Why Do Arteries Get Clogged? It’s Not What You Think

Why Do Arteries Get Clogged? It’s Not What You Think


Cardiovascular disease has been the number
one killer in the world for over a decade and statistically, it’s the number one most
likely thing to kill me, so I’m definitely interested in learning more about it. It brings
to mind one phrase you may have heard now and then, “clogged arteries.” And I’m
going to be completely honest, before I got to college and learned the mechanism behind
this disease, I thought clogged arteries were a direct result of diet. Like if I put too
much butter on my potatoes, that butter was clogging my arteries. But it turns out that’s
not what happens. The term Cardiovascular disease is a catch-all for a bunch of different
diseases, and there are a ton of factors that go into what causes each kind. But the structure
we need to learn to understand these diseases isn’t the heart necessarily, it’s those
arteries. These things are complex, ever changing organs that deliver blood throughout
the body and play a role not just in disease, but in experiencing different climates, exercising,
and maintaining homeostasis. In the last few videos, we’ve been talking about the components of blood, which includes a bunch of specialized cells. We’ve got red blood cells for carrying
and delivering oxygen to hungry body parts, and the white blood cells that make up a big
part of our immune system. But we haven’t talked about the hardware that contains them
and moves them. That’s where the cardiovascular system comes in. If you prefer calling it
the circulatory system, that’s fine too — they’re the same thing. In this video,
I’ll use cardiovascular because the name gives away its pieces: the heart, hence the
cardio portion, and all the blood vessels, which is the vascular part. Now, the heart
is an incredibly complex organ and we could dedicate an entire series to it, but for now,
we’re going to focus on the blood vessels, those tubelike structures that transport blood
around the body. When you take a big picture look at the cardiovascular system, you’ll
notice two distinct loops of blood vessel networks, like a figure eight. One of those
loops carries deoxygenated blood from the right side of the heart to the lungs, picks
up some oxygen, and circles back to the heart. This loop’s pretty straightforward, only
one organ to visit. This pulmonary circulation is where important gas exchange happens, letting
us do something with all the carbon dioxide waste we’ve built up in our blood and capture
that oxygen we breathe in. Once our blood is nice and oxygenated it comes back to the
left side of the heart to be pumped into systemic circulation, the loop that hits everything
that isn’t the lungs. As you can imagine from the everything about this, the systemic
circulation has a little more going on. Right after getting ejected from the left side of
the heart, blood passes through the aorta, the biggest artery we have. This artery is
going to branch off into smaller arteries up into the neck and brain and down the body
into the limbs and abdomen. As they get closer to individual tissues and organs, they’ll
branch off into tiny arterioles, and then into microscopic blood vessels called capillaries.
Some of those capillaries are so tiny that red blood cells have to line up cell by cell
to get through. Not all of our arteries are built the same. Big arteries close to
the heart, like the aorta are under a lot of pressure. And I don’t mean their parents
are hovering over their shoulder checking their math homework, I mean physical pressure
from the pumping heart muscle. To cope with this pressure, they’re built to be more
elastic, letting them expand along with the pressure. As we get to the arteries of the
arms and legs, we see them become more muscular, giving them more control of their diameter.
This is where we start seeing the arteries as more than just static tubes. An artery
itself has three main layers, or tunics: the tunica externa, media, and intima. Literally
the outer, middle, and inner layers of the artery. They all serve a different purpose,
and they all come up again in understanding cardiovascular disease. The tunica externa,
also called the adventitia, gives the artery its general shape and structure. The tunica
media is built of a protein called elastin, which, as you could tell by the name, gives
the artery some elasticity. But it’s also got a layer of contractible muscle around
it. Now, this is a different type of muscle from the skeletal muscles in your arms and
legs. This smooth muscle surrounds the entire blood vessel which provides a little more
support, but more importantly, it regulates how wide the artery becomes. Why is this so
important? Well, the ability to shrink or expand our blood vessels comes in handy in
different situations. Let’s take a look at exercise for example. Right now, you’re
at rest. Your heart is probably beating nice and steady — around sixty to a hundred beats
per minute. At that rate, about five liters of blood will pump out of your heart in the
next sixty seconds. That’s enough to feed all of your oxygen-hungry tissues at rest,
but they get hungrier when you exercise. So in order to ship more oxygen to those tissues,
your body increases its heart rate, or how frequently your heart pumps, and stroke volume,
the amount of blood squeezed out with each pump. For most of us, that means the five
liters of blood we were pumping every minute at rest can get up to thirteen liters a minute
at peak exercise, and even more if you’re a trained athlete. That means your arteries
have to adjust for two and half times more blood volume coming through. They do so by
vasodilating — the smooth muscle of the tunica media relaxes, which expands the diameter
inside the blood vessel. In a totally different situation, your arteries can vasoconstrict
as a way to reduce loss of body heat and stay warm in cold temperatures. Those changes in
diameter are all possible thanks to the tunica media, but there’s still one more layer
to arteries. The innermost layer, or tunica interna, has a little more smooth muscle and
elastin, but most importantly, it’s lined with super smooth endothelial cells. These
cells have a very important job — provide a low friction surface and make sure blood
gets through circulation as smoothly and efficiently as possible. So all in all these arteries
have a thick outer layer, a smooth inner layer, and a middle layer that changes the diameter
of the vessel, which is amazingly useful. All of this sets us up to understand how we
can go from a free flowing, smooth blood vessel to a “clogged artery”. Okay, so this process
isn’t something that happens all at once. Arteriosclerosis is the buildup of plaque
within an artery to the point where it interferes with normal function, and it can happen in
any artery. Some of these conditions get names with a little more pizazz though, a
little more oomph where you’re like “ohh dang, I don’t want that” but the pathogenesis
is the same. Like when the arteries to the brain get blocked, we call that a stroke or
when the arteries to the heart muscle get blocked we call that a heart attack. And when
those organs don’t get blood, they don’t get oxygen, and that can cause severe damage
or sometimes death. There are a few different ways it can begin, but at some point, the
endothelial cells become dysfunctional. Remember from earlier, this layer’s job is to be
as smooth as possible so blood can just flow through. And a bunch of different factors
make this condition more likely — smoking, high blood pressure, diabetes all predispose
an artery to endothelial dysfunction. For instance, smoking reduces the availability
of nitric oxide, a chemical that allows the blood vessels to vasodilate, and increases
some inflammatory factors that make the blockage even worse. But no matter what causes the
dysfunction, now the endothelium lets lipids from the blood sneak under that layer of endothelial
cells and into the intima. That starts a process where immune cells are called to the scene,
where they enter the intima and oxidize those lipids into foam cells. Foam cells sound cute,
but these things are serious. Those immune cells also recruit more smooth muscle to the
area, as well as the tough connective tissue collagen, which is definitely not supposed
to be there. As a result, instead of a soft bump you’ve got a tough, fibrous plaque.
That cycle of plaque stacking can continue until blood can barely get through an artery
and that’s when the tissues it supplies oxygen to really start to suffer. So again,
clogged arteries are the narrowing of arteries from plaque buildup and not some kind of buttery
cholesterol fatberg in your blood vessels. But that doesn’t mean it’s not dangerous. That plaque can break open, which means now there’s a blood clot free floating in your arteries.
That’s why a narrowing of the arteries around the heart is so deadly. If that loose blood
clot gets stuck on some plaque in those arteries, oxygen can’t get to the heart muscle itself
and it can die off. And that’s a heart attack. This is one of the reasons why healthcare
professionals recommend exercise for preventing heart disease. It has the ability to reduce
chronically high blood pressure and lower bad cholesterol, but it also improves your
ability to produce nitric oxide, that vasodilator that improves blood flow. One of the other
benefits of exercise is making more red blood cells, but how does that happen? Tune in to
the next episode in our playlist to find out how. I’m Patrick Kelly, thanks for watching
Seeker.