9.2: Narrowing and Blocking of Arteries

When researchers look at heart disease, strokes, complications of diabetes, and even senility, they see them mainly as the result of a single underlying disease—atherosclerosis. Atherosclerosis is a disease characterized by damaged and narrowed arteries, the blood vessels that carry oxygen-rich blood to every part of the body.

Atherosclerosis is first seen as fatty streaks in the inner lining of an artery. Over time, increased fatty deposits damage the cells that line the arteries, and fibrous scar tissue leads to progressive narrowing (see Fig. 9-1). This process can begin early in life. Early stages of atherosclerosis are commonly seen in autopsies of young American men killed in war or accidents.

Since arteries carry oxygenated blood, severe narrowing can cause blood-and-oxygen starvation to that part of the body the artery feeds. If the arteries feeding the heart (coronary arteries—see Fig. 9-2) don’t deliver enough oxygenated blood, it’s felt as chest pain, and is called angina pectoris (“anger of the breast”) or simply angina.

Angina is commonly triggered by physical activity and relieved by rest. The physical activity causes the heart to beat faster to provide more oxygen to the muscles. The more rapid heart beat increases the heart’s own need for oxygen, but this need can’t be met if the coronary arteries are severely narrowed.

Figure 9-1: Cross Section of Arteries in Atherosclerosis.

In the brain, the effects of an insufficient supply of oxygenated blood depends on which part of the brain is served by the narrowed artery. Possible effects include slurred speech, confusion, weakness, and loss of vision.

Narrowed arteries aren’t the only problem caused by atherosclerosis. As atherosclerosis progresses, the thickened and damaged lining of the artery becomes rigid, often with a rough surface. The rigidity lessens the artery’s elasticity, and the fibrous scar tissue that characterizes advanced atherosclerosis can rupture. A blood clot can form at the rupture and block that narrowed part of the artery. This shuts off the flow of oxygenated blood to the tissue served by that artery, leading to the death of those cells in a very short time.

When such a blockage occurs in the heart muscle, it’s called a “heart attack.” If a significant portion of the heart muscle is damaged in this way, the heart can’t contract, causing sudden death. When the blockage occurs in the brain, it’s called a stroke. The brain damage also could be immediately fatal, or it could cause paralysis, loss of speech, loss of memory, or coma.

Stroke can also be caused by a rupture of an artery in the brain—a hemorrhagic stroke. It’s often preceded by an outpouching of the arterial wall, usually due to a weak spot and/or high blood pressure. The effect is similar, whether the stroke is due to a blockage or rupture of an artery. In both cases, the flow of oxygen to the brain is interrupted.

Figure 9-2: Coronary Arteries Nourish the Heart. They encircle the heart “like a crown.”

Blood Cholesterol

The fatty deposits in atherosclerosis are rich in cholesterol. This is no coincidence. Generally speaking, the higher the level of cholesterol in the blood, the greater the risk of atherosclerosis. But there’s a confounding aspect, related to how the cholesterol is transported. Cholesterol uses different chemical vehicles for transport, which affects cholesterol’s destination, which in turn affects the risk of atherosclerosis.

Cholesterol Transport

Because fat and water don’t mix, fat (lipid) is transported in the blood in combination with protein. These lipid-protein packages are appropriately called lipoproteins, and are classified according to their density. Since fat is less dense (lighter) than protein, the density of a lipoprotein indicates the relative amounts of fat and protein (see Fig. 9-3). Two kinds of lipoproteins that are important in cholesterol transport are low-density lipoprotein (LDL) and high-density lipoprotein (HDL).

Low-Density Lipoprotein (LDL) is mostly cholesterol and delivers cholesterol to the cells for use in making cell membranes, sex hormones, etc. When LDL in blood is excessively high, some of it is taken up by scavenger cells in the lining of arteries. As a result, excessive amounts of LDL can lead to deposits of cholesterol in the arterial lining. For this reason, the cholesterol transported in LDL (LDL-cholesterol) is called “bad” cholesterol. (Again, however, what’s “bad” isn’t the LDL-cholesterol itself. Rather, it’s an excessive amount that’s “bad.”)

Figure 9-3: Lipoprotein composition and size. LDL is bigger and contains more cholesterol.

High-Density Lipoprotein (HDL) is mostly protein, but also contains a fair amount of cholesterol. HDL generally takes cholesterol from cells and to the liver, where the cholesterol can be made into bile acids and secreted into the intestine. (Bile acids are used in digestion, and will be discussed in the next chapter.)

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To remember whether it’s “bad” or “good,” think of LDL-cholesterol as Lousy—high levels raise the risk of atherosclerosis. HDL-cholesterol is Healthy —high levels protect against atherosclerosis.

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Although most of the bile acids in the intestine are reabsorbed back into the bloodstream, some of it gets trapped by dietary fibers in the intestine and is lost in the stool. The loss of cholesterol via bile is the main way in which the body can rid itself of cholesterol. The cholesterol in HDL (HDL-cholesterol) is thus called “good” cholesterol. A high level of HDL-cholesterol in the blood protects against atherosclerosis.

It should be emphasized that the cholesterol itself is the same whether it’s being transported in LDL or HDL. In other words, the description of cholesterol as LDL (“bad”)-cholesterol or HDL (“good”)-cholesterol refers to the lipoproteins carrying cholesterol in the blood. Sometimes people are confused in thinking that there are two types of cholesterol in the diet—“good” cholesterol and “bad” cholesterol. Cholesterol is cholesterol.

Risk Factors

A risk factor is a condition or circumstance that increases the chance of developing a disease or injury. There are many risk factors for atherosclerosis, the primary ones being genetic predisposition, aging, male gender, smoking, high LDL-cholesterol, and high blood pressure. Diabetes also increases the risk. Of course, the more risk factors one has, the higher the risk of atherosclerosis.

Blood-Cholesterol: The American Heart Association (heart.org) recommends that everyone age 20 and older have their blood-cholesterol checked every 4-6 years. Your physician will evaluate your cholesterol values along with other risk factors (e.g., high-blood pressure) to determine whether your blood-cholesterol is too high.

Genetic Predisposition ranges from the subtle to the substantial. A family history of heart disease or stroke suggests a genetic predisposition to atherosclerosis, especially if heart disease or stroke occurred in one’s father or brother before age 55, or one’s mother or sister before age 65. Keep in mind, however, that such relationships may be influenced by other factors; families not only share genes but also tend to share eating, smoking, drinking, and exercise habits.

A genetic predisposition is usually reflected in high levels of LDL-cholesterol in the blood. Fortunately, the high levels—and thus the risk of atherosclerosis—can be lowered by diet and/or medication.

Male Gender: Men of all ages have a higher death rate from atherosclerosis-related diseases than women of the same age and race (see Fig. 9-4), perhaps because women have higher HDL-cholesterol than men. The female sex hormone estrogen can raise HDL-cholesterol, whereas the male sex hormone testosterone can lower it.

Figure 9-4: Heart Disease Death Rate in 2019 by Age, Gender, Ethnicity¹

Smoking: Smoking increases the risk of a heart attack—particularly sudden death from heart attack—even more than it increases the risk of lung cancer. Smoking reduces the amount of oxygen the blood can carry, causes constriction of the blood vessels and damage to the vessel lining, raises blood pressure, and increases the risk of blood clots.

Aging: In this country, the risk of suffering or dying from heart disease increases progressively and dramatically after age 55 (see Fig. 9-4).

However, the age-adjusted death rate from heart disease has fallen dramatically in this country since the 1950s (see Fig. 9-5). A combination of factors, including less smoking by men, improved treatment of high blood pressure and heart disease, and dietary changes have all contributed.

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Age-adjusted death rates adjust for changes in the proportion of older adults in a population. Otherwise, increased death rates can simply be from an increased portion of older adults.

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High blood pressure (130/80 mm Hg or higher)² increases the risk of heart attack and stroke. High blood pressure can cause damage to the lining of arteries and can be a determining factor in the formation and rupture of outpouchings of blood vessels in the brain (hemorrhagic stroke). High blood pressure is much more common among blacks than whites in this country.

Figure 9-5: Age-Adjusted Death Rate for Heart Disease, Cancer (1950-2018).³

The 130 in the 130/80 mm Hg blood pressure reading is the pressure in the arteries when the heart contracts (beats). The 80 is the arterial pressure between heartbeats.

Metabolic Syndrome is having 3 of 5 specific risk factors, which markedly increases the risk of several diseases, including diabetes, heart disease, and some cancers. The 5 risk factors are: (1) high blood pressure, (2) high fasting blood-glucose, (3) high blood-triglycerides, (4) low blood-HDL, (5) high waist-circumference.⁴ A big waist indicates excess abdominal fat (“belly fat”).

The waist sizes that define “abdominal obesity” vary by country. For men in the U.S., Canada, and Europe, abdominal obesity is defined has having a waist size of 40 inches or more, whereas in China and Japan, it’s 33 inches or more. For women, the cut-offs are narrower (31 to 35 inches).⁴ Keep in mind that waist size isn’t the same as belt size. Many people wear their belts below a big belly that obscures their waist!

Figure 9-6: Prevalence of Metabolic Syndrome, U.S. age 20+ in 2011-2016⁵

The prevalence of metabolic syndrome has increased over the years, as expected with the rise in obesity and diabetes; the increase in ages 20-39 is particularly concerning. More than one-third of U.S. adults have metabolic syndrome, with prevalence varying by ethnicity (see Fig. 9-6).⁵