How I Reversed 20 years of Arterial Plaque: Heart Attack Proofing?


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.

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