Ajay V. Srivastava, MD, FACC, identifies Pulmonary Venous Hypertension as the most common form of the disease and recalls how it is a hidden killer, often diagnosed late. Dr. Srivastava reviews how to make the right diagnosis and provide treatment options.
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So our next speaker is another colleague, Dr Shrivastava. Doctor Sevastova came to us from Stanford by way of Yale. Um, he's really a has taken our department by storm. He's He's a dynamo. This Uh huh. Dr. Skouras is, um he's going to be talking to us about patients who have pulmonary venous hypertension, which is the most common type we talked about. Dr. Shah. So is just, uh, promoted. He's our director of temporary mechanical circulatory support is also very interested in shock and heart transplant in l VADs. So, Dr Savas to tell us about left heart disease and pulmonary hypertension. Thank you, Dr Heywood. Thanks for the invite. And, uh, allowing me to be part of this illustrious multi disciplinary panel. Essentially what? Patients with primary hypertension should get access to, um, from cardiology. From pulmonary from rheumatology from adult congenital. This is essentially what, the multidisciplinary team from a clinical viewpoint. Um, and then we factor in, you know, social work and physical therapy and other aspects. But this is this is great. And thank you for doing this conference again. Um, it's great to share input and also learn from colleagues from other subspecialties So my topic is probably Venus. Hypertension. More common than you think. Here are my, um try to move my slides. Okay. Um, so it is the most common cause of hypertension upon my hypertension. So the question is, why is this an important topic? Number one? It is the most common cause. I mean, Dr Mohan just illustrated the W h o classification for primary hypertension, going from group one through five and group to probably hypertension. Otherwise, it's probably Venus. Hypertension is extremely common. Um, for me, Venus, hypertension kills. You know, I put this slide together, actually yesterday, Um, just thinking about why is this topic so important? And then I was looking at the agenda this morning, and I think Dr Heywood's talk was also probably have been a problem hypertension as a hidden killer. And I was like, Okay, well, I felt were totally in sync, like how we manage our patients. But this is how we all feel. Uh, and I'm sure this final feels the same way about probably hypertension. It is more common in general primary hypertension, primary venus. Hypertension is extremely common. And why we do this conference and why we really try to lend emphasis on management of these patients early diagnosis because oftentimes, when we see patients in clinic or effort to us, it's so far late in the game and essentially they get confined to palliative care. We try to get them to transplant. We try different cocktail of therapies, and at times we are successful. But more often our hands are tied because the patients are so late in the disease coast. So we really want to increase awareness. And, uh, I hope after this conference, for those of you just learning about coming hypertension, we all do our bit in sort of increasing our awareness about forming hypertension in general and specifically for the Venus hypertension. And it doesn't have to kill. We can do better, especially if we make an early diagnosis. Think about it at the back of our mind, just like we do. The minute we see an echocardiogram report and we see an ejection fraction of 35% alarm bells go up. We do everything we can in the minute there's a diagnosis of cancer, all hands on deck, and we're taking care of those patients. So the same way I would look at from the hypertension. And Dr Mahan, uh, went through this briefly about the echocardiogram report. One point is just as we think about the ejection fraction as 35% as that number where we separate from doing okay too. We need to do more. Um, the same way I would then add one layer is looking at the P A pressures and STP A pressures are over 35. It doesn't mean the patient needs the right heart cat right away. But if you see a number over 35 it's what spending more time and seeing. Okay, Is there hidden? Probably hypertension is their volume overload. Does this patient need to write out cat? So that number 35 is easy to remember from a dirty workflow perspective. So this busy slide here, um, illustrates concepts from the last two talks. But I wanted to get a little bit more deep into probably Venus. Hypertension, that group to hypertension, essentially probably hypertension from left heart disease. So what does that entail? So if you look over here where it says l V, whether it's reduced LV function or preserve, they'll be function. The what happens is you have diastolic dysfunction, and it happens, obviously, even in the reduce of the function, right, The stiffness of the ventricle, the L E. D. P. Goes up, and that's translated back into the left atrium. So you left. Atrial pressure goes up. Over time, they could be l. A dilation. But even if the L A doesn't look dramatically dilated or enlarged on the echocardiogram, it loses its properties of compliance so it can only accommodate so much volume. It gets a little bit more stiff. That's when you hear about the patient has things like atrial fibrillation and arrhythmias. But ultimately, this fluid then backtracks into the primary vascular system. The primary veins, the lungs, the pulmonary arteries. And then you have you essentially go from left heart disease to post capillary, probably hypertension to a mixed form of hypertension pre and post capillary. And then you get into sort of the arterial hypertensive state, which carries high mortality and extremely poor quality of life for that patient. So, essentially, what I'm hoping to go over in the next 20 minutes or so is the path of physiology of this. How we diagnose this probably Venus hypertension, And why is this, um so crucial? The donuts on the right show the prevalence of heart disease and heart failure across the globe and the United States. Now, yes, this data is from a few years old, and we always hear about this number. There are 67 million patients with heart failure in the United States. And essentially, you know, we have now a large proportion and more and more people with hepatic or preserved ef being diagnosed, all the emphasis I'd say for the last 2030 years was really on reduce CF heart failure. But now we're beginning to see and recognize the importance of preserved EF heart failure, the importance of volume management importance of him. Oh, dynamics and what it really means, You know, also, we are beginning to recognize in the clinical realm that primary hypertension should gain and have as much importance as systemic hypertension. Um, both in terms of patient's quality of life as well as in terms of outcomes. Um, and this takes that concept from an illustration to an echocardiogram just to illustrate. Okay, what is happening? And I think Dr Mohan had a slide very similar, and it shows you that. Okay, so here we have a patient. You have the left ventricle, the right ventricle, both the atrial. You can see this is a chronic high feeling pressure state. Both your atria dilated. And this is a four chamber view and left untreated. And you can tell this has already been going on for a long time by the size of the atria and the size of the ventricles, and then see what happens over here. So now you've caused significant or we've got significant primary hypertension. And then the after load effects on the right ventricle lead the our video dilate, and then it then translates to less flow getting to the left side, and you can essentially now see, the RV occupies most of the space that are a occupies most of the space. And you left ventricle and left atrial are less than the size of the right side, which really illustrates there's not enough flow getting to the left side. So this is pretty much end stage pulmonary hypertension with RV failure. And that same illustration here is shown, uh, in a short axis view of the left ventricle. And this is all the RV. We would never want to see this for any patient, and no patients should be subjected to this. So, really, what we should do is very early on. Be aggressive and diagnosing and treating to prevent patients from even getting to this middle of center stage with evidence of pulmonary hypertension. Um, so first diagnosis. It always starts with a history and clinical probability. Dr. Martin mentioned in his echocardiogram report about how you know you look for indications. Most commonly it's shortness of breath. Fatigue is what we see. We don't see chest pain, and if you see sync api, that's usually, um, bring that patient into the hospital. Admit doing media it right, heart cat. But in this realm, it's shortness of breath. It's fatigue, history and clinical, probably probably the guides to what we do next. So usually it's the echocardiogram that's done. And once you've done the echocardiogram and you look for certain clues, whether it's in this probably Venus hypertension group that the radio CF preserved year, if you're looking at the size of the left atrium and you're looking at tissue Doppler velocities and the P A pressures, if all that fit Or even if you're unsure, the next step you proceed to you is a Swan Ganz catheter measurement, I tell my patients, is a little bit more than putting an I V in. It takes 20 minutes. We do this as an outpatient procedure. I use lidocaine, maybe a little fentanyl. They go home an hour later. In some cases. No sedation. When I'm concerned about the measurements and I want to get really accurate measurements and within a flight, okay, patients don't have any discomfort. So then you get form against capital measurements and what we're looking for. We look at all the variables, right? Right. Atrial pressure, R v p. A wise pressure to start. And then we get into a specific other variables that I will get into in a second but mean peer pressure over 25 millimeters mercury and um which over 15 millimeters mercury. That is sort of the textbook definition for probably hypertension and more specifically, promised Venus hypertension. And we call this otherwise as post capillary farming, hypertension, and we want to make the right diagnosis. A significant percentage of patients can get misdiagnosed as pre capillary arterial hypertension missing the left heart disease portion of it. And why does this happen commonly? Because patients come in for this procedure 12 to 15 hours of fasting. Um, they have not taken their diuretics and maps that morning, and it's not uncommon for these patients to be a bit dry when they come in for the cat procedure. They might be nervous. They might not have had a good meal. So there's a few reasons why they could not represent the true volume state when they come in. And this is as high. I mean, the studies published showing about 20% of patients initially classified as pH, or pre capillary only from hypertension, actually has a mixed picture or a component of post Capri Pompeii hypertension. So it's very important to put the history, the echocardiogram in context. And if there is a suspicion of left heart disease, perhaps consider doing certain maneuvers to make sure that you're not missing the left heart disease of probably hypertension and your unmasking if the numbers are low. And how do we do that two ways. One is very simple saline infusion, and here is one protocol, um, and it might very attachment from program to program but basically half liter of normal saline over 5 to 10 minutes and then reassess you probably capri wedge pressures. If it goes up more than 18 19, that is usually suggestive that that ventricular compliance is compromised. And this patient has a component of, uh, left heart disease. And then you look at the echo where you have maybe some left ventricular hypertrophy decrease tissue Doppler velocities on the echo. The left atrium is dilated and it doesn't have to be severe, but even mild. And you put the case together and then say Okay, well, this patient has a component of left heart disease, especially common as you get, uh, from, you know, for from 40 50 year olds to like 70 80 year olds. Uh, a lot of times patients have a left left out component. Another way to do this. And we do this in our cath lab as well as exercise hemo, dynamic testing. So essentially, we have a symptomatic patient. I have a certain echo. I have an anti BNP that's a touch bit high, but it just doesn't fit. The patient's symptoms are out of proportion to this echocardiogram, and then I may have done a right podcast in the past, which was normal or mildly out, but did not coincide with symptoms. Or I might say, You know, this patient has symptoms and exercise echo is normal from the get go. I might set this up as a right hot cat went exercise. What does that entail? So basically, patient comes in. It's like any other right hard cat that we have a supine bike that's on the cap table. Patient doesn't get any sedation and then we have a protocol we use. We first get through the notion that getting normal resting thermodynamics and then with the feet in the pedal, um, we have this hooked up to a metabolic cart looking at direct V 02 consumption. But also for the purpose of this, we're also looking at the P A cat measurements, with the patient actively exercising. So in normal it is very common, and it should happen that as flow increases as cutting output increases, peer pressures will go up and usually for normal adults and not sort of lance arms from level athletes. You get up to 10 12 liters of cardiac output, your P a systolic gets up to 60 or 65 usually should not go up more than 60 or 65 for the P A systolic. And you mean P. A pressure usually should stay about under 30. And that would coincide with okay, normal exercise induced flow and pressure changes expected. If they're out of proportions, they go more than that. Then you suspect again a competent of left heart disease from a hypertension and in the way. And this is being used more is looking at the total probably vascular resistance, because ultimately, a lot of what drives from the hypertension and the changes happening in the end of helium is lost upon me. Vascular compliance. So, by measuring resistance, um, by in this formula, by taking sort of your factoring in the flow cardiac output and you mean p a pressure and that number should be under three, which is like you probably vascular resistance, basically, and that's what we're looking at. But you're factoring in cardiac output, so you're adjusting it for flow. Um, sorry, this slide doesn't look perfectly clear, but so this is isolated post capital apartment hypertension. So here what we have is basically essentially that the left heart disease preserved already UCF flow back into the primary vascular system. Enough that you're mean. P a pressure is over. 25. Your wishes over 15. You don't call. We don't call this sort of, um, uh, mixed yet because you're not yet affected their RV or you have not affected sort of the pre capillary side. You're probably vascular resistance is under three would units. Um, so, yes, you're getting into parliament Hypertension? Um, yes. This is, uh that's why this is called sort of passive for hypertension. Um, and how do we, um, then different shit. Okay. Are we sort of just with a high wedge, or have we gotten into a high wedge with premier hypertension? And one number of formula is that was sort of variable. That's useful. It's called the diastolic pressure Gradient. What we're looking for is basically okay, So a swan Ganz catheter isn't a p a. And we're looking at the systolic and diastolic pressure, and we look at the difference between the diastolic pressure and the wedge. So normally upon me, artery diastolic pressure closely matches the wedge pressure the minute they start separating, you know, you're causing from a vascular disease and and you start seeing a difference, and usually in any patient without coming hypertension. That difference is less than five minutes. It starts going over seven. Then you know that there is enough amount of from a vascular disease here that that there is that something needs to be done, and this is getting into probably hypertension. So for post capturing, probably hypertension, there are three important points over here, so one is a diastolic pressure gradient. The difference between the public artery diastolic pressure and the wedge should be less than seven in, um, in early or in patients without from hyper ditch the minute it goes over seven. That's the problem. The second one is your transport pressure gradient. This is the mean p a minus the wedge, and this usually should be less than 12, and the third one is probably vascular resistance should be under three would units if we start checking boxes here and patients have an elevated D P. G elevated primary pressure gradient elevated PVR. Now we're going to get into for me hypertension to see, and then we have this combined What I just mentioned is. Okay, So now there's enough flow and going on for enough amount of back time that upon me, off on the arterial after load has increased, putting stress on the right ventricle and keeping in mind that the right ventricle is not like the left ventricle. It's a thin wall structure, exquisitely sensitive to after load. So it just does not like pressure. So we want to keep the pressure as low as possible so the RV can push blood out. The minute that pressure is up, this becomes a problem. So we have to do what we can to decrease pressure in the pulmonary arteries. If its volume its volume, If now you're getting into fix vascular stiffness, then we need to address that. Okay, So now if you have that patient who has sort of pre and post capital department hypertension with increased PVR, um, you're getting into a very, um, uh, defined subset of patients with left heart disease or just hypertension. Now we're getting into a group that has high mortality, and it's crucial here at a few points why we should not miss this phenotype one. Um, what just happened there? Okay. One. Um This is a group What we call a severe problem. Hypertension to these are the patients have a high d p g. That's like putting pressure gradient. Uh, we talked about a high transformative pressure gradient hyperbole, vascular resistance. Um, And when patients have 1234 then they have a pronounced sort of ventilatory response to exercise. Meaning, yes, there s looks, normal blood pressure looks okay, but this patient is profoundly symptomatic because of that uncoupling between the right ventricle and the pulmonary artery. And then they start having V. Q mismatch is because of the vascular change is happening between the alveoli, intercision and the deuterium. And you lose from the artery compliance because this has been going on for X amount of time and ultimately leading to RV failure, uh, and shock. And this then dramatically reduces mortality. We've had 50 60 year old patients we've lost because of just this reason where the LV looks okay. But the RV has taken a toll for me. Artery compliance. So for me, Capri wedge pressure is a reasonable measure of left atrial pressure. It's not perfect, but it works. The thing with PVR is it gives you look at the mean peer pressure. You're looking at the cardiac output, and you're getting a sense. Okay, what is the resistance now? This can vary a lot from patient to patient. You can find to patients who have sort of the same mean peer pressure, same cardiac output in some ways. But who can go better for how much time varies a fair bit. Some patients can decline fairly quick and some patients a little less, and that has to deal with their probably vascular compliance and the surface area of the probably vasculature for that given patient. Another useful formula to look at as a p a possibility, just like with you on the system. Excite for blood pressure where you look at blood pressure 1 20/80 and has a patient gets really sick. Their EF drops to 15 20%. That pulse pressure narrows right. It becomes 80/60 90/60 sort of the same concept on the right side as well. The normal P a pressure, let's say, is around. You know 25 15 35/15. That starts to narrow, you know, And when that starts to narrow that's an obvious sign. This means this right ventricle is extremely at risk. This patients, probably vasculature, is undergoing significant vascular remodeling and stiffness. And you have to act a sap to try to save this patient. And that illustrates over here. So what? This shows you. I showed you the echo picture earlier. And now if you take the hemo dynamic aspects and overlay it with the echo images What you see from the extreme left where? Okay, the diastolic Pommery gradient that difference between the p a diastolic and wedge when it's little. And you just have isolated post capillary hypertension versus when the d. P. G is increasing. And now you're getting into a mixed where you have pre and post capillary hypertension. And then when you have a hyper V vascular resistance, you can see how that overlays, uh, and the stress, Um, it does to the ventricles. And this is a study, uh, well done a few years ago in circulation, looking at the utility of these variables in predicting mortality. So the blue line shows you, uh, the D P G is less than seven, and PVR is less than three. That's the graph on the upper left, um, and Blue Line is a less thick cohort and better survival. And when the D. P G goes over seven and PVR goes over three, you can see how dramatically the survival drops. And this isn't a reduced EF from a venous hypertension population, and then you get into the preserved EF. It's not that different, and in fact it's pretty much looked exactly the same. Um, and it shows you the value of D. P G um, which is more useful in the in the preserved e F population because it's less of a cardiac output. Issues on your PVR can look Okay, so this is a lovely paper done by the group at Pittsburgh some years ago where they took about 10,000 patients who underwent a right heart cat, um, and looked at What is the prevalence of, uh, Tommy hypertension in patients with preserved ejection fraction? And you can see it is a pretty large number and a large number, not with just my elevations and PVR or TPG. Um, if you look at this graph on top, the dark lavender 19% that's the TPG greater than 15. Look at the PVR over four. That's about 12%. And then the same thing for the D. P. G over seven is 78%. A good number of patients, Um and this is looking at among the preserve es population alone. This adds up to be a significant percentage. So you know what looks like pretty benign. Oh, this patient has hypertension, has some volume is a lot more than that going on. And really, I mean, the one lesson I've learned in the last few years, you've got to factor in all variables before coming to a conclusion in these patients with primary hypertension, it is not one given variable D p. G is this. I'm going to go with this now. Let's factor in all and it gives a better assessment overall as to where this patient stands and the mortality risk. So, ultimately, why is volume overload so bad? So stage one. Okay, volume goes up. Increased farmer Venus Hypertension, uh, increase pressures over time. Those Venus pressures affect the entire theory. Um and then it's really the stage three where what happens with this chronic inflammatory state? You have decreased nitric oxide production. You have increased and Italian one, you have decreased process cycling and all of this, along with decreased expression of natural critic peptides basically leads to probably vessel constriction, probably remodeling and high PVR. So what seems as benign? Oh, there's patients. A little volume up shows you how malignant this process can be and how crucial it is to intervene in that stage one with just what seems like volume overload. So the right ventricle, as I mentioned, is exquisitely sensitive to after Load and the other thing to keep in mind this left heart cohort patients with heart disease. A good amount of 2030% of the RVs contraction and force comes from the interplay and dependence of the left ventricle. So the minute the LV loses its force, it takes a toll on the right ventricle, indirectly as well. So not just the volume and the pressure from the back side, but more sort of a direct connection because of the septum between the two ventricles. And then okay, so that's the ventricle. That's the lungs. What not to be forgotten is the other two crucial organs which determine mortality in these patients, the liver and the kidneys and the two organs are affected in terms of two, if you think about it broadly, two ways One is the elevated venous pressures. Chronic congestive happened up with the and chronic congestive net property. You know, we call this as cardiac cirrhosis for the liver with chronic high Venus pressure strike aspect regards station flow into the liver and the same concept for the kidneys. When you have this high chronic venous pressures, it basically, you know, dramatically affects your grandmother filtration rate. There's a state of oedema and, more importantly, information over there. And now you're getting into chronic kidney disease. And that's really a bad sign. And then you have the low cardiac state as well. So that shows you how malignant this processes. And then this very end Stage three is where drug targets are being explode, you know, in terms of what Asians can be used. And we don't have conclusively, you know, in terms of trials, one drug, this is the window. But we do have targets. We understand the path of physiology, and it really comes down. Here is where the role of precision medicine and personalized medicine comes in. Looking at all the data and deciding which drug I'm going to use for which patient in some sort of cocktail when they get into this pre and post Capri Pompeii hypertension with a high PVR. So let's recap my last three slides. One. So which patient and making the diagnosis. The history. As we mentioned, shortness of breath, fatigue, prejudge probability, blood and a high NDP MP should make you think something is going on. Certain clues on the echocardiogram should then lead to a right heart catheterization. Look at the mean peer pressures, look at the wedge and then establishes his pre capillary post capillary looking at the primary Vascular resistance and D. P. G. Next, it's a spectrum. Just because the patient doesn't have a big blown out RV does not mean for me, hypertension does not exist. This this shows the grass on the right. The no PH. The interplay between the submarine Alvin ally in frustration and utility um, is intact. Then you get into isolated post capri from hypertension in the middle, and you can see okay, changes are beginning to happen, and then you get on the right. But you have this combined pre and post capillary when we have attention with high PVR. It's a complete mess, a chronic inflammatory state. Volumes chases over there fiberglass formation, and it becomes more inflammatory disease. And here is my last slide. It's really a multi system condition. We think about it as benign as volume mobile load. It starts there, but it takes a toll on every organ system and very much like cardiac cachexia. We now have a patient who is like cancer cachexia. So it's not benign. Um, the treatment for chronic venous hypertension, diuretics, diuretics, diuretics, diuretics do everything we can to keep this volume load to keep this patient dry. Uh, technology upon the artery sensors has to be magnificent, magnificent for this field. And so we use that to manage these patients and then, case by case, decide which patient would benefit most from ph. Medications. Um, thank you so much for your time and happy to take any questions
