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Cardiovascular Essentials for Advanced Practice Pr ...
Structural Heart Disease
Structural Heart Disease
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Video Transcription
This week, we're talking about valvular heart disease. So we've got you set up to do a fair amount of reading with some guidelines as well as some good physiologic background. But what we're gonna do today is just spend some time reviewing the most recent updated guideline and some of the, I think there's like the top 10 things to remember related to valve disease. So first, just a little bit of anatomy. You know, you've got the four valves, the pulmonary, the aortic, the mitral, the tricuspid. The biggest thing I want you to remember as you think about back to your anatomy days is, you know, the pulmonary and the aortic are pretty simple valves. They're just leaflets. There's not any extra papillary muscles or chordae, tendonae, that kind of thing. So they're pretty, from an architectural standpoint, they're pretty simple valves, which means they're pretty simple to fix. Mitral valves, however, and tricuspid, if you look here, we've got chordae, tendonae, we've got papillary muscles. So to go in and pop in a new valve, if we don't take into account that architecture that was already there, may not be as effective. So a lot of times we hear things like mitral valve repair, we've got mitral clip now, same thing on the tricuspid side. Anytime that that architecture can be preserved and the valve can be repaired versus replaced from a mitral standpoint is much better. So again, just a little bit of background there. So we're gonna start again, kind of top 10 things. So the first one is high-risk patients that are recommended for antibiotic prophylaxis. So endocarditis prophylaxis in our patients with valvular disease, who gets it? And I will tell you, it has changed. Now it's been about five years, maybe a little longer since it's changed, but we used to, anybody that had moderate to severe intrinsic disease, we put them on amoxicillin or Clinda. And now we've cut way back thinking that we likely were over medicating and maybe even led to some of our resistance. But who are the patients? All right, so the prosthetic cardiac valve. If you've got somebody else's tissue or mechanical valve in your chest, then you get antibiotic prophylaxis. Prosthetic materials such as rings, cords, post-cardiac treatment are at greater risk. So those patients. And TAVR patients were recently added to the list. And then certainly if you've had a history of infective endocarditis, you're at risk to having even higher risk of getting it again. And then congenital heart disease. So CHD is congenital heart disease. Those that are unrepaired, so if they've not had a repair or repaired, but what's interesting about repaired is that it's six months post-procedure. So if they've been repaired and there's been opportunity for that area to re-endothelialize and they now don't have any residual effects, they don't need antibiotic prophylaxis. And kind of a thing for you to remember, my husband is an aortic patient where he had a graft put in his aorta. And the whole many years that he was a coarctation patient, he always had to have his amoxicillin. And two years ago, the last time we went to see the congenital heart disease physician, the guidelines had changed. And because it was repaired when he was younger and that graft has been re-endothelialized and there's no residual effects, he no longer needs it. So that was a change in the recent guidelines that those patients that it's only in that first six months post-procedure. And then finally cardiac transplant. Patients need endocarditis prophylaxis. The typical is amoxicillin two grams, PL, so it's four or 500 milligram tablets or clindamycin 600 milligrams PL prior to the procedure. And the most common procedure are dental procedures, but it's really anything that's quote unquote dirty where bacteria could be introduced into the bloodstream. So if you look at the guidelines, the examples of procedures are in there. The next one is anticoagulation for AFib in patients with valvular heart disease. So if you have atrial fibrillation with mitral stenosis, the only indicated agent right now is coumadin or warfarin. It's your agent of choice. The non-coumadin agents such as Pradaxa and several others are not indicated because of that mitral stenosis. If you have atrial fibrillation with other valve disease, then you can follow the CHADS VASC guidelines. And so depending on their CHADS score and then direct oral anticoagulants are the agent of choice. So that would then be a switch. It's no longer coumadin and warfarin, but rather your Pradaxa and those other agents. The next one, aortic stenosis. So TAVR, so we used to only do these in high surgical risk patients, but we now have that it's a viable option for if there's, but a surgical risk profile is required, class one recommendation for high and prohibitive risk patients. So that's the current indication for TAVR. Now bicuspid, unicuspid and non-calcified valves remain excluded from general recommendations for TAVR. So those patients would require an open aortic valve replacement. Mitral regurgitation. So there's two types of mitral regurg, primary and secondary. Primary means there's something wrong with the valve itself. Secondary means the reason the valve, remember in a regurgitation state, the cusps are not coming back together and there's allowing blood to flow back. During systole, it's flowing back into the atria. And so that can either happen because the valve itself is abnormal or because the left ventricle is dilated and it's pulling those valve cuffs apart. The treatment is different in the physiology. Physiology is complex. So again, I just want you to, just because the patient has MR doesn't mean, sometimes they may have MR if they're volume overloaded and if you can get on top of their volume and recheck an echo, the MR may improve. Now here's a question for you. Why does a patient with severe MR and an ejection fraction of 30% have a higher risk of post-op heart failure? So I'm gonna let you think about that for a minute. So here's the deal. The deal with this, to me, this is a bit fascinating, but you're gonna see this. If you're working heart failure or working with structural hearts or working with a high risk surgical program, you're gonna see this. So what happens is we've got severe MR and we've got a reduced ejection fraction. So that left ventricle is not working very well. If we take the patient to surgery and we fix the MR, what happens is we now just shut one door. So before, when the left ventricle had to contract, because of the MR, it emptied into, back up through the MR into the left atrium and it emptied out into the aorta. If we close the mitral valve, we now close a door and we decrease the amount or the area where the blood can empty through to just the aortic valve, we take a left ventricle that's already failing and we almost immediately increase the pressure because it's used to being able to empty out of two doors and we're now only allowing it to empty out of one. Some patients can kind of get through that period. We can support them physiologically with different pressors and that kind of thing. Other patients, they can't tolerate it and they actually end up going into severe heart failure. And in some cases, there's some mortality that can be associated. So there's a concept with MR when it needs to be fixed. It needs to be fixed before the left ventricle fails. What's struggling or what the biggest opportunity or maybe difficulty with managing MR is that not every MR is gonna get to the point where it needs to be fixed. So just because a patient has MR doesn't mean we automatically fix them. But if we wait too long, they can actually become too sick for us to fix. So again, these are one of those things that between the cardiologist and the surgeons, that you may very well be included in some of these discussions and certainly be seeing patients with MR. And at what point do we fix them or can we fix them? The next one is prosthetic valve choice. So thinking about, are we using bioprosthetic or are we using a mechanical valve? So it's a patient-physician shared decision-making that's required. That's the class one recommendation. So we need to both be on the same page. But why would we even give patients a choice and what are the differences? So the reason we give patients a choice is because a bioprosthetic valve does not have a real long life expectancy. Depending on the type of valve, it's somewhere between 10 years. Some of them are longer. But if you're a 40-year-old that needs a new valve and you're gonna give me a valve that has a life expectancy of 10, even 15, even 20 years, that means I'm gonna have to get another one of these probably. And so we start to think about mechanical valves in those patients. Well, the problem with the mechanical valves is that right now they require lifelong anticoagulation and right now it's Coumadin. So now I'm 40, I get my mechanical valve and I get to be in Coumadin the rest of my life. So it almost isn't, you know, which one is you kind of got to, but that's why it's a shared decision-making because the patient really does need to understand what the options are and then what are the potential issues or challenges with those options. So for prosthetic valve antithrombotic therapy, mechanical valves need that higher INR with your Coumadin Warfarin, so a vitamin K antagonist. Bioprosthetic valves just need short-term anticoagulation until the re-endothelialization occurs. So that's usually just several months. Bridging therapy for those mechanical prosthetic valves. So we want to continue anticoagulation for minor procedures. Temporary interruption for those with a bi-leaflet mechanical aortic valve without other risk factors. So what we mean there is if it's a bi-leaflet valve in the aortic position and no other risk factors such as AFib or mitral disease, then we can actually just hold it for the procedure. So temporary interruption, we're not bridging. Everybody else gets bridged with some sort of a heparin agent, so either sub-q Lovenox or IV heparin. So that's our current guidelines for bridging. So I hope that's helpful. Those are kind of the pearls when you think about heart disease that we want you to remember. The actual physiology and the interventions and therapies, you'll learn through the content and through the guidelines this week. But these are probably those key things you want to remember. So again, feel free to reach out if you have any questions. We appreciate you joining us again this week and we hope that you find this information valuable.
Video Summary
In this video, the speaker discusses valvular heart disease and provides an overview of the most recent guidelines and key concepts related to the disease. The speaker explains the anatomy of the heart valves and emphasizes that the pulmonary and aortic valves are simpler in structure compared to the mitral and tricuspid valves, which have additional components like chordae tendineae and papillary muscles. The video also covers topics such as antibiotic prophylaxis for high-risk patients, anticoagulation for atrial fibrillation in patients with valvular heart disease, indications for transcatheter aortic valve replacement (TAVR), different types of mitral regurgitation, prosthetic valve choices, and antithrombotic therapy for prosthetic valves. The speaker emphasizes shared decision-making between patients and physicians when choosing a valve and highlights the importance of timing in the treatment of mitral regurgitation. The video concludes by mentioning bridging therapy for patients with prosthetic valves undergoing minor procedures. This information is intended to provide an overview and further details can be found in the referenced guidelines. No credits were given.
Keywords
valvular heart disease
guidelines
anatomy of heart valves
transcatheter aortic valve replacement (TAVR)
mitral regurgitation
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