Welcome to vasospastic angina. A third and
final type of angina, we, up until this point
have categorized angina as being chest pain,
depending as to whether or not there is rest
or upon exertion. And I told you at the time
that when we were discussing unstable and
stable angina, that we would leave vasospastic
separately because it doesn't necessarily
fall into the same pathogenesis of stable,
unstable and then MI. The spectrum that we
had walked through there and you want to make
sure that you travelled through that pathogenesis
so that as you go through it, you are integrating
the physio; you are looking at the disease
and then how do you want to manage your patient.
With stable angina, do you remember that patient?
There is chest pain upon exertion, nitroglycerin
so that you can relieve some of that pain.
And so by doing so, you are decreasing the
preload, decreasing the afterload and making
it much easier for the heart to then function. Correct?
Unstable angina. My goodness now the atherosclerotic
plaque, key point, atherosclerosis. The plaque
is getting bigger. We went through the pathogenesis
of that and then remember the cardiac enzymes
were negative, black and white. Keep things
simple so that at least you have a definitive
answer and you are confident with your response.
Now clinically, there is always room for overlapping
in that gray area, but at this point let us just
keep things very straightforward.
So with vasospastic as the name implies, formerly
known as Prinzmetal, maybe you have known
it as being variant, but a much more clinically
relevant term would be vasospastic. That's exactly
what is occurring in your coronary artery.
Let us take a look. With focal coronary artery
spasm, the operative word here is spasm. What
is causing this? Well, we'll get to the risk
factors. It is rather, let us say mysterious,
could be because you have to have a atherosclerotic
plaque. How can you confirm that? Take a look
at this. Angiographically there is absence
of narrowing of the coronary artery, which
means what exactly is causing this chest pain
that could mimic angina. ST-segment elevation.
What does that even mean?
Well let's just make sure that we're
clear about the different type of changes
that we've seen thus far. Remember in medicine,
it is about reinforcement and repetition and
we will keep talk about this over and over
again until well whenever a question has been
post to you, you are able to reflexively answer
and you have come up with the right one every
single time. An ST elevation, with anginas,
remember in stable angina at rest, there is
no pain. The EKG looked normal. You were induced
perhaps in your clinic, stress either through
chemical drugs or a treadmill test. Upon doing
so, what did you find on EKG? Find an ST depression.
What? Then you had unstable angina. With unstable
angina, you might have changes there as well,
but it would be non-STEMI. Maybe there is
an ST depression and the pain there occurred
at rest. Now the point is this, cardiac enzymes
were negative with angina because it is not
myocardial infarction. The myocardium has
not been destroyed. You are not releasing
troponin I. Here as well, with vasospastic
angina, has nothing to do with atherosclerosis.
You usually do not find narrowing. The spasms
are taking place. You might find an ST-elevation
but you normally will not find cardiac enzymes.
Is that clear? Now when you hear about ST
elevations, a couple of things that should
come to mind and you need to make sure that
you confirm your findings before you chose
any type of answer. For example, if it is
an ST-elevation and there is no cardiac enzyme,
highly unlikely that this is myocardial infarction.
So what might it be? Was your patient taken
up coccaine, smoking? Was there hypertension?
Things of that nature and if there was, that
ST-elevation would then diagnose your patient
most likely with vasospastic angina. Is that
clear? I hope so. Now the vasospasms could
be superimposed with an atherosclerotic plaque
so that you want to be careful of. So here
once again you might find an ST-elevation
with vasospams. It is important that you go
back and take a look at the history. Is your
patient obese? Then at that point, you are
looking at more of a type of unstable angina
perhaps, especially if the pain of the chest
is occuring at rest. If your patient has a
history of smoking and you find an ST-elevation
with your cardiac enzymes being negative.
Are you listening what I am saying? Then what
is your most likely diagnosis, please? Good.
Vasospastic angina. Let us continue.
Now the clinical manifestations are the following.
Your patients here tend to be younger. That
is key, isn't it? Whereas when we were referring
to unstable angina and company, then those
patients well if it was a male, a little bit
youger than a female, but still 45 and above
in a male, and if it is a female remember that
estrogen is protective, isn't it, for female?
And so therefore 55 and above perhaps, for
atherosclerosis in a female. Now one of the
hyperlipidemias that we referred to was type II
hyperlipidemia or hypolipoproteinemia.
Do you emember type II? What was the problem there?
Good. LDL receptor deficiency. That is where
the problem took place. If the LDL receptors
aren't working properly specifically in the liver,
then how is the LDL ever going to be properly
accepted and absorbed. It is not. You are
going to start accumulating more and more
LDL. Now there could be the familial type
and you then call that what, please? Familial
hypercholesterolemia, is that clear? Now that
patient could be young, granted. All of that
is dealing with atherosclerosis. And by younger
we mean to say that well, autosomal dominant with
type II. In their 40s, that patient would
be heterozygous or homozygous? What do you
remember from genetics? What type of gene
pattern is more dangerous? Homozygous. So
that patient might only, oh boy, 18 to 20, whereas
if he had heterozygous, then you're looking at
a patient maybe perhaps in their 40s. But
that is all atherosclerosis, is that clear?
Our topic at hand is vasospastic and all I
am trying to do here is to make sure that you
have differentials in your mind before you
confirm. How do you confirm your finding is
which you truly asking yourself every single
time. It occurs in an atypical pattern, frequently
at rest and clustered. So that is quite different.
Patients here, the chest pain very much like
angina. What does that mean? Substernal chest
pain, may be radiating up into the jaw and
to the left side and such.
Take a look at the risk factors and pay attention
to this, please. Smoking, cocaine, and maybe
perhaps even diabetes mellitus, but what
kind here please? What kind of patient
most likely is going to then offer insulin
resistance? An obese patient. When those insulin
receptors are not properly functioning, a
type II type diabetic mellitus.
Risk factors are huge here. As you can see,
really has nothing to do with atherosclerosis.