"?><collection xmlns="http://www.loc.gov/MARC21/slim"><record><leader>01000caa a22002652 4500</leader><controlfield tag="001">DOAJ041716337</controlfield><controlfield tag="003">DE-627</controlfield><controlfield tag="005">20230308052048.0</controlfield><controlfield tag="007">cr uuu---uuuuu</controlfield><controlfield tag="008">230227s2021 xx \|\|\|\|\|o 00\| \|\|eng c</controlfield><datafield tag="024" ind1="7" ind2=" "><subfield code="a">10.1002/ehf2.13632</subfield><subfield code="2">doi</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-627)DOAJ041716337</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-599)DOAJ6a316a4df29e4f1fa0ab02a940ffabc1</subfield></datafield><datafield tag="040" ind1=" " ind2=" "><subfield code="a">DE-627</subfield><subfield code="b">ger</subfield><subfield code="c">DE-627</subfield><subfield code="e">rakwb</subfield></datafield><datafield tag="041" ind1=" " ind2=" "><subfield code="a">eng</subfield></datafield><datafield tag="050" ind1=" " ind2="0"><subfield code="a">RC666-701</subfield></datafield><datafield tag="100" ind1="0" ind2=" "><subfield code="a">Quan L. Huynh</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="245" ind1="1" ind2="0"><subfield code="a">Risk factors for left ventricular dysfunction in adulthood: role of low birth weight</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="c">2021</subfield></datafield><datafield tag="336" ind1=" " ind2=" "><subfield code="a">Text</subfield><subfield code="b">txt</subfield><subfield code="2">rdacontent</subfield></datafield><datafield tag="337" ind1=" " ind2=" "><subfield code="a">Computermedien</subfield><subfield code="b">c</subfield><subfield code="2">rdamedia</subfield></datafield><datafield tag="338" ind1=" " ind2=" "><subfield code="a">Online-Ressource</subfield><subfield code="b">cr</subfield><subfield code="2">rdacarrier</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Abstract 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. 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Risk factors for left ventricular dysfunction in adulthood: role of low birth weight

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