as to level of occlusion. Next, let us talk about the
of an atherosclerotic plaque taking place. Let me
explain this figure to you. We have
here on top is going to be lumen of your
blood vessel and here we are going to go ahead
to refer it to this as being the coronary artery.
Is that clear? Now I want you to focus upon
something here, you see that green endothelium.
That is a cap and that is going to be a fibrous
cap in which it is trying to house in this
case, it is trying to prevent that atherosclerotic
plaque. You see what it says cholesterol and
necrotic cellular debris. Well, it is building up
in there, isn't it? As it continues to build,
what is this? This is not hyalin or hyperplastic
type of arteriolosclerosis. This is atherosclerosis
and I have referred to this a few times. Now
with that atherosclerosis, which is building
up, could you imagine what then happens to that
cap? At some point, the fibrous cap, which
is made up of smooth muscle cells, made up
of fibromuscular type of tissues, then the
cap may becomes little thin that it might just
rupture. And if that cap ruptures, then what
then happens to that necrotic debris that
you see in the middle? It is then able
to then escape and then it embolizes. And if
it embolizes, where it going to go? Where are you
right now? Good. You are in the coronary artery
and if you embolize what then happens to the
diameter of the coronary arteries as move distally.
Obviously, it gets smaller. Therefore embolization
of the necrotic debris in the middle. Distally,
you are going to have complete occlusion.
Isn’t that myocardial infarction? Sure it
is. So the protective mechanism of all of
this, at first, begins with pathophys.
So step 1, the endothelium most commonly here
might then become injured. Just goes back
to those concepts of hemodynamics. What do
you mean? Remembering hemodynamics with endothelial
injury. What does that mean to you? You are
then exposing the underlying collagen.
That underlying collagen then is going to express
what? You got this, come on, tell me. Good. Your von Willebrand
factor. So point is if you damage that endothelial
cell, are you not promoting thrombi formation?
Of course, you are, as part of the workout
trial, isn't it?
Next, accumulation of lipoproteins, mainly what type
here, LDL. What does LDL mean to you? LDL
contains what? You remember this from biochemistry.
Good, cholesterol, not triglycerides. Cholesterol,
is that clear. Keep it simple, keep it clear,
always keep it clinically relevant and if
you keep that in mind you will never miss a question.
Let's continue. Number 3, so what then come in? You see these.
These are monocytes. Why am I having you focus
on monocytes? What is that monocyte? Where
am I? In circulation. Your monocyte is part
of where? It is from part of your bone marrow.
Remember all of this is just a continuation.
It is just a story and your bone marrow is
one of your granulocytes, isn't it? And so
therefore, of should I say it is one of your
agranulocytes and it is actually part of your
myeloid lineage. And so monocyte, which is
being released, is traveling in circulation,
but what you call monocyte when you gets embedded
into a tissue? You now call this a macrophage.
So now the monocyte, which then buries itself
into the intima, which is then going to do
what? It is a phagocytic cell. It is trying
to then consume, you see that necrotic debris
that right there in the middle that center
point. It is trying to consume it. So what
do you call macrophage when it's trying
to then consume the cholesterol? It is then
called, please take a look at, foam cells.
Next what do you have? Well the factors released
by macrophages, the platelets, endothelial cells,
all of this is going to recruit the smooth
muscle cells from the intima or should I say
from the media towards the intima and so
of therefore, you are going to help form the
fibrous cap and it is exactly what you have
here, smooth muscle hyperplasia is taking
place, extracellular matrix and all this is
then going to further recruit more lymphocytes.
Then finally as for as the middle is concerned,
this is the necrotic debris. You have created
an environment where everything in there is
then going to perish. And this is made up of
what? Made up of your WBCs, lymphocytes, your macrophages,
your foam cells now, you also have your LDL
and this LDL has now become oxidiser. For
the most part, it behaves like what? It behaves
like a free radical. Is that clear? This is
the process of what? Atherosclerotic disease.
Every one of these points is very crucial
for you to understand of developing atherosclerotic
plaque. As you do so, then what then happens to
the coronary artery? A coronary artery becomes
more and more occluded and depending as to
the percentage, let us keep it at 70 percent
as being the magic number. If it is less than
70 percent and you have occlusion, understand
that you can still may be supply enough blood
to the heart at rest, so the patient is not
going to feel chest pain. However, beyond
that, let us say there is 80 to 90 percent
and the patient is now going to feel pain
even at rest. Welcome to unstable angina.
We'll repeat this over and over again until you
are eventually getting to what is known as
your myocardial infarction. So now we have completed
the supply aspect
of our pathology and what then happens when
it is cut off. It is going to the demand.