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Atherosclerosis in Children

Atherosclerotic cardiovascular disease is the leading cause of death in the adult population of Western societies. It is a process of progressive thickening and hardening of the walls of the arteries as a result of fat deposits on their inner lining. However, the pathological processes and risk factors associated with its development begin during childhood. Environmental and genetic factors such as diet, obesity, exercise, and certain inherited dyslipidemias influence the progression of such lesions.

Atherosclerosis risk factors are present in children and adolescents. Traditional risk factors include obesity, hypertension, and diabetes mellitus. However, endothelial dysfunction is the key event in atherosclerosis with a significant number of young people having advanced coronary artery plaques. As the number of cardiovascular risk factors increases, so does the severity of asymptomatic coronary and aortic atherosclerosis in young people. Also, the degree of atherosclerotic changes in children and young adults can be correlated with the presence of the same risk factors seen in adults. This trend is associated with increasing blood pressure and the occurrence of Type 2 diabetes mellitus in young individuals. Together, these trends may result in increased cardiovascular morbidity and mortality as these overweight pediatric patients become obese adults.

However, only the first stage of atherosclerosis, the highly reversible fatty streak, occurs in childhood. The more harmful second stage of atherosclerosis, the atheromatous plaque, does not appear until after puberty in boys and much later in girls. The association of lipoprotein risk factors with intermediate type atherosclerotic lesions becomes evident in subjects in their late teens, whereas associations with raised lesions become evident in subjects greater than 25 years of age, which is consistent with a transitional role of intermediate lesion in the formation of advanced plaques. Early atherosclerosis is accelerated by lipoprotein risk factors. Thus, long-range prevention of atherosclerosis should begin in childhood and should include measures to control hyperlipidemia.

Systemic inflammation is present in children and adults with obesity. Inflammation associated with obesity appears to be central to the development of insulin resistance and atherosclerosis and may be important in the pathogenesis of other comorbid conditions. However, inflammation associated with obesity declines after weight loss and with exercise. High levels of blood homocysteine may be an important factor of the obesity-induced early arterial atherosclerosis during childhood. High levels of blood homocysteine may be an important factor of obesity-induced early arterial atherosclerosis during childhood. Other atherosclerosis risk factors include (Lp(a), Apolipoproteins A1 and B, and certain markers of fibrinolysis, the process where fibrin clots are broken down.

Rates of overweight and obesity in both adults and children have risen sharply during the past 20 years. Although the reasons for this escalation in obesity are not fully determined, sedentary lifestyle and dietary changes in combination with genetic predisposition are probably involved. Obesity beginning in childhood often precedes the hyperinsulinemic state. Metabolic syndrome is a constellation of disorders that produces a high risk of atherosclerosis. Children of patients with metabolic syndrome have higher values of the serum markers of inflammation, which may be associated with increased risk for development of cardiovascular disease. Current knowledge suggests that better control of blood glucose is likely to lead to improved long-term microvascular and macrovascular outcomes. Thus, the best approach to prevention of future cardiovascular disease in these young patients is early recognition and aggressive therapy.

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