What an amazing set of things we're learning here.
Do you see the patterns yet?
What's the pattern we have?
I mean, I'm both very encouraged to see doctors presenting their cases saying they're able
to help.
I'm horrified to hear that some woman had to spend 123 straight days in the hospital.
So the pattern that's revealing here is that it's possible to do good medicine, but we
have a system that very much is not interested in doing good medicine.
It's interested in something else.
And so very interesting conversations is we all sort of grab at this.
What is this goliath?
What does it want?
Is it just money?
Is it something else?
You know?
Is it evil?
We don't know.
It's interesting to try and figure out how to make sense of all this.
But the patterns do emerge, and it reveals the absolute importance of what we're doing
here today, and being exposed to the straight front line information straight up.
So we're going to shorten that cycle.
I'm really excited for this next talk about microclotting.
This is assessing and treating the emergence of microclotting by Dr. Jordan Vaughn, as you
heard.
What the world leading expert in this who has funded his own techniques and lab to be able
to assess this, Dr. Jordan Vaughn.
After training at the University of Alabama, he brought his medical knowledge of internal
medicine to further expand MedHealth clinics, which was started by his father, Dr. Michael
Vaughn, in 1982, so wow, a lot of experience there, focused on caring for patients in all
aspects of outpatient medicine, acute and chronic body and spirit.
MedHealth clinics at six locations, sees over 190,000 patients a year, wow, employs 18 physicians,
200 healthcare workers.
Dr. Jordan Vaughn is a leading expert at treating long COVID, long VACs, specifically with regard
to the spike protein, and its ability to cause endothelial damage and clotting of the microcapillaries.
And of course, he has also been a key collaborator with Dr. Corey, Corey and Merrick on the eye
recover treatment guidelines.
So with that, let's give a big hand for Dr. Jordan Vaughn.
All righty.
So one thing I want to say first on the healthcare revolution part, you know, as just a kind of
your average internist that actually had his father give him good direction on what it means
to take care of patients, which was always to make sure we have the organization that
allows us to do what we think is best for the patient, not to have a middle manager.
For many years, that meant many different things, whether it was the way we want to treat them
exactly, whether they're billed, you know, whether it has to be paid, the different things
that we need, my dad's always just said, you don't want to have somebody else as your boss.
Not that that is, you know, we all have ultimate bosses in a sense, and our bosses are patients.
But that's a great infrastructure to be in because my dad set that up and let me as another
physician and a son to say, that's one of the most important things that allows him
to do what he does.
And so what we have to do is get back to where our organizations and our ability to treat
patients is not owned or directed by anybody else.
Okay.
And it has to be directed by the patient.
The other thing is, is a lot of the crazy stuff I'm doing is totally because I have
that freedom, because no one has told me, don't buy that crazy microscope.
No one says, don't read that and try it.
And instead, we have a lot of doctors, and I think a lot of really what I get from the
doctors is, well, I just can't do what you do.
Well, if you can't do what I do, maybe you need to change where you're practicing.
Does that make sense?
And I'm not saying that that's in everybody's case, but if you don't have the freedom to
care for the patient, it's kind of hard to care for the patient.
So does that make sense?
So anyway, so what we're going to talk about today is really kind of, again, this is a
little bit old of a topic, but microclotting.
But we're also going to talk about a lot of stuff I think Scott was talking about earlier,
which we've kind of discovered.
And I think it all goes back to the damage to the vascular system.
Okay.
So the vascular system obviously is pretty darn important.
One thing that I have noticed is we pay a lot of attention to the arteries.
We don't necessarily pay a lot of attention to the veins, okay?
And your arterial system has a pump.
It's called the heart.
But the arterial system only contains about 17% of your blood.
Your venous system contains 70% of your blood.
It's a passive low pressure system.
And when it's not working, you're not necessarily going to go to the ER, but your life might
be hell.
So we'll get on to that in a second.
But what I like to talk about is one of the things that kind of stuck out to me as I was
treating people for really acute COVID was what I was seeing with the clotting abnormalities
in the acute disease.
The other thing was, and this is pretty well documented even with my patients, is as my
patients started to go get vaccinated, I started to see people come back to me who I'd seen
for 12, 15 years that would say, hey, I'm short of breath.
Check their D dimer.
I mean, these are otherwise healthy people.
And that was kind of my clue to go search deeper, like what is going on here?
What is so unique about this disease?
And at that time, you were pretty all over the place and what was actually going on.
But I think Risha and Doug, so those are kind of the people that I stand on the shoulders
of, Risha Pretorius and Doug Kell, they had one of the better explanations to me what
was happening because they were able to prove that when you drop the S1 subunit of the spike
protein into people's platelet-poor plasma, you start to get accumulation of amyloid fibrin.
And that is without thrombin.
And so this was an actual protein-protein interaction that was causing a clotting issue.
And that is very unique in disease processes.
They had been studying, really, fibrin aggregates was the fancy word and actually don't necessarily
love the word microclot because every doctor, once they hear the word clot, is going to
try to prove to you there's no clots.
But in reality, we're talking about microscopic clotting.
But in this case, it was that that was happening and was happening in a unique way because
the other thing that's important is when they would apply a trypsin step, and a trypsin
step is something that basically allows you to digest these microclots, they did not go
away.
Now, previous, when they were studying this in inflammatory diseases like rheumatoid arthritis
and other things like diabetes and elderly people, applying trypsin, the actual amyloid
fibrin would go away.
But this didn't.
So it means it's not only there, which is bad enough, but it's pretty darn hard to get
rid of.
So this was kind of what they were finding.
And again, healthy plasma didn't have any of this.
Type II diabetes plasma started to have some of it.
But what's more important is when COVID-19 plasma came along, it came along in droves.
And so again, this is basically using dark field microscopy with immunofluorescence.
And so again, something I don't know how I actually do this now is not anything I would
have ever planned.
I actually had no interest in microscopy or any type of microscope my whole career in
medicine as well as medical school.
It was like the last thing I wanted to do is go to lab.
So the other interesting thing was is they would set up these microfluidic channels that
kind of look like small vessels.
And these actual walls were made out of thrombin.
So when you put somebody's platelet-poor plasma through here, you would get a little
fibrin deposition where this arrow is right here.
There you go.
Anyway, hold on.
Let me do it here.
So right here.
But with a trypsin step again, you would actually get it to go away.
And so what happened was when we took COVID-19 plasma and put it through the same microfluidic
chamber, you would have these long fibrin strands.
But also, in addition, once we exposed them to trypsin, they would stay.
And so the theory was is a lot of this kind of small vessel issues was an accumulation
of basically things that were clogging up.
I use it as a kind of like the word sludge, but in a sense sludge is probably a better
term than microclots.
Because again, if you say microclots to an ER physician, he's going to try to prove to
you that CT NGO doesn't show anything.
So the other thing that was important was these aren't totally occluded.
Obviously, if you occlude vessels, you should have true ischemia and death.
But if you just occluded enough to limit delivery of oxygen and especially dense oxygen.
So we as humans, thankfully, have something called red blood cells.
So red blood cells are uniquely different than a lot of other things like amoebas.
And the red blood cells allow us to deliver oxygen much more densely.
But we also have oxygen that's dissolved in our plasma, right?
So just like an amoeba, an amoeba can kind of exist in some ways because of the dilution
of it into the plasma.
But what makes you able to walk around and do everything, think, heartbeat, those kind
of things is the uniqueness of the fact that we have a dense delivery mechanism.
So we almost have these trains that help.
The other thing is in the spike protein does a similar thing.
So one of the other things that I was going to talk about is how this also relates to
platelets.
So platelets are these a-nucleated cells that you probably have always thought just are
involved in clotting.
Well, they're involved in clotting, but they're involved in a lot of other things.
So they secrete all kinds of things.
They have lots of different receptors on them that, you know, really the more we get into
platelets as well as fibrin, you start to realize that the inflammatory system and the
platelets are, you know, you can't really separate them.
So a lot of times people like to think of it as, you know, the coagulation system is
different than the inflammatory system.
But I would actually posit that the next 10 years it's going to be all about thromboinflammation
or, you know, immunothrombosis, whatever term you want to go.
But they really can't be, you know, disentangled.
So again, what I like to talk about is a nasty sludge of a mess here.
And so what we usually see here, when you take these platelets that are hyperactivated
and then you actually also have these amyloid fibrin-containing clots, you're basically,
you know, you're going to have this kind of nasty sludge of a mess, which is persistent
microclotting, hypercoagulation, inflammation.
And ultimately the most important thing here is something we call endothelial damage, right?
So I was just talking to endocrinologists over here a second ago.
But, you know, the funny thing is about the endothelium, when it's damaged, it releases
tissue factor.
Tissue factor produces thrombin, it also upriculates platelets, it causes a platelet aggregation.
So it's like this nasty kind of continuous cycle, right?
The other thing is, and this is just kind of a busy chart, but when we talk about what
these things do, they're also inflammatory, which I think we'll talk about mast cell activation.
It's one of the probably more underappreciated syndromes that I've ever seen.
It's nothing we even talked about in med school.
But what I've found is, mast cell activation is at the core of a lot of these people's dysfunction.
Stigials are basically, you know, vestigial, I would call it vestigial immune cell that
lives at the interfaces of our environmental interfaces.
So from eyes to nose to oropharynx to lungs to GI tract to skin, and then as Dr. Gazda
talks about, they're also involved in really the microglia and immune system of the brain.
So, but the other thing is, when we talk about low oxygen carrying capacity and tissue dysfunction,
a lot of times, if you can't get dense delivery of oxygen because red blood cells are inhibited
from being delivered there, you're going to have a lot of different symptoms.
And those symptoms are plentiful, so.
So my goal here is basically to say, all of these things combined, if you get vessel damage,
you're going to have issues with getting oxygen delivery.
It's going to cause local tissue hypoxia.
And I can tell you, just really from trying to go up to 18,000 feet right now, a lot of
the symptoms that you associate initially with long COVID are going to be, or even
that's injury, when we talk about, you know, brain fog, feeling a little light headed,
vestibular symptoms, short of breath, those kind of things.
Think about somebody, you know, taking you immediately up to 20,000 feet.
It's a lot of the symptoms that you see in these people are very similar to you to taking
them to very high altitudes.
So that's one of the reasons that they're such overlap.
So if red blood cells can't get to tissues, you get ischemia hypoxia.
And then actually, when you reintroduce oxygen, you can get ischemic reperfusion injury, which
is one of the reasons that we'll talk about it second.
There's some other things that we need to look at with the endothelium.
When we talk about micro circulatory issues, you know, partial pressure of oxygen in humans,
and I didn't know this, at every different level and system, they're different.
So in a sense, the areas that have the lowest amount of partial pressure of oxygen, meaning
they are the most reliant on dense delivery, which would be red blood cells, they are going
to be the ones that are going to be the most impacted.
And when you look at the systems that have the lowest partial pressure of oxygen, brain,
vestibular system, eyes, skeletal muscle, myocardium, and the skin, you can kind of
start to see that a lot of these vaccine injuries as well as symptoms kind of go along with
those areas.
Well, the things that doctors check that aren't demand in the first place, like liver and
kidney, a lot of times look normal, and that's the reason that they're normal, they're not
as dependent.
So a lot of what we've done, and I probably treated about 1,600 people now, on differing
forms of what I would call anti-platelet and anti-coagulation.
Where this came from was Jaco Lobcher in South Africa.
What he was doing was finding that these patients in the cardiac ICU were having, you know,
significant clotting issues.
Now, those people were the people that were getting hypoxic, but the people that would
show up six months after having COVID with these other symptoms, he started to notice
that they had similar pathology, similar microscopy, similar changes in the blood, and he posited
that, I wonder if I use the same thing that I did in the inpatient setting for these very
sick people, if I use it in the outpatient setting, would it work?
And that was kind of the, I guess, the progenitor of a doctor basically using his brain, using
some physiology, using his patients and understanding that they're suffering, and finding out if
actually in, you know, utilizing these therapies would work, and they did.
So and since then, there's another kind of follow-up study they did.
Again, these aren't randomized studies, they're just observational, they're intervention,
and another one about another 100 people that Dr. Lobcher and Assad Khan in England did,
which is also useful.
It helped us another thing that there is a difference, and I think that's one of the
things that we're going to point out now.
So we're going to kind of move from what I would call microclotting to what did I learn
when what I was doing didn't always work, and I think that's one of the more important
things to kind of talk about.
So again, wide triple therapy, we can talk about that later, but again triple therapy
is dual anti-platelet as well as a direct or an equagulant, as well as something to
protect the stomach so they don't have a bleed.
So obviously, endothelial damage dysfunction is at the heart of all this.
So from endothelial injury to blood flow alterations and hypercoagulability, turn into these, again,
the word that I like, which is thromboinflammation in COVID-19.
But also in long COVID, because these symptoms as well as these changes persist.
So most all the data has shown that people, von Wilbens factors elevated, their ratio
of von Wilbens factor to atoms 13 is abnormal.
There's a lot that shows that there's kind of irreversibility of platelet activation.
So again, we're kind of addressing all that at once.
I'm going to move past that.
The one thing that I think has been a new game changer to me, and this is, again, I
think I was talking to Flavia a little bit.
Not all new drugs are bad.
And so one of the things that we have found is endothelial damage and dysfunction.
One thing that really works is a medicine down here, an SGLT2 inhibitor.
And I think a lot of us probably have used those medicines in our diabetics.
A lot of us probably haven't used them in our non-diabetics, okay?
What we can find here is that these SGLT2 inhibitors, basically, this is the endothelium.
And so when we have the endothelium, you have this sodium glucose channel, basically.
And this is the same thing that we usually target in the kidneys when we're talking
about using an SGLT2 inhibitor for diabetes.
But we really didn't know that the endothelium was covered in them until recently.
And the reason we found that out is once everybody started starting their diabetics
on SGLT2 inhibitors, you probably noticed the rep started coming back and saying,
now there's an indication for heart failure and heart issues.
And the reason was is because it affects the vasculature pretty immensely.
But the other thing that you noticed in this study itself was looking at what's going on with these.
And then when the sodium and glucose actually gets taken up by the endothelium,
you get the exact opposite of you want.
You don't want the endothelium to be down-regulating nitric oxide
and up-regulating tissue factor.
You don't want it producing and being more responsive to interleukin-6.
And you don't want basically all the kind of nasty reactive oxygen species to happen.
So interestingly enough, in this study itself, which looked at endothelial cells kind of in vitro,
this again, Giardians or whatever you want to call it, basically when it stops the uptake
of sodium and glucose, you get a down-regulation of all these things
that ultimately you get increase in nitric oxide, which is good for the vessel.
That's kind of the happy thing that it wants.
The other thing that's very useful about this, and it's kind of again happenstance
that we figured it out, was I was using SGLT2 inhibitors for lowering.
At last lecture, we talked about plasmidogen activator inhibitor 1.
And there's some data in the literature that showed that people
that were on these had lower levels of plasmidogen activator inhibitor 1.
Interestingly enough, I started it on some patients who had, you know,
kind of plasmidogen activator inhibitor 1 over expression.
And they were not diabetic historically, but all of a sudden they started to pee sugar.
And that was kind of an interesting finding to me.
And if you actually go back and look at the literature,
SGLT2 inhibitors actually increase endogenous glucose production
and actually help your body have more gluconeogenesis as opposed to glycolysis, okay?
So when we talk about post-exertional malaise, the thing that I could never get these patients
to do was stop it because they say, since I've been on that, I can actually exercise.
So, and I think the actual mechanism for that is not only endothelial healing,
but it's the more availability of glucose in the system.
So, and if you look back at the muscle pathology
that was recently come out of Amsterdam, one thing that they noticed was that the muscles,
especially in the people with long COVID and post-exertional malaise,
went to a more glycolytic stage.
They actually kind of changed the type of muscle that was there.
So in a sense, I think that's probably one of the what's going on
and why the patients love it so much.
The other thing is when you think about POTS patients and those kind of things,
this actually down regulates a lot of adrenergic overdrive and does it without a volume issue, okay?
So when we classically think of these medicines, when you take them,
you're thinking of that uncontrolled diabetic that all of a sudden gets dizzy
because they're peeing like a racehorse.
Well, the problem is in a non-diabetic, that doesn't happen.
And in fact, it down regulates their adrenergic system
and they actually feel better than they did.
So a lot of these POTS patients actually tolerate this very, very well.
So the last thing I want to kind of talk about before we get to venous disease is mastoactivation.
And this has been kind of the humbling part of learning about all of this.
But what I have, this is probably the best diagram I have and I give it to all my patients
because it literally has all the potential triggers down here.
This comes from the infectious analogy, whatever, society.
But then it has so many of these, you know, additional things that are going on.
And so a lot of these patients, you know, all of a sudden have new, I mean,
they've never had allergies before.
They've never been sensitive to anything.
And all of a sudden, they're sensitive to everything.
They feel awful.
Their brain is always tired.
They also, if you talk to them, their eyes itch.
They have, you know, nasal sinus issues.
They think they have a chronic sinus infection.
They also feel like they're more short of breath.
They can also have tachycardia.
They also seem to be more emotional.
They're also told now they have panic disorder.
And the problem is, is actually what's going on is it's like their body is being stung
by a bee all the time.
If you've ever been stung by a bee, your heart races, you get weird stuff on your skin.
You feel a little crazy and in a sense feel that all the time.
Now, the interesting thing is, I have actually, you know, in the mast cell activation world,
a lot of the serologies that we talk about, like histamine, like triptase,
like chromagranin A, are things that we check a lot.
Okay? The kind of mantra in the mast cell community has always been, they're never positive.
Well, I will tell you, histamine is positive a lot.
Okay? And in fact, my histamine was quite elevated.
And I might have had mast cell activation syndrome, you know, to begin with.
My wife probably agrees, you know, in terms of just how I operate it on a day-to-day basis.
So it's just interesting to see that it's a lot more common than you think it is.
And a lot of these people have come up with ways to compensate.
So a lot of times it's the person that, you know, historically,
they ate a very, very clean or limited diet.
You know, that's how they, you know, got their GI issues under control.
And a lot of times they are, you know, so just kind of, you know, looking back at even,
they had a little of the symptoms.
But then there was some kind of event, whether it was the vaccine, whether it was COVID.
And all of a sudden it goes from something that's more of a little bit of a nuance
and more of an annoyance to, oh my God, everything's out of control.
Okay? So this is the last thing I'm going to talk about.
And I think this is really, it'll take me a little while to go through.
But one of the things that we started to see was there's a ton of people that would get better
on triple therapy.
But there was probably about 30% of people that would get better in some ways.
But they also would kind of plateau.
But they also were never able to get back to doing what they wanted to do previously.
And I would kind of give you the example.
A lot of the extreme examples I have in what really kind of drove me to understanding this
was even my first patients for long COVID when I used triple therapy were college athletes.
So their trainer would bring them in and say, we are working them harder and they are getting worse.
And so that was one of the things that basically, not now I don't have to be convinced that someone's tired.
But it's pretty easy to convince me that someone's tired when their times are better than I ever ran any mile.
And people that run four minute miles, those people aren't just all of a sudden going to become depressed
and not be able to run a half mile.
So again, that goes back to believing the patient.
But what we had found was in that, that this would get them better.
But getting them back to running at a collegiate level, it wouldn't do.
They still had significant shortness of breath, significant heart racing.
They still felt pretty crappy in the morning.
I mean, they were better.
They were out of bed.
They were living their life.
They were able to go to class.
They weren't, so they were happy.
But it was like, well, what else is going on?
And what I had found was these people additionally had a venous issue.
And there's a couple of different ways to look at venous issues.
But one of the more major venous issues is what we call maytherner or what I would call,
you know, in a lot of women have been diagnosed with pelvic venous disease
and they didn't really know what it was from.
But so it's common in people that are more hypermobile.
That doesn't necessarily mean you need to be like a contortionist.
I would actually argue that a lot of athletes are hypermobile.
And that's why you're an athlete.
It's why you're better than everybody else at something is
because you can probably open your hips and do things that other people can't do.
But there's also hypermobility that has nothing to do.
I mean, it's not, it's more in the vascular realm.
So there's vascular EDS as well.
A lot of these people are these elite athletes, runner, cyclist,
they're ultramarathon runners.
I'll talk about my theory on why they are those people.
I think they probably self-compensated
for venous insufficiency historically.
A lot of them historically were multi-paras women.
One of the kind of things I say that gives me an idea
that something's going on is the girl that does my interventions,
she probably had done 3,000 stints in her life, okay?
And only three men.
Well, in the 60 people she stinted for me in the last six months,
40% of them are men, okay?
So historically, women happen to have progesterone, estrogen,
uteruses, and babies regardless of what the government says.
That's usually, they have those.
And those things were things that were vascular inflammatory
or pelvic trauma related.
I mean, again, the woman that actually has this kind
of lower extremity issues when she has a baby sitting on her L4, L5,
is going to have some vascular compression there.
She's going to have some, you know, venous swelling.
Men don't have that, and I'm 100% sure about it.
Now, men do get vaccinated.
They do get COVID, and so do women.
So all of a sudden you have this thing
that all of a sudden is becoming more apparent in men, you know,
out of the blue and, you know, somebody who's basically done
pelvic venous disease her whole life,
who'd done basically less than 1% of 1% men, then, you know,
a teeny fraction is getting referred a massive amount.
There's got to be something that's changed.
We all know what that is, but exactly defining it has been a
little bit difficult.
One of the things we're trying to get is some venous.
The other thing back to the original point was no one gives
a crap about the veins.
You know, go search for venous pathology and COVID and look
if anybody's ever even stained it or looked at it
under the microscope, and they haven't.
They've done the arteries, they've done, you know,
all kinds of areas, but no one's actually, you know,
very rarely have they looked at the veins.
There's a couple studies that look at, you know,
before they get coronary artery bypassed,
they've looked at the veins and seen what happened,
but even that's not, you know, just kind of inadequate.
The other thing that's kind of interesting is I'd say 60%
of these men that we're treating have a left scrotal
or testicle history.
It's not something you usually like to discuss
with your significant other, but what we're talking
about is varicoseals kind of above the testicle
or they've had hernia in the area
or they've had one testicle that's larger than the other.
They've never really figured it out,
but they've always said, hey, it's not a big deal,
but, or they've said, how do urologists fix it?
And I think that's one of the things that really helps you
kind of go down that pathway when you're talking about men.
Usually they have lots of lower extremity symptoms.
So I would say that the typical description of it
is somebody that says, you know, my legs feel heavy.
They especially feel heavy when I go up the stairs.
The other thing is they all of a sudden have new symptoms
like restless leg at night.
They also feel like, I mean, I've got plenty of people
that are like my toes or basically when they're recumbent,
not moving, they have a lot of symptoms.
So getting back to what I said earlier,
your arterial system has a pump.
It's called the heart.
Your venous system does not, okay?
And so guess what you don't do while you're asleep.
You don't move, okay?
So if you already have, you know, some kind of compression
or venous insufficiency or venous,
what I would call venous disease, you know,
a lot of the symptoms are definitely worse at night.
And then especially when they put their legs
on the floor in the morning, they feel absolutely awful.
Their brain fog is worse.
They, you know, and so that goes back to the fact
that basically all of this blood has sat there
for whatever amount of time you slept.
And I think of it as sewage.
So again, it's deoxygenated.
It's low oxygen blood.
It's inflammatory blood.
It's basically ready to be cleaned and recirculated.
And instead, you're just holding it in this pond
and keeping it there before you actually move it.
So the other things that go along with this are,
they start to develop other issues,
and we'll talk about why this is in a second,
but they start to have urinary urgency.
Like a lot of these men say,
I mean, I have like a 26-year-old.
It's like I'm waking up four times at night to pee.
Well, that's not normal.
Or we're girls that will say, you know,
I have lots of urinary tract infections,
but they never grow anything.
They're just irritated, urgent, you know.
These kind of, and a lot of them have been diagnosed
because the urologist goes up and looks at the bladder,
and the bladder's inflamed,
and they get the diagnosis of interstitial cystitis.
Well, no one's ever looked at the other side in a lot of ways.
And guess what most of these people have the other side?
A bunch of stagnant venous blood in varicose veins
in the pelvis that's causing inflammation in the bladder.
So as we fix these, a lot of those symptoms get better.
Other thing, heavy menstrual cycles, same reason.
Hemorrhoids, irritable bowel symptoms,
low sacral back pain,
and then kind of the boggy prostate
and nocturine and young men.
So how I like to look at it is if you actually have
some kind of issue that actually impinges on one of these,
mainly it's on this left common iliac vein,
you're gonna basically close down the highway,
and what you're gonna be resolved to do,
your blood's still gonna have to find a way back.
And that way back's gonna go through a lot of smaller vessels
that are easily dilated all through your pelvis.
It also will go up a lot of times the left side.
So sometimes I've got a lot of patients that'll say,
hurts under my left scapula, like under their,
or I actually do have pain,
but it's on the left side primarily,
which is a good signal, but there's something going on.
But one of the reasons the back hurts so much,
additionally, some of my patients ended up having
kind of what I would call lumbar punctures
that had increased protein or blood,
but it was non-diagnostic.
And they also usually are people
that have these kind of Lumbar punctures
that actually don't close off,
so they all of a sudden get like a CSF leak.
So I think a lot of that has to do
with these internal vertebral veins
that are engorged in full of blood,
as well as the sacral veins.
So the other thing when we talk about hemorrhoids,
well hemorrhoids all of a sudden appear,
well guess what you're gonna use
the internal iliac vein for?
You're gonna use it for the rectal plexus
as well as the descending colon.
So a lot of people get constipation,
new irritable bowel symptoms.
Also, when we talk about bladder
and uterine, you know, heavy menstrual cycles,
urinary urgency again,
and we'll show you in a second some of these patients
that the engorgement is a problem.
I mean, inflammatory post-circuit,
what I'd say low oxygen blood or hypoxic blood
is not good to have around.
And then why the left testicle is such an important thing
is when you'll probably remember this,
probably one of the test questions back in anatomy
first year of med school,
but the right side, the right gonadal
and the right ovarian vein is different than the left, okay?
And so the left actually goes instead of going
straight into the inferior vena cava,
it goes up to the left renal vein,
which can produce something else called nutcracker,
but we'll probably not go into that today,
but it's also a valveless vein.
And it has nothing to do with nuts.
It's nutcracker because it's like a nutcracker closing out.
Anyway, sorry.
So this picture of me really put it all together
in terms of what I was trying to do.
And what we get a lot of diagnosis
is of orthostatic intolerance and POTS.
Now, these people do have POTS,
but a lot of times POTS is totally kind of gone over
to it's all dysfunction of the autonomic nervous system,
it's neurological, it's, and I'm not saying it's not,
there is a component of neurological issues.
There's plenty of ways that this is not the cause
of your orthostatic intolerance or POTS.
But in these people, that's what's doing it.
And so what we call Cardiovena syndrome,
a lot of times I like the people to think that
if all of a sudden you're running,
so hold on, and you need more cardiac output, right?
Guess what you also need, cardiac input, by the way.
And so if you have pelvic venous disorder,
which could be mechanical obstruction,
could be a dysautonomia,
so you're not actually clamping down on your veins.
Or, you know, the one-way valves don't work.
Or it could be all three.
When you need more cardiac output,
and there's not an increase in cardiac or venous return
or cardiac input, guess what your heart's going to do?
It's going to beat pretty darn fast.
It's also going to make you short of breath.
The reason it makes you short of breath is because guess
where the blood in the right ventricle goes, to your lungs.
So if you have less blood being pumped to your lungs,
as well as an increased heart rate,
you're going to feel pretty miserable,
especially when you're trying to do stuff
like run around a track really fast.
Does that make sense?
So that's why a lot of these people,
the other thing that's going to happen,
a lot of these people get weird feelings in their arms.
And that's because if they can't get it from below,
it's going to steal it from above, okay?
And so a lot of times blood in their face starts to go away.
They feel like their hands get tingly
when they exercise, those kind of things.
And they're all usually what we call, we call it preload.
So a lot of us don't think about it,
but our heart needs the blood there to pump.
It contracting without blood is very inefficient.
And it's not really the way it's designed.
I don't know if anybody's ever seen a pump
and kind of a chemical engineer historically,
as my undergrad was.
If a pump doesn't have supply, the pump goes nuts.
And that's really, imagine that in the same way, okay?
So the other thing that I found to be useful was,
this is a Polish study looking at women
with pelvic venous disease.
And pelvic venous is this before COVID.
But what they had found was, the blood in their arms
is quite different than the blood that they aspirated
from the varicose veins in their pelvis, okay?
So the blood in their pelvis was much more coagulable.
It was much more inflammatory.
It had increased platelets, it had increased edimer,
it had increased C-reactive protein.
It had increased interleukin-6 and von Wilberns factor.
All those things are bad.
And actually, that's a lot of what we're studying.
And so one of the things that we found was,
is that these people were the people
that once we put them on anticoagulation,
their microclots did not get better.
So instead, they continued to have this kind of daily occurrence
in a sense, and that's, you know,
that they had a reason to have continued fibrin production
or fibrin aggregate production.
And actually, if you look back at recent Doug's work,
one of the things that actually had people
with fibrin aggregates was people with venous disease.
So what I like to kind of look at it,
and these are not the way you look at it at MRI,
but this is a 3D reconstruction.
I didn't think you all wanted to look at the axial views.
But Scott was right.
I feel like I'm probably better at reading MRVs than anybody else
from the venous side because I've been taught
by kind of the world expert over the last, you know, year.
But most radiologists could care less.
They're looking for bigger things.
And even if you ask them to look at it, I mean, I'd say three
out of four of these on the axial, it looks terrible.
But even then, the radiologist
at a very what I would call general radiology practice would say,
oh, it's just normal compression.
But normal compression, we could decide what it is.
But all they're looking for is clots, big clots.
But the problem is that's not the only thing.
Now a big clot, if it's in your iliac vein, you're going
to know your leg's going to be huge.
You're going to have all kinds of pain and pressure.
In a young 25-year-old that's really athletic,
you're not going to have edema.
What you're going to have a lot of times is what we call venous
congestion in the muscle.
And that's going to cause a lot of discomfort and pain almost
like feeling like their legs are heavy or they're full.
And feeling like they want to sit down
as when they're exerting themselves.
And so interestingly enough, I mean, even the third image here is
probably, this is a little 17-year-old, one of my patients.
His mom actually came to me because she actually had a stroke.
I couldn't figure out where it came from.
She ended up having pelvic venous disease.
But at the time, she said, hey, my 17-year-old just been
diagnosed with epilepsy, which is kind of interesting.
He was passing out when he was playing pretty competitive
baseball player, again, the athletic theme here.
And I said, that's kind of interesting.
But then when we got him in and just talked to him,
this kid literally has the most compressed iligophane.
He literally had this non-existent.
And what you can tell is your body starts to form these
collateral.
So he had back pain and other things like that.
But it was probably in the neurologist when I talked to him
eventually, because the other thing that a lot of these people
have is something called a PFO.
And a PFO is basically a hole from your right to left atrium
that if you have microemboline in your pelvis,
it's pretty easy for some of that stuff to get to your head.
That was the source of the mother's stroke.
It's also the source of the son's epilepsy, in a sense,
when he was out on the field.
Because he would have some crazy stuff they could never find.
And actually, the neurologist was like, yeah, that's a lot
better diagnosis than a 17-year-old all of a sudden
getting juvenile myoclonic epilepsy.
But just to show you that it can wreak havoc,
the last thing I want to show you is basically what Brooke does.
And so in a sense, when these people in this one
is actually going to be this last girl right here,
she's a 35-year-old girl, came to us
after getting vaccinated and having COVID.
I mean, just terrible lower extremity pain had been,
again, I don't know if I was Dr. 21,
but I was probably pretty close to up there in terms
of people she had seen.
But so it looks bad enough on MRV.
So I mean, literally, she's got collaterals for days.
And she has basically a non-existent.
And her body is actually trying to find ways.
These are inadequate ways to get Venus returned.
And so when we actually did something called a vinaigram,
so basically, you put contrast into the vessel
down the left leg.
The cool thing about this is it's invasive,
but it's very low.
I mean, it's basically using an IV from above and below.
On the left leg here, what you can see is, is that,
this thing is weird.
Hold on, okay.
It's like, okay, you got to get close to it, okay.
So the blood right here, it's not going up to the IVC
and going back to the heart, okay.
And this is immediately after.
And I'm going to show you in a second what it looks
like 30 seconds later.
And she's already developed these kind of very large,
what we look at, her case called ovarian veins,
as well as lumbar veins, okay.
This is about 30 seconds later, okay.
So again, nothing's getting to the IVC, but instead,
it is using this circuitous, dilated pathway to get the blood
from her left leg up.
And then lastly, a minute later, we got all, I mean,
this is like traffic jam on whatever, whatever road in LA.
It's like using every freaking road available, okay.
And so again, it's finally getting up to the IVC,
so she's getting some venous return.
But I can guarantee you this is not the best route.
And in fact, she even had somebody go the really long pathway
here and anyway, we can talk about what that causes later.
But it's not fun.
So after actual intervention, which basically you can see,
and one of the things that I like Brooke for is she's very,
she's probably the best, what I'd say,
she calls herself a plumber, but this actual stent,
which these venous stents are much better
than they were even 20 years ago, probably even five years ago.
But she stents the whole artery and then she oversized it, okay.
So the goal is to get this where you're creating a new pathway,
but you're also eliminating these bad pathways.
So it's getting things back on the highway.
And you can imagine that when somebody exercises,
they're going to feel a lot better if they actually get blood
back to their heart from their lower extremity.
The other thing I like people to think about is one of the things
that especially when we're talking about people
that have these symptoms, how to get them back to being able
to do stuff has a lot to do with thinking
about where central blood volume is, okay.
So again, 30% of the blood volume is
in the thorax wall supine, okay.
So that's a lot of blood, okay.
But basically, it gravitates towards your abdomen
and lower extremities when you stand.
And one of the things I always tell people is, you know,
I mean when you're laying flat in your bed,
your central venous pressure, your IVC's pressure,
it could be seven, eight, nine millimeters of mercury.
It's 21 to 22 when you stand up.
So more than doubling, okay.
So that's more work for your venous system
that really doesn't work well to begin with,
to be working against, okay.
So one of the things I've learned is these people are able
to do stuff when they're supine.
And it actually is one of the things that, and we'll talk
about in a second on things to help them with,
is that they can do things like recumbent biking,
they can do swimming, they cannot run until you fix the issue
because again, they're going to be working against gravity
and it's hard for them to change that.
So again, when a normal patient stands up, you get this kind
of blood pressure increase and then you get, you know,
the increase in the diastolic pressure as well.
So typically, you're going to have an increase
in heart rate, some vasoconstriction,
immoral activation.
So, and again, I think Alexis Kutchins who's a cardiologist
at Emory that I work with on kind of,
we're trying to define this really well, but in somebody
with venous disease, you get this kind
of hypothetical redistribution.
So in a sense, you're going to have a lot more venous blood
in the lower extremities and in the pelvis, which is going
to mean that there's less kind
of central blood volume in the thorax,
which is kind of where you need the blood to be
when you want to do something.
So, when we talk about non-invasive interventions,
one of the things we're trying to do is kind of a comparison.
Obviously, a lot of the people that we initially sent
to get stented, for this specific thing I've stented
about, not me, Brooke has, about 60 people.
Fifty-five of them have done incredibly well, okay?
Five of them, you know, two of them are still,
they were bed bound to begin with.
I haven't gotten them out of bed yet, but there's hope there.
A lot of times, you know, reprogramming your autonomic system
takes a little bit longer than a couple of days.
So, but, it's been fantastic.
Actually, two of them are college runners
that are back training with their college, okay?
And, which is just kind of nuts.
I mean, they basically went from being collegiate athletes.
One was at TCU.
Her dad's the track coach at Samford here in Birmingham,
and she's back training at Samford for mid-distance running,
when she couldn't run at all, okay?
Pretty amazing.
Of course, anyway, we know what caused it.
There was the vaccine before she got, she had the vaccine,
and then she was at a race,
and her legs wouldn't work anymore.
So, but non-invasive interventions,
obviously, anticoagulation, anti-platelet,
those are things that I like.
These people have what we call post-thrombotic syndrome.
Their blood is different.
It's higher in von Wilberins factors,
higher in looking six, it's higher in fibrinogen.
They are gonna be the more like,
they're the same people that,
they sat on a plane for 14 hours,
they're the ones that get the blood clot in their left leg.
That's the best way to explain it.
So, these people are already hypercoagulable.
Mass cell stabilization is huge,
because this elevation of interleukin,
as well as this ongoing issue with venous return,
causes just, you know, from histamine to triptase
to be elevated, and it is one of the reasons
that they get a lot of their neurocognitive issue.
So, a lot of the reasons they feel crappy
when they wake up in the morning
and put their feet on the ground.
And then endothelial repair,
diosmen is actually in pycnogen,
all those are two kind of natural things
that I use a lot of.
And then, classically, now SGLT2 inhibitors
is a big part of this.
And then increase intravascular volume.
So, it's one of the ways to kind of trick the body,
at least in the short term,
as flugicortisone, salt, hydration, those kind of things.
Physical intervention,
so venous systems low in pressure without a pump,
increase venous return by lower extremity movement.
So, the other thing that I find a lot of these people,
especially the active young men,
they'll be like, you know what,
I can walk the golf course, but I can't run.
Well, and they feel better when they walk the golf course,
okay, makes sense, right?
There's not that mismatch yet,
but when that mismatch happens,
that's when their symptoms go crazy.
So, you know, venous return has,
cardiac output has to be matched by cardiac input,
recumbent biking, and then, you know,
rowing, any kind of, what I would call,
so when you talk about these post exertional malaise patients,
you're scared to get them to exercise.
If they're orthostatically intolerant,
what I've found is most of these do better
when they are parallel to the ground
doing whatever they're doing.
So, that could be swimming,
that could be recumbent biking, that could be rowing.
Intermittent compression is huge.
The other thing that I get these people to do is,
how to make their mornings not as bad,
is to actually use intermittent compression devices
for 30 minutes at night, okay?
So, to get all the venous blood out of their legs.
So, there's less venous blood sitting there
and causing inflammation in the morning,
and a lot of these people are like,
oh, that's a game changer right there, okay?
And then, we're actually trying something actually
with SoftWave.
SoftWave is a high-frequency ultrasound
that they used in lithotripsy
that they've been looking at for erectile dysfunction
and pelvic venous disease historically.
And I called the company and was like,
I think this might, you know,
because there's a couple of different theories
on what's going on.
I could talk about it, but there's three.
But one of them could be that the veins themselves
are in a contracted state, especially the iliac vein,
because of the lack of blood supply to the vasovasorum,
which is the microcirculatory supply
to the muscles in the vein.
And so, actually, one of the guys that's higher up
that I won't name him,
but he thinks that's probably my best theory on this.
But I actually kind of argue with Brooke a lot that,
oh, this is damage, direct damage to the vessel
that's causing it to collapse.
I think that's a little far-fetched.
I think most of these people had some symptoms
to begin with, but again, they were annoyances.
They weren't life-changing.
But then they get issues that cause them to be dysfunctional.
The other thing that I think is athletic people,
why the typical person is somebody that has a history
of running or being athletic.
But you got to think about,
if somebody is running seven days a week
and it makes them feel good, you got to ask why.
And I think one of the things is,
probably these people had some venous insufficiency
to begin with, and their brain learned a long time ago
that if they ran every day, they got a good venous return.
And not only is that also probably why this subset
of people is historically athletic, but it's also one
of the reasons that I think these people suffer so much
when they can't run anymore.
Because they were doing something to compensate for some
of their issues historically, and now they can't run at all.
And they're miserable.
So that's one of the things that kind of goes into this.
You know, again, the other thing is that the veins themselves,
just like the joints being hypermobile, the pliability
or what I call capacitance
of the venous vessels is different in these people.
And I think that's one of the reasons that it's so significant.
So that's all.
All right, Jordan, let's take a seat.
Okay, great talk.
Great talk.
All right, so we're going to turn to questions now.
My first one is you started with microclotting
and then went to IVC, and what is the connection
between COVID and IVC?
How does that tie in here?
So obviously, there's lack of data on looking
at what's happening to the veins.
Again, it goes back to nobody and really cares about the veins.
But someone who I was talking about earlier,
he was talking to the vascular surgery head of Penn
and asking him what he thought about my theory.
He said, well, you know, the vascular, the venous disease
that I'm seeing in the last two years has been 10 times more
than I've seen ever.
And it goes to show that there, I think the spike protein causes
damage to the endothelium of the veins.
The interesting thing is the veins endothelium is very different
than the arterial endothelium, something that I didn't know.
So there's things that it secretes that aren't secreted
in the arterial endothelium.
Things like VEGF that are elevated
when you have arterial issues aren't elevated
when you have venous disease.
Because venous endothelium doesn't secrete VEGF.
So there's a lot of different other ways.
Because again, VEGF is an angiogenic, you know, modulator.
So, you know, on the venous side, they're not sitting there trying
to make new veins to get oxygen.
Instead, you know, it has a whole different function.
So spike protein is the issue.
The spike protein.
Don asked a question here, which is,
how to treat endothelial vascular damage in patients
who've had a TIA?
So one of the things that I've learned is most
of these people, especially when I get parameters on them,
they are hypercoagulable.
And actually, one of the things that I've had, a lot of the patients
that come to me, they've been to neurologists
after having TIAs or even strokes.
And they put them on what we would call typical secondary
prevention.
And guess why they come to me?
Because they've had a second stroke, a third stroke, okay?
It's their hypercoagulability actually is suggestive
that you need to be a little bit more aggressive.
Now, that doesn't mean that you don't need to be, you know,
foolhardy, but what I would say is the only actual patient
that I've had that passed away had an ischemic event
after his third stroke previously,
and he was on triple therapy.
So to actually have a massive ischemic stroke on anti,
do any platelet anticoagulation therapy shows you
how hypercoagulable these people are.
Now, I heard you when you said about the Kell
and Pretorius work that they found these fibrin amyloid
aggregates that were resistant to trypsin,
which my lab days I remember that chewed up everything.
Exactly. That's what's so crazy about it.
And I think that's what's when we talk about typical TIA
or stroke in the context of COVID or the vaccine,
the secondary prevention is inadequate.
I don't have, I mean, it's just, you know,
they're the people that come to me.
Oh, well, the neurologist said I'm good.
And then second stroke, third stroke, they're finally like,
I'm not, I can't trust really what neurologist is saying anymore.
And what, I mean, I think everybody would agree right now,
one of the kind of common threads of COVID is really weird
clotting issues, like things, things clotting that she,
like whether it's the hepatic vein or everything,
you're like, why the heck is that clotting?
And even when we talk about TIAs or even strokes
that are happening in the, in this population,
a lot of them are happening in smaller,
really non-typical areas for stroke.
So they're hitting in the thalamus or in the brain stem.
And those are actually what, what I would argue
as well as it looks like the data would argue
is that's micro thrombosis in situ.
So these small vessels are actually clotting right
in the vessels themselves.
They aren't coming from somewhere.
And that's why a lot of these neurologists are like
looking with echoes and, you know,
and it literally happened right there in the small vessel.
It's a critical insight.
Anonymous is asking a question here.
Do labs such as ESR and CRP display
elevations with micro clotting,
any changes in platelets PT or PTT or INR?
So platelets are kind of unique.
So you can look at MPV, which is mean platelet volume.
That usually tells you how kind of, you know,
aggregated and activated the platelets are.
That's kind of a useful thing.
An actual quantitation of platelets.
Sometimes the platelet actual value is low
when the MPV is high
because the platelets are sticking together.
So that's one of the things that it's kind of,
just because the platelets are low,
don't think that they don't have a hypercoagulable
or hyper platelet issue.
The other thing is, when we talk about PT, PTT,
it's high after I take care, I'm just kidding,
but because I put them on medicine,
but usually it's not abnormal.
CRP and sedrate, I really have never seen
that much of a significant, I mean,
there's a lot of overlap with autoimmune issues as well.
And so sometimes those kind of suggest to me
that maybe I need to look a different area.
So I'm kind of an all abroad looker at the disease process.
I mean, most people would think that all I do
is anti-coagulation and microclotting.
No, I mean, as the venous disease shows,
all the way to the autoimmune dysfunction
to mass selectivation.
I mean, you have to take the patient as they are
and they bring with them, not only most importantly,
their story and what kind of symptoms they're experiencing,
but sometimes things like if the CRP is elevated
and the sedrate's elevated,
it means that there's something else smoldering, I guess.
Yeah, so where do you fall then, Jordan,
on the great Scott Pierre debate?
When somebody's got microclotting this
between one and four, where do you treat?
Well, so first of all, I have two post grads now in a lab
that are, we're basically doing a high throughput
micro well analysis with the fixed volume
and actually have an imaging utilizing AI
to actually give you a fixed,
so three out of four is actually just kind of Jordan's
additional insight.
I mean, it's technically a qualitative test right now,
but we're trying to make it quantitative.
So once we get to the point that we can have
an amount per deciliter or an amount per microliter,
I think that debate will be easier to solve right now.
I feel pretty biased in the debate, so.
Well, it comes to this anonymous question,
which is, are there natural supplements you can take
or maybe we should say, also should you take
for microclotting issues instead of these heavy duty meds?
Such as?
Yeah, absolutely, so, I mean,
the more that I read about the small vessels,
I mean, I almost like tell everybody to take natokinase
or seropeptase, those kind of things.
I take it every day.
The more that I kind of look into it,
I'm like, well, that, you know,
it's almost like kind of preventive cleaning
of your small vessels, you know,
like don't let the sludge muck up.
But those things work.
I will say if the person has a lot of mass selectivation,
the problem with a lot of those things initially is,
typically would have called it kind of
herxheimer reaction, but I actually think it's really,
I mean, especially if they have elevated histamines
and triptase and stuff like that.
I mean, you can start natokinase,
they're not gonna like you,
because when you do, they're just gonna feel like crap.
So a lot of times you have to be more gentle
and definitely address the mast cell.
The first thing I do is address mast cell anyway.
So I usually don't start anticoagulants
or anything like that until they're on femuridine
or something like ketotiphon or, you know,
and then we'll kind of do the anticoagulants,
because what I learned two years ago was,
I would just tell the patients
you're gonna feel like crap for a month,
but patients usually aren't cool with that.
So instead we found a way to kind of like,
kind of dumb down the reaction that their body takes.
But I will say a good signal to me
that you probably have microclotting
is if you take natokinase and your skin crawl.
But anyway, you know,
because you actually have kind of a breakdown in a reaction.
And from what we know from proteomics of these microclots,
they're really inflammatory and really nasty.
Oh, that's fascinating.
We saw when Jo Verone was doing his case study,
he had one chart of lab readouts.
Histamine was way off.
I actually told it, I was sitting over here,
I was like, oh, the histamine's elevated.
Anyway, that's what we find a lot.
And histamine, classically people said,
don't test histamine.
It does matter whether you come in and see me at 8 a.m.,
especially if you're venous disease.
I mean, again, if you have venous disease
and all night you sat there,
your histamine's much more likely to be high in the morning
than it is as you move throughout the day.
But histamine being elevated isn't always,
I mean, there's other things that can release histamine,
like vasophils and stuff like that.
But it's a pretty good indicator to me
that you got to address mass selectivation.
And usually that'll get the patient on board
because once you actually address mass selectivation,
a lot of times they start to say I'm thinking better
and I feel a little bit better
and I'm better able to kind of do what,
you kind of get some street cred, if that makes sense.
Because they've been a year or two with nothing that worked.
Wow, fascinating.
Kate Godley is asking, what tests do we need to do
before referring patients to Brooke?
And can I refer to a local vascular office
in North Carolina, or should we learn how
to do venograms in office?
So if you can do venograms in office, that'd be great.
But I wouldn't, you know, in all honesty,
we probably, Brooke just got a post-grad too.
We're going to put the data together
and publish these the first 60.
But right now, most vascular surgeons and most people
that deal with, or interventional radiologists,
are going to say there's no massive clot there,
so I'm not going to do anything.
And Brooke's been doing pelvic venous disease.
There's another guy in Chicago named Steve Smith.
I think he's retired now.
But they've been doing this for a while
and it's pretty amazing how a stent in the pelvis
can make these people think again.
I mean, I actually have another patient that isn't in Asheville
and I mean, they thought he had dementia.
At C72, he's the oldest person we've stented.
And I mean, the guy's like reading research articles again.
You know, like meaning, and so there's another theory.
I mean, obviously there's the inflammatory issue,
but not getting good cerebral perfusion is not good
for how you think.
And so, you know, just the same way that if you stand
up too quick, your brain's going to, you know,
you might pass out.
But, you know, same thing, if that was kind
of chronically always not perfused well,
you're thinking probably he's going to look like somebody
that might have, you know, that they might say has dementia.
So, doing a Sudoku at 20,000 feet, tough business, right?
Exactly.
So, what I would say is this is new.
Okay, Brooke is the world expert in it.
And as the world expert, I've really learned a lot.
And even I've had to teach Scott a little bit
because sometimes he's, we'll go and find these.
He's like, oh, I'll find somebody in town to do it.
And I'm like, no, they're just going
to frustrate the patient even more.
Now, as we get the data out there, I think it'll be
where people are more likely to do it.
There are people that call me.
I mean, even the head of bachelor's surgery
at Vanderbilt wanted to have a Zoom call with me,
which is interesting because he just wanted
to know what I was doing.
So, the other thing that I will say is as much as we want
to say these doctors out here are crazy, you know, it is,
there are little snippets like Alexis at Emory, Brooke,
or a lot of the people, they work at these great institutes.
And they're the people that are real thinkers
and care about patients.
And there's plenty of them.
They've just probably not been able to openly talk
in the last three to four years.
So, when you find some of those, encourage them,
and continue to communicate because you learn a ton
from them, too.
Well, great.
Another question here, if the left side is worse
on the venogram, do patients have more pain
on the left side, too?
So, not always.
So, as you can see from there, usually the left side is worse.
But if you have reflux across like that did,
all of a sudden you get what we call venous congestion
on the right, too.
The other thing is the anatomy is not always the same.
I've had people that actually have the angulation
of their aorta split off, and it goes all right.
And so, again, these people are already people
that are a little weird in their vasculature.
So, guess what you can predict when you get an MRV?
Their vasculature might be weird.
Yeah. How do they describe that pain?
So, usually, really, leg heaviness,
a lot of times it's worse at night.
They might actually been diagnosed with small fiber
neuropathy or something like that because one
of the reasons you can get small fiber neuropathy has to do
with venous congestion.
It's one of the, you know, and so, a lot of times,
so it's basically that or heaviness.
Usually, they're also worse when they're exerting themselves,
especially going up inclines.
And the other thing that I've found, and this is kind
of a little bit thinking really kind of way out there,
but these athletes that have this,
when I do pulmonary function test on them, their DLCOs are
like 60, okay?
That makes no stinking sense.
Like somebody who's never smoked in their life,
all of a sudden is having a low DLCO
on their pulmonary function test.
Well, if you think about it, the test means
that you have to basically breathe in, hold fullness,
okay? Decrease venous return.
Okay? So, they have venous return issues to begin with.
They're going to get even less venous blood back to their heart.
And their DLCO is going to look crappy
because they're not getting good venous blood
to their lung at all.
And then after we have fixed them on these stents,
it's kind of the cool thing we found is their DLCOs can go
back to normal.
That's a totally like, it's not really,
it tells you anything about, tells you about the pathology,
but it's really just that the test itself is causing the
dysfunction to be elicited.
Does that make sense?
But that's one of the things I found because I couldn't,
and that really led me to this as well.
Because I was like, well, why would somebody
who ran a four or a two mile have a 60 DLCO?
I mean, those are your typical smokers for 30, 40 years.
Incredible. Well, thank you very much.
Big hand for Dr. Jordan Vaughn.
