Atherosclerosis Prevention and Treatment in Children and Adolescents
Atherosclerosis Prevention and Treatment in Children and Adolescents
The atherosclerotic process starts in childhood and studies show its development in fetuses. Clinical manifestation often occurs only in the sixth decade of life. Adolescence is a critical period in the development of atherosclerosis, because fatty streaks may change to transition plaque owing to genetic and environment factors. Healthcare by professionals plays a crucial role in the prevention and treatment of atherosclerosis, identifying poor lifestyle, positive family history of early cardiovascular disease, or other diseases such as dyslipidemia, obesity, arterial hypertension and diabetes. Dyslipidemia in childhood and adolescence should be treating by dietary therapy and change in lifestyle. Children with high-risk lipid abnormalities should be considered for drug treatment.
Based on literature from the last decade, the atherosclerotic process begins early in life and its progression depends on genetic factors that may be influenced by environmental factors.
The earliest pathological finding in atherosclerosis is the presence of fatty streaks in arterial intima, which has been identified as the accumulation of lipid-filled macrophages and a proliferation of vascular smooth muscle cells. The pathogenesis of atherosclerotic disease involves the inflammatory and immune systems. These cells migrate into the arterial intima and form a fibrous plaque that is responsible for clinical outcomes such as ischemic and thrombotic events in adult age. Fatty streaks in arterial intima were found in the fetus of hypercholesterolemic mothers.
Early cholesterol intake may have an influence on cholesterol metabolism later in life, so several surveys have tried to identify the association between infant nutrition, adult lipid profile and cardiovascular risk. Dremmers et al. examined for the first time the endogenous cholesterol fractional synthesis rate (FSR) among human infants, and found that early intake of cholesterol affects the FSR and the plasma lipid levels at 4 months, but the differences observed did not persist at 18 months. This study showed that there is no imprinting of cholesterol biosynthesis at early life-cycle stages with different dietary levels of cholesterol in infancy.
The Bogalusa Study and the Pathobiological Determinants of Atherosclerosis in Youth (PDAY) study showed that the atherosclerosis process starts in childhood. These autopsy studies demonstrated that the extent to which the intimal surface was covered with atherosclerosis was significantly associated with an abnormal lipid profile and the presence of risk factors, such as arterial hypertension and obesity. In the Bogalusa Study, fatty streaks were presented in 50% of the children, increasing with age, and were seen in 85% of adults. The prevalence of fibrous plaque also increased with age, being found in 8% of children and 69% of adults. In PDAY, for every 5-year increase in age, the place of damage is the same, but the grade of atherosclerosis increased from grades I–II to grades IV–V.
The Muscatine study used ultrasonography to evaluate intima media thickness (IMT) of the carotid arteries as a non-invasive indicator of the atherosclerosis process. It demonstrated that the increased carotid IMT in adults was associated with an altered lipid profile and other CVD risk factors in childhood. The adolescents with dyslipidemia have an increased risk of developing high carotid IMT in adulthood (1,6–2,5), and if overweight or obese, they have higher carotid intima thickness in adulthood compared with those who did not have both risk factors.
Abstract and Introduction
Abstract
The atherosclerotic process starts in childhood and studies show its development in fetuses. Clinical manifestation often occurs only in the sixth decade of life. Adolescence is a critical period in the development of atherosclerosis, because fatty streaks may change to transition plaque owing to genetic and environment factors. Healthcare by professionals plays a crucial role in the prevention and treatment of atherosclerosis, identifying poor lifestyle, positive family history of early cardiovascular disease, or other diseases such as dyslipidemia, obesity, arterial hypertension and diabetes. Dyslipidemia in childhood and adolescence should be treating by dietary therapy and change in lifestyle. Children with high-risk lipid abnormalities should be considered for drug treatment.
Introduction
Based on literature from the last decade, the atherosclerotic process begins early in life and its progression depends on genetic factors that may be influenced by environmental factors.
The earliest pathological finding in atherosclerosis is the presence of fatty streaks in arterial intima, which has been identified as the accumulation of lipid-filled macrophages and a proliferation of vascular smooth muscle cells. The pathogenesis of atherosclerotic disease involves the inflammatory and immune systems. These cells migrate into the arterial intima and form a fibrous plaque that is responsible for clinical outcomes such as ischemic and thrombotic events in adult age. Fatty streaks in arterial intima were found in the fetus of hypercholesterolemic mothers.
Early cholesterol intake may have an influence on cholesterol metabolism later in life, so several surveys have tried to identify the association between infant nutrition, adult lipid profile and cardiovascular risk. Dremmers et al. examined for the first time the endogenous cholesterol fractional synthesis rate (FSR) among human infants, and found that early intake of cholesterol affects the FSR and the plasma lipid levels at 4 months, but the differences observed did not persist at 18 months. This study showed that there is no imprinting of cholesterol biosynthesis at early life-cycle stages with different dietary levels of cholesterol in infancy.
The Bogalusa Study and the Pathobiological Determinants of Atherosclerosis in Youth (PDAY) study showed that the atherosclerosis process starts in childhood. These autopsy studies demonstrated that the extent to which the intimal surface was covered with atherosclerosis was significantly associated with an abnormal lipid profile and the presence of risk factors, such as arterial hypertension and obesity. In the Bogalusa Study, fatty streaks were presented in 50% of the children, increasing with age, and were seen in 85% of adults. The prevalence of fibrous plaque also increased with age, being found in 8% of children and 69% of adults. In PDAY, for every 5-year increase in age, the place of damage is the same, but the grade of atherosclerosis increased from grades I–II to grades IV–V.
The Muscatine study used ultrasonography to evaluate intima media thickness (IMT) of the carotid arteries as a non-invasive indicator of the atherosclerosis process. It demonstrated that the increased carotid IMT in adults was associated with an altered lipid profile and other CVD risk factors in childhood. The adolescents with dyslipidemia have an increased risk of developing high carotid IMT in adulthood (1,6–2,5), and if overweight or obese, they have higher carotid intima thickness in adulthood compared with those who did not have both risk factors.