S1: From Kerkow media coming up on the show, the first
S1: patient I saw when I was an intern, I was
S1: at Duke University, I went down to the E.R. to
S1: admit my patient. She was twenty five. She'd come in
S1: the a couple of weeks before pregnant. She was second
S1: trimester tachycardic and short of breath, fast heart rate. Couldn't breathe. Well,
S1: she was told she was anxious from her first pregnancy,
S1: was sent home, came back. I was there to admit her,
S1: but by the time I got it, she'd already had
S1: a cardiac arrest and died. I went to her autopsy.
S1: I have pictures of it to this day. And she
S1: had huge blood clots. One, I never forgot that. You know,
S1: we've both seen a lot of interesting things in medicine,
S1: but that really got my eye that something like this
S1: not only takes the lives of older patients, but can
S1: take the lives of young people who seem to have
S1: no particular risk factors. Dr..
S2: Having trouble catching your breath, slightly dizzy, maybe battling a
S2: small cough, perhaps, that it's probably nothing, right, for the
S2: patients or doctors listening, we're not trying to make you nuts,
S2: but these seemingly benign symptoms might be something that require
S2: a second look. And apparently part of this diagnosis process
S2: comes from perspectives that only come from doctors with years
S2: of experience. A pulmonary embolism has been deemed a silent
S2: killer because most often than not, it's diagnosed only in
S2: an autopsy. Yep, when it's too late. Well, today we're
S2: joined by a renowned doctor from Cedar Sinai whose research
S2: helps lift the curtain behind a disease that plays hide
S2: and seek. It's used to hiding and will only present
S2: itself if you seek it out. It's a sobering lesson,
S2: but it's highlighted with hope. This is medicine we're still practicing.
S2: I'm Bill Kurtis. So first, my co-host, the quadruple board
S2: certified doctor of internal medicine, pulmonary disease, critical care and
S2: neuro critical care, and my very best friend, Dr. Stephen Tayback.
S2: How are you doing, Steve Cable.
S3: Good to see you.
S2: We've got a special guest today that I know you're
S2: going to like because it's just right up your alley.
S2: That's a fact. Our special guest, Dr. Victor Tapson, he's
S2: a professor of medicine and director of clinical research at
S2: the Women's Guild Lung Institute. He's also associate director of
S2: the Pulmonary and Critical Care Division at Cedars Sinai Medical Center.
S2: He's authored more than two hundred peer reviewed manuscripts and
S2: a whole bunch of books and book chapters. We're lucky
S2: to have him here. Vic, I imagine this past year
S2: with covid has been quite a challenge. And I understand
S2: covid creates all kinds of blood clot issues in your patients.
S2: Has it been for the last year?
S1: It's been such a bill as it has for everyone,
S1: but because a lot of problems, a lot of them
S1: involve the lung, of course, and many of them actually
S1: involve specifically a blood clotting in the lung and blood
S1: clotting in other places, too. So we've been trying to
S1: figure out how to deal with how to treat it,
S1: how to diagnose it. It's been a trying, but I
S1: think we've made a lot of progress.
S2: Why does it cause blood clots? How does the virus
S2: do that?
S1: Well, it's interesting, but there's something that go into thulium
S1: cells that line your blood vessels. These are the cells
S1: that line the blood vessels, become very inflamed and irritated
S1: by this virus. And we get something called an endothelial IDUs,
S1: sort of. So these viruses get in there, they inflame
S1: the lining of the cell. And when that happens, it
S1: releases substances from inside the cells. One of them is
S1: called Tissue Factor. It can really get clotting going and
S1: it's more complicated than that. But we certainly learned that
S1: in many blood vessel linings, not just the lungs, this
S1: develops blood clots in their legs called gvt, and they
S1: break off and go to the lungs. We call that
S1: pulmonary embolism. And we've seen a lot of this and
S1: it's been difficult to try to decide who we should
S1: look for that because a fairly high percentage of patients
S1: with Koban do get it.
S3: Back in January, we had 10 deaths a day, and
S3: which is just unprecedented and morale was at an all
S3: time low and just the human tragedy of it. And
S3: the staff was just reeling every day from the terrible
S3: emotional trauma. What did you guys do over the hill?
S3: Over the hill? Because Cedars is over the hill from
S3: where we're at. How did you folks deal with the
S3: social devastation both to the patient's family and also to
S3: your staff?
S1: I can tell you, Stephen, I'm sure you did the
S1: same thing. It was very difficult, especially early in the
S1: pandemic when we weren't putting patients in the room. No
S1: one was coming in. And later the same thing Jan
S1: came along. It was much worse than over the summer
S1: for us to we didn't really notice a really high
S1: death rate the whole first year until that surge after
S1: the holidays. Then we noticed something a little different. I
S1: don't know if that was a variant California variant. We
S1: were getting some of the one one seven Bériot. I
S1: don't know the reason we didn't sequence everything right away.
S1: I could just tell you, though, we saw what looked
S1: like a difference to us and to handle those problems
S1: that you're mentioning, the emotional social issues, me was a
S1: lot of phone calls and we enrolled patients in clinical trials.
S1: And normally we would talk to them and say, well, Mrs. Jones,
S1: we wouldn't like to enroll in this trial. And I
S1: know your husband's on the phone. Let's tell you a
S1: little bit about the study. And it was not just
S1: like a usual study where we would fill them in
S1: on some details. We had tons of questions about Kojm therapy,
S1: everything from other members of our family, how they could
S1: prevent it. So it was a lot of communication, a
S1: lot of phone calls. And I think that's really important
S1: treatment during this kind of thing. And it was family members,
S1: the patients themselves, isolated patients, the rooms. You know, Steve,
S1: it was terrible. It was terrible. A lot of communication,
S1: a lot of handholding.
S2: So I probably can't say the name, but I have
S2: a friend of mine who spent 59 days in your
S2: ICU and was on the ventilator for a long, long time.
S2: And nobody was really too positive about how that was
S2: going to turn out. And you guys sent him home
S2: and he had to relearn to walk. And he lost
S2: all kinds of weight, of course, but you had to
S2: put him back home among his wife and all of
S2: us who love them. And we really appreciate it.
S1: I'm glad he did. Well, boy, I'll tell you and
S1: I'm sure Steve took care of some of the same
S1: kind of folks. We just had some very, very long
S1: hospitalizations that were complicated by subsequent to see someone in
S1: the ICU for a long time or whatever they have
S1: covered or whatever. And then they get a urinary tract infection,
S1: they get a bloodstream infection, they get another kind of pneumonia. So, yeah,
S1: just like you're saying, Bill, these were complicated patients in
S1: many cases.
S3: No question for you. The general public, I think, is
S3: very familiar with the idea that if you've had a
S3: knee replacement, you're going to need to be put on
S3: blood thinners. People have heard they've been on a long
S3: plane flight. They've heard of cases of people developing a
S3: blood clot.
S1: And I think it's
S3: it's just general knowledge that when you're on an airplane,
S3: you should get up and walk around the mechanism for
S3: blood clotting in the covid patients pathologically. Is it? Exactly.
S3: The same as those people who undergo a surgical procedure
S3: or those people who are on a long plane flight
S3: is a blood clot, a blood clot, or is there something,
S3: a nuance to covid patients that we've identified during this
S3: past year?
S1: I think it's a little bit different. I think people
S1: do form clots in their legs. They break off and
S1: go to the lungs. But we're seeing patients that came
S1: in the hospital, as you suggested earlier, are nurse coordinators
S1: drawing blood from cold patients. The two clot it off
S1: and this doesn't happen by the two keeps falling off.
S1: I can't get it quite literally easily. We're seeing something
S1: called micro thrombosis, small clots in blood vessels, blood clots
S1: in the lungs don't start in the lung. They start
S1: in the legs and they go to the lung where
S1: some of these patients getting clots in their lungs. It
S1: might even be building up inside to do some I
S1: don't think know blood clots for forming and veins that
S1: niobium that usually would stay open. And so I think
S1: it was different. Steve, I think this very pro thrombotic,
S1: as we call it, tendency Cauvin was causing problems and
S1: a little different way, not just big macroscopic clots in
S1: the leg veins breaking off and going to the lungs,
S1: but small clots even causing strokes, causing heart problems, causing
S1: kidney problems. So we're seeing multi organ problems and what
S1: we call micro thrombosis, because this organism seems to be
S1: much more pro thrombotic than the flu, more than nerves
S1: or SARS or some of the past infections we've seen,
S3: in addition to the treatment, I should say, of blood
S3: thinning anticoagulation. Have you folks done any research on antiinflammatory agents,
S3: immunotherapy that may have some impact on either prevention or
S3: treatment of blood clots?
S1: We haven't actually done some of the studies on some
S1: of the antivirals. In the early stages, the desert disappear.
S1: We completed a study on a drug called Burset NIB.
S1: There's something called a jack inhibitor. One thing we learn,
S1: as you know, in the Soviet era is that steroids
S1: seem to help. And why do they help? To help
S1: is cytokine storm. These patients get such immune responses and
S1: tremendous inflammation that steroids can tend to kind of shut
S1: that down and calm things down. It put them on
S1: steroids for a long time to early and then they
S1: get covered. Then they're in trouble because their immune system
S1: shut down, can fight the virus. Once they get covered.
S1: Steroids may help. And I think steroids probably help with thrombosis.
S1: But right now, the data don't prove that. One study
S1: published in February suggested that there's no real proof right
S1: now that steroids reduce the chance of getting a clot.
S1: But it's hard to ignore the fact that if you
S1: do the right study, they might because inflammation and coagulation
S1: or clotting are so intimately linked. One way we know
S1: that if look at obesity, obesity, we don't think of
S1: it as an inflammatory disease, but it is obesity is
S1: chronic inflammation. The more we see, the more information there is.
S1: A heavier you are, the more likely you are to
S1: be hospitalized if you got covid and the more likely
S1: you were to get a blood clot. So I think
S1: there's really something to that.
S3: Personally speaking to you and I, we live and breathe
S3: this type of issue in the ICU. Naturally, it's interesting
S3: to us. But was there something in particular that caused
S3: you to pull your focus and to dedicate your life
S3: to dangerous blood clots and pulmonary hypertension?
S1: I could see the first patient. I saw it with
S1: my arm. I was an intern. I was a Duke University.
S1: I went down to the E.R. to admit my patient.
S1: She was twenty five. She'd come in the last couple
S1: of weeks before pregnant. She was second trimester tachycardic and
S1: short of breath. Fast heart rate. Couldn't breathe well. She
S1: was told she was anxious from her first pregnancy, was
S1: sent home, came back. I was there to admit her,
S1: but by the time I got it, she'd already had
S1: a cardiac arrest and died. I went to her autopsy.
S1: I have pictures of it to this day and she
S1: had huge blood clots. I never forgot that. You know,
S1: we've both seen a lot of interesting things in medicine
S1: that really got my eye that something like this not
S1: only takes the lives of older patients, but can take
S1: the lives of young people who seem to have no
S1: particular risk factors sometimes. So it's always been fascinating to me.
S1: I've maintained my interest.
S3: It's one of the most misdiagnosed syndromes in medicine and
S3: one of the most highly litigated syndromes and pulmonary embolism.
S3: Why is it so hard to diagnose? Why is it
S3: that the general population of physicians out there, why is
S3: it that we're still missing so many of these cases?
S1: I think a couple of reasons are I can see
S1: the symptoms, as you know, are very nonspecific. But you're
S1: short of breath. You rarely have coffee. You might have
S1: a cough. You might, in rare cases, cough up blood
S1: not nearly as common with people. You're short of breath.
S1: You listen to the lungs, you don't hear anything. They
S1: sound normal. You don't hear wheezing like you do in
S1: your crackles, like a pneumonia or fibros. You don't hear
S1: decreased breath. Sounds like there's fluid in the lungs. Look
S1: at the chest x ray, chest x rays. Clear, clear
S1: x ray with a big polymorphism, you don't see pneumonia,
S1: heart failure. So people looking at your lungs, they look
S1: your arteries and maybe got a little asthma. Some I'm
S1: not sure what this is. And you're sent home. And
S1: we've learned from four or five autopsy studies, if you
S1: die from pulmonary embolism, more likely than not, you're not
S1: diagnosed until you're dead. And more likely than not, you're
S1: not even suspected until you're dead. So see that that's
S1: right on target and it's still a problem. So I
S1: think we I think we've raised awareness and I. We have,
S1: but we still see this still litigated and it still
S1: poses a huge problem. So you're absolutely right.
S2: So what is the best test at this point to
S2: diagnose this?
S1: One of the best tests off the bat? I'd say,
S1: Bill and I kind of see a tongue in cheek
S1: is using good clinical gestalt. And there's been a study
S1: that's been shown by one of my colleagues over in Belgium.
S1: She did a nice study that showed that you have
S1: these scoring systems as well as well score the revised.
S1: You need to score the perks for to maybe help
S1: you if you're suspecting whether you should do a test
S1: or not. And what Dr. Peñaloza showed was good stock
S1: is better, better even than any of these scoring system.
S1: If you think someone might have P.E. and there's a
S1: reasonable chance they do, you've got to go for a
S1: simple blood test called a dimer. You can do dimer
S1: test is negative. It's very unlikely to have a clot
S1: if it's positive. You can't be sure it's nonspecific, but
S1: you've got to have a low threshold to go ahead
S1: and do a CT scan of the chest. And sure,
S1: you're going to maybe do too many CT scans expected.
S1: Too often you don't want to miss this diagnosis. So
S1: a good gestalt, I think, about the diagnosis and think
S1: about simple things like we've got an unexplained fast heart rate.
S1: Why is your heart rate 110 or 120? Maybe you
S1: are anxious, but maybe it's something else. Maybe it's your
S1: asthma inhaler, but maybe it's pulmonary embolism. So unexplained fast
S1: heart rate, unexplained shortness of breath, even someone's kind of anxious,
S1: a little bit shorter, but I've got to think about it.
S1: So once it comes to your consciousness, I think you're
S1: in better shape.
S3: So let me bring this into the mix, because this
S3: is the era of cost containment and you want to
S3: minimize testing. That's not necessary. And so using a score
S3: like the well
S1: score, which
S3: is supposed to help delineate who's the low risk, mid
S3: risk and high risk, and obviously, if it's a high risk,
S3: you're going to treat the patient. If it's a low risk,
S3: maybe you're going to let the patient leave your E.R.
S3: and certainly a seasoned practitioner such as yourself, your gestalt
S3: means a lot. But for a young practitioner who's making
S3: an assessment, who's relying heavily on a well score, and
S3: who feels pressure to minimize the amount of testing that
S3: they're ordering, what kind of a conundrum is that and
S3: where do we go with that?
S1: It is a conundrum and we do have to think
S1: about that for sure. And in the end, I think
S1: you should use these new scoring systems. I think the
S1: catch is use a scoring system together with a dimer
S1: in a body dimer is negative. You're almost always off
S1: the hook. If your suspicion is somewhat lower moderate, you're
S1: off the hook. If it's very high suspicion, probably nothing
S1: should supersede a very high suspicion. So I think what
S1: you do is you use those things together. And again,
S1: just don't ever second guess a really strong start feeling.
S1: But it's a problem. I think the tests testing make
S1: it better, make it easier. We're using artificial intelligence now,
S1: machine learning. We've done a couple of protocols. Now we've
S1: done with it. Are we able to predict code with
S1: a group we worked with coming up with an AI
S1: program without doing a COBA test? We were ninety nine
S1: point something percent accurate predicting covid. I think the same
S1: thing could be done with pulmonary embolism. And now now
S1: we've got A.I. artificial reading of CT scans, too. But
S1: I think that's going to come into the you may
S1: have seen something on TV using a robot who is
S1: taking histories from people. In the end, it was amazing.
S1: I think using machine learning, artificial intelligence, together with Gestalt,
S1: we're going to do a better job at saving money.
S1: But again, when it gets down to see I've been
S1: really lucky. No one's ever pressured me to save money.
S1: But we do want to use our common sense and try.
S2: But wait a minute. We're the patient here talking. Are
S2: you saying that there are considerations, perhaps with your relationship
S2: with some doctor's relationship with insurance companies that could affect
S2: whether or not you CT scan my dad if you
S2: have a well, let's say a minor suspicion that he
S2: might have a clot.
S1: Part of it is money and part of his resources.
S1: And for example, if you've got a busy day, there's
S1: one hundred people in there being seen. The CT scan
S1: is being used for all kinds of things. And so
S1: it's money and it's also using your resources carefully. But no,
S1: I would never think about money when I really thought
S1: someone that I think in general makes a good point.
S1: You've got to take that into consideration. But when it
S1: gets down to an individual patient to me, I will never,
S1: ever not get a test because I think it might
S1: cost me a little more if I have some doubt.
S3: But there is another consideration, and that is, if so,
S3: the public may say, well, if I'm a little short
S3: of breath, I'm having some chest pain. Everybody should just
S3: get a CT angiogram and and delineate. Is this a
S3: pulmonary embolism? Is it not? But the reality is the dye,
S3: the contrast that are being given with CT scans actually
S3: can have a deleterious effect. It can cause some kidney damage.
S3: And you don't want to, in a cavalier fashion, start
S3: scanning everybody that comes in because you don't want to
S3: miss a pulmonary embolism and wind up causing a certain
S3: percentage of patients to have serious kidney damage. That may
S3: or may not be reversible because you wanted to be
S3: super meticulous about making sure you're scanning everybody. So so
S3: medicine granted should not be it. Certainly in this country,
S3: we should not be thinking resources first by any means.
S3: But we do want to be judicious in our testing
S3: because some of the testing can have some negative impact
S3: on our patients well-being as well.
S1: You've got a screen. You've got you're absolutely right. You've
S1: got to look at that and look at the kidney test.
S1: If it's too high, we can't do the CD. There
S1: is another test you can do called the BQE and
S1: the ventilation perfusion scan. Very good test. Not as accurate
S1: as a CT scan, especially if the X-ray is already
S1: abnormal or the patient has other kinds of lung problems.
S1: But still a good test. But you got. Yeah, you're right.
S1: But look, the lab tests make sure that that's normal
S1: or near normal or you can't do this and you
S1: may have to empirically treat someone you think they might
S1: have until you can do a scan. You may have
S1: to wait a day sometimes to get the kidneys better.
S2: So can I just ask you guys about the treatment
S2: for just a second,
S1: because logic tells
S2: me that if you guys treat a blood clot with
S2: a blood thinner, it would seem that that is going
S2: to reduce the size of the blood clot. Right. Kind
S2: of thin it out. And it would seem that it
S2: could then get dislodged and actually move into a more
S2: destructive location.
S1: They do a couple of things. They don't actually break
S1: the clot down themselves, at least the ones we usually use.
S1: They prevent the body from forming more clot, which is helpful.
S1: They allow the clock to stabilize by keeping it from growing.
S1: It sticks to the wall and is less likely to
S1: break off as it stabilizes like this. The other thing
S1: it does is by thinning the blood, it allows the
S1: blood to flow better. So these remaining channels you have open,
S1: you get blood through better. You've got a blocked off artery.
S1: The heart can't pump the blood as well. If you
S1: can open up some channels by making the blood thinner,
S1: it gets through better so it can help even without
S1: affecting the clot directly. But it takes time for your
S1: own body's fiber optic system or clot busting system to
S1: kind of break down these clots in the blood thinners
S1: will give you a time for that to happen. But
S1: it does happen. You can treat someone and they may
S1: still have another blood clot or form one. But generally speaking,
S1: once they get on, that clot stabilizes and size doesn't
S1: get bigger. And one thing we've learned is blood thinners
S1: save lives. It's one of the dogmatic things we can
S1: say about blood clots is as soon as you get
S1: someone on the blood thinner, their chance of dying gets lower.
S1: It's been shown in one nice research study by a
S1: colleague published in Chest, one of our journals in 2010.
S1: If you're on a blood thinner with an at an
S1: adequate level within twenty four hours, your chances of dying
S1: are far, far lower than if you're not.
S2: And once you're on a blood thinner, very often my
S2: dad and his case, I think warfarin. Was that excessive? Yeah.
S3: We didn't have the docs at the time that your
S3: father was first placed on uncommitted.
S2: OK, but basically once you're on blood thinners, you kind
S2: of stay on blood thinners. Is that the case?
S1: We're doing that more and more nowadays. Why don't we
S1: try to divide clots into what we call promote and unprovoked?
S1: That's a little bit simplified. But the bottom line is,
S1: if you have a really good reason for a clot,
S1: you have a hip replacement and you get a blood clot,
S1: usually will treat you for three months, sometimes six, unless
S1: you have other risk factors. If you fly from Paris
S1: to L.A., actually get a clot. We know the plane
S1: flights increase the risk of clotting, but to me, that's
S1: a minimal increased risk. I've flown my four million miles
S1: of American Airlines. I've never had a clot, I think.
S1: But people are more susceptible, increase their risk, lower the threshold.
S1: They may get a clot, someone that's the only reason
S1: they get a clot because they're flying. I'd be inclined
S1: to treat them long term. I wouldn't say forever, but
S1: I'd say indefinitely. Forever's a long time. And what we
S1: can do now that we've learned with these new drugs
S1: that Steve mentioned, called the Doakes, is we can drop
S1: the dose at six months and reduce the risk of
S1: bleeding dramatically and still offer protection. So no kind of
S1: a new paradigm is to consider many patients treat them longer.
S1: If someone comes in, they have a plot and their
S1: only risk factors, they're obese. We might say, well, we'll
S1: keep you on this drug. We'll drop the dose in
S1: six months. If you lose weight, we'll take you off.
S1: But if you don't want to keep you on the slopes,
S1: there's a lot more versatility nowadays with these new drugs.
S2: OK, well, we're going to take about a 30 second
S2: break here, and when we come back, I'd like to
S2: talk a little about pulmonary hypertension. We'll be right back.
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S2: All right, Vic, pulmonary hypertension. I'm assuming that is high
S2: blood pressure specifically in the lungs. How is that different
S2: than plain old high blood pressure?
S1: So high blood pressure. You measure your blood pressure, your arm,
S1: it's it's 120 over 80 when the heart's squeezing. It's
S1: 120 when it's relaxed, it's eighty. And in the lungs,
S1: you have a separate circulation. Normally in the lungs, the
S1: pressure's much lower because the blood vessels are very dispensable.
S1: They can open up, they can handle more flow. The
S1: pressure might be twenty over ten, much lower pressure. Different
S1: things can make this pressure go up and we call
S1: that pulmonary hypertension.
S3: Now, I had a patient of mine who's become actually
S3: a very good friend of the
S1: family, and
S3: she had a pregnancy and right after she delivered suddenly
S3: became short of breath and she was diagnosed as pulmonary hypertension.
S3: One of my competitors at the hospital said, you know,
S3: you have two years to live and you better get
S3: your affairs in order. And then I walked into the
S3: room and I said, OK, well, things have changed now.
S3: And we obviously put her on some of our newer medications.
S3: It's been ten years and she's doing great. So maybe
S3: give a little bit of history about the earlier prognosis
S3: and where we are today in terms of
S1: the hope and the better
S3: outcomes that we're seeing relative to pulmonary
S1: hypertension. Well, Steve, I'm glad you were there to reassure her,
S1: because you're absolutely right. Things have really changed. Mortality actually
S1: dropped over the years. Just in a very brief nutshell,
S1: kind of five classes of permanent protection once called pulmonary
S1: arterial hypertension. It's the kind of young women tend to
S1: get more commonly than men unknown cause Group two is
S1: from chronic heart disease. That's much more common in older folks.
S1: Gets to FART'S and get heart has more trouble pumping attention.
S1: Group three, you have emphysema, lung fibrosis, scarring in the lungs.
S1: You destroy many of these millions of blood vessels in
S1: your lungs and the pressure goes up. You have to
S1: just treat the underlying disease. Group four is blood clots.
S1: About one in one hundred patients with pulmonary embolism, like
S1: we were talking about, will go on and get chronic
S1: pulmonary embolism. And that's got to be treated differently in
S1: the group. Five is kind of the muscle group. One
S1: is the one I suspect your patient had. It can
S1: be what we call idiopathic pulmonary hypertension, young women probably
S1: for women, for every man it gets it unknown cause
S1: sometimes brought out by pregnancy. And in the old days,
S1: we had no treatments. First patient I saw in nineteen
S1: eighty two, his name was Gary. There's a minister for
S1: South Carolina again. I was an intern. He had severe
S1: pulmonary hypertension of unknown cause. Our attending physician very insightfully
S1: sent them to Berkeley Griffith in Pittsburgh who had already
S1: done about a seven or eight heart lung transplant. Gary
S1: got a heart lung transplant and survived a good three
S1: or four more years after that. Now, we rarely have
S1: to do heart lung transplants, my judgment. And if we do,
S1: patients do much better nowadays. The idea is we have
S1: medications we've studied for the years. It was nineteen ninety six.
S1: We published the first paper on using prostacyclin drug IVI
S1: pulmonary hypertension to be published in England Journal. We studied
S1: eighty patients and 40 of those patients didn't get the drug.
S1: Eight of them died within 12 weeks. The patients that
S1: did get the drug all survive. We learned a lot.
S1: We started doing more and more treatment with that drug
S1: IV with a pump twenty the two we came up
S1: with another drug pill and so on. Over the years.
S1: Now we've got about fourteen pulmonary hypertension drugs. We combine them.
S1: We often have people on one or two or three
S1: at a time and we've just done so much better
S1: than we used to do. So just like you told
S1: your patient, nowadays we can tell people that they can
S1: do well, have a normal life. We don't really like
S1: getting pregnant again if we try to talk them out
S1: of it. But patients can live a much more normal
S1: life now than they used to.
S2: Doctors, how do you test for this? I mean, you
S2: can't put a cuff around the lung, so how do
S2: you know that someone has hypertension specifically in their lungs?
S1: It is harder. And it's it reminds me a lot
S1: of a more chronic form of something like pulmonary embolism,
S1: where you often come in the emergency department suddenly short
S1: of breath, something just happened with pulmonary hypertension. It's often
S1: slowly over months, someone notices I can't walk. My dog
S1: is for a little short of breath walking up the steps.
S1: So you see almost uniformly chronic shortness of breath is
S1: worsened over time, usually at least months. And again, there's
S1: a failure to diagnose. And a lot of cases you're
S1: told you gain weight, you're just you're deconditioned, et cetera.
S1: But what you do, one of the key tests while
S1: you examine someone and if you carefully listen, your loud
S1: heart sounds, you hear this blood's being pumped into the lungs.
S1: The pulmonic valve, one of the heart valves, is slammed
S1: shut by this high pressure. You're allowed second heart stop.
S1: You can pick that up. You do more tests. If
S1: you don't hear that, you still think about doing echocardiogram.
S1: And echocardiogram is the kind of the pivotal test that
S1: gives you a really good clue. If you've got it,
S1: then we do a heart catheterization to prove it. But
S1: you're right. But you got to suspect it first. Then
S1: do consider doing an echocardiogram and you'll be most of
S1: the way there.
S3: Are there any thoughts about what predisposes one individual to
S3: this disease versus another?
S1: Well, I think there's truly some genetics with this group.
S1: One pulmonary hypertension. It's often undiagnosed unknown cause it can
S1: be due to certain connective tissue diseases, lupus, scleroderma, things
S1: like this. It can be from a hole in the heart.
S1: Congenital heart disease, HIV, we learned, can cause from hypertension.
S1: But again, in terms of predispositions, the classic patient that
S1: gets pulmonary hypertension is unknown. Cause probably has genetic some
S1: genetic abnormalities, bumper to gene mutation, one mutation, certain mutations
S1: that some people have, we don't completely penetrate. You might
S1: get this mutation. Not yet. We're still understanding, learning more
S1: about the genetics. But certainly what I can say is
S1: just because someone gets it doesn't mean other people in
S1: the family will. I've taken care of many families with
S1: pulmonary hypertension. One was notably a young woman, forty years old,
S1: that got pulmonary hypertension. And two years later, we diagnosed
S1: her eighty year old grandfather with the same kind of
S1: pull my hypertension. So it's fascinating. But what we can
S1: tell our patients and reassure them is the vast majority
S1: of them will not get it. If they have a
S1: family member that has so well, it may be genetic.
S1: It doesn't mean everyone going to actually get the disease itself.
S3: So because it's on your radar, probably more than everybody else's,
S3: are you seeing more pulmonary hypertension in covid and post
S3: covid Long Pollaers or is there not that association?
S1: It's a great question, Steve. You know, I think it's
S1: a little early to know. So far, we haven't seen
S1: much of it. We've seen patients who have chronic scarring,
S1: lung problems that could easily get pulmonary potentially if this
S1: keeps progressing. So far, though, we haven't seen we've seen
S1: this blood clotting problem we talked about, but so far
S1: we haven't seen or proven that patients are going to
S1: get chronic pulmonary embolism with pulmonary retention or getting any
S1: other form of, like Group three from chronic scarring. But
S1: I think it might be too soon to know that
S1: maybe the next six months or year we'll learn more
S1: about this. If it takes longer to evolve.
S2: I can't help but bring my dad back into this.
S2: And I know both of you guys have had to
S2: deal with this quite a bit. And that's the balancing
S2: act between the treatment that you would like to administer
S2: for a variety of these diseases and someone's kidney function
S2: and whether or not they're capable of withstanding the treatment
S2: that would be best for dealing with pulmonary hypertension or
S2: any other lung issues. Have there been any advancements in
S2: the last number of years that helps you navigate those
S2: balancing act?
S1: Yeah, I think the idea of of kidney function and
S1: liver function, too, is a balancing act because the kidneys
S1: and liver are so important for metabolizing certain drugs. Some
S1: drugs are tablas almost exclusively by the kidney, some of
S1: the liver, some by both. What we don't want is
S1: a beneficial drug to build up in the bloodstream and
S1: cause problems because you got too much of it. And
S1: we usually fine tune these drugs and we try treat
S1: them up to a certain dose. For example, for Pulman hypertension,
S1: but not beyond that. So a careful physician is going
S1: to check a patient's blood test periodically every three to
S1: six months, making sure that kidney functions OK, liver function
S1: is OK, and we don't have to make adjustments, but
S1: we do have new drugs. Now, for example, the proximally
S1: drug that I've inhaled, oral subcutaneous, one of the strongest
S1: medicines we have for Pulman hypertension. And that drug, fortunately,
S1: is not metabolized by the kidneys and you can use
S1: it indiscriminately in patients that have kidney problems. So in
S1: the blood clotting world, we learn you have to be
S1: a little careful. The docs, these newer drugs that Steve
S1: alluded to earlier, one of them, you have got to
S1: stop if the kidney function gets too severe, the other one,
S1: you're probably OK even with severe renal failure if you
S1: dose it carefully.
S2: So, Vic, before we leave, I just wanted to ask you,
S2: over the course of the last, let's say. Three or
S2: four years, what are the biggest breakthroughs that have helped
S2: you with your specialty? And as a warning, I'm going
S2: to ask you for the next three or five years,
S2: what are your expectations?
S1: I think in the past, if you want to go
S1: ten years, the Doakes, we used to use this drug
S1: called Coolman, you mentioned earlier, difficult drug. I mean, we
S1: used it for 50 years. Good drug. But you give
S1: someone an extra dose of Tylenol every day for three days.
S1: Their blood gets way too thin. You put them on
S1: a different drug, it gets too thick. They eat too
S1: much greens, their blood gets too thick. The dough acts
S1: a very few drug and a few critical drug interactions,
S1: you know, but but very few. They're much easier to
S1: use than we used to. And we don't need to monitor.
S1: We don't need a blood test. We don't get INR
S1: every week, every two weeks or every month with these
S1: new drugs. So these drugs have really revolutionized practice, made
S1: them much easier in the blood clotting around another area.
S1: And pulmonary embolism has been we're learning how to treat
S1: blood clots that are really big ones, causing big problems
S1: without using high doses of dangerous drugs that can cause
S1: bleeding without using clot busters or TPA. We can use
S1: lower doses by putting an I.V. or catheter in the
S1: lung and putting low doses in the lung or even
S1: just putting a Katharyn in suctioning the clot out. We're
S1: still learning when that's necessary. We don't want to overdo it.
S1: So those have been big advances, too. And the blood
S1: clotting work in pulmonary hypertension. We've had new drugs. We
S1: have three classes of drugs. Now, the prostate annoys the
S1: endothelium receptor antagonist and the PD five inhibitors. And a
S1: nice paper was just published in the journal. The new
S1: drug called Aricept even has a little bit different mechanisms.
S1: And we've got several other drugs like this that may
S1: be coming soon. So I think that we've just kept pace.
S1: I kind of feel like we're surfing and just staying
S1: on the edge of the wave, just able to kind
S1: of keep up with some of these diseases.
S2: Vic, thank you so much for joining us today. We
S2: certainly appreciated it. How can our listeners follow you if
S2: they want to connect?
S1: I'm on Twitter, Tapson. I don't get a chance to
S1: get on it as often as I like to, but
S1: I try to say something profound every once in a while.
S1: My email address, the typical Cedar's email address. Victor Don
S1: Tapscott Xpress, Doug
S2: Vick, thank you for joining us. And of course, Dr. Tayback,
S2: my good friend. Thank you for doing these shows. We're
S2: Still Practicing is produced and edited by AJ Mosley music,
S2: but we're still practicing as composed and performed by Celeste Anorectic.
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