Although often called “heart disease,” CVD strikes the blood vessels—veins and arteries—as well. But even before people experience major events such as heart attack and stroke, the long-term narrowing and loss of elasticity in blood vessels are caused by atherosclerosis. Atherosclerosis is an inflammatory disease characterized by the accumulation of fatty plaque in the walls of arteries and blood vessels that generally develops over the course of several decades. This process is typically caused by the presence of elevated levels of cholesterol-rich low-density lipoproteins (LDLs) in the blood. As blood levels of LDL rise, they infiltrate the artery wall, where the LDLs are likely to become oxidized (by reacting with unstable oxygen-containing molecules). Oxidized LDLs cause injury to cells that line the vessel wall, and this initiates an inflammatory process that attracts white blood cells called macrophages inside the arterial lining. Other factors, such as smoking or hypertension, can also cause injury to the arterial wall and trigger inflammation. Inside the vessel wall, macrophages take up the oxidized LDLs in a rapid and uncontrolled fashion. These fat-laden macrophages (now called foam cells) die and deposit their accumulated lipids within the wall of the artery, promoting further inflammation.

As a result, the lining of the blood vessel becomes more prone to develop a waxy accumulation of cholesterol and triglycerides, known as a plaque. Over time, plaque development, loss of elasticity, and thickening in the blood vessel walls may make it difficult for blood to flow through the vessel. This “traffic jam” increases the chances of forming blood clots that either block flow at that location or break off and travel through the bloodstream, blocking blood flow elsewhere, causing tissue damage and tissue death. When blood flow is blocked in the coronary artery, which supplies blood to the heart, people experience a heart attack, or myocardial infarction. Most cases of stroke result when a clot impairs the supply of blood to the brain. (INFOGRAPHIC 7.2)

146

Question 7.1

■ ■ ■

For the most part, young people do not have heart attacks (and those that do usually suffer from rare genetic conditions). But just because most teenagers do not die from heart disease does not mean they can ignore heart health. That’s because heart disease can be insidiously gaining a foothold long before we have any obvious symptoms.

147

When Gerald Berenson started his study in 1972, this was far from accepted wisdom. Cardiologists—influenced by the prevailing practice of the day—focused more on the treatment of CVD than on its prevention. But Berenson had been trained in pediatrics as well as cardiology, and he knew that it was important to understand the beginnings of heart disease, as well as its endings.

Question 7.2

He decided to follow children and young people ages 5 to 17 years in the local school system, monitoring them twice yearly. Nurses measured their height, weight, smoking history, blood pressure, and blood lipid levels, among other variables. After age 17, they returned for evaluation periodically, up to age 45. Later, it was decided that any of the study participants who died would be autopsied.

From small beginnings, the study grew to enroll some 16,000 individuals. It is now one of the longest-running CVD studies in the world, the only one with a biracial (black–white) study population. Known as the Bogalusa Heart Study, it was the first study to demonstrate that heart disease begins in childhood.

Although the exact cause of CVD is often unknown, the Bogalusa study has shown there are certain risk factors that increase young people’s chances of developing problems—and the more they have, the higher their risk.