Standardized Procedures and Guidelines for Evidence-Based Practice for Heart Failure Essay

Introduction: Morbidity and Mortality, Etiology, Pathophysiology, and Diagnostic Testing

Heart failure is among the major public health issues worldwide. Approximately 6.3 million adult Americans are currently affected by heart failure (HF) (Wood et al., 2019). Heart failure is also known as congestive heart failure is a condition that results from the inability of the heart muscle to pump blood appropriately. The U.S. and Europe report more than one million patients who develop HF annually. The prevalence and incidence of this condition increase with age. About 20% of the U.S. population is at risk of being diagnosed with this condition at the age of 40 (Long et sl., 2019). The incidence of HF is relatively high among males up to 65 years of age where both genders have equal chances of developing this condition. On average, individuals diagnosed with HF are hospitalized twice annually. Consequently, HF is among the major causes of hospital admission among patients aged 65 years and above in the US. For this reason, the annual medical cost for treating HF is relatively high. The US government spends about $30.7 billion to manage this condition every year. This amount is anticipated to be over $53 billion by 2030 (Long et al., 2019).  The risk of developing heart failure is increased by some pre-existing conditions, including coronary artery disease, high blood pressure, and heart attack among other diseases, which weaken the heart muscle. Additionally, ethnicity is a risk factor for HF. The prevalence of this disease is relatively high among African-Americans compared to other racial groups in the US. African-Americans with HF also register the worst clinical outcomes. Standardized Procedures and Guidelines for Evidence-Based Practice for Heart Failure Essay. The incidence and prevalence of HF are expected to be higher than that of Americans by 2030. About 3% and 3.6% of Americans and African-Americans, respectively are expected to develop HF by the year 2030 (Tillman et al., 2019).

Morbidity and mortality rates are relatively high among Americans with heart failure (HF). HF is one of the deadliest clinical syndromes despite improvement in pharmacology treatments and therapies. The condition is associated with one in eight deaths in the US. Additionally, 20% of total death cases in the country are primarily caused by HF. A steady increase has been reported in the mortality risk following a new diagnosis of HF. The morbidity and mortality rate for individuals diagnosed with HF is increased by various conditions, including renal failure, chronic obstructive pulmonary disease, hypertension, diabetes, coronary artery disease, and kidney failure.

Heart failure is attributed to a wide range of factors, including cardiac conditions, systemic diseases, and hereditary defects. In most cases, individuals diagnosed with HF demonstrate mixed aetiologies that are not mutually exclusive. These aetiologies differ substantially between developed and third-world countries. HF has approximately 17 primary aetiologies. Over two-thirds of all HF cases are associated with four underlying conditions, including ischaemic heart disease, hypertensive heart disease, chronic obstructive pulmonary disease (COPD), and rheumatic heart disease. Chronic obstructive pulmonary disease is mainly responsible for most HF cases. However, the impact of COPD and ischaemic heart disease is relatively low in high-income regions than in low-income areas. Consequently, low-income regions are mainly affected by hypertensive heart disease, cardiomyopathy, myocarditis, and rheumatic heart disease. Other less common etiologies of heart failure include cardiomyopathies, myocarditis, valvular disease, infections, cardiotoxic drugs, systemic toxins, renal disease, male gender, diabetes, older age, and obesity (Long et al., 2019).

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            The primary pathophysiology of heart failure involves a decline in the efficiency of the heart muscle due to damage of valves or overload. Multiple conditions are responsible for these changes. First, myocardial infarction results in the death of the heart muscle due to lack of oxygen. Secondly, hypertension increases the force of contraction, which enables the heart muscle to pump blood. More so, amyloidosis leads to the deposition of misfolded proteins into the heart muscle making it stiff. The increase in workload changes the heart muscle over time making it inefficient in pumping blood (Wright & Thomas, 2018).

The diagnostic testing of heart failure involves conducting various laboratory testing.

A complete blood count is the first laboratory assessment to be conducted. A blood sample is obtained from the patient and analyzed for various important components, including electrolytes (sodium and potassium), albumin, creatinine, and particular biomarkers that might assist to diagnose heart failure (Long et al., 2019). Abnormal results portray a strain on the heart muscle or other body organs, including livers and kidneys, which is caused by heart failure. Secondly, chest x-rays are performed to assess if the heart muscle has been enlarged or the lungs have been congested. Standardized Procedures and Guidelines for Evidence-Based Practice for Heart Failure Essay. Electrocardiogram (ECG) is also obtained rapidly to assess the etiology or precipitating factors of the condition (Long et al., 2019). Finally, cardiac catheterization is performed to view blockages in the coronary arteries or narrowed arteries, which might be damaged or weakened due to lack of blood.

Clinical Presentation related to Objective and Subjective Findings

Heart failure is characterized by typical symptoms, which are evident in objective and subjective findings. Objective findings of a patient suspected of heart failure reveal shortness of breath (dyspnea). The patient experience short of breath especially upon lying down or exerting oneself (Reddy & Borlaug, 2020). An individual also complains of fatigue, weakness, and exercise intolerance. Exercise capacity is limited by excessive tiredness and lack of adequate blood in the muscles. Muscle fatigue and dyspnea in patients with heart failure are caused by abnormalities in peripheral blood flow, skeletal muscle, endothelial function, and lung function. Additionally, extreme tiredness occurs due to the inability of the heart to supply the muscles with enough blood. Moreover, swelling (edema) in the legs, feet, and ankles is reported (Long et al., 2019). Patients reveal that a thumb leaves a dent in case it’s pressed against the flesh due to retention of fluid. Some patients also report unintentional weight loss due to reduced appetite following a buildup of fluid in the liver and gut. Retained fluids make one feel full or bloated. Palpitations are also reported by some patients who are suspected to have HF. An individual claims that he or she can feel the heart beating faster than normal. Finally, some patients claim to experience lightheadedness or dizziness due to the inability of the heart muscle to pump adequate blood to the head.

Furthermore, clinical presentations of heart failure are revealed in subjective findings. A healthcare provider notices refractory volume overload during physical examination. Recurrent ventricular arrhythmias, hypotension, and some signs of inadequate perfusion such as low pulse pressure are noted during the examination. Palpitations are also noticed during the examination. In addition to physical examination, diagnostics reveal clinical symptoms of HF. Enlargement of the heart muscle or congestion of the lungs is revealed by chest x-ray. Blockages in the coronary arteries or narrowed arteries are also seen during cardiac catheterization.

Diagnostic Criteria and Management

Diagnostic Criteria

The diagnostic criteria for heart failure involve taking a patient’s medical history, physical examination, and laboratory testing. The healthcare practitioner starts by taking the medical history and symptoms of a patient with suspected AHF. Physical examination involves taking a patient’s blood pressure, weight, and listening to the heart and lungs using a stethoscope. However, the history and physical examination of patients with HF varies significantly due to the complex pathophysiology. In most cases, individuals diagnosed with HF vary in various aspects, including the structure and functioning of the heart muscle, the heart failure’s etiology, comorbidities, the precipitant of the AHF exacerbation, and current medications. These variations are likely to result in misdiagnosis in case diagnosis is delayed leading to adverse outcomes or death. About one-third of patients with HF are misdiagnosed upon initial presentation. Although the likelihood of HF cannot be reduced by a single examination finding or historical factor, initial clinical gestalt has reported sensitivity and specificity of 61% and 86%, respectively for the diagnosis (Long et al., 2019). Standardized Procedures and Guidelines for Evidence-Based Practice for Heart Failure Essay.

Significant diagnostic and prognostic information for a patient with suspected HF is gathered through laboratory assessment in which multiple tests are performed. A complete blood count is the first laboratory assessment to be conducted. A blood sample is obtained from the patient and analyzed for various important components, including electrolytes (sodium and potassium), albumin, creatinine, and particular biomarkers that might assist to diagnose heart failure (Long et al., 2019). Abnormal results portray a strain on the heart muscle or other body organs, including livers and kidneys, which is caused by heart failure. Secondly, chest x-rays are performed to assess if the heart muscle has been enlarged or the lungs have been congested. Electrocardiogram (ECG) is also obtained rapidly to assess the etiology or precipitating factors of the condition (Long et al., 2019). Moreover, cardiac catheterization is performed to view blockages in the coronary arteries or narrowed arteries, which might be damaged or weakened due to lack of blood. In other words, this test indicates the efficiency of the heart muscle in pumping blood. An echocardiogram (echo) is also performed to assess the capacity of the heart muscle to relax and pump blood. Additionally, this ultrasound reveals the condition of the heart valves and how the blood flows across them, and variations in pressure inside heart chambers. Another test that is conducted is the Multigated Acquisition Scan (MUGA scan) to evaluate the efficiency of the lower chambers of the heart muscle (ventricles) in pumping blood. Finally, the stress test is performed to assess how the heart reacts to stress.

Management

            The management of heart failure includes both clinical preventive services and treatment plans.

 Clinical Preventive Services

Clinical preventive services involve advising individuals to practice healthy living. First, people are advised to check their diet. The building up of fluids in the body is caused by excess salt (sodium). Consequently, the heart muscle works harder while pumping blood to other body parts leading to heart failure. Some clinical symptoms of HF, including shortness of breath and edema, are caused by excess fluids. Therefore, avoiding excess salt will prevent fluid from building up in the body, thus reducing the possibility of developing heart failure. In addition to salt, one should limit the intake of calories and carbohydrates to avoid becoming overweight. According to Wali et al. (2020), the risk of cardiovascular disease and diabetes is increased by a high intake of fats. These conditions, in turn, increases the risk of heart failure. Secondly, individuals are advised to stay active. Exercises enable the heart muscle to work efficiently. Thus, one should engage in various aerobic activities, including walking, jogging, and, running to reduce the chances of heart failure. Moreover, individuals are advised to quit smoking. Blood vessels are damaged by smoking, thus reducing the amount of oxygen the blood making the heart muscle to beat too fast and work harder to pump blood, which might result in heart failure. Individuals are also advised to avoid emotions, which is likely to strain the heart making it work harder leading to heart failure. Persons should also keep a track of body weight to avoid becoming overweight. The heart works harder to pump blood when a person is overweight increases the risk of HF.

Treatment Plan

The evidence-based treatment plan for heart failure includes lifestyle modifications, pharmacological treatment, and procedures. Lifestyle changes include regular exercise to burn excess calories and exercise the heart muscle, quitting smoking, effective management of high blood pressure through medication, active lifestyle, and low-sodium diet, managing obesity by avoiding high cholesterol and avoiding taking alcohol or other illegal drugs.

Secondly, pharmacotherapy treatment for this condition is based on neurohumoral inhibition of the adrenergic system and the renin-angiotensin-aldosterone system (Berliner et al., 2020). This pharmacological treatment involves the use of various medications. Renin-angiotensin-aldosterone system inhibitors (RAASi) are the primary pharmacological treatment for heart failure (Fonseca et al., 2020). This medication is prescribed to the patients to minimize strain on the heart and reduce blood pressure improving blood flow. It is usually preferred over ACE inhibitors due to their efficacy and safety (Burnett et al., 2017). Also, ACE inhibitors are prescribed to patients with heart failure to minimize strain on the heart and reduce blood pressure. Consequently, the heart pumps blood efficiently improving blood flow. Moreover, a diuretic is prescribed to eliminate excess fluid from the body to reduce swelling of the feet and the ankles. According to Lee et al. (2019), a diuretic is primarily prescribed to patients diagnosed with edema to eliminate excess fluid from the body, thus reducing the swelling. Standardized Procedures and Guidelines for Evidence-Based Practice for Heart Failure Essay. Digoxin is also prescribed to enable the heart to pump more blood with every beat, thus facilitating the movement of oxygenated blood throughout the body. Besides, an aldosterone antagonist is given in case of advanced heart failure to alter hormones, which damage the heart, thus preventing it from straining.

Lastly, different procedures are performed depending on the detected cause of heart failure. For instance, valve disease or coronary artery disease procedures are performed in case of artery and valve problems to improve blood flow. Bypass surgery is also performed to allow blood to flow inside a clogged artery (Crespo‐Leiro et al., 2018). Another surgery performed in case of this problem is valve surgery. This procedure is conducted to replace or repair faulty valves to facilitate the proper flow of blood. On the other hand, particular devices are utilized in treating rhythm problems. These gadgets are usually attached to the heart to improve a slow or regulate an abnormal heart rhythm. This prevents the heart from straining while pumping blood.

References

Berliner, D., Hänselmann, A., & Bauersachs, J. (2020). The Treatment of Heart Failure with Reduced Ejection Fraction. Deutsches Aerzteblatt International, 117(21), 376–385. https://doi.org/10.3238/arztebl.2020.0376

Burnett, H., Earley, A., Voors, A. A., Senni, M., McMurray, J. J., Deschaseaux, C., & Cope, S. (2017). Thirty years of evidence on the efficacy of drug treatments for chronic heart failure with reduced ejection fraction: a network meta-analysis. Circulation: Heart Failure, 10(1), e003529.

Crespo‐Leiro, M. G., Metra, M., Lund, L. H., Milicic, D., Costanzo, M. R., Filippatos, G., … & Ruschitzka, F. (2018). Advanced heart failure: a position statement of the Heart Failure Association of the European Society of Cardiology. European journal of heart failure, 20(11), 1505-1535.

Fonseca, C., Brito, D., Branco, P., Frazão, J. M., Silva-Cardoso, J., & Bettencourt, P. (2020). Hyperkalemia and management of renin-angiotensin-aldosterone system inhibitors in chronic heart failure with reduced ejection fraction: A systematic review. Revista Portuguesa de Cardiologia (English Edition), 39(9), 517–541. https://doi.org/10.1016/j.repce.2020.03.010

Lee, G., Cho, J. H., Son, C. G., & Lee, N. (2019). Successful treatment of refractory edema with traditional herbal medicine: A case report. Medicine, 98(41).

Long, B., Koyfman, A., & Gottlieb, M. (2019). Diagnosis of Acute Heart Failure in the Emergency Department: An Evidence-Based Review. The Western Journal of Emergency Medicine, 20(6), 875–884. https://doi.org/10.5811/westjem.2019.9.43732.

Reddy, Y. N. V., & Borlaug, B. A. (2020). Heart Failure with Preserved Ejection Fraction: Where Do We Stand? Mayo Clinic Proceedings, 95(4), 629+. https://link.gale.com/apps/doc/A623573459/ITBC?u=uphoenix&sid=ITBC&xid=d07e5377

Tillman, F., Kim, J., Makhlouf, T., & Osae, L. (2019). A comprehensive review of chronic heart failure pharmacotherapy treatment approaches in African Americans. Therapeutic advances in cardiovascular disease, 13, 1753944719840192.

Wali, J. A., Jarzebska, N., Raubenheimer, D., Simpson, S. J., Rodionov, R. N., & O’Sullivan, J. F. (2020). Cardio-Metabolic Effects of High-Fat Diets and Their Underlying Mechanisms—A Narrative Review. Nutrients, 12(5), 1505.

Wood, R. L., Migliore, L. A., Nasshan, S. J., Mirghani, S. R., & Contasti, A. C. (2019). Confronting Challenges in Reducing Heart Failure 30-Day Readmissions: Lessons Learned with Implications for Evidence-Based Practice. Worldviews on Evidence-Based Nursing, 1, 43. https://doi.org/10.1111/wvn.12336. Standardized Procedures and Guidelines for Evidence-Based Practice for Heart Failure Essay.

Wright, P & Thomas, M. (2018). Pathophysiology and management of heart failure. The Pharmaceutical Journal. https://www.pharmaceutical-journal.com/cpd-and-learning/cpd-article/pathophysiology-and-management-of-heart-failure/20205742.cpdarticle?firstPass=false

Background: Chronic congestive heart failure is a common condition that, if untreated, markedly impairs the quality of life and is associated with a high risk of recurrent hospitalization and death. Methods: This review is based on articles retrieved by a selective search in PubMed, as well as on relevant guidelines. Results: Evidence-based treatment options are available only for congestive heart failure with a low ejection fraction. Pharma – cotherapy is based on neurohumoral inhibition of the renin-angiotensin-aldosterone system and the adrenergic system. The prognosis of patients with this condition has been further improved recently through the introduction of combined angiotensin receptor antagonists and neprilysin inhibitors. Modern implantable devices are a further component of treatment. Implantable defibrillators and special pacemakers for cardiac resynchronization are well established; the utility of alternative devices (baro – reflex modulation or cardiac contractility modulation) needs to be investigated in further studies. It was recently shown that the catheter-based treatment of secondary mitral regurgitation with a MitraClip improves the outcome of selected patients. Conclusion: The treatment of chronic systolic heart failure as recommended in the relevant guidelines, with drugs and implanted devices if indicated, can significantly improve the clinical outcome. Cite this as: Berliner D, Hänselmann A, Bauersachs J: The treatment of heart failure with reduced ejection fraction. Dtsch Arztebl Int 2020; 117: 376–86. DOI: 10.3238/arztebl.2020.0376 Chronic heart failure is one of the most frequent causes of death and reasons for hospitalization in industrialized countries. If left untreated, patients have a poor prognosis (1). The introduction of new drugs and the rigorous implementation of evidence-based recommendations in the guidelines on heart failure has led to a reduction in recent years in mortality and frequency of hospitalizations in patients with heart failure and reduced ejection fraction (HFrEF) (2). In addition, established devices such as implantable defibrillators and resynchroni – zation therapy have improved patients‘ symptoms and prognosis. Newer devices are currently being investigated in studies or have already shown early success in smaller studies. The aim of this article is to provide an overview of current drug therapy while taking into account new treatment approaches as well as to outline the possibilities presented by various device-based treatments. Department of Cardiology and Angiology, Hannover Medical School: Dr. med. Dominik Berliner, Dr. med. Anja Hänselmann, Prof. Dr. med. Johann Bauersachs Learning objectives After reading this article, the reader should: ● Be familiar with the problem of the rising prevalence and, if left untreated, poor prognosis of the syndrome of heart failure ● Be able to name current drug therapies used to treat heart failure ● Be familiar with the most important device-based treatments and their indications. Method A selective literature search was conducted in an international database (PubMed). The authors took into consideration the current guidelines of the European Society of Cardiology (ESC) and the German Cardiac Society (Deutsche Gesellschaft für Kardiologie, DGK), as well as the German national treatment Prevalence Heart failure is common: The prevalence of heart failure in the western world is approximately 1–2%. Different types of heart failure A distinction needs to be made between three different types of heart failure depending on left ventricular ejection fraction. 376 Deutsches Ärzteblatt International | Dtsch Arztebl Int 2020; 117: 376–86 MEDICINE guideline (Nationale Versorgungsleitlinie, NVL) on heart failure.Standardized Procedures and Guidelines for Evidence-Based Practice for Heart Failure Essay.  Epidemiology The prevalence of heart failure in western industrialized nations is around 1–2% and increases steadily with advancing age—from below 1% in under 55-year-olds to approximately 10% in over 80-year-olds (3). Due to changes in age structure, a significant increase in the prevalence of heart failure is forecast in the coming years—accompanied by the anticipated economic consequences. The prognosis of affected patients is poor: approximately 50% of patients diagnosed with heart failure die within 5 years (e1). European data from the ESCHF pilot study show a 17% overall mortality rate and 44% rehospitalization rate in the first 12 months following hospital stay (4). Pharmacological treatment approaches A distinction is made between three different types of heart failure depending on left ventricular ejection fraction (LVEF) (Table 1) (2). All types of heart failure are associated with a reduction in stroke volume and cardiac output. There is differing evidence to support the treatment of the various types. Due to a lack of studies, the current ESC recommendations provide no clear recommendations on the treatment of patients with heart failure with mid-range ejection fraction (HFmrEF). There are analyses based only on post-hoc analyses from studies on HFrEF and/or HFpEF (heart failure with preserved ejection fraction, [diastolic heart failure]) using subgroup analyses of patients that are now classified as HFmrEF (5). Furthermore, no treatment strategy in HFpEF patients has shown a significant improvement in prognosis as yet. Other studies, particularly in relation to the latter, are currently underway and their results are eagerly awaited. In everyday routine, HFpEF patients are often prescribed the same drugs as patients with HFrEF, for which, however, there is no scientific basis, given that the evidence is neutral. Nevertheless, HFmrEF patients appear to benefit from beta- blockers and renin-angiotensin-aldosterone system (RAAS) blockade (5). There are clear recommendations on HFrEF treatment that have been demonstrated in numerous randomized studies and which are therefore evidence-based. As a result of the reduced ejection fraction and reduced stroke volume, a “vicious circle” is set in motion (Figure 1). The goal of pharmacological management of HFrEF, as well as that of some devices, is to interrupt these harmful maladaptive processes (e2). Prognosis The prognosis of affected patients is poor: Approximately 50% of patients diagnosed with heart failure die within 5 years. Evidence-based treatments Evidence-based treatments are available only for heart failure with reduced ejection fraction (HFrEF). TABLE 1 Classification and frequency of the different types of heart failure according to the extent of left ventricular dysfunction*1 * 1 Modified from (2, e23) * 2 From numerous randomized studies ESC, European Society of Cardiology; HF, heart failure; LAE, left atrial enlargement; LVEF, left ventricular ejection fraction; LVH, left ventricular hypertrophy Abbreviation HFrEF HFmrEF HFpEF Description HF with reduced ejection fraction HF with mid-range ejection fraction HF with preserved ejection fraction Frequency in the ESC Heart Failure Long Term Registry (e22) 59.8% 24.2% 16% Characteristics Symptoms Symptoms ± signs Symptoms ± signs Symptoms ± signs LVEF <40% 40–49% ≥ 50% Other criteria 1. Elevated serum levels of natriuretic peptides 2. At least one additional criterion: a) Relevant structural heart disease (LVH and/or LAE) b) Diastolic dysfunction 1. Elevated serum levels of natriuretic peptides 2. At least one additional criterion: a) Relevant structural heart disease (LVH and/or LAE) b) Diastolic dysfunction Evidencebased therapy +*2 – – Deutsches Ärzteblatt International | Dtsch Arztebl Int 2020; 117: 376–86 377 MEDICINE The basic principle here—besides treating the underlying cause (for example, by means of revascularization or heart valve surgery)—is neurohumoral inhibition by means of ACE inhibitors, angiotensin II receptor blockers (ARB), or angiotensin receptor neprilysin inhibitors (ARNI), as well as mineralocorticoid receptor antagonists (MRA) and beta-blockers. Numerous randomized studies have demonstrated the efficacy of these treatment approaches (2). The basis of drug therapy Treatment with ACE inhibitors and beta-blockers has led to a significant improvement in the prognosis of heart failure patients. What is important is to appropriately increase the dose to the respective target dose. A large European study (BIOSTAT-CHF) only recently demonstrated once again the prognostic relevance of appropriate dosing of ACE inhibitors and beta-blockers (6). ARB represent an alternative for patients unable to tolerate ACE inhibitors due to cough or angioedema. Table 2 provides an overview of the effects of heart failure treatment. The treatment is supported by diuretic therapy tailored to the patient‘s symptoms. The prognostically beneficial effect of MRA is also established—not only in patients with severe symptoms using spironolactone (NYHA III–IV [7]), but also in those with less severe symptoms using eplerenone (NYHA II [8]). According to the current guidelines, all patients with an LVEF ≤ 35% that remain symptomatic under treatment with an ACE inhibitor as well as a beta-blocker should receive an MRA (2) (Figure 2). Compared to eplerenone, spironolactone is a non-selective MRA that also activates progesterone and androgen receptors and can therefore lead to gynecomastia, impotence, and menstrual disorders (9). Furthermore, since the blood pressurelowering effect of spironolactone is stronger than that of eplerenone, the latter can be preferentially used in the case of low blood pressure. Treatment with the direct renin inhibitor aliskiren is not recommended in heart failure treatment, since it has not been demonstrated to be superior to ACE inhibitors (2, e3, e4). Angiotensin receptor neprilysin inhibitors Angiotensin receptor neprilysin inhibitors (ARNI) combine the established inhibition of the renin–angiotensin–aldosterone system (RAAS) with inhibition of the degradation of endogenously released natriuretic peptides. Natriuretic peptides are released upon cardiomyocyte hypertrophy and cause an increase in intracellular cyclic guanosine monophosphate (cGMP), natriuresis, as well as a reduction in renal renin secretion and a weakening of the angiotensin II-induced hypertrophic signal transduction in cardiomyocytes (e5). The only substance available in this drug group is the combination comprising the angiotensin II receptor blocker valsartan and the neprilysin inhibitor sacubitril. Neprilysin (synonym, neutral endopeptidase [NEP]) breaks down natriuretic peptides and various other vasoactive substances (for example, bradykinin, endothelin-1, and adrenomedullin). The PARADIGM-HF study on patients with symptomatic HFrEF (NYHA II–IV; LVEF ≤ 40%, modified during the course of the study to ≤ 35%) and elevated levels of natriuretic peptides, compared sacubitril/valsartan therapy with treatment using the ACE inhibitor enalapril (10). Sacubitril/valsartan therapy resulted in a significant reduction in the primary endpoint of cardiovascular mortality and hospitalization due to heart failure (21.8% versus 26.5%). In addition, cardiovascular mortality (13.3% versus 16.5%), overall mortality (17.0% versus 19.8%), and The basis of drug therapy Treatment with ACE inhibitors and beta-blockers remains the basis of heart failure therapy. The drug aliskiren Aliskiren is not recommended in the treatment of heart failure. FIGURE 1 Simplified representation of the vicious circle in heart failure ultimately responsible for the disease‘s poor prognosis. The aim of drug therapy as well as device-based therapy is to stop or interrupt this downward spiral. Standardized Procedures and Guidelines for Evidence-Based Practice for Heart Failure Essay. Activation of structural, neurohumoral, cellular, and molecular mechanisms Worsening of cardiac function Volume overload Sympathetic activity ↑ Cardiac remodeling Inflammation Reduced stroke volume 378 Deutsches Ärzteblatt International | Dtsch Arztebl Int 2020; 117: 376–86 MEDICINE Achieving target doses Achieving target doses of ACE inhibitors and beta-blockers is prognostically relevant. Mineralocorticoid receptor antagonists In the case of persistent symptoms (NYHA ≥ II) and LVEF ≤ 35% despite ACE inhibitor and beta-blocker therapy, treatment should be complemented by a mineralocorticoid receptor antagonist. TABLE 2 Effects and typical side effects of the various heart failure drugs*1 * 1 In combination with ACE inhibitors, *2 vs ACE inhibitors, *3 the mentioned side effects relate to the results of the DAPA-HF study (dapagliflozin vs. placebo in addition to an existing pharmacological heart failure treatment); modified from (10, 13, 21, e24–e26, 38) ARNI, angiotensin receptor neprilysin inhibitors; CI, confidence interval; HR, hazard ratio; MRA, mineralocorticoid receptor antagonists, NNT, number needed to treat; SGLT2, sodium-glucose linked transporter 2 Drugs ACE inhibitors (e25, 38) Angiotensin receptor blocker (e25, 38) Beta-blockers (e25, 38) MRA (e25, 38) If channel blockers (e24) ARNI (10, e26) SGLT2 inhibitors (21)*3 Overall mortality HR [95% CI] 0.84 [0.67; 1.01] 0.89 [0.61; 1.27] 0.58 [0.34; 0.95] 0.58 [0.36; 0.90]*1 0.96 [0.87; 1.05] 0.84 [0.76; 0.93]*2 0.83 [0.71; 0.97] NNT for mortality (standardized for 36 months) 26 9 6 NA 35*2 22 Heart failurerelated hospitalizations HR [95% CI] 0.52 [0.32; 0.76] 0.53 [0.26; 1.03] 0.45 [0.13; 1.39] 0.36 [0.12; 0.96]*1 0.81 [0.73; 0.89] 0.79 [0.71; 0.89]*2 0.70 [0.59; 0.83] Typical side effects Impaired renal function, hyperkalemia, hypotension, cough, angioedema Impaired renal function, hyperkalemia, hypotension Bradycardia, hypotension, impaired peripheral perfusion, bronchoconstriction Hyperkalemia, impaired renal function, hypotension (primarily spironolactone); gynecomastia, impotence, menstrual disorders (spironolactone) Symptomatic bradycardia, impaired vision (phosphenes, blurred vision), atrial fibrillation Impaired renal function, hyperkalemia, hypotension, angioedema Genital infections, urinary tract infections, hypoglycemia (when combined with sulfonyl – ureas or insulin), diabetic ketoacidosis, dysuria, polyuria, volume depletion Typical active substances Captopril Enalapril Lisinopril Ramipril Trandolapril Candesartan Losartan Valsartan Bisoprolol Carvedilol Metoprolol succinate Nebivolol Eplerenone Spironolactone Ivabradine Sacubitril/ valsartan Dapagliflozin Empagliflozin Initial daily dose 3 × 6.25 mg 2 × 2.5 mg 1 × 2.5–5.0 1 × 2.5 mg 1 × 0.5 mg 1 × 4–8 mg 1 × 50 mg 2 × 40 mg 1 × 1.25 mg 2 × 3.125 mg 1 × 12.5–25 mg 1 × 1.25 mg 1 × 25 mg 1 × 25 mg 2 × 5 mg 2 × 49/51 mg 1 × 10 mg 1 ×10 mg (increasing if appropriate to 1 × 25 mg) Target daily dose 3 × 50 mg 2 × 10–20 mg 1 × 20–35 mg 1 × 10 mg 1 × 4 mg 1 × 32 mg 1 × 150 mg 2 × 160 mg 1 × 10 mg 2 × 25 mg 1 × 200 mg 1 × 10 mg 1 × 50 mg 1 × 50 mg 2 × 7.5 mg 2 × 97/103 mg – Deutsches Ärzteblatt International | Dtsch Arztebl Int 2020; 117: 376–86 379 MEDICINE heart failure-related hospitalizations (12.8% versus 15.6%) were significantly improved (10). Subanalyses of the study also show that sacubitril/ valsartan reduced the frequency of heart-failure– related rehospitalizations and significantly improved quality of life (e6). In addition, the rate of ventricular arrhythmias was lower in an observational study (e7). More recently, another observational study, the PROVE-HF trial, demonstrated a positive effect on cardiac remodeling (e8). The current ESC guidelines recommend sacubitril/valsartan for all patients (class IB recommendation) that would have fulfilled the inclusion criteria and that remain symptomatic despite treatment with an ACE inhibitor or ARB, a betablocker, and an MRA (2) (Figure 2 and Box). Typical side effects of sacubitril/valsartan therapy compared to the comparison substance in the PARADIGM-HF study, enalapril, include the onset of (symptomatic) hypotension, whereas an elevated serum potassium levels as well as increased retention values were more often found with enalapril (10). Hyperkalemia as a relevant side effect—which, under RAAS inhibitors, often prevents the uptitration of heart failure medication in clinical routine—could be treated in future with potassium binders such as patiromer. However, further studies are required here in order to demonstrate that patiromer is associated with an improvement in prognosis in the treatment of heart failure. Less is more: heart rate monitoring As a result of the reduced cardiac output due to the reduced ejection fraction, the heart rate increases as a reflex. In heart failure patients, an elevated heart rate leads to less economical ventricular function and has been repeatedly associated with a poorer prognosis (e9). Treatment with the If channel blocker ivabradine is able to achieve a rate reduction in patients in sinus rhythm without the blood pressure-lowering effect of beta-blockers. In the SHIFT study, treatment with ivabradine, in addition to the guideline-based heart failure therapy including beta-blockers, resulted in: ● A significant reduction in heart failure-related hospitalizations and cardiovascular mortality (hazard ratio [HR]: 0.82; 95% confidence interval [0.75; 0.90]) (11) ● An improved quality of life (e10) ● An improvement in left ventricular function and a reduction in left ventricular volume (12). The combined primary endpoint of the SHIFT study was largely driven by the reduction in hospitalizations (Table 2). The current ESC guidelines (national treatment guideline) recommend treatment with ivabradine for HFrEF patients (LVEF ≤ 35%) in sinus rhythm with a heart rate of ≥ 70 (≥ 75) beats/min that remain symptomatic despite therapy with an ACE inhibitor or angiotensin II receptor blocker, a beta-blocker, and a mineralocorticoid receptor antagonist (2, 13) (Figure 2). Standardized Procedures and Guidelines for Evidence-Based Practice for Heart Failure Essay. Still unclear: the value of cardiac glycosides Although cardiac glycosides have long been used in heart failure, their role is unclear and they are classified in the ESC guidelines as well as the German national Sacubitril/valsartan compared to the ACE inhibitor enalapril In the PARADIGM-HF study, sacubitril/valsartan led to a significant reduction in mortality and hospitalization rates compared to the ACE inhibitor enalapril. Heart rate monitoring An elevated heart rate is associated with a poorer prognosis. BOX Treatment recommendations for routine practice ● Switch ACE inhibitor to angiotensin receptor neprilysin inhibitor sacubitril/valsartan When switching an ACE inhibitor to the angiotensin receptor neprilysin inhibitor sacubitril/valsartan, ACE inhibitor use needs to be discontinued at least 36 h before the first use of sacubitril/valsartan. The background to this is that both substances—neprilysin and ACE—degrade bradykinin. Therefore, in principle, the simultaneous use of ACE inhibitors and sacubitril can lead to an accumulation of bradykinin and, thus, to angioedema. An angiotensin II receptor blocker can be directly swapped for sacubitril/valsartan. ● Important to note with digoxin Due to the narrow therapeutic range in patients with impaired renal function, the use of digitoxin should be preferred in this patient group, since digoxin is excreted primarily via the kidneys. Serum levels should be determined 4–6 weeks following initiation of treatment with cardiac glycosides (39). In general, doses should be lower than those commonly previously used (i.e., digoxin 0.1–0.2 mg/day, digitoxin 0.05–0.07 mg/day) (40). Target level: Digoxin: 0.5–0.9 ng/mL Digitoxin: 8–18 ng/mL ● Indication for cardiac resynchronization therapy For the indication to cardiac resynchronization therapy, the current ESC guidelines on the treatment of heart failure (2) give a: – Class I recommendation for patients with a left bundle branch block (LBBB) and a QRS duration of ≥ 150 ms (IA) or 130–149 ms (IB) – Class II recommendation for patients with non-LBBB morphology – Class III recommendation (contraindication) for patients with a QRS duration of <130 ms 380 Deutsches Ärzteblatt International | Dtsch Arztebl Int 2020; 117: 376–86 MEDICINE treatment guideline on heart failure as a “back-up drug” in advanced symptomatic heart failure under existing optimal drug therapy (2, 13). The only large ran – domized study, the DIG trial (14), on digoxin in heart failure patients was deemed neutral, since the primary endpoint of overall mortality was not affected by the treatment; however, heart failure-related hospitali – zations and mortality were significantly reduced. Subgroup analyses showed a mortality benefit for patients with low serum digoxin levels compared to patients with high levels (15). A meta-analysis on the studies available to date on digitalis in heart failure revealed that treatment with digitalis reduces hospitalizations and improves the symptoms of heart failure (16). In older, multimorbid patients with reduced renal function, digoxin poses the risk of accumulation and possible toxicity. The alternative cardiac glycoside, digitoxin, is less dependent on renal function and appears to be beneficial in patients with reduced renal function (Box). A large randomized study to investigate the role of digitoxin in heart failure patients in addition to a modern, up-to-date drug therapy is currently underway: the DIGIT-HF study (DIGitoxin to Improve ouTcomes in patients with advanced chronic Heart Failure, EudraCT-Nr.: 2013-005326-38) (17). Treating comorbidities The comorbidities of heart failure warrant particular attention. For example, iron deficiency reduces physical capacity and is associated with a poorer prognosis (18). In proven iron deficiency (ferritin <100 mg/L or ferritin 100–299 μg/L and transferrin saturation <20%), iron replacement therapy even in the absence of anemia led to improved quality of life and physical capacity (19, 20). The current guidelines recommend intravenous iron therapy in symptomatic patients with heart failure and confirmed iron deficiency (2). The FAIRHF2-DZHK5 study is currently investigating the prognostic effect of iron therapy on mortality and hospitalizations. The SGLT2 inhibitors (sodium-glucose linked transporter 2) are a highly promising drug group in patients with heart failure with and without diabetes mellitus. The 2016 ESC guideline stated that empagliflozin should be considered in patients with type 2 diabetes in order to prevent or delay the onset of heart failure. This recommendation was recently expanded to include the alternative SGLT2 inhibitors canagliflozin and dapagliflozin (5). The results of the DAPA-HF study have also been presented, showing a The value of cardiac glycosides The value of cardiac glycosides in the treatment of heart failure has not been fully elucidated as yet; they are used especially in patients with atrial fibrillation and high ventricular rate. Primary prevention defibrillator implantation In symptomatic patients with an LVEF ≤ 35% defibrillator implantation is recommended in order to prevent sudden cardiac death. FIGURE 2 Overview of drug therapy and possible device-based therapies for heart failure with reduced systolic left ventricular function (HFrEF) (modified from [2, e27]). To treat symptoms, diuretic therapy should be additionally used, as well as implantation of a cardioverter- defibrillator due to the risk of malignant cardiac arrhythmia in persistently reduced left ventricular function (LVEF <35%). In the case of intolerance due to cough, an ACE inhibitor should be swapped for an angiotensin receptor blocker. Color denotes the level of recommendation: green, class I recommendation; yellow, class II recommendation; gray, no clear level of recommendation in the 2016 ESC guidelines *Consider therapy ARB, angiotensin II receptor blocker; ARNI, angiotensin receptor neprilysin inhibitor; BAT, baroreflex modulation therapy; CCM, cardiac contractility modulation; CRT, cardiac resynchronization therapy; HF, heart rate; HTx, heart transplantation; LBBB, left bundle branch block; LVAD, left ventricular assist device; LVEF, left ventricular ejection fraction; MRA, mineralocorticoid receptor antagonist; non-LBBB, non-left bundle branch block; NYHA, New York Heart Association class Devices CCM/BAT* Patient with symptomatic HFrEF NYHA ≥ II LVEF ≤ 35% Treatment with ACE inhibitors and beta-blockers Administration of MRA NYHA ≥ II LVEF ≤ 35% ACE inhibitors/ARB well tolerated at a sufficient dose Sinus rhythm HR > 70/min QRS <130 ms QRS ≥ 130 ms Non-LBBB LBBB Digitalis LVAD HTx In the case of persistent heart failure, check other therapeutic options CRT Check ARNI Ivabradine Deutsches Ärzteblatt International | Dtsch Arztebl Int 2020; 117: 376–86 381 MEDICINE significant reduction in mortality and heart failure- related hospitalizations in HFrEF patients under dapagliflozin treatment irrespective of the presence of diabetes (HR 0.74; [0.65; 0.85]; p <0.001) (Table 2) (21). Novel treatment approaches Two new treatment approaches in chronic heart failure include vericiguat, a stimulator of soluble guanylatcyclase (sGC), and omecamtiv mecarbil, a myosine activator. In the recently published VICTORIA study, the primary composite endpoint of death from cardio – vascular causes and heart failure-related hospitalization was significantly reduced in HFrEF patients under vericiguat treatment (HR 0.90; [0.82; 0,98]; p = 0.02) (e11). For omecamtiv mecarbil, further studies are still required to demonstrate its value in current modern heart failure therapy. The results of the GALACTICHF study on the relevance of omecamtiv mecarbil in HFrEF are expected in 2021. Devices in the treatment of heart failure Implantable cardioverter-defibrillators To avoid sudden cardiac death, primary prevention defibrillator therapy (implantable cardioverter- defibrillator [ICD]) is recommended in patients with LVEF ≤ 35% despite optimized drug therapy (2, 22). For optimally treated patients (including cardiac resynchronization therapy) with non-ischemic heart failure, the DANISH study showed no significant difference in relation to all-cause mortality (21.6% versus 23.4%; HR 0.87; [0.68; 1.12], p = 0.28) (23), whereas the onset of sudden cardiac death was significantly reduced (4.3% versus 8.2%; HR 0.50; [0.31; 0.82], p = 0.005). However, in a subgroup analysis, a significant survival benefit was demonstrated for patients ≤ 70 years also in terms of all-cause mortality (HR 0.70; [0.51; 0.96], p = 0.03) (24). The authors of the German national treatment guideline on heart failure do not infer from this “a specific recommendation for the use of implantable cardioverter-defibrillators in the primary prevention indication in patients with non-ischemic cardiomyopathy,” but instead recommend “establishing an individual indication by appropriately specialized cardiologists” (13). In patients with advanced heart failure (NYHA class IV) to whom therapeutic options such as resynchronization therapy, a left-ventricular assist device (LVAD), or transplantation are not available, implantation of a cardioverter-defibrillator is currently not recommended (22). Standardized Procedures and Guidelines for Evidence-Based Practice for Heart Failure Essay. This needs to be discussed critically with the patient and their relatives. As a bridging measure, i.e., as protection against malignant arrhythmias during the optimization phase of drug therapy, a wearable defibrillator can be prescribed in the first months (25). Cardiac resynchronization therapy In patients with heart failure, a left bundle branch block (LBBB) causes intraventricular (between the interventricular septum and the posterolateral left ventricular wall), as well as an interventricular (between the right and left ventricle) dyssynchrony. This worsens ventricular remodeling, cardiac output per minute, and existing functional mitral insufficiency. Cardiac resynchronization therapy (CRT) using specialized pacemaker systems equipped with an additional left ventricular lead implanted in the coronary sinus makes it possible to resolve or reduce this dyssychrony. This achieved an improvement in heart failure symptoms and physical capacity, as well as having a positive effect on cardiac remodeling (e12, e13, 26) and positive effects on heart failure-related hospitalizations and mortality (HR 0.63; [0.51; 0.77]; p <0.001) in the CARE-HF study (CRT) compared to optimal drug therapy; (HR 0.66; [0.52; 0.84]; p <0.001) in the MADIT-CRT study (CRT+defibrillator compared to ICD) (27–30). A high percentage (target: 98%) of LV pacing is crucial to treatment success (2). Mortality and morbidity increase with each percentage decline in left ventricular stimulation (31). Patients with a broad QRS complex of >130 ms but non-LBBB morphology do not benefit from cardiac resynchronization therapy to the same extent in the large studies (28, e14, e15). However, a recently conducted registry analysis found that cardiac resynchronization may be beneficial in patients with a QRS duration of more than 180 ms irrespective of QRS morphology (e16). In the case of a narrow QRS complex (<130 ms) despite echocardiographically confirmed mechanical dyssynchrony, no prognostic improvement was conferred by cardiac resynchroni – zation therapy—on the contrary, an excess mortality was seen in the cardiac resynchronization therapy arm (e17). This gives rise to the recommendations in the current ESC guidelines shown in the Box. Devices in narrow QRS complex Only around 20% of patients have a QRS duration of >120 ms (e18), meaning that cardiac resynchronization therapy is not indicated in the majority of HFrEF patients. Since modulation of the autonomic nervous system by means of vagal nerve stimulation was Resynchronization therapy Resynchronization therapy in patients with left bundle branch block significantly reduces heart-failure–related hospitali – zations as well as cardiovascular and overall mortality. Success of resynchronization therapy A high percentage of LV pacing is crucial to treatment success. 382 Deutsches Ärzteblatt International | Dtsch Arztebl Int 2020; 117: 376–86 MEDICINE unsuccessful (e19), baroreflex activation therapy (BAT) and cardiac contractility modulation (CCM) could represent potential alternative therapies in the future for patients with a narrow QRS complex. Both therapies are relatively new devices for heart failure and could be considered for HFrEF patients with a narrow QRS complex that remain symptomatic despite optimal guideline-compliant drug therapy. The Food and Drug Administration has already approved baroreflex activation therapy and cardiac contractility modulation in the USA to improve HFrEF symptoms. Hard data on improvement of prognosis (mortality) are currently still pending. The German heart failure treatment guideline (NVL) deems the available evidence on baroflex activation therapy and cardiac contractility modulation as hitherto insufficient for the purposes of making specific recommendations (13). Both devices currently play a secondary role in the clinical treatment of heart failure patients and are only used on the basis of individual assessments in specialized centers. Secondary mitral regurgitation Patients with HFrEF frequently develop secondary mitral regurgitation (MR); in patients with an LVEF ≤ 35%, mitral regurgitation of at least moderate severity was detected in 49% of cases (32). Typically, the valve itself is intact in secondary mitral regurgitation. The regurgitation is the result of an imbalance between the closing and tethering forces on the valve due to changes in left ventricular geometry (e20). The prognosis of patients with HFrEF worsens with increasing severity of mitral regurgitation (32, e21). Treatment comprises optimal heart failure drug therapy, as well as cardiac resynchronization therapy where indicated (2). The value of isolated surgical treatment of secondary mitral regurgitation has not been elucidated as yet and is viewed with caution in the current guidelines (2). Alternatively, interventional procedures have been available for some years; MitraClip therapy in particular is an established treatment option. In 2018, two studies were published on the value of MitraClip therapy of severe secondary mitral regurgitation in HFrEF: The French MITRA-FR study (33) found no significant difference between treatment with MitraClip and optimal drug therapy on the combined endpoint of all-cause mortality and heart failure-related hospitalizations following MitraClip therapy. In the COAPT study, on the other hand, interventional mitral valve repair conferred an improvement in prognosis in selected patients with heart failure (LVEF 20–50%) and moderate-to-severe mitral regurgitation following previously optimized heart failure treatment, with a reduction in hospitali – zations and death (34). Quality of life was also significantly improved (35). Possible reasons (e22) for these differing results could lie on the one hand in the severity of mitral regurgitation, which was greater in the COAPT study. Another difference lay in the fact that the left ventricular end-diastolic volume was higher in the MITRA-FR study, i.e., patients with more advanced heart failure and a higher degree of LV dilatation were included. These two studies resulted in the coining of the term “proportionate” as compared to “disproportionate” functional mitral regurgitation compared to the size of the left ventricle (36). The COAPT study primarily included patients with the latter, meaning that these patients appear more likely to benefit from the MitraClip intervention (5). The results of the COAPT study demonstrated, for the first time, a significant improvement in prognosis as a result of interventional therapy in patients with severe secondary mitral regurgitation. The number needed to treat for mortality in this study is six. Therefore, the possibility of MitraClip therapy should be assessed in patients with HFrEF, optimal heart failure therapy, and severe secondary mitral regurgitation in order to improve prognosis in this group. Implementing treatment recommendations in the outpatient sector Particularly in the outpatient sector, recommendations on the treatment of HFrEF are not sufficiently implemented in daily routine. Uptitration of heart failure drugs is often inadequate. Comorbidities (for example, COPD, depression, sleep apnea) hamper the diagnosis and treatment of heart failure, are often not taken into account, or are underestimated in terms of their prognostic effect. Therapy needs to be optimized by means of heart failure networks made up of specialized heart failure practices, clinics, and supraregional centers in order to guarantee the best possible treatment of heart failure patients. The German Cardiac Society (DGK) certifies appropriate facilities (37). Specialized heart failure nurses and medical assistants play an important role here, as do telemedicine approaches, which are able to indicate overhydration early on (for example, CardioMEMS, a pressure sensor that is implanted in the pulmonary artery), and could help to promptly identify decompensation and prevent hospitalizations in the future. Alternative device-based therapies Alternative device-based therapies in patients with a narrow QRS complex comprise baroreflex activation therapy and cardiac contractility modulation. MitraClip therapy A positive effect on mortality and hospitalization rates was seen for MitraClip therapy in selected patients with secondary mitral regurgitation. Deutsches Ärzteblatt International | Dtsch Arztebl Int 2020; 117: 376–86 383 MEDICINE Conclusion Further advances have been made in the treatment of HFrEF in recent years and the prognosis of these patients has significantly improved. In addition to the introduction of angiotensin receptor neprilysin inhibitors, new pharmacological approaches such as SGLT2 inhibitors and sGC activators, as well as novel devices, are showing promise. 10. McMurray JJ, Packer M, Desai AS, et al.: Angiotensin-neprilysin inhibition versus enalapril in heart failure.Standardized Procedures and Guidelines for Evidence-Based Practice for Heart Failure Essay.   N Engl J Med 2014; 371: 993–1004. 11. Swedberg K, Komajda M, Böhm M, et al.: Ivabradine and outcomes in chronic heart failure (SHIFT): a randomised placebo- controlled study. Lancet 2010; 376: 875–85. 12. Tardif JC, O‘Meara E, Komajda M, et al.: Effects of selective heart rate reduc tion with ivabradine on left ventricular remodelling and function: results from the SHIFT echocardiography substudy. Eur Heart J 2011; 32: 2507–15. 13. Bundesärztekammer (BÄK), Kassenärztliche Bundesvereinigung (KBV), Arbeitsgemeinschaft der Wissenschaftlichen Medizinischen Fachgesellschaften (AWMF): Nationale Versorgungs-Leitlinie Chronische Herzinsuffizienz –Langfassung. 3. Auflage. 2019 (last acessed on 31 October 2019). 14. Digitalis Investigation Group: The effect of digoxin on mortality and morbidity in patients with heart failure. N Engl J Med 1997; 336: 525–33. 15. Adams KF, Butler J, Patterson JH, et al.: Dose response characterization of the association of serum digoxin concentration with mortality outcomes in the Digitalis Investigation Group trial. Eur J Heart Fail 2016; 18: 1072–81. 16. Hood JWB, Dans AL, Guyatt GH, Jaeschke R, McMurray JJV: Digitalis for treatment of heart failure in patients in sinus rhythm. Cochrane Database Syst Rev 2014; 4: CD002901. 17. Bavendiek U, Berliner D, Davila LA, et al.: Rationale and design of the DIGIT-HF trial (DIGitoxin to Improve ouTcomes in patients with advanced chronic Heart Failure): a randomized, double-blind, placebo- controlled study. Eur J Heart Fail 2019; 21: 676–84. 18. Jankowska EA, Rozentryt P, Witkowska A, et al.: Iron deficiency: an ominous sign in patients with systolic chronic heart failure. Eur Heart J 2010; 31: 1872–80. 19. Anker SD, Comin Colet J, Filippatos G, et al.: Ferric carboxymaltose in patients with heart failure and iron deficiency. N Engl J Med 2009; 361: 2436–48. 20. Ponikowski P, van Veldhuisen DJ, Comin-Colet J, et al.: Beneficial effects of long-term intra-venous iron therapy with ferric carboxymaltose in patients with symptomatic heart failure and iron deficiency. Eur Heart J 2015; 36: 657–68. 21. McMurray JJV, Solomon SD, Inzucchi SE, et al.: Dapagliflozin in patients with heart failure and reduced ejection fraction. N Engl J Med 2019; 381: 1995–08. 22. Priori SG, Blomström-Lundqvist C, Mazzanti A, et al.: 2015 ESC guidelines for the management of patients with ventricular arrhythmias and the prevention of sudden cardiac death: The task force for the management of patients with ventricular arrhythmias and the prevention of sudden cardiac death of the European Society of Cardiology (ESC) endorsed by: Association for European Paedi – atric and Congenital Cardiology (AEPC). Eur Heart J 2015; 36: 2793–867. 23. Kober L, Thune JJ, Nielsen JC, et al.: Defibrillator implantation in patients with nonischemic systolic heart failure. N Engl J Med 2016; 375: 1221–30. 24. Elming MB, Nielsen JC, Haarbo J, et al.: Age and outcomes of primary preven tion implantable cardioverter-defibrillators in patients with nonischemic systolic heart failure. Circulation 2017; 136: 1772–80. 25. Duncker D, Veltmann C: Role of the wearable defibrillator in newly diagnosed heart failure. Curr Heart fail Rep 2018; 15: 368–75. 26. Abraham WT, Fisher WG, Smith AL, et al.: Cardiac resynchroni – zation in chronic heart failure. N Engl J Med 2002; 346: 1845–53. 27. Moss AJ, Hall WJ, Cannom DS, et al.: Cardiac-resynchronization therapy for the prevention of heart-failure events. N Engl J Med 2009; 361: 1329–38. 28. Tang AS, Wells GA, Talajic M, et al.: Cardiac-resynchronization therapy for mild-to-moderate heart failure. N Engl J Med 2010; 363: 2385–95. 29. Cleland JG, Daubert JC, Erdmann E, et al.: The effect of cardiac Results of the COAPT study The results of the COAPT study demonstrated, for the first time, a significant improvement in prognosis as a result of interventional therapy in patients with severe secondary mitral regurgitation. Conflict of interests Dr. Berliner received consultancy fees from Novartis. He received funds for the preparation of scientific meetings from Orion Pharma, Abbott Vascular, and Novartis Pharma GmbH. He received funds to conduct clinical trials from Zoll Medical Corporation, CVRx, and Novartis. Dr. Hänselmann was reimbursed for congress participation fees as well as travel and accommodation costs by Bayer and Böhringer Ingelheim. She received funds for the preparation of scientific meetings from Novartis. Prof. Bauersachs received consultancy fees from Astra Zeneca, Bayer, BMS, Böhringer Ingelheim, Novartis, and Servier Vifor. He was reimbursed for travel and accommodation costs by Bayer, Böhringer Ingelheim, and Servier. He received funds for the preparation of scientific meetings from Abiomed, Astra Zeneca, Bayer, BMS, Böhringer Ingelheim, CVRX, Medtronic, MSD, and Novartis. He received funds for a research project of his own initiation as well as to conduct clinical trials from Abiomed, Bayer, Böhringer Ingelheim, CVRX, Medtronic, MSD, Vifor, and Zolll. Manuscript submitted on 2 June 2019, revised version accepted on 29 January 2020. Translated from the original German by Christine Rye. References 1. Lindenfeld J, Albert NM, Boehmer JP, et al.: HFSA 2010 Comprehensive heart failure practice guideline. J Card Fail 2010; 16: e1–194. 2. Ponikowski P, Voors AA, Anker SD, et al.: 2016 ESC guidelines for the diagnosis and treatment of acute and chronic heart failure: The task force for the diagnosis and treatment of acute and chronic heart failure of the European Society of Cardiology (ESC). Developed with the special contribution of the Heart Failure Association (HFA) of the ESC. Eur J Heart Fail 2016; 18: 891–975. 3. Mosterd A, Hoes AW: Clinical epidemiology of heart failure. Heart 2007; 93: 1137–46. 4. Maggioni AP, Dahlstrom U, Filippatos G, et al.: EURObservational Research Programme: the Heart Failure Pilot Survey (ESC-HF Pilot). Eur J Heart Fail 2010; 12: 1076–84. 5. Seferovic PM, Ponikowski P, Anker SD, et al.: Clinical practice update on heart failure 2019: pharmacotherapy, procedures, devices and patient management. An expert consensus meeting report of The Heart Failure Association of the European Society of Cardi – ology. Eur J Heart Fail 2019; 21: 1169–86. 6. Ouwerkerk W, Voors AA, Anker SD, et al.: Determinants and clinical outcome of uptitration of ACE-inhibitors and beta-blockers in patients with heart failure: a prospective European study. Standardized Procedures and Guidelines for Evidence-Based Practice for Heart Failure Essay. Eur Heart J 2017; 38: 1883–90. 7. Pitt B, Zannad F, Remme WJ, et al.: The effect of spironolactone on morbidity and mortality in patients with severe heart failure. N Engl J Med 1999; 341: 709–17. 8. Zannad F, McMurray JJ, Krum H, et al.: Eplerenone in patients with systolic heart failure and mild symptoms. N Engl J Med 2011; 364: 11–21. 9. Zannad F, Gattis Stough W, Rossignol P, et al.: Mineralocorticoid receptor antagonists for heart failure with reduced ejection fraction: integrating evidence into clinical practice. Eur Heart J 2012; 33: 2782–95. 384 Deutsches Ärzteblatt International | Dtsch Arztebl Int 2020; 117: 376–86 MEDICINE resynchronization on morbidity and mortality in heart failure. N Engl J Med 2005; 352: 1539–49. 30. Bristow MR, Saxon LA, Boehmer J, et al.: Cardiac-resynchronization therapy with or without an implantable defibrillator in advanced chronic heart failure. N Engl J Med 2004; 350: 2140–50. 31. Hayes DL, Boehmer JP, Day JD, et al.: Cardiac resynchronization therapy and the relationship of percent biventricular pacing to symptoms and survival. Heart rhythm 2011; 8: 1469–75. 32. Koelling TM, Aaronson KD, Cody RJ, Bach DS, Armstrong WF: Prognostic significance of mitral regurgitation and tricuspid regurgitation in patients with left ventricular systolic dysfunction. Am Heart J 2002; 144: 524–9. 33. Obadia J-F, Messika-Zeitoun D, Leurent G, et al.: Percutaneous repair or medical treatment for secondary mitral regurgitation. N Engl J Med 2018; 379: 2297–306. 34. Stone GW, Lindenfeld J, Abraham WT, et al.: Transcatheter mitral-valve repair in patients with heart failure. N Engl J Med 2018; 379: 2307–18. 35. Arnold SV, Chinnakondepalli KM, Spertus JA, et al.: Health status after trans – catheter mitral-valve repair in heart failure and secondary mitral regurgitation. COAPT Trial 2019; 73: 2123–32. 36. Grayburn PA, Sannino A, Packer M: Proportionate and disproportionate functional mitral regurgitation: a new conceptual framework that reconciles the results of the MITRA-FR and CO-APT trials. JACC Cardiovasc Imaging 2019; 12: 353–62. 37. Ertl G, Angermann CE, Bekeredjian R, et al.: Aufbau und Organisation von Herz – insuffizienz-Netzwerken (HF NETs) und Herzinsuffizienz-Einheiten („Heart Failure Units“, HFUs) zur Optimierung der Behandlung der akuten und chronischen Herz – insuffizienz. Der Kardiologe 2016; 10: 222–35. 38. Yancy CW, Jessup M, Bozkurt B, et al.: 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. 2013; 62: e147–e239. 39. Bavendiek U, Aguirre Davila L, Koch A, Bauersachs J: Assumption versus evidence: the case of digoxin in atrial fibrillation and heart failure. Eur Heart J 2017; 38: 2095–9. 40. Bavendiek U, Aguirre Davila L, Schwab J, et al.: P6168Digitoxin serum concentrations affecting patient safety and potential outcome in patients with HFrEF–analyses of the ongoing DIGIT-HF-trial. Eur Heart J 2017; 38. Corresponding author Dr. med. Dominik Berliner Klinik für Kardiologie und Angiologie Medizinische Hochschule Hannover Carl-Neuberg-Straße 1 30625 Hannover, Germany [email protected] Cite this as Berliner D, Hänselmann A, Bauersachs J: The treatment of heart failure with reduced ejection fraction. Dtsch Arztebl Int 2020; 117: 376–86. DOI: 10.3238/arztebl.2020.0376 ►Supplementary material For eReferences please refer to: www.aerzteblatt-international.de/ref2120 Further information on CME ● Participation in the CME certification program is only possible online: cme.aerzteblatt.de. The submission deadline is 21.5.2021. Submissions by letter, e-mail, or fax cannot be considered. ● The completion time for all newly started CME units is 12 months. The results can be accessed 4 weeks following the start of the CME unit. Please note the respective submission deadline at: cme.aerzteblatt.de. ● This article has been certified by the North Rhine Academy for Continuing Medical Education. CME points can be managed using the “uniform CME number” (einheitliche Fortbildungsnummer, EFN). The EFN must be stated during registration on www.aerzteblatt.de (“Mein DÄ”) or entered in “Meine Daten” and consent must be given for results to be communicated. The 15-digit EFN can be found on the CME card (8027XXXXXXXXXXX). Deutsches Ärzteblatt International | Dtsch Arztebl Int 2020; 117: 376–86 385 MEDICINE Deutsches Ärzteblatt International | Dtsch Arztebl Int 2020; 117: 376–86 | Supplementary material I Supplementary material to: The Treatment of Heart Failure with Reduced Ejection Fraction Dominik Berliner, Anja Hänselmann, Johann Bauersachs Dtsch Arztebl Int 2020; 117: 376–86. DOI: 10.3238/arztebl.2020.0376 e15. Zareba W, Klein H, Cygankiewicz I, et al.: Effectiveness of cardiac resynchronization therapy by QRS morphology in the multicenter automatic defibrillator implantation trial-cardiac resynchronization therapy (MADIT-CRT). Circulation 2011; 123: 1061–72. e16. Sundaram V, Sahadevan J, Waldo AL, et al.: Implantable cardioverter-defibrillators with versus without resynchronization therapy in patients with a QRS duration > 180 ms. J Am Coll Cardiol 2017; 69: 2026–36. e17. Ruschitzka F, Abraham WT, Singh JP, et al.: Cardiac- resynchronization therapy in heart failure with a narrow QRS complex. N Engl J Med 2013; 369: 1395–405. e18. Shenkman HJ, Pampati V, Khandelwal AK, et al.: Congestive heart failure and QRS duration: establishing prognosis study. CHEST 2002; 122: 528–34. e19. Gold MR, Van Veldhuisen DJ, Hauptman PJ, et al.: Vagus nerve stimulation for the treatment of heart failure: the INOVATE-HF trial. J Am Coll Cardiol 2016; 68: 149–58. e20. Baumgartner H, Falk V, Bax JJ, et al.: 2017 ESC/EACTS guidelines for the management of valvular heart disease. Eur Heart J 2017; 38: 2739–91. e21. Bursi F, Barbieri A, Grigioni F, et al.: Prognostic implications of functional mitral regurgitation according to the severity of the underlying chronic heart failure: a long-term outcome study. Eur J Heart Fail 2010; 12: 382–8. e22. Pfister R, Hausleiter J, Boekstegers P, et al.: Role of percutaneous edge-to-edge repair in secondary mitral regurgitation after MITRA-FR and COAPT : a comment by the section of AV-valve treatment of the Working Group of Interventional Cardiology (AGIK) of the German Society of Cardiology (DGK). Clin Res Cardiol 2019; 108: 969−73. e23. Chioncel O, Lainscak M, Seferovic PM, et al.: Epidemiology and one-year outcomes in patients with chronic heart failure and pre – served, mid-range and reduced ejection fraction: an analysis of the ESC Heart Failure Long-Term Registry. Eur J Heart Fail 2017; 19: 1574–85. e24. Fox K, Komajda M, Ford I, et al.: Effect of ivabradine in patients with left-ventricular systolic dysfunction: a pooled analysis of individual patient data from the BEAUTIFUL and SHIFT trials. Eur Heart J 2013; 34: 2263–70. e25. Komajda M, Böhm M, Borer JS, et al.: Incremental benefit of drug therapies for chronic heart failure with reduced ejection fraction: a network meta-analysis. Eur J Heart Fail 2018; 20: 1315–22. e26. Srivastava PK, Claggett BL, Solomon SD, et al.: Estimated 5-year number needed to treat to prevent cardiovascular death or heart failure hospitalization with Angiotensin Receptor-Neprilysin inhibition vs standard therapy for patients with heart failure with reduced ejection fraction: An analysis of data from the PARADIGM-HF trial. JAMA Cardiology 2018; 3: 1226–31. e27. Duncker D, Veltmann C: Device therapy in heart failure with reduced ejection fraction—cardiac resynchronization therapy and more. Herz 2018; 43: 415–22. eReferences e1. Benjamin EJ, Blaha MJ, Chiuve SE, et al.: Heart Disease and Stroke Statistics-2017 Update: A report from the American Heart Association. Circulation 2017; 135: e146–e603. e2. Ferrari R, Ceconi C, Tavazzi L, Ghio S, Boffa G, Fucili A: Heart failure: 150 questions & answers. 2nd ed. Neuilly-sur-Seine Cedex: Servier; 2011. e3. Gheorghiade M, Bohm M, Greene SJ, et al.: Effect of aliskiren on postdischarge mortality and heart failure readmissions among patients hospitalized for heart failure: the ASTRONAUT randomized trial. JAMA 2013; 309: 1125–35. e4. McMurray JJ, Krum H, Abraham WT, et al.: Aliskiren, Enalapril, or Aliskiren and Enalapril in heart failure. N Engl J Med 2016; 374: 1521–32. e5. D‘Elia E, Iacovoni A, Vaduganathan M, Lorini FL, Perlini S, Senni M: Neprilysin inhibition in heart failure: mechanisms and substrates beyond modulating natriuretic peptides. Eur J Heart Fail 2017; 19: 710–7. e6. Lewis EF, Claggett BL, McMurray JJV, et al.: Health-related quality of life outcomes in PAR-ADIGM-HF. Circ Heart Fail 2017; 10. e7. de Diego C, Gonzalez-Torres L, Nunez JM, et al.: Effects of angiotensin-neprilysin inhibition compared to angiotensin inhibition on ventricular arrhythmias in reduced ejection fraction patients under continuous remote monitoring of implantable defibrillator devices. Heart rhythm 2018; 15: 395–402. e8. Januzzi JL, Jr, Prescott MF, Butler J, et al.: Association of change in N-terminal pro-B-type natriuretic peptide following initiation of sacubitril-Valsartan treatment with cardiac structure and function in patients with heart failure with reduced ejection fraction. JAMA 2019; 322: 1085–95. e9. Böhm M, Swedberg K, Komajda M, et al.: Heart rate as a risk factor in chronic heart failure (SHIFT): the association between heart rate and outcomes in a randomised placebo-controlled trial. Lancet 2010; 376: 886–94. e10. Ekman I, Chassany O, Komajda M, et al.: Heart rate reduction with ivabradine and health related quality of life in patients with chronic heart failure: results from the SHIFT study.Standardized Procedures and Guidelines for Evidence-Based Practice for Heart Failure Essay.  Eur Heart J 2011; 32: 2395–404. e11. Armstrong PW, Pieske B, Anstrom KJ et al.: Vericiguat in patients with heart failure and reduced ejection fraction. N Engl J Med 2020 [epub ahead of print]. e12. Cazeau S, Leclercq C, Lavergne T, et al.: Effects of multisite biventricular pacing in patients with heart failure and intraventricular conduction delay. N Engl J Med 2001; 344: 873–80. e13. Auricchio A, Stellbrink C, Sack S, et al.: Long-term clinical effect of hemodynamically optimized cardiac resynchronization therapy in patients with heart failure and ventricular conduction delay. J Am Coll Cardiol 2002; 39: 2026–33. e14. Gervais R, Leclercq C, Shankar A, et al.: Surface electrocardiogram to predict outcome in candidates for cardiac resynchronization ther – apy: a sub-analysis of the CARE-HF trial. Eur J Heart Fail 2009; 11: 699–705. Copyright of Deutsches Aerzteblatt International is the property of Deutscher Aerzte-Verlag GmbH and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder’s express written permission. However, users may print, download, or email articles for individual use.

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Each state has its own requirements for advanced practice registered nurse (APRN) practice. Employers, likewise, may have additional limitations for APRN practice, such as standardized policies and procedures, chart review processes, supervising physician agreements, etc.

Use your findings from this week’s Standardized Policies and Procedures Research learning activity (SEE Instructions BELOW) for this assignment.

• Write a 2,200-word evidence-based practice paper that you would consider submitting for publication on the evaluation, assessment, diagnosis, and treatment of the topic selected of “Heart Failure”.

• Apply appropriate national guidelines and evidence-based practice guidelines (See BELOW for some Referenced Material …)

Include the following components regarding Heart Failure:

1. • Introduction, morbidity and mortality, etiology, pathophysiology, and diagnostic testing
   • Clinical presentation, relevant objective and subjective findings
   • Diagnostic criteria and management, including clinical preventive services and treatment plan (treatment plans must follow evidence-based practice and national guidelines when available) Standardized Procedures and Guidelines for Evidence-Based Practice for Heart Failure Essay.

Include a minimum of 10 references from the most current national guidelines from professional sites and sources including peer reviewed articles in the last five years (preferable in the last three years).

Format your assignment according to APA guidelines.

National Guidelines and Evidence-Based Practice Guidelines

[ https://www.heart.org/en/professional]

Please use these Articles researched for the paper…., but remember to include the other ones from reliable sources: 

• Berliner, D., Hänselmann, A., & Bauersachs, J. (2020). The Treatment of Heart Failure with Reduced Ejection Fraction. Deutsches Aerzteblatt International, 117(21), 376–385. https://doi.org/10.3238/arztebl.2020.0376
• Fonseca, C., Brito, D., Branco, P., Frazão, J. M., Silva-Cardoso, J., & Bettencourt, P. (2020). Hyperkalemia and management of renin-angiotensin-aldosterone system inhibitors in chronic heart failure with reduced ejection fraction: A systematic review. Revista Portuguesa de Cardiologia (English Edition), 39(9), 517–541. https://doi.org/10.1016/j.repce.2020.03.010
• Long, B., Koyfman, A., & Gottlieb, M. (2019). Diagnosis of Acute Heart Failure in the Emergency Department: An Evidence-Based Review. The Western Journal of Emergency Medicine, 20(6), 875–884.  Standardized Procedures and Guidelines for Evidence-Based Practice for Heart Failure Essay. https://doi.org/10.5811/westjem.2019.9.43732
• Reddy, Y. N. V., & Borlaug, B. A. (2020). Heart Failure With Preserved Ejection Fraction: Where Do We Stand? Mayo Clinic Proceedings, 95(4), 629+. https://link.gale.com/apps/doc/A623573459/ITBC?u=uphoenix&sid=ITBC&xid=d07e5377
• Wood, R. L., Migliore, L. A., Nasshan, S. J., Mirghani, S. R., & Contasti, A. C. (2019). Confronting Challenges in Reducing Heart Failure 30-Day Readmissions: Lessons Learned With Implications for Evidence-Based Practice. Worldviews on Evidence-Based Nursing, 1, 43. https://doi.org/10.1111/wvn.12336
• Yancy, C. W., Jessup, M., Bozkurt, B., Butler, J., Casey, J. D. E., Colvin, M. M., Drazner, M. H., Filippatos, G. S., Fonarow, G. C., Givertz, M. M., Hollenberg, S. M., Lindenfeld, J., Masoudi, F. A., McBride, P. E., Peterson, P. N., Stevenson, L. W., & Westlake, C. (2017). 2017 ACC/AHA/HFSA Focused Update of the 2013 ACCF/AHA Guideline for the Management of Heart Failure: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines and the Heart Failure Society of America. Journal of the American College of Cardiology, 70(6), 776–803. https://doi.org/10.1016/j.jacc.2017.04.025

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Learning Activity

• Standardized Policies and Procedures Research Locate and download the board of nursing sample template for standardized policies and procedures for your state of practice FLORIDA.

Please follow the grading criteria (See Below), when writing this paper.

Grading Criteria:

Standardized Procedures and Guidelines for Evidence-Based Practice for Heart Failure Essay