Atherosclerosis: Arterial Disease

What are the stages of atherosclerosis?

There are several stages of atherosclerosis (described below). Each stage involves changes in your artery wall. These changes are so tiny that you can’t see most of them without a microscope. But they add up to cause serious damage to your artery.

The stages of atherosclerosis happen over many years. And they often go undetected.

Stage 1: Endothelial damage and immune response

Atherosclerosis begins when damage occurs to the inner layer of your artery wall. This layer is called the intima. The surface of your intima is lined with endothelial cells. This thin lining, called the endothelium, is the barrier between your blood and your artery wall.

Many things can harm your endothelium. The most common culprits include:

High levels of LDL (“bad”) cholesterol circulating in your blood.

Toxins, like those from cigarette smoke.

High blood pressure that persists for a long time.

Once your endothelium is damaged, several things happen:

Cholesterol from your blood starts gathering at the site of injury.

These cholesterols become oxidized (a chemical process) and trigger an immune response.

This immune response causes many white blood cells to travel to the area. These white blood cells are called monocytes. They gather and lead to inflammation within your artery.

Stage 2: Fatty streak

A “fatty streak” is the first visible sign of atherosclerosis. It’s a yellow streak or patch formed from dead cells at the site of endothelial damage.

Here’s how it forms:

The monocytes that moved to your artery turn into cells called macrophages. Macrophages surround and consume invaders to get rid of them. In this case, your macrophages consume the cholesterol.

As your macrophages fill up with cholesterol, they take on a foamy appearance. So, they’re then called “foam cells.”

After the foam cells consume cholesterol, they die.

As the foam cells die, your body sends more and more white blood cells to the area. Those cells continue consuming cholesterol, get foamy and die. As this process continues, it damages your endothelium more.

All the dead foam cells form a bulge underneath your endothelium. This “fatty streak” is the beginning of plaque formation.

Stage 3: Plaque growth

More dead foam cells and other debris continue building up at the site of the fatty streak. The fatty streak slowly gets bigger and forms into a larger piece of plaque.

Your artery’s smooth muscle cells form a layer on top of this plaque. This is called a fibrous cap. The fibrous cap covers the plaque. It prevents bits of plaque from breaking off into your bloodstream. Meanwhile, the plaque keeps growing. It gains calcium, which makes it harder.

For a while, your blood still has enough room to pass through. That’s because your artery wall expands outward to make space for the plaque. But it can only expand outward so far. As the plaque gets too big, the opening of your artery becomes narrower and narrower. There’s less room for your blood to flow through.

The plaque may stay stable for a long time. But eventually, it can rupture.

Stage 4: Plaque rupture

In this final stage, the plaque ruptures and causes major problems in your body. At this point, the plaque has been in your artery for a long time — perhaps many years. It has grown in size and taken up more space in your artery. But the fibrous cap has kept the plaque from breaking open until this point.

When the fibrous cap breaks open, the plaque inside comes into contact with your blood. This can trigger a blood clot to form. This blood clot (known as a “thrombus”) blocks your blood flow and leads to a heart attack or stroke.

Researchers are still learning how these ruptures happen and who’s at risk. A thin fibrous cap may be more likely to rupture than a thicker one. The size of the plaque itself may not matter as much. In some cases, smaller plaque bulges lead to a heart attack.

What causes atherosclerosis?

Damage to your artery’s inner lining (endothelium) causes atherosclerosis to begin. The damage usually occurs slowly and over time.

Risk factors for atherosclerosis

Some conditions can raise your risk of developing atherosclerosis. These include:

Hyperlipidemia (high cholesterol).

Hypertension (high blood pressure).

Hyperglycemia (high blood sugar).

Immune response and inflammation. Smoking is a major cause.

What are the symptoms of atherosclerosis?

Atherosclerosis often doesn’t cause any symptoms until an artery is very narrow or entirely blocked. Many people don’t even know they have the condition until a medical emergency, such as a heart attack or stroke.

You may start noticing symptoms if your artery is more than 70% blocked. The blockage causes your blood flow to slow down. As a result, your body isn’t getting enough oxygen.

Some early warning signs include:

Chest pain (angina) while exercising. This pain stops when you rest.

Leg cramps when walking (intermittent claudication).

Transient ischemic attack (TIA). This is a “mini stroke” that has the same symptoms as a stroke. But it goes away within a day and doesn’t damage your brain. If you have a TIA, you’re at risk of having a stroke within days or weeks.

If you have a blood clot or sudden blockage, you may have a heart attack or stroke. Symptoms of a heart attack include:

Chest pain. It may be mild discomfort or severe, crushing pain.

Pain in one or both arms or shoulders.

Discomfort in your neck or jaw.

Nausea or vomiting.

Heart palpitations.

Anxiety or a feeling of “impending doom.”

Sweating.

Dizziness or fainting.

Women and people designated female at birth (DFAB) may also experience shortness of breath, fatigue and insomnia. These symptoms might begin days, weeks or even months before the heart attack.

The blood clot or blockage can also lead to a stroke. Symptoms of a stroke include:

Sudden numbness or weakness in your face, arms or legs, especially on one side of your body.

Sudden trouble speaking or understanding others.

Slurred or confused speech.

Trouble seeing in one or both eyes.

Severe dizziness or loss of balance.

Trouble walking.

Sudden and severe headache.

How is atherosclerosis diagnosed?

To determine whether you have atherosclerosis, your healthcare provider will start with:

Family medical history.

Personal medical history.

Physical exam, listening with a stethoscope for weak or absent pulse or an abnormal sound in your arteries called bruit.

Blood tests, which can measure the amount of fat, cholesterol, sugar and protein in your blood.

What tests diagnose atherosclerosis?

Your healthcare provider may order additional tests to diagnose atherosclerosis and plan the best treatment for you. These tests include:

Angiography. This test uses special X-rays to locate and measure blockages. Your healthcare provider will inject a contrast dye into your arteries to help the blockages show up on the X-rays. Your healthcare provider will insert a catheter (thin tube) into one of your arteries, usually in your groin or arm.

Ankle/brachial index. This test compares the blood pressure in your ankle to the pressure in your arm to measure blood flow in your limbs.

Chest X-ray. A chest X-ray takes pictures inside of your chest.

CT scan. This scan takes pictures inside of your body and can show any hardening and narrowing of your large arteries.

Echocardiogram (echo). An echo takes pictures of your heart’s valves and chambers and measures how well your heart is pumping.

Electrocardiogram (EKG). An EKG measures your heart’s electrical activity, rate and rhythm.

Exercise stress test. This test measures your heart function while you’re physically active.

Carotid ultrasound. This test takes ultrasound pictures of the arteries in your neck (carotid arteries). It can detect hardening or narrowing of these arteries as blood flows to your brain.

Abdominal ultrasound. This ultrasound takes pictures of your abdominal aorta. It checks for ballooning (abdominal aortic aneurysm) or plaque buildup in your aorta.

What specialists might I need to see for atherosclerosis?

If you have atherosclerosis, your healthcare provider may recommend you see a specialist, such as:

Cardiologist, who specializes in the heart.

Nephrologist, who specializes in the kidneys.

Neurologist, who specializes in the nervous system (brain and spine).

Vascular specialist, who specializes in blood vessels.