Small size at birth predicts decreased cardiomyocyte number in the adult ovine heart

Vranas, S.; Heinemann, Gary; Liu, Hong; Blasio, Miles J. De; Owens, Julie A.; Gatford, Kathryn L.; Black, M. Jane

doi:10.1017/s2040174417000381

Cited by 23 publications

(28 citation statements)

References 47 publications

(107 reference statements)

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“…The comparable results in cardiac morphometry and function as well as in cardiac biomarkers between AGA and SGA infants is reassuring and suggests that these alterations may become more apparent later in childhood or occur exclusively in infants with abnormal perinatal trajectories and/or born preterm . Along these lines, the decrease in cardiomyocyte number observed in animal models after prenatal growth restraint seems to have an impact on cardiac functional reserve only in adulthood . Also, the association between birth weight and specific indices of cardiovascular performance experience an amplifying trend with age .…”

Section: Discussionmentioning

confidence: 74%

The sequence of prenatal growth restraint and postnatal catch‐up growth: normal heart but thicker intima‐media and more pre‐peritoneal fat in late infancy

et al. 2018

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Summary Background The sequence of prenatal growth restraint and postnatal catch‐up growth leads to a thicker intima‐media and more pre‐peritoneal fat by age 3–6 years. Objectives To study whether carotid intima‐media thickness (cIMT) and pre‐peritoneal fat differ already between catch‐up small‐for‐gestational‐age (SGA) infants and appropriate‐for‐gestational‐age (AGA) controls in late infancy (ages 1 and 2 years) and whether such differences – if any – are accompanied by differences in cardiac morphology and function. Methods Longitudinal assessments included body height and weight; fasting glucose, insulin, Insulin‐like growth factor (IGF‐I), high‐molecular‐weight adiponectin; body composition (by absorptiometry); cIMT, aortic IMT, pre‐peritoneal fat partitioning (by ultrasound); cardiac morphometry and function (by echocardiography) in AGA and SGA infants at birth, at age 1 year (N = 87), and again at age 2 years (N = 68). Results Catch‐up SGA infants had already a thicker cIMT than AGA controls at ages 1 and 2 years, and more pre‐peritoneal fat by age 2 years (all p values between <0.01 and <0.0001); all cardiac and endocrine‐metabolic results were similar in AGA and SGA infants at ages 1 and 2 years. Conclusions From late infancy onwards, catch‐up SGA infants have a thicker cIMT and more pre‐peritoneal fat than AGA controls, but their cardiac morphology and function remain reassuringly similar.

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Section: Discussionmentioning

confidence: 74%

The sequence of prenatal growth restraint and postnatal catch‐up growth: normal heart but thicker intima‐media and more pre‐peritoneal fat in late infancy

et al. 2018

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“…; Vranas et al . ). Thus, although we did not measure cell number, it probably was reduced in the PUN hearts and contributed to the smaller hearts.…”

Section: Discussionmentioning

confidence: 97%

“…This deficit persisted after nutritional rehabilitation, consistent with the fact that cardiomyocyte proliferation is minimal after PN21. Sheep, in which cardiomyocyte maturation occurs prenatally, developed smaller hearts with fewer cardiomyocytes when there was IUGR and these differences persisted postnatally even with adequate nutrition (Stacy et al 2009;Vranas et al 2017). Thus, although we did not measure cell number, it probably was reduced in the PUN hearts and contributed to the smaller hearts.…”

Section: Heart Sizementioning

confidence: 93%

“…; Vranas et al . ). However, the extent to which alterations in cardiac cell size, number and nucleation/ploidy are impacted when a nutritional deficit occurs only after birth, i.e.…”

Section: Introductionmentioning

confidence: 97%

“…Thus, the extent of cardiac maturation that occurs after birth will depend on the degree of prematurity, which could be substantial, and subject to the postnatal nutritional state. In sheep and rodents, newborns that experienced prenatal growth impairment have fewer cardiomyocytes (Corstius et al 2005;Stacy et al 2009;Master et al 2014) and their capacity to recover appears to depend on the developmental stage at recovery (Bai et al 1990;Lim et al 2010;Black et al 2012;Botting et al 2012;Vranas et al 2017). However, the extent to which alterations in cardiac cell size, number and nucleation/ploidy are impacted when a nutritional deficit occurs only after birth, i.e.…”

Section: Introductionmentioning

confidence: 99%

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Postnatal undernutrition alters adult female mouse cardiac structure and function leading to limited exercise capacity

Ferguson

Monroe

Heredia

et al. 2019

The Journal of Physiology

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Key points Impaired growth during fetal life can reprogramme heart development and increase the risk for long‐term cardiovascular dysfunction. It is uncertain if the developmental window during which the heart is vulnerable to reprogramming as a result of inadequate nutrition extends into the postnatal period. We found that adult female mice that had been undernourished only from birth to 3 weeks of age had disproportionately smaller hearts compared to males, with thinner ventricle walls and more mononucleated cardiomyocytes. In females, but not males, cardiac diastolic function, and heart rate responsiveness to adrenergic stimulation were limited and maximal exercise capacity was compromised. These data suggest that the developmental window during which the heart is vulnerable to reprogramming by inadequacies in nutrient intake may extend into postnatal life and such individuals could be at increased risk for a cardiac event as a result of strenuous exercise. Abstract Adults who experienced undernutrition during critical windows of development are at increased risk for cardiovascular disease. The contribution of cardiac function to this increased disease risk is uncertain. We evaluated the effect of a short episode of postnatal undernutrition on cardiovascular function in mice at the whole animal, organ, and cellular levels. Pups born to control mouse dams were suckled from birth to postnatal day (PN) 21 on dams fed either a control (20% protein) or a low protein (8% protein) isocaloric diet. After PN21 offspring were fed the same control diet until adulthood. At PN70 V̇O2, max was measured by treadmill test. At PN80 cardiac function was evaluated by echocardiography and Doppler analysis at rest and following β‐adrenergic stimulation. Isolated cardiomyocyte nucleation and Ca2+ transients (with and without β‐adrenergic stimulation) were measured at PN90. Female mice that were undernourished and then refed (PUN), unlike male mice, had disproportionately smaller hearts and their exercise capacity, cardiac diastolic function, and heart rate responsiveness to adrenergic stimulation were limited. A reduced left ventricular end diastolic volume, impaired early filling, and decreased stored energy at the beginning of diastole contributed to these impairments. Female PUN mice had more mononucleated cardiomyocytes; under resting conditions binucleated cells had a functional profile suggestive of increased basal adrenergic activation. Thus, a brief episode of early postnatal undernutrition in the mouse can produce persistent changes to cardiac structure and function that limit exercise/functional capacity and thereby increase the risk for the development of a wide variety of cardiovascular morbidities.

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Preterm Birth and Heart Failure in Infancy and Beyond

Belfort

Sacks

2021

JAMA Pediatr

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The past 30 years have seen major advances in the medical care of preterm neonates such that currently more than 95% of the approximately 400 000 preterm infants born each year in the US survive to discharge from the neonatal intensive care unit (NICU). For even the smallest and least mature infants (extremely preterm infants born <28 weeks' gestation), survival is approximately 90%. 1 Given these successes, the focus must now shift from reducing mortality to improving long-term health outcomes in this vulnerable population.Shifting the focus to long-term health requires a clear understanding of the risks that preterm infants face once they leave the NICU. Most pediatricians are aware of the heightened risk of neurodevelopmental impairments, including motor, cognitive, language, and behavioral difficulties. To address these needs, existing infrastructure includes multidisciplinary high-risk infant follow-up clinics and communitybased early-intervention programs, which complement the care provided within the pediatric primary care setting. Typically, high-risk infant follow-up care does not extend beyond childhood.A less well-recognized area of risk for surviving preterm infants is in their cardiometabolic health. Epidemiologic evidence has linked preterm birth with risks of hypertension 2 and type 2 diabetes, 3 with smaller and less mature infants facing the greatest risk of developing these conditions in young adulthood. Some but not all studies have found that preterm birth is also associated with an increased risk of ischemic heart disease in adulthood. 4,5 In contrast with neurodevelopmental concerns, which often lessen in severity over time, particularly when appropriate supports and therapies are in place, cardiometabolic risks may be invisible during early childhood, only to emerge in adolescence, young adulthood, or even middle age.In this issue of JAMA Pediatrics, Crump et al 6 substantially extend our understanding of the cardiometabolic risks faced by infants born preterm by investigating a previously understudied condition, heart failure. In a populationwide study that included more than 4 million participants observed throughout more than 40 years, they found that preterm birth at less than 37 weeks' gestation was associated with a 2.7-fold increased incidence of heart failure compared with full-term (age 39-41 weeks) birth. Stratified analyses revealed several clinically relevant results. First, the risk of heart failure was increased not just for heart failure during infancy (age <1 year, 4.5-fold increased risk) and childhood (age 1-17 years, 3.4fold increased risk), but also for heart failure that presented during adulthood (age 18-43 years, 1.4-fold increased risk).

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Small size at birth predicts decreased cardiomyocyte number in the adult ovine heart

Cited by 23 publications

References 47 publications

The sequence of prenatal growth restraint and postnatal catch‐up growth: normal heart but thicker intima‐media and more pre‐peritoneal fat in late infancy

The sequence of prenatal growth restraint and postnatal catch‐up growth: normal heart but thicker intima‐media and more pre‐peritoneal fat in late infancy

Postnatal undernutrition alters adult female mouse cardiac structure and function leading to limited exercise capacity

Preterm Birth and Heart Failure in Infancy and Beyond

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