Chapters Transcript Video Outpatient Medical Management of HF Back to Symposium Good morning everyone. Great to be here. Thank you Doctor uh Yusupov and Doctor Talreja for inviting me to be uh a speaker another year on this conference. Great to see familiar faces and get to meet new faces as well. Thank you for supporting our, uh, program. So we'll talk today about outpatient heart fre management, uh, for patients with heart fail and reduced ejection fraction. These are my disclosures. So what is heart failure? Basically, the heart is unable to pump enough blood and oxygen to meet the body's demand. This can be because the heart is too weak to do that or the heart is too stiff, and there are new, uh, basically classifications for heart failure. Heart failure with reduced ejection fraction, be it ejection fractions and 40%, might reduce ejection fraction between 40 and 49% and preserve ejection fraction. More than 50% we'll talk today between uh EF less than 40% have one of my other colleagues Doctor Jordan in the afternoon who'll be talking about ejection fraction more than 40%. So just in a word or two on heart failure, it's around 6.8 million adults with heart failure in the United States, and this number is anticipated to continue to increase year after year. We're having a lot of patients with risk factors such as diabetes, hypertension, dyslipidemia, um, and others, and. You know this all these can increase your risk of developing heart failure. Also, the number of hospitalization rate continued to increase, as we can see around like 1.3 million hospitalizations attributed to heart failure, and it's the number one diagnosis for 30 days readmission and it's a contributing cost around 450,000 deaths in the United States and 45% of the total cardiovascular death in 2021. So the number continues to increase and we say now 6.8 million, probably it's more than that. By 2030 it's gonna be around 8.5, maybe even more because of all the risk factors we have more and more patients living with heart disease. In the past, patients with heart attacks used to pass away, but now we have stents, we have surgical revascularizations, we have a lot of options that can keep patients alive, but when they're alive, they're having, uh, the symptoms of heart failure and they live with heart failure. So the lifetime risk of developing heart failure is 1 in 4 people, 1 in 4, of patients or adults will have heart failure, and this number is more commonly gonna be in African American or black patients or Hispanics. They are higher incident, higher risk for developing heart failure. And this is uh from the latest publication like in August of last year showing that the death from heart failure uh continues to go as you can see here this per per ages, but the death from heart failure slides went down but then slightly go back up from 2011. It peaked around COVID time in 2020, 2021 and then went down slowly but it's still, it's above the target that we want them to be. And with increased uh mortality there's also hospitalizations for heart failure. This is uh also all recent data we see that patients with heart failure had increased in hospitalization, but during COVID patients older than 65 years old usually stayed home and they didn't go to the hospital. But, um, the hospitalization rate for this patient population more than 65 was lower, but younger than 65 there was increase in hospitalization. Um, African American and black patients continue to tend to also have higher risk of heart fail hospitalizations and worse outcomes compared to others. Um, and also there was again, uh, we, if you're in a rural area, the hospitalization rate is usually lower compared to urban areas because technically people don't have access to care or do not go to the hospital in those regions. Why hospitalizations are important to highlight is because whenever patients get hospitalized for heart failure, their overall survival drops. After one hospitalization for heart failure, the 5 year survival for this patient drops around 25%. So, and this has been shown and proven in multiple trials. Again, the more you get hospitalized for heart failure, the worse your outcomes. So we need to find a way where we can improve survival and reduce heart failure hospitalizations as well. And this is a scheme from the straight from the American Heart Association about how to manage patients with heart failure. We're not gonna go into it too deeply, but knowing that if you're symptomatic with EF less than 40%, there are 4 pillars of GDMT, including ARNI, which is, uh, secondhibitor valsartan. MRA being spironolactone or elienone, SGLT2 inhibitors be depagilflozone and pilflozin, and beta blockers, which could be carvedilol, bisoproro, or metoprolol succinate. And after we put these patients on the medications, we tend to check their ejection fraction. If the ejection fraction is more than 40%, you keep following them up. If their ejection fraction less than 40% and these patients remain symptomatic from heart failure, if they're African Americans, you can consider hydralazine and Isordil. If their EF less than 35%, you can refer them for ICD or CRTD. And if the patients remain to be symptomatic with uh heart failure with low EF, then you have to think about advanced heart for surgical options, be it durable mechanical circuitry support or heart transplantation. So this is also, uh, that shows and can answer some questions basically if somebody's on ACE inhibitors, you have to wait 36 hours off ACE inhibitors to start them on ANI or accubior valsartan. If you start them on MRA, you have to check a BMP within 1 week of starting on the medicine because you want to check their potassium levels, your creatinine levels, and if you know they're SGL-2 inhibitors, it's straight one fixed dose of 10 mg. And that should be sufficient. You don't need to check any labs for it. And if they are an ACER, we check usually a BMP in a couple of weeks to make sure the kidney function and electrolytes are fine. And for those patients who are still symptomatic, again, you can, and they're tachycardic. The heart rate is more than 70 on maximum targeted beta blocker, you can consider starting them on varidine, which is a medicine that can help slow down the heart rate, because again, heart rate when it's usually more than 70 in patients with heart failure is associated with worse outcomes or if they had recent heart failure hospitalization, you can consider starting them on Verisigwat or Vercuvo, uh, with low EF as well. So this is um how and the uh the sequence of uh these medications being approved and went into the guidelines beta blocker made it to the guidelines in 2001. Then after that in 2005 MRAs and 2016 the AI and 2022 the SGLT2. I remember all these times at 2014 and 2019 when. Arni came out in the market and was a big uh shift in measure for heart failure patients because it was the first medicine after years and years that have shown to improve survival in the Paradigm trial. In 2019 I was at HFSA Heart Fest of America meeting and uh DAPAHF and uh Emperor Reduced came out at that time and SGL-2 inhibitors were basically, uh, shown to improve outcomes in patients with reduced ejection fraction. So what is the prevalence of heart failure nationally we talked about 6.8, but worldwide on 30 million and look out of these patients of the eligible patients to be on beta blocker, 33 patients are on beta blocker on AI, only like 11% of patients are on ANI and only like 43%. On MRA and 9% of patients on SGLT2 inhibitors, so there is a lot of need and a lot of work needs to be done to ensure that our patients get on GDMT. And why is that? It's not because we wanna add another pill. I don't tell my patients I'm not a pill pusher. I'm not doing it for the sake of giving you medicine. I have no, uh, stocks in the companies or anything. Because you know it's important to highlight that because the mortality rate without these medications is significantly high as you can see here, patients discharged from heart from the hospitalization for heart failure, around 82% of patients qualify for the four medicines, but out of these patients who are, uh, you know, qualify, only 15% of patients get these medications. For those who get the quadruple therapy, you can see how their risk for mortality drops significantly. Here and compared to patients without GDMT, you know, the mortality rate is significantly higher than when you're taking the medications. And this is a slide I like to show all the time when I give talks for, uh, heart failure is that when you add medication one after the other, so you add AI, the two year mortality drops from 35% to 25%, add a beta blocker, it drops to 16%, Aldoster antagonist 11, and as you inhibitor, the two year mortality is 9.5. It is less than 35%, but still it is high, and that says a lot. We have residual risk of death and mortality despite medical therapy. But again, When you put them on these medications, these patients gain around 7 to 10 years of extra life to their. Longevity basically and not just survival, these patients stay out of the hospital with reduction of hospitalization by 85% risk reduction and absolute risk of 33%, and you need to treat 3 patients with these medications to prevent one hospitalization, which is huge because again hospitalization is not just a nuisance for us it's not just getting taking a bed away from patients who might need it. Or is not to get it basically uh another HMP or orders for the patients. No hospitalization is critical because every time a patient is hospitalized for heart failure their overall mortality drops significantly, their morbidity is high they feel worse, the depression is worse, the caregivers, uh, increase burden on them. So again it's important to reduce hospitalizations. And if you don't put these patients on these medications, you see also mortality, hospitalizations, so we need to do a better job with that. How do we start these patients on the medications we have what we call the rapid sequence initiation. And the best way, and you have the captive audience when patients are hospitalized for heart failure, you start the 4 medications. You don't have to start the full dosages. You start with the lowest doses of the medicine with a beta blocker and ANI. You can start with a simple dose of uh spironolactone or elione, the standard dose, and standard dose of SGLT2 inhibitors, and all the trials have shown that when you start the patients inpatient on these medications, the chances for them to stay on these medications significantly higher than you start them in an outpatient setting because again you get make sure this patient get these medicines they pick it up from pharmacy because in outpatient setting. We say, oh, we're gonna start this medicine, let's see how they do our next visit, and some patients fall through the cracks not getting these medicines. What we do in outpatient setting after we start these medications, we can up titrate the dosages. Out of these 4 medicines, the only one of the main medications have shown improved benefit with higher dose initiate uh target dosage is a beta blocker. So we can start low, but we have to optimize the beta blocker dosages with RE you can start with a lower dose and not much significant difference in outcome being the highest and the lowest, but the beta blockers have the most significant benefit. You can start low and go slow, but make sure you put these patients on the 4 medications. OK, people say we can't do these medications. Why we're not utilizing the medicine, and these are some of the reasons people and providers do not initiate the medicines clinical inertia. Well, you know, ain't broke, don't fix it. They're doing OK. Why add another medicine, which happens all the time, and it's a conspiracy that happens between that both the physician and the patient agree on the physicians don't wanna add a new medicine because they have to follow up on the medicine. And the patient did not wanna start a new medicine, so it's like, OK, so let's not start and see how you do and see you later and you know they don't get the medicine. So also when you start some medication you're gonna check labs, so lab monitoring, checking their potassium, an extra step, but again we need to figure it out and dynamic concern oh the blood pressure is 100, 110, like I don't wanna start this Entresto or this, uh, go up with the beta blocker because I don't want them to get dizzy. OK, how do you know if you don't. Try to push the medicine and see how they do so again we should not be just worried about what can happen we wanna see if it happens first polypharmacy worry. We have a lot of pharmacists in the room again, patients, we should tell patients we're not pushing medicine. We are putting these medications because they can improve your outcomes and survival. So they're already on too many medications. My heart failure patients, when they come and see me in clinic, they are at least on 5 or 6 medications because now heart failure is not just a single isolated disease, it's a disease associated with multiple comorbidities diabetes, hypertension, dyslipidemia, uh, you know, all the other stuff, obesity. So again. And I added pill. It's not just a pill, it's a pill that can show improved outcomes, cost and access. I was giving a talk about this morning and we talked about access and getting this medication approved and nowadays all these medications, the pillars of GDMT are class one and so. Basically all insurance companies should approve these medications. Frailty and age, we have this bias against against older patients, and now old is very subjective. But again, if somebody's more than 70 years old, it's like, oh, I don't wanna start them on a, uh, SGLT-2 because they can develop a UTI. Well, again, would you prefer to have a UTI or you wanna prefer to have cardiovascular, uh, mortality or hospitalization? You have to weigh the risks and the benefits for these patients. Again, we're worried about the side effects. We, you know, discharge rush. We can get him out of the hospital because we need this bed and we don't tend to get these patients on medications also because sometimes we don't dose them correctly. We don't, we said we doubt that guidelines, so. Again, there are a lot of reasons not to, but on the other hand, there should be all reasons why to, and this is a slide that I got it also is that how this medication cost the four pillars of GDMT currently should cost the patient on $420 a year. I know it might be not too, too much for us, but. For some patients could be, you know, big burden for them, but again, if you're gonna look at this cost of medication compared to where their hospitalization would be or their mortality when the family members have to struggle with that, it's all worth it. So whenever you see a patient and you want to prescribe them GDMT or the four pillars or wanna push medicine dosage on the medicine, you have should should have two ideas in your mind. One of them is kind of like the good angel, the bad angel, the one to say like, oh, I wanna, I worry about the side effects and, you know, the adverse events. Let's not do it. But on the other hand, should be thinking about the survival, hospitalization, quality of life, and symptoms and improving the symptoms what these patients can get. So We talked about I wanna add something different this year which is device therapy in heart failure management too because it's not just about medications we are living in day and time where we have devices that can also improve outcomes for patients when to think about device therapy, and this is a, uh, paper we published in the Journal of Cardiac failure last year think about HF device, this smnemonic. If these patients are hospitalized for heart failure, they have functional impairment, they have dyspnea. EF is abnormal. Uh, they have velar disease inbulatory GDMT and congestion, elevated ipro BMP or BMP. These patients might qualify for device therapies. What are the device therapies? So this is basically, um, how heart failure goes. Patients, when they get diagnosed with heart failure initially, you put them on medications, they feel better, but they're gonna be a period of time where they start feeling worse. You can go up on dose, lower the dose. But when they get hospitalized and the quality of life goes down, you start thinking about other stuff for these patients, you know, we are living in day and time. We, for example, in Centerra and other institutions, we have a beautiful and great uh structural heart team we do. Of work for mitral valve, which is a tricuspid valve leakages of that regurgitation, we can put, you know, clip there or, you know, all these procedures if they have significant aortic stenosis we can also adjust, uh, take care of these patients percutaneously other than like open heart surgeries. Also we have remote monitoring which we're gonna talk about the cardiograms or, you know, there's autonomic nervous system modulators or cardiac contractility modulators too which we also use uh in our system. So I wanna talk to you about in a second. So this is also uh work we've done to to go through an algorithm on how and who are the patients can benefit from device therapy. So first of all, before considering device therapy, these patients should be on GDMT, the four pillars, and if they remain symptomatic despite that, consider device therapy. We talked about the CCM, BAT, the BAT, and also Carioms. So we start with cardiac contractility uh modulator or CCM impulse optimizer. Heart failure patients, the pathogenesis pathogenesis for these patients with reduced CF or contractility is calcium, intracellular calcium. If there is imbalance between intracellular calcium, it can affect contractility. So what does this device do? It's implanted on the usual, if they have an ICD on the right side and delivers signals to, it's a biphasic signal goes to the ventricular septal wall during the refractory phase, and basically it can on the absolute refractory period. What happens, it does not result in contraction, it can lead to structural and functional changes in the myocardium. There's no changes with that. It can increase contractility without increasing myocardial oxygen demand. It can reduce the volume, and this is mainly through intracellular calcium. So the trial that got CCM approved was fixed HF trial. They went through 12345, A and B, and until C. This CCM device has shown it can improve quality of life for these patients that it was trends toward hospitalization. And as you can see here this is the ICD on this side and this device on the right side where you have multiple wires definitely coming in into the patient's right ventricle and there's one goes to the right atrium where it stimulate the timing of the contractility again in the last uh American uh Heart Fair Out of America annual scientific meeting in October of last year. There was a uh abstract uh that was uh presented which showed that there's reduction in heartware hospitalization and, uh, LAD and transplant but again still it's only for quality of life. What about autonomic nervous system modulation in heart for patients there's definitely imbalance between the parasympathetic. And sympathetic nervous system, the sympathetic nervous system can increase heart rate after load and stress on the heart, and the parasympathetic can lower that. So there's imbalance in heart failure. There's more sympathetic, lower parasympathetic. So what does bear stem do? As you can see here, it can modulate that it's a again device with a uh generator implanted in the right side of the heart, and there it there's a wire that's tunneled under the skin in the neck and it goes into the carotid bear receptors and it stimulates these receptors and when it does that it can increase the parasympathetic nervous system and lower the sympathetic so that's the main goal reduce sympathetic and increase parasympathetic. And this is how it looks like. And this is the chest X-ray of how a bear stem can see the generator and the wire goes up into the carotids, and it got approved by the trial called BAHF trial which uh randomized patients with EF less than 35%. To standard of care and uh the Beristem and they found that patients who were received the Beristem device there is reduction in their NYCHA classification they're symptomatically feeling better, decrease in anti-R BMP and tend to reduction in heart forre hospitalization. and it's also approved in 2019 for these patients with NHA class 3 or two who are private 3 with the have less than 35%. We have a lot of patients who are embarrassed and who felt significantly better, had improved their quality of life with this device as well. Uh, lastly we're gonna talk about, uh, pulmonary artery pressure sensor monitors. Patients when they come and see you, because again, heart failure is kind of digress a little bit, 60% of all heart failure patients are managed by patients in the commu by primary care physician in the community. You guys tend to see these patients when the patients come to see an advanced heart failure cardiologist or a cardiologist. These patients technically have been seen by multiple other times by PCPs, and if they see us, they're usually in really not ideal situation. So you guys tend to see these patients it's important to know about these therapies as well. So before patients tend to develop the symptoms of shortness of breath or the weight gain, these patients have increased in the fill pressures because volume is pressure when you have more fluid in your body. The pressure inside your lungs will go up and that's reflected on the devices that we're gonna see later on so high pressure, high volume, and that can lead to changes in the heart parameters and then you can have the weight change, then you're gonna have the symptoms and then patient eventually get hospitalized for heart failure. So CarMMSs, which is a pulmonary artery pressure sensor monitor, as you can see like a butterfly, uh, which basically, uh, it's a sensor sensor we do a right heart catheterization we find an area in the pulmonary artery and we drop it there and basically when it's there it. Delivers and transmit uh signals we give patients a pillow the the patients lay on a pillow and that pillow will be used to transmit the signal from the sensor through the pillow to a computer. Where it's checked by our nurse practitioners or providers twice a week. If there is a trend to increase in pressures, which again volume is pressure, more higher pressures means more they're retaining more fluid, then we contact the patient if it's high for 2 days that, hey, take an extra diuretic, how you doing? salt, diet, you know, and medications. Through Carioms, it has shown that there is a reduction of heartfare hospitalization up to 30% in 6 months. And when you when physicians have managed patients solely by cardioms, there's a reduction in hospitalization as well, but also quality improvement in quality of life. But again, for this to work, patients have to do the reading, have to lay down on a pillow. As simple as it is, not many people and patients do that. They, so to work you have to do it. Lastly, Cordella, which is similar to Cardim's, it's a pressure sensor monitor which is implanted in the right pulmonary artery. Our center was involved in that trial, the proactive trial, and this trial has shown that basically patients who are managed through Cordella or, you know, with the pressure pulmonary artery pressure sensor, these patients have lower hospitalization rate for heart failure. So in conclusion, the M and GDMT is not just pharmacotherapy, it is also device therapy and in appropriately managing these patients. They are both synergistic rather than in competition with each other. So not just take the medicine, but also we are living in a day and time where device therapy can also improve outcomes for these patients. So don't be a Scrooge and you know take your time and also maybe prescribe these medications and overcome that inertia of not prescribing the medicine and it's not true if it ain't broke don't fix it no we wanna make sure we provide our patients with medication that can improve survival and quality of life so on that I thank you for your attention. Published June 30, 2026 Created by Related Presenters Amin Yehya, M.D. Sentara Advanced Heart Failure Center View full profile
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