Atherosclerosis, or plaque, is the process in which the arteries in the body become narrowed. Unstable plaque can sometimes rupture and lead to blood clots which cause a heart attack.
In nerd speak, atherosclerosis is referred to as atherosclerotic cardiovascular disease (ASCVD).
Understanding Plaque and Angina Symptoms
It’s normal for patients to have some plaque buildup in their coronary arteries as they age. Stable plaque rarely causes any medical problems.
The coronary arteries are under a lot of pressure, and their anatomy and blood supply make them a perfect target for plaque buildup.
Combine that with a person’s lack of exercise and stiffness of the arteries, and you can get a condition called angina, an overtreated diagnosis that we’ll discuss in future articles.
Angina is the medical term for heart-related pain. It’s when the heart doesn’t get enough oxygen temporarily when it has extra demand.
When the person stops exercising, or their anxiety level comes down, the heart’s oxygen demand goes down, and enough blood passes through the narrowed coronary arteries, stopping the chest pain.
A Heart Attack from Lack of Oxygen
A heart attack differs from angina in that the heart gets no oxygen whatsoever due to unstable plaque. It also remains starved of oxygen long enough that damage occurs.
If stable plaque is lining a coronary artery and it becomes unstable, it could break off. In its place is left a raw area on which clotting occurs.
This blood clot can grow and completely block off the artery. Without anything to break up the clot or manually open up the artery, that part of the heart muscle will die off.
That’s a heart attack.
Understanding Atherosclerosis & Cholesterol
Cholesterol is what we commonly measure in the blood. The total cholesterol value, for example, tells me how much total cholesterol is floating around in my bloodstream.
LDL cholesterol (LDL-C) tells me how much cholesterol my LDL particle carries.
Triglycerides (Tg) are a different lipoprotein altogether, not cholesterol; though they carry quite a bit of cholesterol. Tg isn’t as important when it comes to understanding atherosclerosis.
Other tests, such as HDL cholesterol and VLDL cholesterol, tell us how much cholesterol those particular proteins carry.
High cholesterol leads to atherosclerosis
The above statement is not fully accurate. Higher apolipoprotein B (apoB) directly increased atherosclerosis.
The cholesterol measurements are just surrogates for this ApoB molecule. For whatever reason, we aren’t accustomed to measuring this in the blood.
The Goal of Treating Atherosclerosis
To understand atherosclerosis, it’s important to realize that apoB is the main molecule that must be managed.
We aren’t trying to lower LDL-C or Triglyceride or raise HDL; none of that! It’s important to understand how those relate to the apoB molecules, but they don’t correlate in some individuals.
Some patients have high cholesterol, and they have no atherosclerosis. Others have low cholesterol and a lot of atherosclerosis.
This isn’t confusing. Remember that the vehicle is the lipoprotein – the apoB – while the passengers are the cholesterol molecules.
When we measure the LDL-C, then we are only told how many passengers exist on the bus. But the bus is what actually causes atherosclerosis.
We can look for symptoms like angina or signs of limb ischemia which can tell us there is atherosclerosis.
X-rays of the body will sometimes show calcified vessels. This is the calcium deposit inside atherosclerotic arteries.
Coronary CT Angiogram
CT angiograms aren’t the most accurate studies for visualizing coronary arteries. But they have a place in certain populations.
Angiograms visualize the coronary arteries by injecting dye into the coronary artery directly.
Some studies show that a CTA can show high-risk plaque and help us identify those at the highest risk of plaque rupture.
Coronary Calcium Load
Another common test is the coronary artery calcium measurement; often referred to as the CAC score. This also utilizes a CT scan to calculate the amount of calcified plaque in the coronary arteries.
When understanding atherosclerosis, it’s important to point out that in most coronary vessels, calcified plaque makes up about 20% – or the tip of the iceberg – while fibrotic plaque and lipid-rich plaque make up the other 80%.
The most accurate measurement is intravascular ultrasound, but that’s not yet a viable option.
Developing Atherosclerotic Plaques
How do these “atheromatous plaques” develop?
There are many theories, but we know that something inflames the inner endothelial lining of the arteries, making it susceptible to fatty deposits.
The floating LDL particles (different from LDL-Cholesterol) can enter the endothelium. The cholesterol particle might then release and oxidize there, which starts the inflammatory cascade.
HDL particles can extract some of this cholesterol and return it back to the liver. But that process wouldn’t be enough on its own. Which is why raising HDL doesn’t help.