Association of Low Birth Weight With Subclinical Cardiovascular Disease in Adulthood

2021 ◽  
Vol 30 ◽  
pp. S174
Author(s):  
Q. Huynh ◽  
A. Venn ◽  
C. Magnussen ◽  
H. Yang ◽  
T. Dwyer ◽  
...  
Keyword(s):  
Cardiovascular Disease ◽  
Birth Weight ◽  
Low Birth Weight ◽  
Subclinical Cardiovascular Disease

MORTALITY FROM CONGENITAL CARDIOVASCULAR DISEASE IN OREGON

PEDIATRICS ◽  
1967 ◽  
Vol 40 (3) ◽  
pp. 334-344
Author(s):  
Victor D. Menashe ◽  
Harold T. Osterud ◽  
Herbert E. Griswold
Keyword(s):  
Cardiovascular Disease ◽  
Birth Weight ◽  
Low Birth Weight ◽  
Life Span ◽  
Normal Birth Weight ◽  
Parental Age ◽  
Cardiac Malformation ◽  
Death Rates ◽  
Normal Birth ◽  
Weight One

Over one half of the deaths from all congenital malformations were due to congenital cardiovascular disease. There were 496 individuals who died of congenital cardiovascular disease in Oregon during 1957 thru 1961, and three fourths of the deaths occurred in infants under 1 year of age. More males were affected by congenital cardiovascular disease than females, but, when congenital cardiovascular disease was present, the length of survival, as measured by life span, did not differ by sex. One out of every four infants dying of congenital cardiovascular disease was of low birth weight; of these, 60% were over 37 weeks' gestation. However, there was no difference in the life span of low birth weight and normal birth weight infants who died with congenital cardiovascular disease. This would imply that the significant factor of death in these infants was the cardiac malformation rather than the low birth weight. One out of every three infants who died with congenital cardiovascular disease had malformations of other systems. Fewer deaths than expected were identified among first born. Fetal deaths were noted more frequently in the population of mothers of children with congenital heart disease than in the overall population. The parental age in this group was significantly higher than in the general population and death rates of infants with congenital cardiovascular disease increased with advancing parental age. Thirty-two percent of the infants who died with congenital cardiovascular disease had single lesions. Early diagnosis and treatment is to be stressed if mortality is to be reduced.

scholarly journals A post‐weaning Western‐style diet exacerbates early programming of cardiovascular disease in low birth weight Yucatan miniature pigs

2009 ◽  
Vol 23 (S1) ◽  
Author(s):  
Semone B Myrie ◽  
Leslie L McKnight ◽  
Bruce N Vliet ◽  
Sukhinder K Cheema ◽  
Robert F Bertolo
Keyword(s):  
Cardiovascular Disease ◽  
Birth Weight ◽  
Low Birth Weight ◽  
Miniature Pigs ◽  
Early Programming

Low birth weight and cardiovascular disease: myth or reality?

1998 ◽  
Vol 9 (4) ◽  
pp. 309-312 ◽  
Author(s):  
Susan Elizabeth Jones ◽  
Jens Randel Nyengaard
Keyword(s):  
Cardiovascular Disease ◽  
Birth Weight ◽  
Low Birth Weight

Sexually dimorphic effects of maternal alcohol intake and adrenalectomy on left ventricular hypertrophy in rat offspring

2003 ◽  
Vol 285 (1) ◽  
pp. E31-E39 ◽  
Author(s):  
Jennifer Slone Wilcoxon ◽  
Jeff Schwartz ◽  
Fraser Aird ◽  
Eva E. Redei
Keyword(s):  
Cardiovascular Disease ◽  
Birth Weight ◽  
Low Birth Weight ◽  
Left Ventricular Hypertrophy ◽  
Ventricular Hypertrophy ◽  
Alcohol Exposure ◽  
Female Offspring ◽  
Left Ventricular ◽  
Placental Weight ◽  
Mrna Levels

In humans, low birth weight and increased placental weight can be associated with cardiovascular disease in adulthood. Low birth weight and increased placental size are known to occur after fetal alcohol exposure or prenatal glucocorticoid administration. Thus the effects of removing the alcohol-induced increase in maternal corticosterone by maternal adrenalectomy on predictors of cardiovascular disease in adulthood were examined in rats. Alcohol exposure of dams during the last 2 wk of gestation resulted in significantly decreased fetal weight and increased placental weight on gestational day 21. Adult female, but not male, offspring of alcohol-consuming mothers exhibited left ventricular hypertrophy. Placental 11β-hydroxysteroid dehydrogenase-2 (11β-HSD-2) mRNA levels, measured by Northern blot, were decreased in females but not males. Adrenalectomy of alcohol-consuming dams reversed the increase in placental weight and the decrease in female placental 11β-HSD-2 expression and eliminated the left ventricular hypertrophy of adult female offspring. These data suggest that alcohol-induced changes in placental 11β-HSD-2 mRNA levels and left ventricular weight are coupled in female offspring only and depend on maternal adrenal status.

Accelerated senescence in kidneys of low-birth-weight rats after catch-up growth

2009 ◽  
Vol 297 (6) ◽  
pp. F1697-F1705 ◽  
Author(s):  
Valerie A. Luyckx ◽  
Catharine A. Compston ◽  
Thomas Simmen ◽  
Thomas F. Mueller
Keyword(s):  
Reactive Oxygen Species ◽  
Cardiovascular Disease ◽  
Birth Weight ◽  
Low Birth Weight ◽  
Reactive Oxygen Species Generation ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Normal Birth Weight ◽  
Normal Birth ◽  
Catch Up

Epidemiological studies show a strong association between low birth weight and hypertension, renal, and cardiovascular disease, especially after catch-up growth. Senescence is an important contributor to the progression of chronic disease. Developmentally programmed premature senescence may be a link among low birth weight, catch-up growth, and adult disease. Low birth weight was induced by feeding pregnant rats a low-protein diet from day 12 of gestation to 10 days postdelivery. Low- and normal-birth-weight male offspring were weaned onto regular or high-calorie diets to enhance catch-up growth. Kidneys and hearts of offspring were analyzed for RNA and protein markers of stress-induced senescence (p16, p21, p53, Rb). Markers of mitochondrial stress (p66Shc) and activation of endoplasmic reticulum protein secretion (Ero1α) were analyzed as regulators of reactive oxygen species generation. Reactive oxygen species are known to be associated with premature aging. Senescence markers were not different in low- or normal-birth-weight kidneys at birth. During rapid catch-up growth, p16 and p21 increased significantly in low-birth-weight kidneys and hearts ( P < 0.01). Renal p16 levels increased progressively and were significantly higher in low-birth-weight kidneys at 3 and 6 mo ( P ≤ 0.02). Renal p66Shc and Ero1α were significantly higher in low- compared with normal- birth-weight kidneys at 6 mo, suggesting reactive oxygen species generation ( P ≤ 0.03). Low-birth-weight rats exhibit accelerated senescence in kidneys and hearts after rapid catch-up growth, a likely important link between early growth and subsequent hypertension, renal, and cardiovascular disease.

scholarly journals Akt signaling as a mediator of cardiac adaptation to low birth weight

2017 ◽  
Vol 233 (2) ◽  
pp. R81-R94 ◽  
Author(s):  
Kimberley C W Wang ◽  
Kimberley J Botting ◽  
Song Zhang ◽  
I Caroline McMillen ◽  
Doug A Brooks ◽  
...  
Keyword(s):  
Cardiovascular Disease ◽  
Birth Weight ◽  
Low Birth Weight ◽  
Adult Life ◽  
Epidemiological Studies ◽  
Left Ventricular ◽  
Postnatal Life ◽  
Risk Of Death ◽  
Expression Of Genes ◽  
Increased Risk

Intrauterine insults, such as poor nutrition and placental insufficiency, can alter cardiomyocyte development, and this can have significant long-term implications for heart health. Consequently, epidemiological studies have shown that low-birth-weight babies have an increased risk of death from cardiovascular disease in adult life. In addition, intrauterine growth restriction can result in increased left ventricular hypertrophy, which is the strongest predictor for poor health outcomes in cardiac patients. The mechanisms responsible for these associations are not clear, but a suboptimal intrauterine environment can program alternative expression of genes such as cardiac IGF-2/H19, IGF-2R and AT1R through either an increase or decrease in DNA methylation or histone acetylation at specific loci. Furthermore, hypoxia and other intrauterine insults can also activate the IGF-1 receptor via IGF-1 and IGF-2, and the AT1 receptor via angiotensin signaling pathways; both of which can result in the phosphorylation of Akt and the activation of a range of downstream pathways. In turn, Akt activation can increase cardiac angiogenesis and cardiomyocyte apoptosis and promote a reversion of metabolism in postnatal life to a fetal phenotype, which involves increased reliance on glucose. Cardiac Akt can also be indirectly regulated by microRNAs and conversely can target microRNAs that will eventually affect other specific cardiac genes and proteins. This review aims to discuss our understanding of this complex network of interactions, which may help explain the link between low birth weight and the increased risk of cardiovascular disease in adult life.

scholarly journals Could Low Birth Weight be Associated with Cardiovascular Disease in Adolescence?

2016 ◽  
Vol 38 (04) ◽  
pp. 189-195
Author(s):  
Priscila Alves ◽  
Ana Henriques ◽  
Francisco Carvalho ◽  
Edward Araujo Júnior
Keyword(s):  
Cardiovascular Disease ◽  
Birth Weight ◽  
Low Birth Weight
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