This is part 2 in the Personal Prevention Experience series. This is
another Bale/Doneen slide. It's talking- there- it makes a couple of good points.
The first one is the focus on education. Again, education is the biggest part of
this. It's like the old Sims commercial and many other commercials. The best
customer, the best client, the best patient is clearly somebody that knows
what's going on- is the educated, smart consumer. Now, another thing that's very
helpful to see on this slide is something that you wouldn't notice
unless it's pointed out or you're already aware of it. This is- a picture of
an artery with blood flow going through it. Now, this middle one is the best one
to look at and the bottom one is- has got a couple of problems; but the middle one
is- shows the blood going through the artery and it shows that the plaque is
not in the lumen. The plaque is inside the artery wall itself; and in fact the
vast - the vast majority of that plaque is LDL. So that's what leads to a lot of the
misperception that cholesterol in your diet or LDL is what causes plaque. Again,
that's wrong. Here's what actually happens. You get inflammation of that
lining right there, which you can hardly see. It's a single cell layer. It's called
the intima or endothelium of the artery. When you get inflammation of that, you
get holes and nicks in it. Then, LDL, cholesterol that's in the blood actually
goes through those holes and nicks and lodges in that artery. Let's go to
another issue- event reality. Here's the major point that- that this makes- that
99% of all plaque is going away from the hole, in other words in the artery itself.
Now, most heart attacks and strokes are caused by plaque that is not blocking
the flow of blood. Again, we- the obvious common logic is that it's like hair
clogging the drain of a shower or a bathtub. It's inside the lumen. That's not
what happens. It's inside the- the artery wall as we just showed on the last slide.
That's why you can't predict a heart attack or a stroke. As we've said many
times, half of heart attacks- the patient first finds out about it by dying. Now,
here's a picture of- a diagram of a clean artery with no disease. The major areas
that we want to look and think about are the intima or that endothelial layer.
It's what keeps things like cholesterol from soaking into the artery- the artery
wall itself. Then the media is the second layer, it's a muscle layer that provides
strength to keep that intima layer, which is so thin it would blow apart
with the pressure that's inside a typical artery. We don't worry about that
adventicia. It just keeps the artery in place. It's when this intima gets-
irritated and burned and has holes in it that cholesterol starts to seep through
those holes. The cholesterol then, can't go on through the media, so it gets stuck
between the intima and media layers. Here are a couple of images in these next two
slides- of the progression of this disease. The first slide just- I mean the
first on the left, basically shows a normal artery, an artery without plaque.
Each successive cut shows more and more plaque. It also talks about some of the
enzymes that you start to see. On the inflammation panel, for example, you'll
see LP PLA 2 / plaque-2. If you haven't taken the course, the free inflammation
course, go back to our videos, just google Ford Brewer
inflammation course. It should come up. If you haven't, make a comment below and
I'll help you find the- find the course; but LP PLA 2 is that one of the labs
that we look at in the inflammation panel. That starts to happen along this
area as shown here. It's- it's an enzyme released by the immune system, is it's
trying to get this plaque out of here. Your immune system recognizes that
plaque and knows this should not be happening. It's when this happens over on
the right that you get a heart attack or stroke. You get damaged- the- the immune
system attacks this plaque; that's where you start to see these little red spaces
and actually it's green, some enzymes called MPO,
just like plaque 2. I'll show you that in the next slide; but you start getting
this what we call necrotic or dead material because the immune system is
releasing enzymes which degrade and dissolve this plaque, trying to get rid
of it; but here's the problem. That and that necrotic material, if it
releases out into the bloodstream as this has in this diagram, will cause a
clot. So it's not- in the clot- the clot, if it's big enough and goes to the heart,
caused a heart attack. If it's big enough and goes to the- to the brain, it causes a
stroke. Now, so it's not the plaque itself that's blocking off the artery wall and
causing the heart attack like so many people think, again, just using common
logic. That's why you can't predict it by doing a stress test or angiograms. You
cannot predict this. It's because of this acute episode where you get the
leak. Now that's called- and you'll hear it multiple times, we call it a hot
plaque. Let me go back to a comment, well actually we'll make that. We'll go back
to it a little bit later. I mentioned that some of the- the drawing
in the artery wall is a little bit different. May not all be red, as you
start getting into some of the release of these enzymes. In fact, some of them
are green. Pardon the- what's the word I would use-
maybe ugly imagery. I'm gonna- but I'm gonna connect a couple of dots here.
We're talking about MPO here- Myeloperoxidase. It's another enzyme, another
lab test. It's green and you may recognize this when you have a cold or a
child has a cold and and they have mucus coming out of their nose. It's got a
greenish tint to it. That's Myeloperoxidase; and it's the same thing. It is
enzymes that are released by white cells. A certain type of white cell releases
MPO. Another type of white cell releases plaque 2. So those are some of the key
tests within the inflammation panel; and as you see in this image, again, it's the
release of this liquid plaque with all of these inflammatory markers in it, that
causes a clot, which causes the heart attack. Now, that was all images. Let's
just look at the- the reality. This is- this is an artery. This is- and this is a
picture of a real one. It's on a microscope. They've cut it sideways like
this. So you can see the lumen, which is inside. This is where the blood flows. You
can see this red tint. That's that media layer that we talked about earlier.
That's the muscle. That's the structure that holds holds the artery.
Now, this thin layer right here is the intima. You can barely see it, but right
here you can see it very well. In fact, there's nothing but intima right here,
between this area- this light colored area, and this lumen where there- where
the artery blood flow is. All of this is plaque; but we can tell by
looking at it, it is state- this part of the plaque is stable.
It's a waxy substance. It's not going to break loose but look again and let's
look deeper at this- inflamed plaque. This was liquid. It's inflamed plaque and the
reason we know that is- that it's liquid, is it has retracted some away from the
rest of the tissue, when you put it in the- on the slide preparation. So now you
begin to realize, you've got hot liquid plaque with those inflammatory immune
cytokines biomarkers in the- in this plaque right here; and the only thing
standing between that and the flow of the blood is that intima layer. Now if
that breaks through, it can cause a clot. And that's exactly what happened here.
This is a different type of preparation but as you can see it's a- it's a real
artery. In this one, the- the muscular or artery wall, the media layer is this more
clear looking area. This yellowish waxy looking stuff is stable plaque. These
brown areas are hot liquid plaque areas. And look what happened here. Again, as you
can see this is a Bale/Doneen slide. Brad and Amy tend to call this
"intima," the tennis court, because your body has several- has the equivalent of
several tennis courts; but here's the the most important part. Look at how that has
cracked. This area used to look like this one; and the intima cracked and this
liquid came out. Now, that's not the liquid. That black thing is a clot. The
clot formed when that hot liq- liquid plaque-
when this crack happened in the intima layer, and the hot liquid plaque touched the
blood stream, therefore, causing the clot. That clot went on back up into
this area and in fact as you can see, well you can't see, the reason they were
taking this artery out, is because this patient has died. He's died from a heart
attack and it came from the clot that was formed here. One other thing to note,
is that you've got this brown spot up here. As you can see, this inflammatory
process is a systemic process. If you find it in one place, you'll find it in a
bunch of others. Now, that's a logically very helpful for us to remember and
here's why: We take a look for hot plaque in the neck using the CI-MT (Carotid
Intima-Media Thickness Test). So what we're looking for on the Carotid
Intima-Media Thickness Test is the thickness between this intima and media
area. And as you can see in different parts of the artery, it too varies. So
that gives you some of the clue regarding some of the challenges in
getting an appropriate and accurate CI-MT. Another thing that the you see, when
we're looking for CI-MT, is we're looking for these hot liquid plaque areas. On
this- on this image again, we're looking for that CI-MT, the intima-media
thickness area, and we're also especially looking for these hot liquid areas. When
you get a normal carotid ultrasound, they would show- this would show as negative;
because it doesn't really- a normal carotid ultrasound, as opposed to a CI-MT,
the normal one, the routine one that 99% of them that are done out there, is only
positive if you have obstruction of the flow. And that create- that takes up to
two-thirds of the decrease of the size of the lumen. So these are some of the
things that help you understand, a little bit more about what's going on with a
Bale/Donee type of evaluation, some of my preventive evaluations, and it starts
to get into what actually causes a heart attack. If
you've made it this far, as usual, thank you so much for your interest!
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