Drs. Birgersdotter-Green, Heywood and Yeang address questions from the audience.
Back to Symposium Page » another question and this could come up for I think all of us to be a part of. It's a great way to transition into the panel discussion. Can you briefly speak to impulse dynamic therapy and if you are considering this in your patients who are not candidates for CRT. Yes. So impulse dynamics. It's it's um it's a therapy that is um it's a very different type of therapy where you put a device in and you put a lead in and the way that the therapy works is that it enhances calcium release. And by doing that it's the thought is it will improve contract ill, it's at the heart and improve ejection fraction. So that's impulse dynamics and the two second background. Um It is in clinical trials and it's FDA approved. It's being implanted now. Um I think we don't have nearly enough data yet to say If it works and who will it work for? The hope is that this could potentially work in the borderline ejection fraction patients. So in the less than 35 you know they're going to get a defibrillator. But is there something we can do for the 35 to 50 percent heart failure patients? Or even those with diastolic dysfunction couldn't do something there. So those are the questions that come up with this type of therapy and and um we don't have the data yet. The problem with us is the data is set is very small. The outcomes are more kind of clinical outcomes like six minute walks and quality of life which are important. But we don't have it's easy when the device saves your life. That's an easy question. But this is less sure and heart failure is such a moving target. Now with the therapies like the S. G. L. T. Two inhibitors, the Cupertino val started and presto cardio memes. We have these really important therapies that make that have pretty I think more measurable effect. And so the baseline keeps going at the bar keeps going up so you're going to put a device in that has maybe marginal benefit and patients keep doing better and better than it gives you pause and there's more things to do. So I think they're going to have a little bit of a tough road for a while until they get really compelling data, compelling data. But even when we have compelling data we still don't. So we have that's exactly right if a particular synchronization therapy we have compelling data and so that I don't know 6 10,000 patients and randomized clinical trials and we still can't get that out and being used the way it should be. So this I mean there are so far behind again and that kind of data set you know the you know just to underscore what Ricky said, you know women that have left bundle branch block and cardiomyopathy there the effect with CRT is nothing short of miraculous. Often I see patients whose es go up 20% and they almost need no medical therapy anymore. So I'm really uh you know even if a woman says they might say well I don't really want this, I'll ask them repeatedly, you know you know this is often along an ongoing discussion with them two to say you know this would benefit you so much. You really need to strongly consider this. I see much better effects with CRT and women than I see. And men typically they often are non ischemic, what is it? Non ischemic, woman left bundle branch block. Those are the super responders with CRT. It's interesting the once the impulse dynamics received FDA approval, their marketing people are just littering social media. So it it seems like it's so it's it's why are we not on the bandwagon yet? Why are we not implanting this every day? I think like you said Ricky that we just don't have all the data for everybody to feel comfortable just to dive in headfirst. Yet. We may get that, but we don't have it yet. Uh And um there is a I think Ricky this question was for you are our overall women getting less devices. Does it have anything to do with age? You know, it's uh in general women tend to come in at an older age to see the cardiologist. This is true for for all aspects of cardiology and the atrial fibrillation justice as much. So it's it's possible that that does contribute a little bit. But all the data would suggest that the older women benefit as much as an older man. So there's that there's no difference there at all. Gotcha tom. You mentioned we were you talked so well about the different pharmacologic therapy for Hef ref and FPF. And so talking about the Hedgpeth that preserved ejection fraction heart failure patients. Um you talked about the different medications that are used. And the question I think that often comes up in the office space of cardio practice of cardiology is. Well here we have a patient that's maybe they were hospitalized diaries and sent home but maybe they're presenting to the office there a little volume overloaded and they're not on any medical therapy. What what is what is your sort of playbook as far as starting? What's the first drug you would start them on? Is it the S. G. L. T. Two inhibitor? Is it interest? Oh is it spironolactone? What sort of your if they're not on anything? Ejection fractions preserve their in heart failure? What's your playbook as far as how that's going to how you gonna treat? But I think one of the important things that we've done in half path is there are many types of health path and you have to think about this why I like being a doctor because every patient's a little bit different than you have to tailor your therapy to them. So if I'm seeing a patient that was hospitalized with heart failure, their EF is normal. I want to know what their EF is and uh and you know what their gender plays a role here as well. Uh The really important thing to look at is what their P. A pressure is. The higher their P. A pressure is the sicker they are. And this is where we have this intersection of electrophysiology and heart failure because so many people have a fib for such a long time the atrium dies. The atrium gets stiff. The pressures go up because the RV has to push blood into the stiff left atrium. They get R. V. Failure. They get Tr and you get the spectrum. That's why I'm quite aggressive with a fib. I don't want patients to stay in a fib because eventually they're atrium will die and then their RV will die and I don't want because we don't have good therapies for RV. Dysfunction. So what's their phenotype? So their phenotype is an E. F. Less than 55. They have some blood pressure there. BMPs internal BMPs elevated and the volume overloaded. I'm probably going to start with uh cooper travel certain and depending on how volume overloaded they are. I don't like to start to major drugs at once so I might do some cooper travel certain, maybe a little diuretic, see them back in two weeks and then consider it an S. G. LT two inhibitor. If they have coronary artery disease and diabetes then I'm probably going to use the SDLP two inhibitor first because the data if you have coronary disease and diabetes, uh the S. G. L. T. Two inhibitor is absolutely life saving for those patients. So I look at Vienna types, coronary disease, gender. What their Ef is. Uh the important thing with them is to try to make them you've Olynyk and to normalize the ph pressures and if I get them on good therapy and they still have elevated pressures then I would consider cardio members for those patients especially enrolling them in the guide trial. That's still ongoing to see if BNP but this patient's been hospitalized if they haven't been hospitalized were using BNP. But really we have much more options and we're seeing patients more because we have to titrate these things. It's not just one and done you have to do this but to see patients improved to stay out of the hospital. Uh really it's really a blessing for patients and a lot of fun. Yeah. And along those lines tom another question and Calvin, I have a discussion, I want to start with you in just a moment. So don't feel like you're being left out. But this question kind of goes along with what you were talking about tom. The question comes in. Um if the ejection fraction improves to over 57%, do you need to stop and presto? I don't think so. You know, it's like, oh the medicine works so let's so I would continue on unless there's a compelling reason to stop it. Um You know so we we've we've done studies where we stopped wrasse blockade in people with so called recovered ejection fractions. And a number of those patients decline and sometimes we can't get them back. So I think it's it's a small price to pay to take a couple of medicines that actually worked and to give you, you know and there's other effects of these drugs, they're polymorphic effects. Uh cooper Brossard lowers your risk of developing diabetes which we don't know, it lowers arrhythmic risk significantly. There's a sudden death benefit from being on sick. Uber drove al certain it lowers uric acid. So there's you know, we don't really know why all these drugs work or how they work. We think we do, but there's really the body is very complicated and when we start affecting mechanism within the body uh that's why we have to do these large trials to say what's the outcome, That's not just what we think is going to happen. But what what you know how many people are in the hospital, how many people die? Uh That's really how this field has progressed and that's really the gold standard. Yeah dr yang question came in from one of our attendees and I want to ask a question that I was gonna ask first because then I think that next question will lead into that. Um You know, a lot of times in the practice of clinical office space cardiology. We're seeing patients to discuss their risk factors or their family history or perhaps they've had some chest discomfort and we're working that up or and we order if it's not been ordered, we ordered the lipid panel and a comprehensive metabolic profile. Um Some people may order lipid panels, some people may order the particle size panels. The question I would have is is that in those patients who are looking at risk factors, maybe they're in uh they, for whatever reason they were referred to go over their risk factors. Or as a primary care physician or an advanced practitioner may say, well let's get your risk factors associated assessed and they check a lipid panel and the hemoglobin a one C etcetera should lipoprotein a be a part of that. And everybody. Yeah, that's a great question. Um so the key is, you know, atherosclerosis or even the aortic valve disease, it's not really a one risk factor disease, it's really a confluence of all these multiple risk factors in the patient's. So I think if the goal is to really understand comprehensively what risk the patient is that, then it does make sense to measure all the cause of risk factors are likely cause of those factors. Um So in this way I think the L. P. A. Can be additive to risk stratify people for the risk of either developing atherosclerotic disease or even aortic stenosis and progression of the auditor notices. Um This is kind of a personal opinion at this point though because it hasn't, the guidelines have recommended checking L. P. A. And certain patients mainly in patients with family history of cardiovascular disease because it's such a strong genetically determined risk factor and also in patients who have had their events. So they have an M. I. And you won of all the traditional risk factors and nothing was found. Um I think that is uh certainly a reasonable approach. But it is kind of a shame I think if you find out someone's risk only after they had the events, uh, and you know, you kind of missed the opportunity to prevent that risk. So in that way it might make sense to track the L. P. A. Um, in patients who you believe are at risk or who are you trying to do a comprehensive risk evaluation for now? I guess the question with this, this is uh, uh, kind of going into the realm of screening here. So the question is, what do you do with the information if you screen patients and you find that they have high Okay. Uh, well, I think that's something that really needs to be addressed with randomized clinical trials. And we need to know if L. P. A. Lowering through randomized clinical trials does improve cardiovascular events. And I think if we know that we can make the justification for finding patients with high opa and treating them to lower the L. P. A. But I think even short of that, if you find patients who are at higher risk because of L. P. A. Or other risk factors that might have come up through a comprehensive evaluation. Um, you know, we know that we can reduce overall risk by modifying independent risk factors meaning regardless of what the um primary ultimate risk factor is reducing the LDL cholesterol down linearly reduces risk and modifying other risk factors such as blood pressure or lifestyle risk factors independently reduces risk as well. So even if we don't know for sure that okay lowering might reduce risk in a patient, we kind of know what to do to modify risking my patients. Another question that came in along this discussion is there's actually two questions and one is would you ever hold off on a statin and do APCSK nine inhibitor instead if lipoprotein it was elevated? Yeah, that's a good question. Um You know, personally I don't think I would because the data with the data from the PCSK nine inhibitor trial. Sure. And benefit. Or in the context of those, all the trial participants in those trials were heavily treated with statins. More than 70% were already on a statin. So I'm not sure we know the effect of PCSK nine inhibitors alone on LP immediate arrest and even those times raised the L. P. A. The effect is generally marginal. Some patients it doesn't go up And some patients it might go up 10 at most 20%. Um So the effect is kind of marginal and the benefit that you would miss out on with LDL cholesterol lowering if you did not have a stand on board, that might be a real missed opportunity. And I think that the benefits seen with PCSK nine inhibitors in attenuating LP immediate risk. I think that's partly due to getting the LDL cholesterol down, very, very low down to 30 mg per destiny arrange and usually do need a stand on board to get there too. So I think it's probably a combination of a PCSK nine inhibitor plus this time, that will work. And then thank you. And and then another question along the lines of life, a protein, any treatments given the current technology for measuring L. P. A. That you went over. Can you explain how I explain again how to arrive at the and this is in quotes on the question, correct L. P. A. Oh yeah, yeah, yeah. This is uh this is kind of an emerging concept. So there's the issue of what is the correct LDL um because the L. P. A. Particle carries cholesterol on it and the L. P. A. Particle carries cholesterol on its LDL like morty. So essentially L. P. A. Is an LDL like particle and all clinical laboratories that measure and report LDL cholesterol. They aren't able to distinguish the cholesterol that's coming from okay or LDL. So the LDL cholesterol is the way that we understand all the clinically it's part of the lipid panel that we all check in our patients. And the point I was trying to make was that the LDL cholesterol you get from the clinical laboratory, whether it's scripts UCSD or any laboratory uh does not accurately reflect LDL particles. It's really a combination the summation of LDL plus LP particles because these are different particles that have different path of physiology and they respond differently to lipid lowering therapies. Uh It might not be the best idea to really think of those as a composite in LDL cholesterol. But it may be this is kind of just food for thought. But it may be better if we can with the right technology to separate out what is correct of the from what is L. P. A. Cholesterol from what we're being told is of the cholesterol. Good. Um Dr Heywood tom there's a question that came up for you Can the S. G. L. T. To be given to non diabetic patients? Yes. Um So the data initially started with diabetic patients and show this profound heart failure reduction. And so there's been several heart failure trials now that have given to a combination of diabetics and non diabetics. The effect of the S. G. L. T. Two inhibitor uh is fairly mild on hemoglobin. A one c it's about 10.5. And as your diabetes gets less and less than the effect on the diabetes is lower. And there's almost no hypoglycemia with these agents. So the risk is quite low. So in the data with so but we had to do heart failure studies per se. And the heart failure studies are positive. Now they're not as positive as people with coronary disease and diabetes. Those trials were profound. But what I think is the most important message I could give people is that in the heart failure studies, per se there was a marked reduction in renal outcomes. So these agents are very real protective and that may be one of the major ways that they benefit patients. So Anything that reduces the need for dialysis and stage renal disease by 50 has profound implications both for the patient and for society. So the data is uh, I think these agents are going to be a lot like statins that they started in highest risk patients and we move to lower his patients. I suspect that the next field they will be used in is the metabolic syndrome patient who has high blood pressure, prediabetes, et cetera because they cause you to lose weight and when patients have trouble deciding well, do I really want to take another met? Would you like to lose eight or £10? Yes please. And then they go on it. So that side effect of weight loss is very important. And some of the other diabetes drugs have marked weight loss benefits as well. In fact, it's interesting in the diabetic world. The drugs that make you lose weight do better than the drugs that make you gain weight or promote heart failure. So there are a combination of so called diabetic drugs That will be used in non diabetic patients that might lower your you know, cause as much as £20 weight loss in patients with diet and exercise. So, and obesity is such a huge problem in the United States. And this is important data. So, yes. The answer is yes. Non diabetic patients now in women, there's glucose in the urine. So they have more yeast infections. You have to warn them. It's not. Most women do not get infections, but some do. So. They have to be warned if that happens to treat them and not surprised. Yeah. I don't think very many people have said ever. I don't want to lose 10 or £20 be included. So, um is there a role for SGL T two for valvular heart failure, Valvular related heart disease? Uh So we haven't looked at that specifically, you know uh might regurgitation? Try husband regurgitation goes along with heart failure. Is the heart gets bigger? The ventricles dilate that pulls the valves apart? You get regurgitation? So I think the secondary regurgitation that we see from heart failure per se might get better. I don't think that that specifically looked at. We have looked at using super travel certain in M. R. With heart failure and it does get better and the left atrium gets smaller too. So so so that's another of these benefits, you know. Hi. I tell the fellows that your job in the 21st century is to figure out how to make the right ventricle work better and how to keep the left Atrium alive. If we could keep the left atrium normal sized and functional in our patients, the amount of disability that would be prevented is just hard to hard to underestimate. We do not have real therapies for the left atrium at the present time and we desperately need them. So there's a lot more work in cardiology left. We haven't figured out all the answers yet. Yeah. And uh that's what makes it all fun. Right? It's we're learning with all this new technology, this new pharmacology all the time. Ricky. I have a question for for you and in our world, you know, over the years there's been a lot of uh get with the guidelines bridge the gap. Um No your E. F. Sort of campaigns to try to help that under representation that you showed so well in receiving. I see therapy for both for both male and female patients. Um But I don't think and if it has if it exists I haven't seen that much of it. And I do try to look for all these things. Has there ever been a campaign specifically addressing addressing the gender disparity from, you know, most of that comes from industry, but it's brought into the communities, but I'm not aware of that. I have not seen that at all that there there is, as you say, so industry is recognizing it definitely more um but not not anywhere to a point where this is out there as a, as a discussion in the community at all. Yeah, maybe something, you know, do what they did and that tom was talking about uh have a just a reminder and electronic medical records reminder. You know, best practice alert come up. That would be fantastic. If that could be something many institutions would would start going after. Yeah, well, it would also be a click that I'd be happy to do. You know, I'm trying to reduce my clicks, but that would be a good click. Send the patient for ICD evaluation please. God, yeah, that was not going to add to the clinical tunnel syndrome. Right. Great. Well, everybody, we have just about three minutes left. I I think that this has been a great discussion. Um um well, we did have a quick question come in tom and this could be for all of us. But I think to you, would you just would you just continue SGL T two inhibitor if patients develop yeast infection or U. T. I and would you resume after treating the U. T. I. And yeast infection that came in from one of our audience members? I probably just continue it and treat the infection. Um you know, it's always risk benefit, nasty to have an infection, nasty to have heart failure and be in the hospital and die. So, you know, I don't want to underplay you know, and a number of women tell me, you know, I have infections all the time and I just really negative and you know, people have to make individual choices about their therapy. But uh I think we, you know, we have to be providers of information to our patients and say this is this is the benefit to you. This is the risk, this is how we'll deal with problems. A lot of my job is to be a problem solver problems come up. I don't want to take this medicine because well what can I do about it if I reduce your other medicine or I reduce your diuretic or I let you have more solved. Well that allow you to stay on your medicine. So the easy way out is the patient says, well, I don't want to take this medicine. I don't like it. Just say okay fine. I think that's kind of lazy. I think we have to work with the patients and say, you know, again remind them why we take this. Okay. So why are you adding this medicine? I said well, because I like you would like to keep you around for a while. We like to keep you out of the hospital. Okay? And then, you know, they have a problem with it. Okay. What was the problem? That that's not unexpected but we can deal with it and you know, as long as we're allies with them, give them good information, be helpful available to them. I think we can work through mostly. But sometimes you can't use them and you know, everybody's that's why we're not going to be replaced by robots anytime soon. There's there's too many variables in this. I'm glad they like this. Come see us. That's, that's nice. It's rewarding. You know, what you have to say this, this field, you know, the things that we can offer patients just can transform their lives if you do well. Nice, nice. John All right. One of the pets, you know, so I'm glad people are here. I hope you embrace these, these therapies because they really will make a big difference in your patients lives. Well, this panel has been amazing, Ricky Calvin tom, thank you all very much for, for doing such a wonderful job. I learned so much and I've got pages of notes here for myself and um, we really appreciate all of you, your expertise and your willingness to share and spend sunday morning and such great presentations. Thank you very much. So, um, we're now going to take a break before we start the last session. Uh, they feel free to view the exhibits virtually, And we'll see you back here at 10:30.