Alright, so we've given you the
overview, we fast forward you through that.
Now this is the slow motion replay, okay.
I want you to be very clear how this happens
so you understand the medications we use,
the dietary recommendations
that we make the patients.
This is all part of you having a whole
complete picture so you're better equipped
to help your patients make healthier choices.
So here we go with slow motion.
So you know that first, the
artery lining is injured - we got that.
Now the response to the injuries,
we're going to talk about next.
So these fatty materials,
let me give you a list of those:
LDL, cholesterol, triglycerides
- these are fatty materials.
They're good things, I know they have a bad
reputation in some areas however, we need them
and they do do good things in the body but in this
case, when there's too much of them, it can cause damage,
injury, then you have a response to the injury with
the fatty materials plus the inflammatory mediators.
Now that's the combination when in excess, when there's
too much inflammatory responses, now we've got a problem.
So the fatty materials then we've got the
inflammatory mediators, right - you know those,
the microphages, the white cells, they all
infiltrate the lining of the damaged artery.
Damage - response so what
are the two groups that respond?
the fatty materials right and inflammatory mediators
and they infiltrate into the lining of the damaged artery.
Now what happens is the platelets
release growth factor at the site.
Okay, so when platelets release
growth factor, things happen
and that smooth muscle that we talked
about earlier - that is stimulated to proliferate.
Proliferate just measns it's gonna
get bigger and bigger and bigger.
So you've had that damaged area, we had the responders and
the platelets release this growth factor right at the site
so the smooth muscle is stimulated to proliferate.
Now the lipids, eccetera are trapped in the
wall so you got a great drawing for you there.
Look you've got the epithelial lining, you saw
where the damage was, we saw the responders.
Now because of that proliferation,
all that is trapped right in the wall.
So the lipids and everything else are trapped
in the wall of the artery and it's getting thicker
When the wall get thicker, the area for blood
flow gets smaller so becomes increasingly smaller
and the opening becomes that much
smaller so as this process is going on,
we've got more and more and more impeding blood flow.
So that's how you go from fatty deposits to
plaque, right we've got this process started
Now we're looking at over time those
fatty deposits that are trapped in there, right?
Proliferated, they're trapped in there, now they've become
hard - that's what becomes the tough and fibrous plaque.
So that was a lot of information.
Before we finished on this slide, I want
you to pause and go back and review,
what you know from how do we move from
damage to the endothelial lining till we get to this point?
Okay, so pause the video, walk
through that in your own mind,
jot some quick notes so you're just up to
speed with us again, great place to review.
Alright, thanks for taking the time to do that.
The reason we give you those study breaks,
is that we know this is a lot of information.
This is really important stuff but you
can't process it as fast as we think we can so
we'd encourage you to teach you as you're studying on your
own, that you would pause, take those breaks and reflect.
That'll supercharge your study habits and
help you retain and recall important information
Now we're talking about how do you go from
these fatty deposits, remember they're trapped in there,
how we go from fatty deposits to plaque?
and why is plaque such a bad thing?
Well because it's really tough and
fibrous and it's a pretty significant blockage
so that's why it's a problem, it's
making that area of blood supply smaller.
So let's look at these deposits.
They can be there just on one side or they
can be all the way around the lumen of the artery.
There's not always a rhyme
or reason as to why it happens.
It just depends on the extent of the injury,
where it occurred and how the body responded.
But as the blood flow decreases, the arteries
just can't supply enough enough oxygen-rich blood
to meet the demands of the heart muscle.
There's the problem or do we
say, "Aye,there's the rub right there"
Because we don't get enough oxygen to the
heart, that's the source chest pain, ischemia
and the worst case scenario - myocardial infarctions.
So the patient usually will start to
experiencing ischemia or chest pain
and they have an increased risk of myocardial infarction.
As this progresses, as it becomes worse, see ischemia is a sign
to let us know not all is well with that patient's blood supply.
We can intervene as early as possible and try and turn that
situation around because our goal is to minimize ischemia,
because we don't want ischemia or chest
pain to progress to myocardial infarction,
because that's dead tissue.
So hopefully this helps you start to understand why in some
patients, chest pain symptoms are so kind of intermittent.
They start, they stop, why we
see them, what the causes are -
all this requires you to understand the
process that's actually going on in their arteries.