The story of a plaque: from cholesterol to a heart attack

A heart attack feels sudden, but the story behind it usually starts decades earlier. It is the story of a plaque, a fatty lump in the wall of an artery. Understanding how a plaque is born, grows and finally breaks helps explain why your doctor cares so much about your LDL cholesterol, even when you feel perfectly well.

How does the story begin?

A healthy artery has a smooth inner lining, a bit like the inside of a new water pipe. Blood flows easily, and the lining keeps itself clean.

Over the years, several things can injure this lining:

• High LDL cholesterol
• High blood pressure
• Smoking or chewing tobacco
• Diabetes and high blood sugar
• High triglycerides, often linked to belly fat and fatty liver

Once the lining is irritated, LDL particles from the blood slip into the wall of the artery and get trapped there. The more LDL in the blood, and the longer it stays high, the more gets trapped. This is why lifelong exposure to LDL matters.

How does a plaque grow?

The trapped cholesterol acts like an irritant, and the body sends in clean-up cells called macrophages. They swallow the cholesterol and swell up into “foam cells”. When foam cells die, they release their fatty contents and form a soft, cholesterol-rich core inside the artery wall.

To wall off this core, muscle cells from the artery build a layer of tough fibrous tissue over it, called the fibrous cap. Calcium can also be laid down over time. Together, this lump of fat, dead cells, fibrous tissue and calcium is the plaque. Doctors call the whole process atherosclerosis.

As the plaque grows, it can narrow the artery. In the heart, this is coronary artery disease. A narrowed artery may cause chest discomfort on exertion, called angina, because the heart muscle is not getting enough blood when it needs more.

Why do some plaques burst?

Not all plaques behave the same way.

• Stable plaques have a thick fibrous cap. They grow slowly and may narrow the artery, but they rarely burst.
• Unstable plaques have a large soft fatty core and a thin cap, with a lot of inflammation. They may not narrow the artery much, so they often cause no symptoms, but they are fragile.

This is an important point. Many heart attacks come from plaques that were not very large. A normal treadmill test does not always rule out a risky plaque.

What happens during a heart attack?

When the thin cap of an unstable plaque cracks, the fatty core is exposed to the blood. The body treats this like a wound. Platelets rush in and a blood clot forms on the plaque within minutes.

If the clot blocks the artery completely, the heart muscle beyond it gets no oxygen. Heart muscle starts to die within about twenty to thirty minutes, and the damage spreads over the next few hours. This is a heart attack, or myocardial infarction.

How much muscle is lost depends on which artery is blocked, how long it stays blocked and, above all, how quickly treatment starts. Opening the artery early, with clot-dissolving medicine or angioplasty, saves heart muscle. This is why chest pain should never be “watched” at home.

How do statins change the story?

Statins reduce the amount of cholesterol your liver makes. The liver then pulls more LDL out of the blood, so your LDL falls. Statins help in several ways:

• Less LDL enters the artery wall, so plaques grow more slowly.
• Less inflammation inside the plaque.
• Stronger caps. The plaque’s soft core shrinks and the cap thickens, making it less likely to crack.
• Some shrinkage. With strong LDL lowering, imaging studies have shown plaques can shrink a little.

Interestingly, statins can make plaques show more calcium on a scan. This is often a sign of healing, not worsening, so a higher calcium score on a statin needs careful interpretation by your doctor.

Where does ezetimibe fit?

Ezetimibe blocks cholesterol absorption from the gut, so it lowers LDL in a different way from statins. Added to a statin, it brings LDL down further. In the IMPROVE-IT trial, adding ezetimibe to a statin after a heart attack led to fewer repeat heart attacks and strokes. You can read more in how ezetimibe works.

Other medicines, such as newer injections that lower LDL, are used for people at very high risk who do not reach target. Your doctor will discuss what suits you.

Does treatment make the plaque disappear?

Usually not completely. Treatment works more like healing than erasing. The plaque becomes smaller, calmer and better covered, and far less likely to burst. Some risk remains, which doctors call residual risk, and that is why blood pressure, sugar, smoking and weight all still matter.

Why does this matter for Indians?

Heart disease in India tends to start about a decade earlier than in many Western countries. Diabetes, belly fat, low HDL and high triglycerides are common together. The Lipid Association of India therefore recommends fairly strict LDL targets for many Indians, especially those with diabetes. Your waist size is a useful clue to this risk, so check your waist-to-height ratio. If you have diabetes, keeping sugar in range also protects your arteries; read whether diabetes can go into remission.

What should you ask your doctor?

• What is my overall heart risk, and what should my LDL target be?
• Do I need a statin, and would I benefit from ezetimibe or other medicines?
• How often should I repeat my lipid profile?
• Should anyone in my family be tested for high cholesterol?

Cholesterol problems often come with diabetes, thyroid problems or obesity, which endocrinologists treat. See who an endocrinologist is or book a consultation.