Pediatric Precursors of Adult Atherosclerosis

Brook Belay; Peter Belamarich; Andrew D. Racine

doi:10.1542/pir.25-1-4

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Brook Belay, MD*
Peter Belamarich, MD†
Andrew D. Racine, MD, PhD‡

^*Fellow, Division of Pediatric Nephrology, Department of Pediatrics
^†Associate Professor of Clinical Pediatrics, Department of General Pediatrics, Division of General Pediatrics
^‡Professor of Clinical Pediatrics; Director, Division of General Pediatrics, Department of Pediatrics, Albert Einstein College of Medicine/Children’s Hospital at Montefiore, Bronx, New York

Objectives

After completing this article, readers should be able to:

Describe the development of atherosclerotic plaque.
Discuss the two-pronged approach to addressing pediatric hypercholesterolemia advocated by the National Cholesterol Education Program and the American Academy of Pediatrics.
Describe the criteria for using lipid-lowering medication in children.
List risk factors for coronary artery disease that should be addressed in pediatric patients.

Introduction

Despite significant declines in death rates from heart disease in recent years, this continues to be the leading cause of death in the United States. In 1999, heart disease was responsible for more than 30% of all deaths, with ischemic heart disease representing 65% of this total. With improved mortality rates of coronary artery disease (CAD) has come greater understanding of how atherosclerosis arises and may be prevented.

This review summarizes recent findings regarding the development of cardiovascular disease and alerts pediatricians to how they can screen patients for precursors of CAD. It provides primary and secondary prevention strategies to manage risk factors when they are detected and directs readers to sources that include detailed guidelines for the risk factors that are discussed.

Current Understanding of Atherosclerosis

Central to an appreciation of childhood risk factors for adult heart disease is an understanding of how the principal feature of coronary artery disease—the atherosclerotic plaque—develops. Rather than a simple accumulation of cholesterol on the intimal surface of vessel walls, the atherosclerotic plaque represents the culmination of a complex series of events involving inflammatory mediators, macrophages, and activated T lymphocytes in addition to circulating lipoproteins.

The sequence begins when low-density lipoprotein (LDL) particles, those composites of lipid and protein designed to transport cholesterol from the liver and intestine to other organs, accumulate beneath the endothelial layer of the arterial wall. There, the central lipid portion of the LDL particle undergoes oxidation, and the proteins on the surface of …