Cardiovascular Risk in Pediatrics: A Dynamic Process during the First 1000 Days of Life
Abstract
:1. Introduction
2. Methods
3. Prenatal and Neonatal Cv Risk Factors
3.1. Fetal Growth Restriction
3.2. High Birth Weight
3.3. Prematurity
3.4. Maternal Cardiovascular Disease Risk Factors
3.5. Mode of Delivery
3.6. Sex Differences
3.7. Congenital Heart Disease
4. Early Childhood Cardiovascular Risk Factors
4.1. Rapid Catch-Up Growth
4.2. Adiposity Rebound
4.3. Early Obesity
4.4. Infants Antibiotics Exposure
5. Preventative Measures
6. Conclusions
Author Contributions
Funding
Institutional Review Board Statement
Informed Consent Statement
Data Availability Statement
Conflicts of Interest
References
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Risk Factor | Reference | Results |
---|---|---|
Prenatal and neonatal CV risk factors | ||
Fetal growth restriction | Syddall et al., 2005 [14] | Syddall et al. underscored, in their cohort study, a significant association between lower birthweight and an elevated risk of circulatory disease-related mortality in both men and women. |
Lawlor et al., 2005 [15] | There is a reverse relationship between birth weight and the risk of coronary heart disease and stroke in a population born during a period when environmental conditions, as reflected by low infant mortality rates, were comparatively favorable for infants. | |
Faienza et al., 2016 [18] | SGA individuals showed vascular abnormalities and subtle cardiac changes compared with AGA individuals, increasing their cardiovascular risk. | |
Brodszki et al., 2005 [32] | Inadequate intrauterine growth due to placental insufficiency appears to result in impaired vascular development that persists into early adulthood, affecting both males and females. The smaller dimensions of the aorta and the elevated resting heart rate observed in adolescents who experienced IUGR could have implications for their future cardiovascular well-being. | |
Dodson et al., 2014 [33] | Intrauterine growth restriction resulting from placental insufficiency leads to heightened vascular stiffness through remodeling at the end of gestation, potentially laying the groundwork for changes in vascular growth and development. | |
Verburg et al., 2008 [35] | Reduced fetal growth is linked to adaptive adjustments in fetal cardiovascular function. The alterations in cardiac structure and cardiac output align with a progressive rise in afterload and diminished arterial flexibility, even before clinical signs of fetal growth restriction become evident. These early changes may play a role in the heightened risk of cardiovascular disease in adulthood. | |
Leipälä et al., 2003 [36] | IUGR is linked to changes in cardiovascular adaptation and the development of septal and left ventricular hypertrophy in low-birth-weight newborns. While the findings suggest that SGA fetuses can undergo significant cardiovascular adaptation, there may still be an elevated risk of circulatory issues in the future. | |
Tintu et al., 2009 [37] | This study explored the impact of prenatal hypoxia on chick embryos, revealing that it leads to cardiomyopathy characterized by enlarged heart chambers, reduced heart muscle mass, and increased cell death. These cardiac abnormalities persist into adulthood and are associated with elevated VEGF levels. The findings underscore the significant role of VEGF in hypoxia-induced cardiomyopathy, which poses a lasting risk for cardiovascular diseases in affected individuals. | |
High birth weight | Cnattingius et al., 2012 [48] | Prenatal factors play a significant role in the obesity epidemic, and preventing LGA births could help break the cycle of intergenerational obesity. |
Rashid et al., 2019 [49] | High birth weight is associated with an increased risk of heart failure and potential mortality, regardless of traditional risk factors. Therefore, it is important to inquire about a history of high birth weight in both young and older adults as a preventive measure for heart failure. | |
Prematurity | Willemsen et al., 2008 [27] | In a group of short children born SGA, preterm birth has varying impacts on multiple cardiovascular risk factors. Specifically, preterm SGA children exhibited elevated systolic and diastolic blood pressure but lower levels of body fat. They also displayed increased insulin secretion and a higher disposition index compared with their term-born SGA counterparts. |
Bensley et al., 2010 [52] | Pre-term birth initiates changes in myocardial structure, ultimately leading to long-term cardiac vulnerability. | |
Maternal cardiovascular disease risk factors | Lazdam et al., 2012 [54] | Early-onset preeclampsia is associated with elevated postnatal diastolic blood pressure, a greater increase in blood pressure over the years, and higher nocturnal blood pressure in later life. Offspring born to mothers with early-onset preeclampsia also have higher systolic blood pressure compared with those born to mothers with late-onset preeclampsia. |
Geelhoed et al., 2010 [55] | Gestational blood pressure disorders are linked to higher blood pressure in offspring. The mechanisms connecting preeclampsia and gestational hypertension to offspring blood pressure may differ, with preeclampsia possibly affecting intrauterine growth restriction. | |
Lawlor et al., 2012 [56] | Preeclampsia and gestational hypertension elevate offspring blood pressure in infancy, indicating shared risk factors between mothers and infants, unrelated to cardiometabolic abnormalities. These effects are not solely due to long-term consequences of pregnancy hypertensive disorders. | |
Youssef et al., 2020 [57] | Fetuses of preeclamptic mothers, regardless of their growth patterns, displayed cardiovascular issues similar to fetal growth restriction. More research is required to understand the mechanisms behind fetal cardiac adaptation in these cases. | |
Barker et al., 2007 [131] | Hypertension can develop through two distinct pathways: fetal malnutrition (making the child susceptible to postnatal stress) and maternal metabolic dysfunction, particularly in protein metabolism. | |
Bogdarina et al., 2007 [132] | Offspring from mothers fed a low protein diet exhibited increased expression of AT1b receptor mRNA and protein in the adrenal gland. The increased AT1b receptor expression is believed to play a role in hypertension development and may result from fetal programming. | |
Khan et al., 2004 [133] | In this study, researchers examined ‘predictive adaptive’ responses in rodents with adult offspring from fat-fed mothers displaying metabolic syndrome traits. When these offspring were raised on a high-fat diet, their vascular function and heart rates improved, but elevated blood pressure persisted in female offspring. Therefore, predictive adaptive responses may not completely prevent high blood pressure. | |
Geelhoed et al., 2011 [59] | Adaptive alterations in fetal arterial resistance could be part of the mechanisms connecting maternal smoking during pregnancy to both low birth weight and cardiovascular developmental changes in their children. | |
Oken et al., 2005 [60] | Mothers who smoked before or during early pregnancy had children with slightly higher systolic blood pressure, but only those who smoked during early pregnancy had more overweight children. The mechanisms linking smoking to child weight gain and blood pressure may differ. | |
Vik et al., 2014 [69] | Researchers examined the influence of parental factors on cardiovascular risk factors in their offspring. They compared the associations between fathers and offspring and mothers and offspring. The results showed that these associations were largely similar, suggesting that there are no strong maternal effects transmitted through intrauterine mechanisms. | |
Mode of delivery | Begum et al., 2022 [70] | C-section-born children had higher scores (waist circumference, systolic blood pressure, HDL cholesterol levels, fat mass index, and a composite metabolic syndrome score) for several CVD risk indicators compared with those born vaginally. Additionally, children with a high BMI trajectory had increased CVD risk, particularly in the C-section group. This suggests that C-sections were independently associated with elevated CVD risk profiles in children, which were further exacerbated by a high BMI trajectory. |
Sex differences | Grigore et al., 2007 [73] | In a rat model of late gestational reduced uterine perfusion, male offspring with IUGR developed high blood pressure. The study investigates the role of the RAAS in this process. Researchers found that early RAAS blockade using an ACE inhibitor prevents hypertension in adult IUGR male offspring, highlighting the RAAS’s involvement in established hypertension. They also observed temporal changes in the RAAS in IUGR offspring, particularly in the intra-renal RAAS, which may be influenced by factors like sex hormones and which contribute to the development and persistence of hypertension in this model. |
Ojeda et al., 2006 [134] | In a rat model of IUGR induced by placental insufficiency, only male IUGR offspring develop hypertension in adulthood. This study investigates the role of testosterone and the RAAS in this hypertension. At 16 weeks of age, male IUGR offspring have higher testosterone levels and elevated BP. Gonadectomy reduces BP in IUGR males but not in controls. Treatment with an ACE inhibitor, enalapril, lowers BP in both intact and castrated IUGR males, but the response is more significant in intact males, suggesting that testosterone, in conjunction with the RAAS, contributes to hypertension in adult male IUGR offspring. | |
Congenital heart disease | Goldstein et al., 2020 [78] | In adults with CHD, mortality risks vary depending on the severity of their condition. Severe CHD is associated with a higher likelihood of early mortality. Individuals with nonsevere CHD tend to have longer life expectancy but still face risks of mortality from both cardiovascular and non-cardiovascular causes. It is crucial to undergo long-term follow-up, including personalized screening and risk management strategies. |
Giannakoulas et al., 2009 [79] | In adults with CHD, the risk of developing CAD increases as they age. CAD prevalence in adult CHD patients is similar to the general population. Traditional CVD risk factors applied to this population emphasize the importance of CAD prevention | |
Early childhood CV risk factors | ||
Rapid catch-up growth | Lurbe et al., 2018 [85] | In this prospective study, researchers explored how BW, growth patterns, and cardiometabolic risk factors were interconnected within a cohort monitored from birth to age 10. While BW served as a reflection of early fetal experiences and exhibited enduring effects, the pace of weight gain emerged as a pivotal factor in the development of obesity, metabolic disorders, and cardiovascular issues. |
Ong et al., 2004 [87] | Lower BW may contribute to IR, particularly when coupled with rapid early weight gain. Additionally, smaller birth size, lower IGF-I levels, and shorter childhood stature were associated with reduced compensatory insulin secretion. | |
Li et al., 2021 [88] | The study provided strong evidence that the influence of BMI trajectories on CMR operated indirectly through concurrent BMI. Researchers should select the appropriate analytical method based on their study hypothesis to accurately assess the overall or direct impact of growth patterns on cardiometabolic disease risk in children. | |
Adiposity rebound | Hughes et al., 2014 [92] | The study aimed to explore the relationship between the timing of AR in childhood and adiposity indicators (BMI and fat mass) at age 15. The findings revealed that early AR, occurring between 3.5 and 5 years, was strongly associated with higher BMI and fat mass during adolescence. Interventions to prevent excessive adiposity should focus on addressing modifiable factors in early childhood to delay the timing of AR. |
Totzauer et al., 2022 [93] | Infants fed with lower protein formula had lower BMI trajectories compared with those fed with conventional higher protein formula. Therefore, feeding infants with lower protein formula can lead to healthier BMI outcomes and similar values at adiposity rebound as observed in breastfed infants. | |
Wibaek et al., 2019 [95] | Early childhood growth patterns are linked to the development of obesity and CMR, emphasizing the importance of interventions targeting young children with unfavorable growth patterns in low-income countries. | |
Early obesity | Guzzetti et al., 2019 [97] | Gender and puberty affect the frequency of CVRF abnormalities, even during prepubertal stages. Identifying individuals with a higher risk of metabolic complications is crucial for the development of tailored prevention strategies. |
Wardle et al., 2008 [106] | Genetic factors play a substantial role in BMI and abdominal adiposity in children born during the pediatric obesity epidemic. To address obesity effectively, early prevention may target family dynamics, while long-term weight management will require individual commitment and broader societal efforts to modify environments, especially for genetically predisposed children. | |
Mantzorou et al., 2022 [109] | Breastfeeding exclusively for at least 4 months has favorable outcomes, including a reduced risk of childhood overweight and obesity, along with benefits for postnatal maternal weight control. It is important to convey these advantages to expectant and new mothers and implement supportive measures to promote breastfeeding initiation and continuity for all mothers and their babies. | |
Yan et al., 2014 [110] | Breastfeeding is a significant protective factor against childhood obesity. | |
Weber et al., 2014 [112] | Choosing a low-protein infant formula has demonstrated a correlation with reduced BMI and a lowered risk of childhood obesity among school-aged children. Therefore, it is crucial to avoid infant foods that offer excessive protein intake as a potential approach to address childhood obesity. | |
Gingras et al., 2019 [113] | Introducing CF early is related to elevated adiposity measurements in both breastfed and formula-fed children, while introducing CF later was associated with increased adiposity in formula-fed children. | |
Infants antibiotics exposure | Ternak et al., 2005 [118] | The usage of antibiotics, both in humans and animals, has significantly increased over the years. Animal studies have demonstrated that antibiotics can promote growth by affecting gut flora, and there are indications that similar effects might occur in humans. This hypothesis warrants further research. |
Trasande et al., 2013 [120] | Early antibiotic exposure during the first 6 months of life is associated with increased body mass from 10 to 38 months, but later exposures in infancy show no consistent link to body mass changes. Given the prevalence of antibiotic use in infants and rising concerns about childhood obesity, further research is needed to explore the long-term effects on body mass and cardiovascular health. | |
Azad et al., 2014 [121] | In boys, early-life antibiotic use was linked to a higher likelihood of being overweight and having excess central body fat during preadolescence. This suggests the importance of prudent antibiotic usage, especially in infancy. |
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Calcaterra, V.; Mannarino, S.; Garella, V.; Rossi, V.; Biganzoli, E.M.; Zuccotti, G. Cardiovascular Risk in Pediatrics: A Dynamic Process during the First 1000 Days of Life. Pediatr. Rep. 2023, 15, 636-659. https://doi.org/10.3390/pediatric15040058
Calcaterra V, Mannarino S, Garella V, Rossi V, Biganzoli EM, Zuccotti G. Cardiovascular Risk in Pediatrics: A Dynamic Process during the First 1000 Days of Life. Pediatric Reports. 2023; 15(4):636-659. https://doi.org/10.3390/pediatric15040058
Chicago/Turabian StyleCalcaterra, Valeria, Savina Mannarino, Vittoria Garella, Virginia Rossi, Elia Mario Biganzoli, and Gianvincenzo Zuccotti. 2023. "Cardiovascular Risk in Pediatrics: A Dynamic Process during the First 1000 Days of Life" Pediatric Reports 15, no. 4: 636-659. https://doi.org/10.3390/pediatric15040058
APA StyleCalcaterra, V., Mannarino, S., Garella, V., Rossi, V., Biganzoli, E. M., & Zuccotti, G. (2023). Cardiovascular Risk in Pediatrics: A Dynamic Process during the First 1000 Days of Life. Pediatric Reports, 15(4), 636-659. https://doi.org/10.3390/pediatric15040058