You don’t really need to remember all of the nitty-gritty details on the various types of cholesterol, just the bottom line: If your cholesterol levels are out of whack, you’re heart disease risk is increased. Exactly how cholesterol wreaks havoc is fairly complicated.
All cells have receptors, or “doors,” that suck LDL into them. If you have too much cholesterol in your blood, the cells make fewer receptors so they can avoid, quite literally, drowning in cholesterol. This, in turn, leads to more cholesterol floating in your bloodstream. While some of it gets returned to your liver for disposal via the garbage-bearing HDL, some of it stays in the bloodstream. [fit hangs around long enough, it may become oxidized. And some of it burrows into your artery walls, where it’s even more likely to become oxidized.
To understand oxidation, think about what happens to a metal chair when it’s left out in the backyard: It rusts. That’s what happens to cells in the body when they’re attacked by free radicals—unstable molecules that damage cells, Free radicals are a by-product of just about any bodily process that involves oxygen.
Why doesn’t cholesterol in the bloodstream always become oxidized? Because of wonderful compounds called antioxidants, which do just what their name implies; more on antioxidants in later chapters.
Your body has a system to deal with this oxidized cholesterol, dispatching specialized white blood cells called monocytes to gobble it up. If there’s too much oxidized cholesterol, however, the monocytes get stuffed. They take on a foamy appearance, hence their new name, “foam cells.” These foam cells collect in the blood vessel wall, where they turn dangerous and begin producing free radicals, which further oxidize the cholesterol, Eventually a fatty streak forms—the dreaded plaque. This is stage I of atherosclerosis, or hardening of the arteries.
Nearly everyone, regardless of their diet or lifestyle, will have at least a low level of damage in their blood vessels by the time they die. And thanks to growing rates of obesity and physical inactivity, even children under 10 are now susceptible.
Stage II Heart Disease
Eventually this mess of cholesterol, foam cells, and other debris builds up, pushing outward from the artery wall. This cholesterol-rich “bump” looks like the pus that develops in.an open wound. As with such wounds, white blood cells rush to the site to repair the damage, forming a hard coating, or cap, over it. Meanwhile, the bump continues to grow, eventually becoming so big it narrows the artery, decreasing blood flow and the supply of oxygen and mutrients to the heart. If your heart doesn’t get enough oxyger-rich blood, you may feel a squeezing sensation in your chest. This is called angina. It often happens when you exercise, because that’s when your heart needs additional oxygen
Stage III Heart Disease
To understand what may happen next, visualize a rushing mountain stream. As it flows, it knocks aside rocks, plants, and other debris in its way, sending that debris downstream. The same thing can happen in your blood vessels. As the blood flows, it can “nip” the cap off the plaque, letting the pus out just as if you nipped the scab off a wound. The larger the plaque, the more likely it is to rupture. Also, the type of LDL that makes up the plaque could play a role in how easily it bursts; recent research shows that very small, dense LDL particles make these plaques more fragile.
Once a plaque bursts, blood platelets begin sticking to the exposed surface of the ruptured plaque, eventually blocking flow through the vessel altogether and triggering a heart attack or stroke (or, if these blockages occur in the arteries leading to yourlegs, peripheral artery disease).
Unfortunately, there may not be any waming signs of heart disease before a heart attack occurs, especially in women. Some people experience angina, but others only machines, and a nurse leaning over them telling them about the heart attack they just suffered. That’s why it’s so important to identify your risk factors, such as high cholesterol, and do what you can to tilt the odds in your favor.
Examining Your Arteries
Is there any way to tell how much plaque you have before a heart attack occurs? If you’re having angina or have several risk factors for heart disease, your doctor may order a series of tests to determine if you have coronary artery blockages. These include:
Electrocardiograms, In this test, known as an ECG or EKG, electrodes are attached to your chest to detect any irregular heart rhythm or damage from a heart attack and determine whether your heart is getting enough blood and oxygen.
Imaging techniques. These can determine if you have any artery blockages and if so, how severe they are. The most Common ones are:
Radioisotope scan. A radioactive dye is injected into the bloodstream, and a special machine takes pictures of your heart and arteries as the dye passes through,
Echocardiogram. This test uses sound waves instead of dye or X-rays to trace a picture of your heart, revealing any damage to the muscle or abnormal blood flow.
CT scan. A more advanced form of X-ray, the CT machine takes detailed pictures of your heart from various angles, providing a cross-sectional view,
MRI. Using a magnetic field and radio waves, MRI records energy signals emitted by the atoms that make up the cells of the body. MRI can measure blood flow through arteries, providing information about blockages.
Cardiac catheterization, or angiography. In this procedure—an invasive test—a pencil-sized plastic tube is threaded through an artery in your groin. A catheter is then passed through the tube toward the heart and into a coronary artery. lodine based dye is then injected, and a special camera takes pictures to show any blockages.
EBCT. This sophisticated test measures calcification of the arteries, a possible indication of CHD.(Go to this chapter)
Once your doctor determines you have plaques, the goal is to stabilize them and prevent a heart attack. But it’s far better to prevent the plaques in the first place. Bringing down your cholesterol is a key strategy for both. For instance, having 60 percent of the surface area of a coronary artery covered in plaque is considered significant atherosclerosis. If your cholesterol is 150 you’ll be 80 years old before you get that much plaque. But if your cholesterol is 300 you’ll reach that level before you hit 40.
Of course, cholesterol isn’t the only factor that plays a role in the development of heart disease. In Chapter 2 we’ll explore some of the other factors—inflammation, high blood pressure, even germs—that can significantly affect your risk.
