Chapters Transcript Video Low Flow, Low Gradient Aortic Stenosis um So we've we've discussed and we are discussing several special challenges that are unique to structural heart. The one that I'm going to discuss today is something that is occurring or at least we're experiencing and seeing at increased frequencies um which is low flow, low gradient aortic stenosis. So I'm hoping to demystify this a little bit. We did something similar at grand rounds a few months ago but I'm gonna walk you through um oh yes sorry I'm gonna walk you through my approach to these patients and how I produce a framework for understanding this concept of low flow low gradient aortic stenosis. So the true definition is the presence of truly severe aortic stenosis that we're not capturing by bivalve dynamics either in the cath lab or more typically on echocardiography. And we're not capturing them meaning they're typically below the thresholds or with some sort of discordance between the typical scenario we see which is normal flow, high gradient aortic stenosis. And really it comes down to differentiating between true severe es with abnormal flow hydrodynamics from non severe aortic stenosis is what we call pseudo stenosis. Um from true severe aortic stenosis. So the causes have to do with abnormal flow. And so I think about it in three ways. Um flow is dependent on stroke volume which is of course dependent on contract Illini pre load after load. And so any of those things that are affecting stroke stroke volume can impact your assessment of aortic stenosis. Whether it be cardiomyopathy which is what we most commonly experienced patients with reduced ejection fraction but it can also be amyloid restrictive cardiomyopathy, small LV chambers and and one of the things we'll talk about as well as this concept of after load mismatch with hypertensive patients. It could be a common source for underestimation of aortic stenosis. Um But also mitral regurgitation is not just abnormal stroke volume but abnormal forward flow. So the reason this is important is because estimates on the incidents of these different subtypes of eric stenosis that it's a very common problem and we're seeing it at increasing frequencies as I mentioned in our structural heart clinic. So again we're all familiar with the normal flow scenarios and the criteria that we use to differentiate patients with different severity of Eric Stenosis, peak velocity of 440 d. I have less than .25 or an area of less than 1.0. So those are probably things that are familiar familiar to you all when you see a patient with stenosis as far as how we're quantifying the severity. But when we talk about abnormal flow, that's what I just mentioned, we have things like classic low flow, low gradient aortic stenosis which is reduced ejection fraction, paradoxical low flow, low gradient aortic stenosis, severe mmr. But we also have to take into account the fact that there may be measurement errors and pseudo stenosis. Typically it's defined by a lack of stroke volume index above 35 with an avia of less than one. I don't want to be labor, ultrasound physics and calculations and things like that on a saturday morning but include this only to say that objective numbers can only be relied on based on how they are acquired. And so if we're using those strict criteria for assessing superiority notices were obligated to understand where the pitfalls and sources of errors may occur and one of the most common ones are our best estimate is peak velocity over four can vary by up to 15% with certain regulations on the probe. And when we're sampling the flow away from the left ventricle, A mean grading of over 40 is generally the next most commonly used number requires a tech very accurately tracing not just getting normal flow parallel with the flow on their Echo probe, but also tracing it accurately. So it's dependent on the same sort of features and is prone to the same pitfalls. Dimension list index is a ratio and so it tends to be by definition dimension list, which is important and differentiating from aortic valve area which is dependent on measures and flow. And so it can be solved for in the continuity equation. And as such it's prone to several different areas. So once we've eliminated or assessed for potential areas of pitfalls and miss measurements then we really look at is their pseudo stenosis or is the severe aortic stenosis with abnormal flow. And we typically define these scenarios with again a stroke volume index less than 35 a V eight less than one. And I mean gradient less than 40. We're seeing low gradients in the causes as I mentioned, have to do with stroke volume and abnormal forward flow. We do things where we used to do things like stress echo to see if we can augment that stroke volume so we can capture the true state of the aortic valve and how static it is in practice. We don't do that much anymore. It doesn't eliminate the fact that patients may not have what's called contract. I'll reserve that they can't augment their stroke volume by at least 20%. So it doesn't necessarily eliminate the fact that you have true aortic stenosis and low gradients without contractor observe versus reduced eF without contract our reserve obviously with low pressure measurements. Ultimately one of the things we used very commonly when these numbers don't make sense. As we look at the valve itself, which I think is the most common and the most important part of all of this. You can look at it obviously on echo when we see the discordance, this is what we're talking about. As far as collecting additional data, we can do things like calcium scoring. We can use other or additional clinical information like BMP strain imaging, we can get a VHS from symmetry by T, which is a little less accurate. And then I'll talk really briefly about the caveats with cardiac cath. So this is a little bit more complex as far as the understanding of this paradoxical low flow low gradient A. S. When you see low flow low gradient A. S. Most people just think of the cardiomyopathy reduced ef. In actuality it's far more common to run into a scenario where patients have normally f but some sort of other reason for abnormal stroke volume and again stroke volumes depending on pre load after load and contract ill itty. So in these patients it can be very difficult to diagnose. It can be very controversial as far as we went to treat important thing. And this isn't, the guidelines is optimizing people's blood pressures and that's that you avoid this after load mismatch problem. Using ct scanning is very important in these patients. You can consider invasive as a dialect testing. Again focused on after load but ultimately it's important to differentiate these because there's a cardiomyopathy underlying all this and you have to diagnose that cardiomyopathy and treat the underlying causes. And then M. R. Is something that we see in structural heart quite a bit incompetent poly valvular disease, moderate severe M. R. Is present in almost 30% of patients with low flow, low gradient aortic stenosis when the E. R. O. A. Is greater than 00.4 which is what we consider severe stroke volume is decreased from 70 to 47. So almost cut in half. The main gradient has decreased from 57 to 33. The peak velocity has decreased by 51238. Um And the A. V. A. And D. Are unchanged but there's still significant with less decrease in the E. R. O. A. So it's very important to understand and recognize that when you're looking at aortic valve that doesn't look normal to also look at whether it's the presence of mitral regurgitation, affecting some of the numbers that you're relying on to guide your therapies. The guidelines tell us that for paradoxical low flow gradient A. S. To normalize the blood pressure, we measure for classic low flow low gradient S. They still recommend with the two a indication dsc or invasive provocative testing, dimensional index and cT scoring are also two indications. But this is this is the most important part. All of these numbers. All of caveats to these numbers. All of the pitfalls and measurements all that's very very important for a subset of aortic stenosis. But there's an entirely other subset of aortic stenosis that really highlights the fact that these are clinical diagnosis and the decisions you make are based on your clinical diagnosis. If you look at the guidelines as far as the workflow and patients due to aortic stenosis if the F. Is less than 50% and the Eva is less than one and you're not getting contract our reserve it ultimately comes down to is a s the most likely cause of the symptoms. So you see a bad valve, you hear a bad valve clinically it makes sense and you're not getting the numbers and you look through all of these things, it's still a clinical diagnosis. You keep reaching for additional clinical data to reconcile the differences in what you're seeing and what these tests are showing. Speaking to cath. It's a class three to cross valves unless there's discrepancy in these numbers and that's because there's an inherent stroke risk. When you look at the fusion weighted imaging on these MRI's after cats in general, you can get abnormalities up to 22% of patients and then prognosis is poor in these patients. We've long known that the prognosis in many situations is worse than classic low flow low gradient. So to summarize things, does my patient have severe aortic stenosis? We all know the common and more frequently used measures of that there are pitfalls to those. If you're not seeing. When you evaluate a patient with a bad looking valve and a bad sounding valve and you're concerned for stuff. You should not seeing the numbers that you would expect. You have to look at our their technical errors is the f normal or abnormal, calculate the stroke volume index is the concomitant severe M. R. L. V. H. Or evidence of amyloid which is very common in these paradoxical low flow low gradient patients and then consider additional testing. Ultimately it's a clinical diagnosis and rigid adherence to non invasive valve hydrodynamics leads to delays in patients getting appropriate therapies that are evidence based as far as their impact on the patient themselves. To highlight this is a case that we had in the hospital a few weeks ago as a patient with an ejection fraction of 12% newly diagnosed came in with decompensating heart failure. That valve is not normal, doesn't look normal, it's not opening, it's calcified patient has aortic stenosis. The question is, how severe is it? And is the cardiomyopathy the cause or is the cardiomyopathy the reason that we're not seeing the numbers that we would expect for a valve that looks like that. These are the numbers. The main gradients on this patient was 19. The peak philosophy was 2.9. A lot of people would look at just the report and say that's not severe aortic stenosis. And I don't don't think that that captures the true picture. When you look at the cT scan, he had a high valves calcium score and he presented with hypotension, hypoxia, respiratory failure without other clear causes. DR Tower did a beautiful baby facilitated and supported Pc on this incredibly sick patient. Got him through that treated his multi vessel disease and then he underwent TF tavern. This was last month and he's been able to get out of the hospital. He's revascularization. He's got improving ejection fraction already a month out. Um and we made the diagnosis without the typical criteria that you would use to qualify someone for a trans Katharina replacement. Thank you. Published Created by Related Presenters Matthew Summers, M.D. Sentara Cardiology Specialists Dr. Matthew Summers performs complex coronary and structural interventions, including transcatheter aortic valve replacements, coronary stent procedures requiring mechanical support and chronic total occlusion interventions. View full profile