Begin with aortic stenosis. So this referred
to a few times. How is the patient feeling?
Walking through the door and your patient tells
you, well I gave you that patient earlier. It was 32 years
of age with aortic stenosis. How is it possible
that 32 year old is having aortic stenosis?
How is that possible that the aortic valve
has already undergone so much damage that
is now accumulating dystrophic calcification?
In basic pathology, we talked about the differences
between dystrophic calcification and metastatic
calcification. You have done that plenty of
times. What is the difference? Dystrophic calcification would be
damaged, D; dystrophic D, damaged tissue occurs
first. Where is the damaged tissue here? The
aortic valve. So you have normal amounts of
calcium that deposits on damaged tissue resulting
in, well what kind of characteristic would calcium
then give that tissue when it starts accumulating?
Rigid, hard. So now we have an aortic valve,
which is hardened due to dystrophic calcification,
but still doesn't answer the question why
a 32 year old? Because now your patient might
have been only born with how many cusps of
the aortic valve? Only two. How many should it
normally have? Every single valve in the heart
except the bicuspid has three cusps. So now the
aortic valve only has two. That is congenital
bicuspid disease resulting in early dystrophic
calcification. This patient, 32 years of age,
young, is having fatigue and tiredness upon
exertion. If there is enough muscle build-up,
a concentric hypertrophy of the left ventricular
wall may result in angina maybe even chest
pain upon exertion. Are you with me? Increased
afterload. Tell me about that murmur. Where
is it located? Where would you hear it? Second
intercostal space point to it please, the right parasternal.
Where else might you hear it? That murmur, not the blood
then may radiate up in the carotid. Is that
clear? Increased pressure. So what are you
going to do with all this? Take a look at
physiology and with physio it is important
that you take a look at the cardiac cycle.
It is important that we then compare this
to pressure volume overload. Is this important?
Yes and you know as well as I do as to how
often that is asked on every single level
of medical education. There are three main
causes. Senile calcification.
So who is this patient? Not 32 year old probably
would not take kindly to the fact that he
or she is going to be referred to as being
senile. Next, so senile would have to be someone
who is 70-some. As we get older, our tissues, unfortunately,
do get tired, old, damaged and may result
in what kind of calcification? Senile dystrophic
calcification. What is our topic? Aortic stenosis.
That would be the most common cause obviously.
Can we prevent age from taking place? Not
that I know unless you're Johnny Depp from Pirates of the
Caribbean and he was looking for fountain of youth, you know
his entire life got old in the process though,
even he was not successful. Incidents increases
with advancing age obviously. What is happening?
The aortic valve was becoming damaged. How
many cusps does this patient have? Three,
which is getting old, damaged. Calcification,
this is the 32 year old that I have been referring
to a couple of times now. Congenital bicuspid
aortic valve. Now what I do want you to pay attention
to is don't just take a look at congenital
and give it a generic name. What kind of congenital,
or maybe the Down syndrome? Is that congenital? I believe
so. What about Turner syndrome, XO? Would you have bicuspid?
Of course these are congenital
conditions. So any congenital anomaly might
then also give rise to a bicuspid aortic valve
and now prone to what? Dystrophic calcification
at what age? Young and by young we are talking
about 20s and 30s. Next, what else? In developing countries,
not developed countries, the most common cause
of aortic stenosis would be rheumatic heart
disease. Is that clear? Now, what do you want
to do with rheumatic heart disease? Be careful
and the reason I say that is number 1, couple of
ways in which your patient may develop this.
We will talk about in greater detail and obviously
hit upon this in microbiology. And you have
a child that might have pharyngitis and that
pharyngitis was caused by group A streptococci
pyogenes and the pharyngitis was not properly
treated and two to four weeks later ended
up developing issues in the heart. So we have rheumatic
fever, part of this might have been endocarditis.
Or maybe it was impetigo. Impetigo could be caused
by staph, but in this case streptococci pyogenes
and may give rise to heart. Not so much. We will
talk about that in more being with post-streptococcal,
but at this point what I want to firmly or plant a seed
in your head is the fact that streptococci
infections do not only limited to pharyngitis.
It could also involve the skin, but each one
of those would be giving rise to different
types of diseases. So here we go. With rheumatic
heart disease, if it is early on and damage
to the valve. Listen to what I'm saying, early
is the operative ward, then it would be a
regurgitative issue. What is my topic? Stenosis.
What do you think
stenosis might mean in a rheumatic heart disease
patient? It just caused damage. At some point
in time, don't you think that repair process is
kicking in. Of course it is. What does the
repair process mean to you? Collagen coming
in, deposition of fibrosis. So what does fibrosis
mean to you? Hardening. Is that clear? Do
not memorize this. So when you talk about
rheumatic heart disease, 95 percent of your
patients will have issues with the left-sided
heart valves. "Dr. Raj, what about the right
side?" Of course the right side could be involved
with a measly five percent. So do you want
to spend time on things that are uncommon?
Why would you want to do that? Why would you
want to make your life more difficult? So
95 percent of time, it would be the left side.
On the left side, it would be aortic and mitral.
So those are the valves that will be affected
early on it will be regurged. Our topic here is
stenosis. Where is your patient coming from?
Developing countries. What if there was a
developed country? Congenital bicuspid or
older 70-some, what kind? See now. Are you
putting things together or are you creating
differentials based on the history and demographics
of your patient? Here with calcification, nice little cartoons,
between a normal and then you find calcification.
How many cusps do you see here? One, two, three.
So it was normal and how old was this
patient presenting with aortic stenosis and
dystrophic calcification? Old, has to be senile.
Three cusps. What if you only find
two cusps? Then it will be young patient.
Guaranteed. Is that clear? Here you only have
two cusps. Do you see them? This is the aortic
valve. This is not the bicuspid. That is the
problem and so therefore at the age of 30-some
ends up developing dystrophic calcification,
aortic stenosis and let us go one step further.
How does the left ventricle going to respond
please? Hypertrophy and the left ventricle
is lifting weights and what are the weights?
The aortic stenosis. What is it going to do?
Undergoes hypertrophy. What kind? Concentric
hypertrophy. Let us go one step further. If
that left ventricular wall becomes thickened,
What is the size of the chamber, please? Reduced.
When you have reduced size of the chamber
because of increased thickness of the left
ventricular wall, you cannot accommodate for
more blood to come in. Is that a diastolic
or systolic dysfunction? It is a diastolic
dysfunction. In fact, clinically speaking,
there is something called heart failure with
preservation of your ejection fraction. HF
heart failure. Preservation P. EF ejection
fraction. So you can actually have heart failure
with aortic stenosis early on, ejection fraction
is normal. It still would be around 55 percent.
Is that clear? I will talk more about that
later. You have discussed that in physio,
but it is important that you bring it into