Hello, this is Sandy McCrary, I'm a physician assistant, and we're going to continue by looking at some heart failure case studies. The first case study, we'll call patient a, and I'm making a little easy for all of these case studies because I'm giving you the answer up front. This is a 76 year old male, and his diagnosis is ischemic cardiomyopathy. He has a past history of CAD, he's had prior cabbage, he's had COVID infection, he's diabetic, hypertensive, hyperlipidemia, former smoker. He had a stress nuclear study in 2019 that showed a normal ejection fraction of 60% and the perfusion was also normal. So he presented to the hospital recently with a two week history of shortness of breath, chest pain and was diagnosed with non steamy. You can see the results of his EKG here, his chest x ratio pulmonary edema. He had a troponin peak of 11.5, and TSH was normal, chemistry panel, EGFR was normal. His home medications included enalapril, metformin, metoprolol tartrate, rosuvastatin, and aspirin. So he underwent an emergent cath, and this showed that three of his four grafts were patent, but the saphenous vein graft to OM1 and 2 was compromised. So because of this, he underwent PCI with the drug eluting stent to this culprit lesion. An echocardiogram showed that his ejection fraction is 30 to 35%. There was also wall motion abnormalities consistent with his CAD. There was grade two diastolic dysfunction, mildly dilated left atrium, and RBSP was 30 to 35. He also had mild to moderate MR. So during the admission, his enalapril was discontinued. He was then placed on valsartan. His metoprolol tartrate was changed to carvedilol because of its indication with LV dysfunction. He was started on spironolactone, half tablet daily, and then prior to discharge, he was switched from valsartan to Entresto. And at this point, 36 hours had passed since his last dose of enalapril. So frequently what happens when the patient goes into the hospital, if they are found to have an LV dysfunction upon admission and they are presenting with a home medication of an ACE inhibitor, that will be stopped. They will be switched over to an ARB. And on that ARB, the patient can be switched directly to Entresto without a washout period, but that allows them to be on the ARB and allows the ACE inhibitor to have that 36-hour washout. So the patient was seen by our heart failure coordinator and set up with an initial appointment in our heart failure clinic. Of course, she went over educational materials with the patient. So at our first visit, which was two weeks after discharge, blood pressure was running high. You know, with heart failure, you ideally want that, certainly want that blood pressure to be less than 120 systolic. His heart rate was also high. It was 97. Ideally with heart failure with reduced ejection fraction, that heart rate should be more in the 50s to 60s. He was taking carbidolol, 6.25 BID, low-dose Entresto, half a tablet of spironolactone, torcimide, relenta, statin, and aspirin. So during the first visit, we increased his Entresto to 49.51 BID, hoping to achieve better blood pressure reduction. We also added Farxiga, decreased his torcimide to 20 milligrams daily PRN. He was euphelemic on this visit, and obtained a BMP two weeks later, and you can see the results there. So he came back for his second visit. This was two weeks later. Blood pressure looked much better. Heart rate was also much better, but still high. His medications included the carbidolol 6.25, the mid-dose Entresto, spironolactone, half a tablet, as well as Farxiga, torcimide, relenta, Crestor, and aspirin. So at this visit, we increased his carbidolol to 12.5 milligrams BID, and we also increased the spironolactone to a full tablet daily. He came back at visit three, which was three weeks later. Blood pressure looked good. Heart rate was 75. He was taking 12.5 carbidolol, still on the middle dosage of Entresto, spironolactone, full tablet, as well as the Farxiga, torcimide, relenta, rosuvastatin, and aspirin. You can see his lab work here, which everything looks stable. So we recommended that he increase the carbidolol to 25 milligrams BID at this visit. At visit four, when he came in, blood pressure looked really good. Heart rate was now 65. He was taking full-dose carbidolol, mid-dose Entresto, full tablet of spironolactone, as well as Farxiga, torcimide, PRN, but had not required any, relenta, Crestor, and aspirin. His labs looked stable, and we recommended at this visit that he increase Entresto to full-dose, which is 97-103 BID. So he came back for visit number five, which was three weeks later. Blood pressure looked really good. Heart rate was excellent. His medications were great. He was on full-dose carbidolol, full-dose Entresto, spironolactone, Farxiga, had not required any torcimide, was taking his relenta, Crestor, and aspirin, thankfully. Lab work looked good. He was tolerating all of his medications. He had some mild lightheadedness with sudden change of position, but said that it was tolerable, and so we again discussed the importance of orthostatic precautions. So the patient is now on optimum medical therapy with guideline-directed medical therapies, and so we ordered an echo. So when he came back for visit number six, which was three weeks later, his hemodynamics looked really good. Drug therapy was excellent. His echo had been done, which is now more than three months post-PCI, and it showed that his ejection fraction had improved from 30-35% to now 40-45% on the follow-up echo. So the take-home points for this patient is that this patient had a history of CAD, had prior CABG, but his EF had remained normal up until this current admission. His stress nuclear study three years prior had shown a normal ejection fraction with normal perfusion. So his current presentation was for a non-STEMI, and he had a new decline in his ejection fraction. A CAD showed that three of the four grafts were patent, but the saphenous vein graft to OM1 and OM2 was compromised, and so this culprit lesion was treated with PCI drug-eluting stent. So in this situation, guideline-directed medical therapy needed to be initiated and titrated as efficiently as his hemodynamics and renal function allowed, and he did have an improvement in his EF to where it is now greater than 35%. Remember, it was 30-35% previously. It's now 40-45%. The importance of this for this patient is that now puts him at the level that he does not require consideration for ICD therapy based on his ejection fraction. If that ejection fraction improves to 35% or greater, then the patient's risk for ventricular arrhythmias and sudden cardiac death goes down significantly. So patient B is a 57-year-old male who has non-ISCHEMIC cardiomyopathy, and his is tachycardia-mediated. He has a history of diabetes, hypertension, hyperlipidemia, family history of coronary disease, he has a history of tobacco usage, he has COPD, sleep apnea, and is not on CPAP, reflux. His echo was done two years ago because of dyspnea, and it showed a normal ejection fraction of 55-60%. When he presented, he was taking atorvastatin, 40-hydrochlorothiazide, and losartan. So he presented to his primary care office with a one-week history of shortness of breath, PND, orthopnea, and profound fatigue, which had been going on for at least three weeks. He had an EKG, which showed atrial fibrillation with rapid ventricular response. His heart rate was in the 150s, and this was a new finding for him. So he was sent to the hospital and admitted. At the hospital, his D-dimer was abnormal, so he had a CTA of the chest, and it showed no PE. He had bilateral lower extremity ultrasound, which was negative for DVT. His labs, you can see sodium-potassium normal, EGFR was 61, troponins were negative, thyroid was normal, but his NT-proBNP was markedly elevated at 67-51. He was initially treated with a cartosome drip. Remember, he had heart rates in the 150s, the 8-fib with RBR. He was placed on IV diuretics, Lovenox, and heart rate after initiation with this treatment was now in the 80s. His echocardiogram showed that his EF was 20%. He had severe global hypokinesis, diastolic function could not be assessed, he had borderline left ventricular enlargement and right ventricular enlargement, severely reduced RB function. Remember, his previous echo that was done two years prior showed a normal ejection fraction, and it is now 20%. So he was seen by cardiology. The cartosome was stopped because of the negative inotrophic effects that calcium channel blockers can have and potentially cause hemodynamic compensation in patients that have reduced ejection fraction. So he was started on metoprolosustenate and continued on Losartan and Lovenox. He had a Lexascan NUC that showed EF 32% on the NUC and no evidence of ischemia. So a TEE cardioversion was attempted, but the TEE when it was performed showed that his ejection fraction was 15 to 20%, but there was also spontaneous echocontrast with thrombus in the left atrial appendage. So the cardioversion was canceled and plan was to reconsider doing a TEE guided cardioversion after he had been on anticoagulation for four to six weeks if the atrial fibrillation persisted. So he was discharged on SGLT2 inhibitor, metoprolosustenate, Lasix, Losartan, Eloquus for anticoagulation, and atorvastatin. He was seen during the admission by our heart failure coordinator, given heart failure education, and scheduled into our clinic. And our first visit with him, which was two weeks after discharge, blood pressure looked good. His heart rate was 53 at this visit. He was taking metoprolosustenate 150 milligrams daily, Losartan 100 milligrams daily, Jardiance, Lasix, and Eloquus. You can see his labs here. So on this first visit, we switched his Losartan to Entresto 2426BID. We also added spironolactone, and we decreased his Lasix from taking it daily to taking it on a PRN basis only. So he came back two weeks later for his second visit in heart failure clinic. You can see his blood pressure is 98 over 58 sitting, 102 over 60 standing, and heart rate is 85 on the EKG. His medications, again, include the metoprolosustenate 150 daily, Entresto, Jardiance, spironolactone, Lasix, PRN, but he had not required any, and Eloquus. And you can see his labs here. So seven weeks after discharge, he underwent a TEE cardioversion. The TEE showed that EF was 15 to 20%, but there was no thrombus, no spontaneous echo contrast noted in the left atrial cavity or appendage. So he was able to undergo a successful DC cardioversion of his atrial fib with restoration of sinus rhythm. So he came in then for his third heart failure clinic visit, which was three weeks after his cardioversion. You can see his blood pressure readings, heart rate is 53, EKG shows sinus rhythm, and his rate is 55 on EKG. Patient was taking maximum tolerated doses of metoprolosustenate with 150 milligrams daily, Entresto, Jardiance, and Spironolactone. We really did not consider that we could increase the metoprolol any further because his heart rate is 53, or the Entresto because of his blood pressure readings. He was tolerating the doses he was on, but we did not feel that he could tolerate higher doses. So we did a repeat echo, and this was about 10 weeks from the onset of symptoms. So we did a repeat echo, and this was about 10 weeks from the onset of symptoms. And on the repeat echo, his ejection fraction was 25 to 30%. So because it was still 35% or lower, we made referral to our EP colleagues to consider ICD placement. So the take-home points with this patient are that calcium channel blockers have a negative inotropic effect and may cause hemodynamic decompensation with patients with reduced ejection fraction. If you see a decline in an ejection fraction from prior studies, his prior EF two years before on echo done because of shortness of breath was normal, but is now 15 to 20%. He had no history of CBD, and his cardiomyopathy was likely felt to be tachycardia-mediated, but we still need to do an ischemic evaluation. In this case, a Lexiscan nuclear study showed normal perfusion. The atrial fibrillation needs management with oral anticoagulation therapy, as well as preferably restoration of sinus rhythm. Now, in some cases, the sinus rhythm cannot be immediately restored, such as this case, because he had a left atrial appendage thrombus. So the restoration of sinus rhythm had to be delayed. So in that situation, our treatment recommendation was for oral anticoagulation and rate control. His EF, when he was able to have a repeat TE with cardioversion and restore the sinus rhythm, his EF had improved, but it still remained 35% or lower after being on optimal medical therapy with guideline-directed treatments with beta blocker, ARNI, MRA, and SGLT2 inhibitor. So because of this, he needs to be considered for device therapy, so we referred him to our EP colleagues. Finally, we'll move to patient C. She is a 60-year-old female with HEF-PEF. She has no history of coronary artery disease. No prior cardiac testing was done. She is obese. Her BMI is 35.43. She has what she describes as diet-controlled diabetes, hypertension, family history of CAD, and history of smoking a pack and a half for 30 years, COPD with oxygen dependence, arthritis, and chronic back pain. Her home medications included metoprolol tartrate and gabapentin. She initially presented to the emergency department after a ground-level fall in her garage. Radiograph images were consistent with thoracic and lumbar compression fractures. She was noted on exam, however, to have 2-plus bilateral lower extremity edema, and during the assessment, she became hypoxic, and she required increased levels of oxygen and eventually BiPAP. She had a chest X-ray, which was abnormal, and her ABGs were also abnormal. Her labs included a COVID viral fourplex, which was negative, but her NT-proBNP was elevated at 69.57. Troponins were negative. Her potassium was low. Renal function was normal, and you can see the other lab values here. Her EKG showed sinus rhythm. There were no old studies to compare, and she underwent an echo, and this demonstrated a normal injection fraction, 55-60%. There was grade 2 diastolic dysfunction. There was moderately dilated RB and RA and mildly dilated left atrium, and her RBSP was 35-40. She was managed in the hospital by the hospitalist team. They replaced her potassium and magnesium during the hospitalization, and then the levels were followed as an outpatient. She was treated with empiric antibiotics and steroid for her COPD exacerbation, as well as diuretics. Initially with IV diuretics, transitioned to PO prior to discharge because of the exacerbation and symptomatic heart failure with preserved ejection fraction. She was also treated, of course, with calcium, vitamin D, and physical therapy for her thoracic and lumbar compression fractures. Outpatient heart failure clinic appointment was requested by the hospitalist, and she was seen by her heart failure coordinator prior to discharge for education regarding heart failure and initial scheduling. So when she came in for her first visit in heart failure clinic, this was three weeks after discharge. Blood pressure was 132 over 72, sitting, her heart rate was 81, BMI was 31, so she had reported to have lost 25 pounds since discharge. She had no further lower extremity swelling, and she was euphemic on exam. Her cardiac medications included metoprolol tartrate, 25 milligrams BID, Lasix, and potassium. And let me just say that metoprolol tartrate in her situation is fine. She is HEF-PEF, and so this does not require one of the three beta blockers indicated for HEF-REF, but the metoprolol tartrate is fine in her situation because her ejection fraction is preserved. She had not smoked since discharge. She had a history significant for probable sleep apnea. She had excessive daytime drowsiness. She needed daytime naps. Her sister reported that she snored, and you can see her labs here. So at the first visit, we recommended that her Lasix be changed to PRN. She was now euphemic. She had had a 25-pound weight loss, which was probably mostly fluid. We added spironolactone, 25 milligrams daily because of its benefit in HEF-PEF. We also added Jardiance, 10 milligrams daily because of its benefit in HEF-PEF. We also added a statin drug and stopped the potassium supplement. We recommended sleep evaluation, but she declined. We did our usual heart failure education, reiterated the importance of sodium restriction, continued smoking cessation, and went to call us at the clinic if symptoms arose. So she came back three weeks later for her second heart failure clinic visit. You can see her blood pressure readings and heart rate is 76. She had continued to abstain from smoking. Her cardiac medications included, she was still on metoprolol tartrate, 25-BIV. The Lasix was now PRN, and she had not required any. She was taking Jardiance, spironolactone, and her statin drug. You can see her labs here. We recommended that she continue the same cardiac medications. We also again recommended sleep evaluation, but she again declined. We educated and reiterated the importance of sodium restriction, daily weights, continued smoking cessation, and went to call the clinic. So the take-home points with this patient C who has HFPEF is, number one, we need to very effectively manage the volume status, diuretics as needed. Number two, the medications need to include the SGLT2 inhibitors and MRAs were tolerated. We also need to adequately manage the blood pressure and may need to consider ACE, ARBs, or ARNIs for benefit in blood pressure management. And we also repeat educational information and discussion with that patient at each visit, and this includes smoking cessation. And I just want to point this out, and I should discuss this with her. It made quite an impact on her. When we did her 10-year ASCBD risk assessment while she was smoking, her 10-year risk for ASCBD was 24.9%. By quitting smoking, she decreased her 10-year ASCBD risk from 24.9% to 12.5%. That's a huge difference, and it was very motivating for her, and she, at least at this point, has continued to abstain from smoking. So that is the end of our case studies. Thank you so much for joining us and for your time.

physician assistant

heart failure

case studies

ischemic cardiomyopathy

ejection fraction

medication adjustments