Hello this is Dr. Ford Brewer - with state-of-the-art preventive medicine,
heart attack, cancer, and stroke prevention. Today we're going to talk
about removal of plaque from artery walls. Everybody knows you can't do
that, right ? Well, that's not right! Actually I'm a poster boy for getting
plaque out of my artery walls. I'm going to show you my CIMT results from two
years ago. As you see here that's my C IMT. It was done in February of 2015. I
was 57. I had a plaque here and a discreet plaque there.
Well, that wasn't good news. If you look at my arterial age, it was estimated at 73 (years old.)
Here are the normo- grams for the (predictable amount of) thickness that you
expect to see for males and females. And there's mine. So again, I was not a happy
camper! That's an emotional event, whenever a patient sees a plaque in
their arteries. And for me that was a surprise. expected
to have crystal clean arteries. I'd always been the the poster boy for a
good heart attack and stroke lifestyle nobody expected me to have that. I
started off as an ER doc very early - in my early 20s. I got very frustrated
seeing too many early heart attacks. I went to Johns Hopkins to learn prevention. I loved it, did well, and
ended up running the program in prevention. I've taught a couple of the
past presidents of the American College of Preventive Medicine. (Or maybe I should say they taught me!) So I know
prevention . And I've always basically practiced it- good diet, good lifestyle,
good exercise. (I followed a) plant-based diet
all according to the standard recommendations (at that time. The science keeps improving. )
Now what I'm getting ready to show you is plaque - so you can understand what
that is. You can see that in a couple of my other videos as well. To understand
plaque you need to understand the artery. There are two layers of the artery that
we need to look at :one is the intima (or endothelium) layer; the other is the media layer.
Normally LDL ( the small dense LDL particles) can go through this intima (or endotheliel
layer). Then, when they do, they'll go straight on through the media layer. But in
arteries that have inflammation, they lose the ability to pass through this
media layer. That's research by the way that's only just a couple of months old.
It was done by a mentor and friend Brad Bale along with Amy Doneen and David
Vigerust. So what you're looking at here in a CIMT is the Carotid rtery
Intima Media Thickness test. So again that's where you're going to get plaque
laid down. Let's look at it in terms of plaque progression. This end of
the picture is a normal healthy artery with very little plaque. As you see it
progress, you get more and more plaque. One of the things you may notice - is that
the flow is not compromised until there is a deep level of plaque.
So that's why flow studies like angiograms
and stress tests are way too late. They don't really look at doing any kind of
intervention (because their interventions are surgery focused). They don't look at
that (surgery) until you get a 50% occlusion ( occlusion means blockage of flow). As you can see, with this kind
of plaque you still have very little occlusion(or blockage of blood flow). So we're saying: Wait; Move back
up here; and Start thinking about the determinants(the things that make your
plaques inflamed, the things that cause deposition
of plaque). Here's a a couple of views from patients that have heart attacks. This is
the intima(endothelial) layer - that narrow layer, the lining. This is the media layer. So
everything in between those two is plaque (mostly LDL - or "bad cholesterol" that has gotten stuck between the intimar & media layers). That's what they're
measuring. With me they were measuring the thickness and saying, "Look, even though
you're 57 years old you've got enough plaque here to where you fit
the normo- gram (or the average) of a 73 year old. This shows another thing - it
shows inflamed plaque. What is inflammation of plaque? Inflammation of plaque is -
where your immune system attacks it (the LDL in the plaque between the intima & media layers). White cells from our immune cells go in ( to the LDL in the plaque)
with antibodies. They release enzymes. (These enzymes are meant to digest & dissolve the plaque.) We can actually measure a couple of those
enzymes: myeloperoxidase (also called MPO) and LP-PLA2 (also called "plack2") - all in blood tests. This is what causes the
heart attack - not this. This is a waxy, stable substance. This is a liquid. As
you see from here this is liquid. (When they dry this sample for the microscope - the liquid
retracted away from the from the slide.) You can also see there is very little
standing between the blood flow and that hot plaque! Here's why
that's the problem: hot liquid plaque - when it touches blood
will cause a clot. It's not regular plaque that causes the heart attack. It's
the clot. In well over 90 percent of the cases, the clot comes from
liquid plaque that has gotten out and touched the blood. That's exactly what
happened with this patient. As you see, this is the intima layer. And The media
layer's out here. This is plaque. The intima has a few cracks in it. We
actually look at that (the intima - or endothelial layer) when we're looking for MACR - (
Micro-Albumen/ Creatinine Ratio). That's one of our tests for inflammation. (This test - MACR is used by most internists. Although most know it's important, not as many know we're checking for holes in the intima. That's because the intima is the membrane filter of the kidneys - see other videos,)
I'll talk about that in another video. But you see here - this "hot", or liquid plaque
has leaked into the bloodstream. And this is a clot. The majority of this clot
broke off & went up to the heart. It caused the heart attack and killed this patient!
(The fact that this clot is) down in here shows evidence that the blood actually seeped through
the cracks in the in the intima and formed the clot inside that area (inside
the wall as well.
I'm still standing! I didn't have that happen. But what did I
do about it? Obviously there was not a whole lot that I could do (or so I thought at the time I taped this video) for my
73 years worth of plaque (deposition of LDL and my artery
wall) - in terms of lifestyle because my lifestyle was pretty good. (Or so I thought at the time). Soon
that I began to realize that if I had not had a good lifestyle I very well
could have had an event and all the bad things that go along with having a
cardiovascular event now. (The reality is that I should I have focused more on my dietary high-glycemic carbs). I did have some other things and you might be
guessing genetics. Yes, I did I had some genetic challenges. I had (& obviously still have) 9P21.
The 9 stands for the number of the chromosome. I've got 23
chromosome pairs (like most humans). Chromosome 9 has a section on it called p21 which has a lot
of heart attack gene problems(called SNPs - or Single Nucleotide Polymorphisms. These are sort of like mutations. Except these are stable variations seen in a lot of the population.) In fact, if you look at Brad (Bale) & Amy( Doneen's) book BEAT THE
HEART ATTACK GENE, that's the one they're talking about -9p21 I also have
4q25. That one (4q25 - again on the fourth chromosome) is really an atrial
fib risk gene. My mother has atrial fib. I have atrial fib.(Atrial fibrillation is the most common cardiac rhythm problem.) We have some
predisposition (genetic tendency) for that (atrial fib). (I also ran marathons on weekends. It has recently been found that prolonged, intense conditioning can also increase the risk for atrial fibrillation. In retrospect, that may not be a good idea for someone with 4Q25.)
it's not all just atrial fib, though. Current evidence is beginning to
indicate that it also has some risk (with 4q25) associated with heart attack and stroke
as well. Fortunately for me I had HAP 1,1. Haptoglobin 1,1 .
I have a series on cardiovascular genetics.
We can talk about those later
What else did I have? ApoE 3,3 - so not a lot of risk associated with ApoE 4.
I didn't have that allele (or that ApoE4 gene). I did have high blood pressure. And as I've
mentioned a couple of times before I had insulin resistance. (I didn't know about my insulin resistance until it had already caused this plaque. If anyone should have known - it was me.) One of the major
associations with 9 p21, by the way, is diabetes. (Another reason I should have discovered my IR earlier.) So that could I have a genetic
predisposition for both diabetes and heart attack & stroke.
(Again, at that time, I followed standard practices in this area. Now, on fasting & low carb diets, I'm keeping my blood sugar, insulin & HgA1c at much better levels.) So what did I do
I did do a couple of lifestyle things. I did a little tune-up. I started eating
salmon everyday (more like 3 days/week now. I realize the salmon/mercury haters out there believe this is a problem) - to get omega 3s.
I added niacin. Niacin is a supplement which improves HDL, decreases LDL and
decreases triglycerides. Niacin is an over the counter you get up to about 2
grams daily. It is the only thing that we have so far that has such a widespread
(or broad) effect on all our cholesterol values. Was it the niacin? I don't think - well, it
could have been - I think the niacin helped. I don't think so (I don't think the niacin was the major change, but contributed.) There were
a couple of other medication modifications I made. One was ramipril. I
had high blood pressure I was on an ARB (a related type of blood pressure medications). I switched to an ACE
inhibitor. We've mentioned that before we'll mention that again in other videos.
ACE inhibitors, like statins, do more than what they're prescribed for. ACE
inhibitors are prescribed for high blood pressure. They actually decrease
inflammation. Inflammation causes arteries to lay down
plaque. Likewise with statins. I think that's
where I made the biggest change. (I've made bigger changes since then by getting control of my previously unknown blood sugar problem.) I had been avoiding (delaying, refusing) taking statins - like most
of my patients - because of the side effects. I went ahead and
"bit the bullet" and took the Crestor (rosuvastatin). I took a very low dose of Crestor - 5 milligrams.
(Since getting better control of my blood glucose through dietary carb control, I have dropped the Crestor to 2.5 mg 2 times/week.)
I could take a lower dose. The lower doses impact (decrease) inflammation. They don't
impact (or cause) diabetes at the lower doses. And I think that's what made the
difference. By the way what was the difference? A year ago my (plaque age) my
artery age was 59. A few months ago my artery age was 52. (2 years ago my artery age was 73 - for a total drop of 21 years in about 2 years.) A few weeks ago, it was 52 so you can't
reverse plaque, right? I don't believe that! Thank you
This sounds like my major focus is medications. It never was before. And it isn't now. Please understand my point. Research & experience show that lifestyle is far more important. But sometimes - like when I was unknowingly building plaque with dietary carbs - meds can help.