What are the stages of atherosclerosis?

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:

1. Cholesterol from your blood starts gathering at the site of injury.
2. These cholesterols become oxidized (a chemical process) and trigger an immune response.
3. 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:

1. 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.
2. As your macrophages fill up with cholesterol, they take on a foamy appearance. So, they’re then called “foam cells.”
3. After the foam cells consume cholesterol, they die.
4. 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.