Cardiovascular disease is the leading cause of death in the United States and has origins in childhood. Familial hyperlipidemia, childhood obesity, and certain systemic diseases increase the risk of atherosclerosis in childhood. Hyperlipidemia in childhood and adolescence should be identified and treated with medication in the setting of genetic hyperlipidemia or the presence of multiple cardiovascular risk factors. Healthy lifestyle choices should be stressed to all families, especially those who are a high risk for cardiovascular disease.(1)

Hyperlipidemia can alter vascular endothelial function and impair some of its pro-fibrinolytic and anti-thrombotic regulatory properties, as well as initiate the atherosclerotic process. There are strong links between vascular changes and hyperlipidemia in children, both from pathologic and non-invasive assessment studies.(2)

Atherosclerosis begins in childhood as deposits of cholesterol and its esters, referred to as fatty streaks, in the intima of large muscular arteries. In some persons and at certain arterial sites, more lipid accumulates and is covered by a fibromuscular cap to form a fibrous plaque. Further changes in fibrous plaques render them vulnerable to rupture, an event that precipitates occlusive thrombosis and clinically manifest disease (sudden cardiac death, myocardial infarction, stroke, or peripheral arterial disease). (3)

We now have evidence that serum lipoprotein concentrations, smoking, obesity, and hyperglycemia are closely associated with fatty streaks in the second decade of life. The same risk factors, along with hypertension, are associated with raised lesions in the third decade of life. These results indicate that the long-range
prevention of CAD should begin in childhood with control of the risk factors for CAD to limit the extent of juvenile fatty streaks and, more critically, to prevent or retard their progression to raised lesions.(3)

Chronic renal insufficiency (CRI) is associated with a characteristic dyslipidemia. Findings in children with CRI largely parallel those in adults. Moderate hypertriglyceridemia, increased triglyceride-rich lipoproteins (TRL) and reduced high-density lipoproteins (HDL) are the most usual findings, whereas total and low-density lipoprotein cholesterol (LDL-C) remain normal or modestly increased. Qualitative abnormalities in lipoproteins are common, including small dense LDL, oxidized LDL, and cholesterol-enriched TRL. Measures of lipoprotein lipase and hepatic lipase activity are reduced, and concentrations of apolipoprotein C-III are
markedly elevated.(4)

1.Gidding, Z. F. a. S. (2009). "Lipid Management in Children." Endocrinol Metab Clin N Am 38: 171-183.

2. McCrindle, B. (2006). "Hyperlipidemia in children." Thrombosis Research 118: 49-58.

3. McGill HC, C. M., EE Herderick, et al (2000). "Origin of atherosclerosis in childhood and adolescence." Am J Clin Nutr 72(suppl): 1307s-15s.

4. JM Saland,HG Grindle. (2007). "Lipoprotein metabolism in chronic renal insufficiency." Pediatr Nephrol 22: 1095-1112.