ACC SAP 11 Heart Failure and Cardiomyopathies PDF

Question 1 of 70 A 39-year-old woman is referred from her primary care clinician for dyspnea on exertion. She feels short of breath after climbing one flight of stairs, whereas 6 months previously she could climb the stairs without difficulty. She has two children, 18 months of age and 4 years of ag...

Question 1 of 70 A 39-year-old woman is referred from her primary care clinician for dyspnea on exertion. She feels short of breath after climbing one flight of stairs, whereas 6 months previously she could climb the stairs without difficulty. She has two children, 18 months of age and 4 years of age, and she is having trouble keeping up with them due to shortness of breath. She underwent lumpectomy for ductal carcinoma in situ 1 year earlier without radiation therapy. Her only medications are tamoxifen and a daily multivitamin. She is a lifelong nonsmoker, drinks alcohol socially, and does not use illicit drugs. Her family history is remarkable for a mother who died suddenly at 52 years of age; she had had a pacemaker implanted in her 40s. i o ) On examination, her blood pressure is 127/83 mm Hg, pulse is 90 bpm, and oxygen saturation is 95% on room air. The examination is remarkable for a normal S1 and S2, a a rd faint grade 1/6 systolic flow murmur that does not change with Valsalva, a jugular venous C o) pressure (JVP) of 10 cm H2O, and trace bilateral lower extremity edema. S P d i F C ar d Which one of the following is this patient's most S C (likely diagnosis? o o CP m F A. Ischemic cardiomyopathy. ah an ( M rh B. Chemotherapy-induced rcardiomyopathy. D r Fa C. Familial dilated cardiomyopathy. D. Peripartum cardiomyopathy. D E. Heart failure with preserved ejection fraction.  Correct Answer C Commentary This patient is presenting with exertional dyspnea, elevated JVP, and lower extremity edema, all signs of clinical heart failure. Her family history is remarkable for her mother likely having had early conduction system disease requiring a pacemaker, followed by sudden cardiac death in early life. This is suspicious for a genetically mediated familial dilated cardiomyopathy. Although ischemic cardiomyopathy accounts for about one-half of cases of heart failure with reduced ejection fraction, this patient has no symptoms or risk factors for coronary artery disease, making it less likely. She is 18 months postpartum and did not develop symptoms until 6 months earlier. Peripartum cardiomyopathy typically occurs within 5 months postpartum and is therefore not the most likely cause of her cardiomyopathy. o ) Although she has a history of breast cancer, she has no history of treatment with i a rd anthracyclines or trastuzumab, so chemotherapy-induced cardiomyopathy is not the correct answer choice. Although heart failure with preserved ejection fraction would fit her C o) symptoms, her family history makes familial dilated cardiomyopathy the best answer S P d i choice. Moreover, a laterally displaced point of maximal impulse suggests left ventricular C ar enlargement, more consistent with a dilated cardiomyopathy. F References d ( SC o o Heart 1. Bozkurt B, Colvin M, Cook J, et al.; American C PAssociation Committee on Heart m on(FClinical Cardiology, Council on Failure and Transplantation of the Council ah Council Cardiovascular Disease in the Young, a n on Cardiovascular and Stroke Nursing, Council on Epidemiology andM h Prevention, Council on Quality of Care and Outcomes r Research. Current diagnostic D a r and treatment strategies for specific dilated F Dr cardiomyopathies: a scientific statement from the American Heart Association. Circulation 2016;134:e579-e646. Key Point A large proportion of dilated cardiomyopathy is likely related to a genetic cause; however, routine genetic testing is likely low yield in the absence of a strong family history of cardiomyopathy or typical presentation. Related Text Click the title below to read text related to this question in the Heart Failure and Cardiomyopathies chapter/Cardiomyopathies module. Dilated Cardiomyopathy Question 2 of 70 A 42-year-old woman is admitted to the hospital with shortness of breath. She notes onset of fevers 1 week earlier with subsequent chest pain and myalgias. She has no past medical history and is on no medications. Her blood pressure is 98/76 mm Hg, heart rate is 112 bpm, temperature is 39.2°C, and oxygen saturation is 94% on room air. Examination reveals bibasilar crackles. Heart sounds are tachycardic with no murmurs. There is mild bilateral lower extremity edema. Her electrocardiogram shows sinus tachycardia. Laboratory studies are notable for white blood cell count of 18,200/mm3 and troponin I of 8.2 ng/mL. An echocardiogram reveals a left ventricular ejection fraction of 25%. i o ) a rd S C o) P d i her presentation? Which one of the following pathogens is most likely responsible for F C ar A. Parvovirus. d ( SC B. Reovirus. o o CP h m (F C. Rhabdovirus. a a n r M r h D. Poxvirus. D rF a E. Escherichia coli. D  Correct Answer A Commentary Parvovirus is the correct answer choice. The patient's presentation is consistent with acute viral, or lymphocytic, myocarditis given the infectious symptoms, heart failure findings, and reduced left ventricular function in combination with elevated troponin. Classically, enteroviruses such as coxsackievirus have been the most frequently detected viruses in endomyocardial biopsies from such patients. More recent data using polymerase chain reaction techniques have shown that parvovirus B19 and human herpesvirus 6 may be more common organisms causing myocarditis today. Reoviruses such as rotavirus primarily cause gastrointestinal infections in children. Rhabdoviruses are rarely pathogenic in humans apart from rabies. Poxviruses, including smallpox and molluscum, display prominent skin findings. None of these viruses have any o ) notable association with myocarditis. Escherichia coli also does not typically result in i myocarditis. a rd References S C o) 1. Kindermann I, Barth C, Mahfoud F, et al. Update on myocarditis. P d i J Am Coll Cardiol 2012;59:779-92. C Circ a r ( 2. Fung G, Luo H, Qiu Y, Yang D, McManus B. Myocarditis.F C Res 2016;118:496-514. o d PS Key Point m o are Fviruses. C The spectrum of identified viruses The most frequently identified pathogens has changed, with enteroviruses a less n ( h frequently identified. Parvovirus B19 and human M herpes virus 6 are the most common h a viruses identified by gene amplification in the United r D r Fa States and Europe. Influenza is also r an important cause of fulminant heart failure. Related Text D Click the title below to read text related to this question in the Heart Failure and Cardiomyopathies chapter/Myocarditis module. Etiology of Myocarditis  Question 3 of 70 A 65-year-old man with known chronic systolic heart failure (HF; left ventricular ejection fraction [LVEF] 30%) presents to the office with worsening dyspnea on exertion. Over the prior 6 months, he has developed dyspnea with ambulating 22.86 m or with any incline. He denies weight gain or worsening lower extremity swelling, but does need two pillows to sleep comfortably at night. His past medical history includes hypertension, hyperlipidemia, type 2 diabetes mellitus, obesity, and obstructive sleep apnea. He currently is taking aspirin 81 mg daily, lisinopril 40 mg daily, metoprolol succinate 100 mg daily, spironolactone 25 mg daily, furosemide 40 mg daily, and metformin 1000 mg twice daily. i o ) His vital signs include blood pressure of 100/62 mm Hg and heart rate of 60 bmp with normal oxygen saturation. His heart sounds are distant with a faint S1 and S2 and a a rd grade 2/6 holosystolic murmur best appreciated at the apex. He has 1+ pedal edema and C o) his jugular venous pressure is 15 cm H2O. Recent laboratory values are normal except S P d i for an elevated B-type natriuretic peptide. An electrocardiogram is performed (Figure 1). F C ar He is referred for right heart catheterization with d S C angiography. Coronary ( coronary angiography reveals mild nonobstructiveocoronaryPartery disease. Right heart o FC catheterization hemodynamics are as follows: m Right atrium: 15 mm Hg a h n( Right ventricle: 64/12 mm Hg Mof 42rmm h a Hg) Pulmonary artery: 66/30 (mean r Dpressure:a mean 35 mm Hg (Figure 2) Pulmonary capillary wedge r F Cardiac output: 3.5 L/min Cardiac index 1.6 L/min/m2 D  i o ) a rd S C o) P d i F C ar d ( SC o o CP m F ah an ( r M rh D r Fa D (Figure 1)  i o ) a rd S C o) P d i F C ar d ( SC o o CP m F ah an ( r M rh D r Fa D (Figure 2) Which one of the following is the best next step to reduce this patient's mortality? A. Mitral valve surgery. B. Cardiac resynchronization therapy. C. Intravenous nitroprusside. D. Intravenous dobutamine. E. Transcatheter edge-to-edge mitral valve repair. Correct Answer B Commentary This patient presented with decompensated systolic HF. He was on guideline-directed medical therapy (GDMT), which includes an angiotensin-converting enzyme inhibitor inhibitor, angiotensin II receptor blocker (ARB, or angiotensin receptor–neprilysin inhibitor ARNI), beta-blocker, and mineralocorticoid-receptor antagonist (if indicated). Diuretic therapy is indicated as needed to treat volume overload. Based on his history and clinical findings, he had evidence of volume overload. His right heart catheterization revealed a low cardiac output and postcapillary pulmonary hypertension (i.e., a mean pulmonary arterial pressure ≥25 mm Hg and a pulmonary arterial wedge pressure [PCWP] of >15 mm Hg) that is secondary to elevated left-sided pressures. On the PCWP tracing, the v waves are very tall and consistent with severe mitral regurgitation (MR; Figure 2). Thus, the patient has decompensated HF with concomitant severe functional MR. i o ) The patient's electrocardiogram revealed a left bundle branch d ≥150 msec. Cardiac resynchronization therapy (CRT) is recommendeda r block (LBBB) with a QRS for patients who have an LVEF of ≤35%, sinus rhythm, LBBB with a QRS C duration)of ≥150 msec, and New P York Heart Association (NYHA) class II, III, or ambulatoryS IV d io on GDMT (Level of symptoms Evidence A for NYHA class III/IV [38,78,116,594];C r Level ofaEvidence B for NYHA class II). Thus, CRT is the correct answer choice. ( F C o d PS Intravenous nitroprusside acts to reduce m opreloadF C and afterload but is primarily reserved for ah aisn an( effective hospitalized patients with acute decompensation alone. Similarly, intravenous dobutamine and would not alter this patient's mortality inotrope that is typically used for r M hospitalized patients with severe r h systolic HF, hypotension, and a decreased cardiac output or as a palliative agent inD a stage D HF who remain symptomatic despite patients with F r GDMT and are not eligible for advanced therapies (i.e., ventricular assist device or Dof these choices is the best next step given the clinical transplantation). Thus, neither scenario. This patient has severe functional MR due to chronic systolic HF. In patients with dyssynchrony, CRT improves secondary MR. In the MIRACLE (Multicenter InSync Randomized Clinical Evaluation) trial, the long-term benefit of CRT was established, which included significant reductions in left ventricular dimensions and a reduction in MR. Invasive strategies for severe functional MR (3+ to 4+) can be considered in patients with symptomatic systolic HF (NYHA class II, III, or IV [ambulatory]) despite GDMT and/or CRT (if indicated). There is limited evidence on the safety and efficacy of isolated mitral valve surgery for MR. No randomized trials have assessed medical versus surgical therapy, but no differences in survival have been noted between surgery and medical therapy in observational studies. Thus, mitral valve surgery should be reserved for patients undergoing cardiac surgery for a different indication. The evidence for benefit of transcatheter edge-to-edge mitral valve repair (TMVR) over medical therapy in patients with moderate-to-severe or severe secondary MR and an LVEF of 20-50% with NYHA class II, III, or IV (ambulatory) HF despite GDMT and/or CRT was demonstrated in the COAPT (Cardiovascular Outcomes Assessment of the MitraClip Percutaneous Therapy for Heart Failure Patients With Functional Mitral Regurgitation) trial. TMVR significantly reduced mortality (29.1% vs. 46.1%) and HF hospitalizations (35.8% vs. 67.9%) at 24 months compared with medical therapy alone. TMVR may be a reasonable option for this  patient if the MR persists despite CRT. References 1. Yancy CW, Jessup M, Bozkurt B, et al.; American College of Cardiology Foundation, American Heart Association Task Force on Practice Guidelines. 2013 ACCF/AHA guideline for the management of heart failure: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. J Am Coll Cardiol 2013;62:e147-239. 2. Management and prognosis of chronic secondary mitral regurgitation (UptoDate website). 2020. Available at: //www.uptodate.com/contents/management-and-prognosis-of-chronic- secondary-mitral- regurgitation?search=heart%20failure%20miral%20regurgitation&topicRef=121085&source=see_link#H Accessed 6/26/2020. 3. Abraham WT, Fisher WG, Smith AL, et al. Cardiac resynchronization in chronic heart failure. N Engl J Med 2002;346:1845-53. i o ) with heart failure. N Engl J Med 2018;379:2307-18. a rd 4. Stone GW, Lindenfeld J, Abraham WT, et al. Transcatheter mitral-valve repair in patients S C o) Key Point P d i r for patients with C be indicated a decompensated heart failure who are not responding F Currently, invasive right heart catheterization would ( SasCexpected when decision making is based on noninvasive methods (persistent o d P symptoms, hypotension, renal failure despite o apparent volume overload) and in patients in whom m F C therapies with significant risks ah an (inotropes, left ventricular assist devices, ( transplant) are being considered. Related Text r M rh D Click the title below to read F a to this question in the Heart Failure and text related Dr Cardiomyopathies chapter/Hemodynamic Assessment module. Invasive Assessment of Hemodynamics: ESCAPE and the Role of RHC in the Post- ESCAPE Era Question 4 of 70 A 55-year-old man presents to the emergency department with new-onset dyspnea on exertion. His symptoms started several weeks earlier. The shortness of breath has progressively worsened to the point that he is now breathless at rest. He also notes swelling in his ankles and difficulty sleeping at night for the previous few days that required sleeping in his recliner. He has no prior medical history and is on no medication. His physical examination demonstrates a man with obesity and a thick neck. Jugular venous pulsations are difficult to visualize. Heart sounds are regular but distant. There is 1+ lower extremity edema bilaterally. i o ) A chest X-ray demonstrates pulmonary vascular congestion. His initial laboratory studies are normal except for an elevated brain natriuretic peptide. Bedside echocardiography a rd reveals a normal ejection fraction without significant valvular abnormalities. S C o) P d i Which one of the following clinical developments(F C ar you to pursue right heart catheterization (RHC) for this patient? d S C would prompt o o CP m F ah an ( A. Development of atrial fibrillation. B. Pulmonary edema requiring r Mbilevelrhpositive airway pressure. C. Initiation of intravenous F a Dfurosemide. D r D. Fevers and hypotension requiring vasopressor support. E. Worsening renal function on intravenous furosemide.  Correct Answer E Commentary In the scenarios provided, the only clinical scenario that warrants invasive monitoring/ assessment is worsening renal function despite intravenous furosemide. In this scenario, RHC can help determine the cause and/or therapeutic intervention required to improve symptoms and renal function in a patient who is failing medical therapy. Patients with pulmonary edema and/or requiring higher levels of respiratory care (e.g., bilevel positive airway pressure) do not require routine invasive hemodynamics to diagnose and/or guide therapeutic interventions. Additionally, initiation of intravenous furosemide does not warrant routine RHC unless the patient fails medical therapy. RHC in the setting of septic shock is not routinely recommended but may be considered in selected patients with a concern for concomitant cardiogenic shock and/or unknown o ) volume status. The development of atrial fibrillation may be seen in the setting of volume i a rd overload but does not indicate a need for invasive monitoring. Routine use of invasive hemodynamic assessment with RHC is not warranted for patients with acute C o) decompensated heart failure. It should be reserved primarily for patients with an S P d i indeterminate volume status and/or persistent symptoms that are refractory to medical therapy. F C ar d ( SC Invasive hemodynamic monitoring shouldobe considered (Class IIa) in patients with: o C P 1. Presumed cardiogenic shock requiringh mescalating ( F pressor therapy and consideration of mechanical circulatory support; a a n 2. Severe clinical decompensation r M r h in which therapy is limited by uncertain contributions of a and vascular tone; elevated filling pressures,Dhypoperfusion, F 3. and D r Apparent dependence on intravenous inotropic infusions after initial clinical improvement; 4. Persistent severe symptoms despite adjustment of recommended therapies. References 1. Yancy CW, Jessup M, Bozkurt B, et al.; American College of Cardiology Foundation, American Heart Association Task Force on Practice Guidelines. 2013 ACCF/AHA guideline for the management of heart failure: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. J Am Coll Cardiol 2013;62:e147-239. Key Point Invasive hemodynamic assessment via right heart catheterization allows direct measure of the pulmonary capillary wedge pressure and cardiac output, but careful attention to detail when performing this procedure is necessary to obtain reliable information. Related Text Click the title below to read text related to this question in the Heart Failure and Cardiomyopathies chapter/Hemodynamic Assessment module. Invasive Assessment of Hemodynamics Question 5 of 70 A 55-year-old woman is referred by her primary care clinician for dyspnea on exertion. She works as a physical education teacher in the local middle school, and reports shortness of breath this year while demonstrating sports and activities to her classes. She denies chest pain with exertion, palpitations, presyncope, or syncope. She does endorse slight swelling in her feet after a long day, which has been present for 3 years. She has no significant past medical history and takes no medications. On physical examination, her height is 152.4 cm, weight 83.9 kg, body mass index is 36 kg/m2, heart rate is 65 bpm, and blood pressure is 145/84 mm Hg. Physical examination is remarkable for a normal S1 and S2 with a grade 2/6 early peaking systolic murmur o ) appreciated at the right upper sternal border, as well as trace bilateral ankle edema. i a rd Limited echocardiography views are shown (Videos 1, 2, 3). S C o) P d i F C ar d ( SC o o CP m F ah an ( r M rh D r Fa D Video 1 Apical Four-Chamber View  i o ) a rd S C o) P d i F C ar d ( SC o o CP h m Video ( F2 a an Short-Axis View Parasternal r M rh D r Fa D  i o ) a rd S C o) P d i F C ar d ( SC o o CP h m Video( F3 a an Long-Axis View Parasternal r M rh D r Fa Which one of the following mechanisms is most likely responsible for her dyspnea on exertion? D A. Elevated transaortic pressure gradient. B. Elevated transmitral pressure gradient. C. Increased airway reactivity. D. Dynamic left ventricular outflow tract gradient. E. Abnormal ventricular relaxation.  Correct Answer E Commentary The correct answer choice is impaired relaxation. In patients with obesity and reduced exercise tolerance, heart failure with preserved ejection fraction (HFpEF) caused by impaired left ventricular (LV) relaxation and/or increased stiffness should be in the differential diagnosis. This woman also has hypertension, which is often present with HFpEF. The echocardiogram shows preserved LV ejection fraction with LV hypertrophy and left atrial enlargement. Although no measures of LV relaxation are provided among these limited echocardiographic views, the aforementioned findings along with a lack of explanatory valvular pathology are concerning for HFpEF. o ) The aortic valve is clearly trileaflet with good mobility, so an elevated transaortic gradient is i a rd unlikely to be present. Her grade 2/6 early peaking murmur at the right upper sternal border is likely a flow murmur and not due to aortic valvular pathology. There is concentric C o) hypertrophy without narrowing of the left ventricular outflow tract (LVOT) noted on the S P d i parasternal long-axis view, making the presence of a dynamic LVOT gradient unlikely. C ar There is no echocardiographic evidence of mitral stenosis, so a high transmitral gradient is F ( SC not likely. There are no signs or symptoms to suggest reactive airway disease. d References o o CP 1. Pieske B, Tschöpe C, de Boer RA, etm ( Fto diagnose heart failure with preserved ejection fraction: the HFA–PEFF a h al. How n diagnostic algorithm: a consensus recommendation from the Heart Failure Association M a (HFA) ofhthe European Society of Cardiology (ESC). Eur D r Far Heart J 2019;40:3297-317. r Key Point D Patients with heart failure with preserved ejection fraction have true heart failure, defined as increased cardiac and pulmonary filling pressures and vasoconstriction of the systemic and pulmonary circulations. The pathophysiology of this disease appears to be distinct and not merely a continuum with heart failure with reduced ejection fraction. Related Text Click the title below to read text related to this question in the Heart Failure and Cardiomyopathies chapter/Basic Mechanisms and Pathophysiology of Heart Failure module. Heart Failure With Preserved Ejection Fraction Question 6 of 70 A 45-year-old woman is referred to you for shortness of breath. She has shortness of breath that is worse with exertion. She also reports a dry cough and hoarse voice. She takes no medications. She is a life-long nonsmoker. Her vital signs include pulse of 78 bpm, respirations of 14 breaths/min, and blood pressure of 116/80 mm Hg. Physical examination reveals scleral and conjunctival injection. There is a tender rash on the upper arms. There are diminished breath sounds at the right lung base. Cardiac examination is remarkable for an S3 gallop and no murmurs. There is mild (1+) edema of both ankles. i o ) Her electrocardiogram shows sinus rhythm with first-degree atrioventricular delay. Chest X-ray shows bilateral perihilar fullness and ill-defined opacity along the right tracheal a rd border. Echocardiography reveals thinning and akinesis of the basal interventricular septum. S C o) P d i F C ar d Which one of the following is the best next step S C (in the management of this patient? o o FC P m ah an ( A. Cardiac magnetic resonance imaging. B. Pyrophosphate scan. r M r h D rF a C. Metaiodobenzylguanidine scan. D D. Computed tomography pulmonary angiography. E. Gallium-67 scan.  Correct Answer A Commentary Sarcoidosis is a granulomatous disease of unclear etiology that affects multiple organ systems. Pulmonary involvement as suggested by the chest X-ray with bilateral perihilar and right paratracheal lymphadenopathy ("lambda sign"), as in this case, is the most common manifestation, but clinically significant cardiac involvement occurs in ≥5% of cases. Cardiac involvement can be confirmed with cardiac magnetic resonance imaging, which usually shows midmyocardial and epicardial late gadolinium enhancement, particularly in the basal septum and basal lateral wall; T2 imaging can also detect active inflammation in some cases. Positron emission tomography with 18F-fluorodeoxyglucose (FDG-PET) can also confirm active inflammation in a pattern suggestive of sarcoid. i o ) Technetium-99–labeled pyrophosphate scanning can detect transthyretin amyloid in the heart, and there are no features in this patient suggestive of amyloid. 131I- rd methyliodobenzylguanidine was developed for localizing extra-adrenal production of a C o) adrenaline in paragangliomas and may have a role in risk stratification of systolic heart S P d i failure by imaging the adrenergic innervation of the heart but would not confirm or exclude C ar the diagnosis of infiltrative disease. Computed tomography pulmonary angiography would F d ( SC not have had a role in the evaluation of this patient for whom there is suspicion of cardiac sarcoid involvement. Gallium-67 scanning for inflammation imaging was previously used to o o CP confirm pulmonary sarcoid; this has been supplanted by computed tomography and FDG- m F PET, both of which have better sensitivity and specificity as well as lower radiation exposure. ah an ( References r M rh 1. Birnie DH, Nery PB, Ha AC, F a RS. Cardiac sarcoidosis. J Am Coll Cardiol D Beanlands 2016;68:411-21. Dr Key Point Cardiac magnetic resonance imaging may be a useful intermediate step in evaluation of patients with possible inflammatory or infiltrative cardiomyopathy, and may help identify patients who would benefit from endomyocardial biopsy. Related Text Click the title below to read text related to this question in the Heart Failure and Cardiomyopathies chapter/Cardiomyopathies module. Dilated Cardiomyopathy/Primary Causes: Myocarditis Question 7 of 70 A 70-year-old man returns to clinic for routine follow-up of heart failure with reduced ejection fraction (left ventricular ejection fraction of 35%) due to a nonischemic cardiomyopathy. He mentions mild fatigue and dyspnea walking up a flight of stairs. His medications include losartan 50 mg daily, carvedilol 12.5 mg twice daily, furosemide 40 mg daily, and spironolactone 25 mg daily. His examination reveals heart rate of 68 bpm, blood pressure of 122/80 mm Hg, and oxygen saturation of 96% on room air. He has no pulmonary congestion and his cardiac examination is benign except for grade 1-2/6 apical systolic murmur that has been present for a long time. i o ) His creatinine is normal at 0.9 mg/dL and his N-terminal pro–B-type natriuretic peptide is a rd ferritin level is 250 ng/mL minimally elevated at 950 ng/mL. His hemoglobin is 13.6 g/dL, (normal 24-336 ng/mL), and iron saturation 16% (normal S C>20%). o ) A colonoscopy 3 years earlier showed no polyps. P rd i C F Ca ( od CPSfor the management of this patient? Which one of the following would be mostoappropriate a hm n (F A. Intravenous iron sucrose. r M rha B. Transfuse packed redD a blood cells. F C. Oral ferrous sulfate. Dr D. Oral vitamin C. E. Subcutaneous erythropoietin.  Correct Answer A Commentary The correct answer choice is that this patient should receive intravenous (IV) iron sucrose or ferric carboxymaltose until the iron saturation is >20%. Both the 2016 European Society of Cardiology (ESC) Guidelines for the Diagnosis and Treatment of Acute and Chronic Heart Failure and the 2017 American College of Cardiology/American Heart Association/ Heart Failure Society of America (ACC/AHA/HFSA) Focused Update of the 2013 ACCF/ AHA Guideline for the Management of Heart Failure suggest that IV iron therapy should be used when there is New York Heart Association (NYHA) functional class II or III heart failure and either one of the following criteria are met: 1) the ferritin level is 55%), cardiac siderosis (T2