Atherosclerosis causes narrowing and hardening of the arteries, creating slowdowns in blood flow. Even worse, atherosclerosis can trigger sudden blood clots. Heart attacks and strokes are the often-deadly result.
If we could see what was going on in our arteries, we might think twice about our lifestyle choices. Could atherosclerosis be clogging your arteries? Take a look on this amazing voyage into your body's highway system.
Atherosclerosis: Certain Arteries More Vulnerable
The entire body depends on arteries for blood flow. Atherosclerosis acts throughout the body but is more selective as to where it becomes serious.
"One of the paradoxes of atherosclerosis is that although it acts diffusely, blockages tend to form only in certain places," according to Saul Schaefer, MD, professor of medicine at the University of California-Davis.
- The coronary arteries bring blood to the heart. A sudden blood clot in a coronary artery can cause a myocardial infarction, or heart attack. Stable blockages here can sometimes cause angina, or chest pain.
- The carotid, vertebral, and cerebral arteries carry blood to the brain. Atherosclerosis here can cause strokes.
- The femoral arteries carry blood to the legs. Atherosclerosis in these arteries, or their branches, can cause peripheral arterial disease.
The Endothelium: Canary in a Coal Mine?
All our arteries are lined by special tissue called endothelium. Healthy endothelium dilates arteries widely during exercise. It also prevents atherosclerosis or blood clots from developing.
Using tests not widely available, researchers can detect problems in the endothelium before atherosclerosis ever develops. "Most likely, damaged areas of endothelium are where atherosclerosis begins," says Schaefer.
You can't feel problems in your endothelium. But "if you're sedentary, smoke, have diabetes, high blood pressure or cholesterol, you likely have some endothelial dysfunction," according to Schaefer. That can set you up for developing atherosclerosis.
Atherosclerosis: What's in Your Arteries?
Over years, continued exposure to risk factors tends to cause atherosclerosis. The process works like this:
1. Fatty Streaks
Low-density lipoprotein (LDL or "bad" cholesterol) works its way into the walls of arteries. Once inside, LDL is like toxic waste: hard to detect, hard to dispose of, and potentially disastrous down the road.
If we could see inside arteries, the LDL at this point would be visible in the wall as a fatty streak, like a smear of grease. Autopsies of young people show that fatty streaks develop as early as the teenage years.
2. Plaque Formation
Over time, more cholesterol accumulates in the artery. The body sends leukocytes, a cleanup crew of white blood cells. The cholesterol and the cells responding to it evolve into a "bump" on the artery wall. This is called a plaque.
3. Plaque Growth
Unfortunately, the ongoing "cleanup" doesn't shrink the plaque. In fact, just the opposite: as more cholesterol and cells gather, the plaque grows. What happens next inside your arteries can be a matter of life and death.
Growing Plaques: Arteries' Extreme Makeover
As plaques grow, arteries remodel themselves to keep blood flow. They thicken their walls, making room for the enlarging plaque. "The plaque grows but stays out of the way, like a car stranded at the side of the road," explains Schaefer.
Eventually, some plaques grow slowly into the flow of blood. Even so, they rarely cause symptoms until the artery is more than 70% blocked. "Given enough time, arteries can create collateral channels, a natural bypass around the blockage," says Schaefer.
When a plaque does limit blood flow, pain with exertion is the most common symptom. In the coronary arteries, this causes angina (chest pain), and in the legs, claudication (muscle pain).
Surprisingly, these near-complete blockages aren't the most dangerous plaques.
"Another paradox of atherosclerosis is that these severe blockages don't usually cause heart attacks," explains Schaefer.
Atherosclerosis: "Stable" and "Unstable" Plaques
In general, severe blockages that have occurred over decades are stable. They're the bad neighbor who everyone's gotten used to living with. (Or you just don't know he's there.)
Rather, the plaques to watch out for are the young punks down the block. "Most heart attacks occur because of sudden changes in plaques that only block 20% or 30% of an artery," says Jeff Borer, MD, professor of cardiovascular medicine at Weill Cornell Medical College in New York.
These small but deadly plaques are hard to detect, even with advanced tests for atherosclerosis. "Generally, we just have to infer they're there from the presence of bigger blockages elsewhere," says Borer.
Learning why these smaller plaques rupture is a key focus of ongoing research. Studies over the past decade have demonstrated that inflammation inside the plaque is the key
Atherosclerosis: Inflammation in Your Arteries
How does a plaque become inflamed? As plaques grow, leukocytes and muscle cells gather inside. The leukocytes attempt to digest the LDL cholesterol.
That may sound like a good thing. But leukocytes' job description includes releasing chemicals that can be destructive. The local muscle cells also release damaging substances.
The result can be a dissolving of the interior of a stable plaque, rendering it unstable. If the cap of the plaque breaks off, dangerous materials inside are exposed to blood flowing by. A blood clot forms rapidly in the artery, causing a heart attack or stroke.
Severe but stable blockages can often be seen on a stress test or coronary angiogram. However, smaller, dangerous plaques usually go undetected. And with current knowledge, "it's impossible to determine when these plaques are inflamed and therefore more likely to rupture," explains Borer.
Using a marker in the blood called C-reactive protein (CRP), doctors can get a general idea of the level of inflammation in the body. This test can't predict heart attacks or strokes with accuracy, though.
Atherosclerosis: Calcium and Hardening of the Arteries
Why is atherosclerosis often described as "hardening of the arteries?" As plaques grow and evolve in the artery walls, calcium deposits inside them. The calcium makes the plaque firm and the artery stiffer. In general, stable plaques contain more calcium.
A relatively new test called electron-beam computed tomography (EBCT) can calculate the amount of calcium in the coronary arteries and help predict the risk of heart attack in certain people.
Atherosclerosis: Reducing Your Risk
Atherosclerosis is frightening because its complications can be both unpredictable and deadly. However, it's worth remembering that up to 90% of the risk of a first heart attack is preventable. The risk factors are well known, and most can be prevented or treated.
Smoking: Tobacco smoke damages endothelium and accelerates atherosclerosis. Smoking also increases inflammation, the process that makes plaques unstable. On the other hand, "if you quit smoking, after a few years your risk falls nearly to that of a nonsmoker," says Borer.
Sedentary lifestyle: Exercise keeps arteries' endothelium healthy. This helps explain why frequent exercise dramatically reduces the risk of atherosclerosis. Exercise also reduces the risk of diabetes, another cause of atherosclerosis. Thirty minutes a day provides a large benefit, but any exercise is better than none.
High blood pressure and cholesterol: If you're leaving your blood pressure untreated, your arteries are taking the pounding. Lowering cholesterol to healthy levels is proven to reduce the risk of heart attacks. Some people can achieve healthy blood pressure and cholesterol levels with lifestyle changes alone. Many, though, will require medicines to reduce the risk.
What you don't see can hurt you. Until we can see inside our arteries, the best advice is to start lowering your risk for atherosclerosis now.
"Without question, reducing your risk factors will lower your chances of dying from cardiovascular disease," the most common killer of Americans, says Schaefer.