Today I want to give you some basic large look overview. And what we're
talking about? David will tell you in a few minutes or maybe he's already told
you. I don't know about medical standards. This is something that I learned from
David. He's he taught me about how it was 200 years before a lime became the use
of lime for a prevention of scurvy. To became a standard, it took a hundred
years for metformin. I looked him up, checked him out on it, and he's right.
And at this point, it still takes 20 years or so... 15, 20 years even in the age
of internet. Why is that the case? I've been involved in medical standards when
I was at Hopkins and ran the prevention program. I had my students, my student
doctors that I was teaching, did the science reviews for the US Preventive
Services Task Force. Those guys sit around the table and have to argue with
each other over who should have discovered something, who hasn't,
why they haven't. It's a human political process and they also have to prove that
these things are right. So it takes time. Now
there are three areas where the standards have not quite caught up to
the science and that's what we're going to talk about today. One of them has to
do with plaque. The next one has to do with insulin resistance (the most common
cause of plaque). And the third has to do with inflammation (cardiovascular
inflammation) and it's proximal most urgent cause of heart attack and stroke.
Now it's not gonna be missed. It's not gonna be in that order. I'm gonna start
off with some discussion about inflammation then we'll give we'll jump
around a little bit. Please be patient with me as we do. If you look at Time
magazine way back in 2004, they had a cover article on inflammation and its
cause of heart attacks, cancer, Alzheimer's, and other critical diseases.
If you look at medical magazines, they're still mentioning it. But as we just said,
the medical standards have not caught up yet. In fact, most cardiologists do know
that there's something about cardiovascular inflammation in it
causing heart attack. But this study that came out two years ago still caught the
the world's cardiology leadership flat-footed. The most common thing they
said was, "You know, I knew that cardiovascular inflammation had
something to do with it, but I didn't know this." And this what they're talking
to is Paul Ridker, a very smart guy,
cardiologist at Harvard who's been preaching this inflammation message for
decades. Actually, was able to give a a very strong anti-inflammatory medicine
used for inflammatory diseases which we won't go into but he gave that to people
all over the world and actually decrease their heart attack and stroke activities
the rate of heart attack and stroke. So I'm not gonna go any deeper in that.
I'll just show a picture of Paul Ridker. Again, maybe the godfather of
cardiovascular inflammation in terms of this space and the name of the trial was
the CANTOS trial. You can see that in Scientific American magazine as well as
the New England Journal that I just talked about. But again, let's focus on
what we're here to learn today. First is, "Do you have plaque?"
Unfortunately, the standards of medicine are not that great on helping you
understand that, and that's the most important first thing to find out. That's
why we're having the CIMT. I'm gonna go quickly through these items and talk
about the pros and the cons. Framingham is basically where your cardiologist or
your primary care doctor will start. It's not a measurement, it's a guess, and it's
a bad guess. Then usually most people will say, "Well, I got a stress test."
5,000,000 stress tests are being done each year. There are a huge number of
false positives as in like 30% depending on where you get them. And if false
positive leads you to the cath lab, they're also an even worse a huge number
of false negatives. Again, you'll see literature say up to 30% here. The bottom
line is with a stress test, it's not gonna be... it's not going to show you a
positive unless you have over 50% blockage of your artery. Well, guess what?
68% of heart attacks and strokes occur in people that don't have 50% blockage
of their arteries. Again, that's why we're here
looking CIMT and getting a CIMT. PC angiogram,
in other words "percutaneous," going through the skin. And welcome to the cath
lab, that's not where we want to go if we can avoid if we want to. Calcium score is
a big improvement over these. It's a great first group. It's a great think
tool for screening. It's not great for following progress, and there is
radiation involved. So it's available. It's just not as good as CIMT. CT
angiogram is expensive. It's coming out of the blocks now as a very good test.
Again, it's expensive and part of the problem of the CT angiogram is you don't
know whether you're... if you see plaque, you don't know whether it's soft or
stable. Hence, the CIMT. Again, I've mentioned it
a couple of times. I'm not going to cover it any deeper today. Todd's gonna cover
that in his presentation. And again, you've got David here to give you a
little bit more detail. I just want to give you the perspective from a
physician in terms of the advantages and disadvantages. I did an article a video
recently on ABI (ankle brachial index). It's a great do-it-yourself one except
for the following problem. A negative is not going to tell you that much. And if
you have a positive, most people already know their results before they have this
test. It's an accurate test. It's a do-it-yourself. It's very inexpensive,
unfortunately. And it's a great test. If you haven't done it for yourself, look it
up on my video and do it. Unfortunately again, it doesn't you already know most
of what you're gonna find out from an ABI. I'm gonna skip over these
questions because we have a lot that I'd like to cover for you today and let's go
again a little bit more deeply into cardiovascular information. First of all,
this is where we're going in deeper and deeper in terms of scope or granular
granularity in terms of what's going on and where
we're looking from the heart and cardiovascular system to a single artery
then getting into layers of the arteries and then getting into glycocalyx. Now
again, very minimal high level. Look the heart and the arteries. We're looking at
the intima and media. The intima is the lining. It says it's a slick lining but
it again it has that glycocalyx area. The glycocalyx is sort of like the edge of a
marshland that area where you have marsh next to the river, that's where the real
metabolic activities occur both in our body as well as in the marshland. And
this is a picture under this is a cross-section of the artery
showing that hairy-looking glycocalyx. Here's a diagram of the glycocalyx, and
here's a healthy glycocalyx right here. Now what happens with inflammation
is this. Let's say you are a smoker or you have inflammatory disease like
rheumatoid arthritis or most commonly like over half of us as adults, you have
insulin resistance. In other words, you eat carbs and your body stays at a 180
or above for hour after hour in terms of your blood glucose level. Look what
happens. That tends to destroy that glycocalyx. This is a healthy glycocalyx
up here. And down here out here, these are systemic effects occurring from
inflammation. Once that happens, it becomes much easier to understand how
small dense LDL can make it through that hairy glycocalyx and lodge into the
cells of the intima and pass through them and lodge into the artery wall. Once
that happens, we get inflammation the body's immune system. It's taking from
you're taking friendly fire the body's immune system recognizes this plaque and
says, "This should not be here." It sends in immune cells: T-cells,
monocytes, polymorph... and I'm not going to name all the different types of cells.
But we will talk about two of them a little bit later because we can actually
measure their activity. That's part of the inflammation test. All of that's
actually not bad because the immune system is doing what it should do.
It's liquefying something that shouldn't be there so it can remove it. So this is
the cross-section of an artery. This is the media, the muscular layer. This
is the intima, the lining with that glycocalyx. And this is plaque that has
gotten stuck between the intima and media layers. But here's the problem. Well
one more thing, this little this is a liquid area that's why I sort of
retracted away from the slide. Now this hot liquid area that again all of that
stood up until this point and here's the problem you go back to these cells these
cells and what and some of the chemicals that they release can cause a clot. If
they touch blood (and that's exactly what happened here), this is another view of
someone who died from a heart attack, just like this one and this is a larger
view. It's a little bit different preparation. This is the media of the
artery wall out here. This is the intima as you see. There are a couple of broken
places. This black thing is not hot plaque, it is the clot that the blood
formed when that hot plaque touched the blood. The larger part of this clot is
what killed the patient. It floated on up to the heart. And again this is
not plaque. This is... pardon the image, there are the mislabeling.... this is the
clot that's gone on up into the area where that hot plaque was here. You see
there's another hot plaque pocket right here. So that shows that this is a
systemic issue. In other words, it's happening one place in the body. It's
happening all over in the body. That's why, we can look and tell whether
you have hot plaque by looking at your neck instead of your heart we've
actually done studies so we haven't done them they've been done many many times.