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Dec.18.2021

Heart Failure

Synopsis

Key Points

  • Heart failure is a clinical syndrome characterized by structural or functional impairment of ventricular filling or ejection of blood resulting in insufficient perfusion to meet metabolic demands and clinically manifested as edema, dyspnea, and fatigue
  • Diagnosis is suspected based on a thorough history and physical examination. Measurement of natriuretic peptide levels, 2-dimensional echocardiography with Doppler, and chest radiography support the diagnosis of heart failure
  • Functionally categorized as either heart failure with reduced ejection fraction (left ventricular ejection fraction of 40% or less) or heart failure with preserved ejection fraction (left ventricular ejection fraction of 50% or more). Patients with values of 41% to 49% are classified as having borderline reduced ejection fraction
  • Coronary artery disease is the predominant cause of heart failure with reduced ejection fraction, which most commonly results in left ventricular dilation; hypertension is the predominant cause of heart failure with preserved ejection fraction, which is usually associated with left ventricular hypertrophy
  • Treatment of heart failure with reduced ejection fraction depends on disease stage and functional classification; recommended pharmacologic classes include ACE inhibitors, β-blockers, and aldosterone antagonists for most patients, with diuretics for volume overload
    • Angiotensin receptor blockers or angiotensin receptor–neprilysin inhibitors may be indicated instead of ACE inhibitors in selected patients
    • Vasodilators, ivabradine, and digoxin may be added for appropriate patients with continued symptoms
  • Recommended therapies for heart failure with preserved ejection fraction are symptom-directed or for management of comorbidities, especially hypertension, that may worsen heart failure
    • Although diuretics are recommended for fluid overload, there is no evidence that other treatments recommended for heart failure with reduced ejection fraction are efficacious for heart failure with preserved ejection fraction
  • Device therapy (with implantable cardioverter-defibrillator or cardiac resynchronization device) is sometimes indicated as adjunctive therapy in select patients; temporary inotrope support, mechanical circulatory support with a ventricular assist device, and heart transplant are indicated in select advanced cases refractory to other treatment
  • Complications include malignant ventricular arrhythmias, atrial fibrillation, and thromboembolic events
  • Prognosis of patients hospitalized with heart failure, and especially those with serial readmissions, is poor r1r2
    • Mortality rate for patients with heart failure is approximately 50% within 5 years of diagnosis; for those with advanced heart failure, the 1-year survival rate is 50%

Urgent Action

  • Life-threatening conditions (eg, acute coronary syndromes, cardiac arrhythmias) may precipitate acute decompensated heart failure and must be treated emergently

Pitfalls

  • Treatment of advanced heart failure is often palliative; reevaluation of quality of indicators is necessary to avoid prolongation of futile efforts
  • There is no evidence of benefit from antiplatelet drugs (including aspirin) in patients with chronic stable heart failure unless concomitant coronary artery disease is present. Likewise, oral anticoagulants are not recommended unless atrial fibrillation or known cardiac thrombus is present r3

Terminology

Clinical Clarification

  • Heart failure is a complex clinical syndrome caused by structural or functional impairment of ventricular filling or ejection of blood resulting in insufficient perfusion to meet metabolic demands
  • Characterized by progressive cardiac remodeling with left ventricular dilation, left ventricular hypertrophy, or both
  • Cardinal clinical manifestations include pulmonary and/or systemic venous congestion and/or inadequate peripheral oxygen delivery with edema, dyspnea, and fatigue

Classification

  • Staging by American College of Cardiology Foundation/American Heart Association guideline (based on structure and progression of disease as evidenced by ECG and echocardiography) r2
    • Stage A
      • At high risk for heart failure without structural heart disease or symptoms, based on risk factors of hypertension, dyslipidemia, diabetes, obesity, and exposure to cardiotoxic agents (eg, doxorubicin)
    • Stage B
      • Structural heart disease (eg, ventricular remodeling, previous myocardial infarction) without signs and symptoms of heart failure
    • Stage C
      • Structural heart disease with prior or current symptoms of heart failure
    • Stage D
      • Heart failure refractory to optimal goal-directed medical therapy
  • Functional classification by New York Heart Association (based on symptom severity) r2
    • Class I
      • Heart disease with no symptoms or limitations on physical activity
    • Class II (mild)
      • Comfortable at rest, but symptoms of heart failure during ordinary activity
    • Class III (moderate)
      • Comfortable at rest, but symptoms of heart failure with minimal exertion
    • Class IV (severe)
      • Symptoms at rest
      • Unable to carry on any physical activity without symptoms
  • Classification based on ejection fraction
    • Heart failure with preserved ejection fraction r2
      • Approximately half of all patients with heart failure r4
      • Ejection fraction 50% or more r2r5
      • Filling of ventricles is impaired owing to abnormal relaxation or stiffness and decreased diastolic distensibility
      • Historically described as diastolic heart failure
      • European guidelines have additional criteria that include elevated levels of natriuretic peptides and either relevant structural heart disease or diastolic dysfunction r3
      • Patients often have left atrial enlargement and increased left ventricular wall thickness but usually do not have left ventricular dilation
    • Heart failure with mid-range ejection fraction: borderline (alternative terminology is heart failure with borderline ejection fraction) r2r3r5
      • Ejection fraction of 41% to 49%, with characteristics similar to patients with heart failure with preserved ejection fraction r2r5
      • European guidelines have additional criteria that include elevated levels of natriuretic peptides and either relevant structural heart disease or diastolic dysfunction r3
    • Heart failure with preserved ejection fraction: improved (or recovered) r2r5
      • Ejection fraction has improved to more than 40% in a patient previously classified as having heart failure with reduced ejection fraction r2r5
    • Heart failure with reduced ejection fraction r2r3r5
      • Ejection fraction of 40% or less r2r3r5
      • Historically described as systolic heart failure
      • Left ventricular contractility is impaired and is often dilated
  • Classification based on timeline
    • New (de novo) heart failure r3
      • Acute onset
        • May present suddenly as a result of acute insult (eg, myocardial infarction)
      • Subacute onset
        • Gradual onset of symptoms
        • Occurs when transitioning from asymptomatic to symptomatic heart failure
    • Chronic heart failure r3
      • Stable
        • Treated heart failure, signs and symptoms are unchanged for more than 1 month (ie, compensated)
      • Decompensated
        • Symptomatic deterioration of stable chronic heart failure, often requiring hospitalization
        • Decompensation may occur acutely owing to a precipitating event (eg, myocardial infarction, atrial fibrillation, noncompliance with medical therapy) or subacutely

Diagnosis

Clinical Presentation

History

  • Common symptoms of heart failure include:
    • Dyspnea r2c1
      • Dyspnea on exertion; dyspnea at rest often occurs in advanced heart failure c2c3c4
      • Orthopnea c5
      • Paroxysmal nocturnal dyspnea c6
    • Fatigue r2c7
      • Exercise intolerance c8
      • Increased recovery time from activity
    • Peripheral edema r6c9
      • Ankle swelling c10
    • Ascites causing any of the following: r6c11
      • Anorexia c12
      • Early satiety c13
      • Gastrointestinal discomfort c14
      • Increased abdominal girth c15
      • Scrotal swelling c16
    • Change in weight r6c17
      • Rapid weight gain suggests volume overload c18
      • Weight loss may occur in advanced disease c19
  • Other symptoms of heart failure may include:
    • Nonproductive cough during recumbency r6c20
    • Confusion, especially in elderly people r7c21
    • Palpitations r8c22
    • Syncope r6c23
  • Family history of cardiomyopathy may suggest underlying cause; ask patient about heart failure in family members going back 3 generations c24

Physical examination

  • Specific signs include: r2r6r8
    • Prominent jugular venous distention c25
    • Positive hepatojugular reflux c26
    • Laterally displaced apical impulse c27
    • Presence of S₃ gallop with systolic heart failure; may have S₄ gallop with diastolic heart failure c28c29
  • Less specific signs include the following (may be associated with many other conditions): r2r6r8
    • Tachypnea and tachycardia c30c31
    • Narrow pulse pressure c32
    • Cool extremities c33
    • Crackles/rales (may be absent in advanced chronic heart failure) c34
    • Wheezes c35
    • Peripheral edema, ascites, and hepatomegaly c36
    • Cachexia in advanced disease c37

Causes and Risk Factors

Causes

  • Most common causes of heart failure are hypertension and ischemic coronary artery disease r6r7
    • Hypertension is the single most important modifiable cause of heart failure r2c38
    • Risk increases 8- to 10-fold after myocardial infarction r6c39
    • Patients with heart failure with preserved ejection fraction (usually older and female) more commonly have hypertension and less commonly have coronary artery disease c40c41
    • Patients who have heart failure with reduced ejection fraction are more likely to have coronary artery disease (approximately two-thirds of cases), with hypertension a contributing factor
  • Other causes of heart failure with reduced ejection fraction include valvular disease and cardiomyopathies
    • Valvular disease c42
      • Predominantly mitral and aortic valve disease (eg, mitral regurgitation, aortic stenosis, aortic regurgitation) r9c43c44c45c46c47
    • Cardiomyopathies c48
      • Idiopathic dilated cardiomyopathy r2c49
        • Large group of dissimilar myocardial disorders with common characteristics including ventricular dilation and depressed myocardial contractility in absence of abnormal loading conditions (eg, hypertension, valvular disease) r2
      • Familial cardiomyopathy c50
        • 2 closely related family members must meet criteria for idiopathic cardiomyopathy r2
        • 20% to 35% of presumed idiopathic cardiomyopathies are now recognized as familial r2
      • Toxic cardiomyopathy c51
        • Heart failure may result from toxic effect on cardiac preload, cardiac afterload, or myocardial contractility r10
        • Heart failure may be reversible (eg, secondary to propofol), irreversible (eg, secondary to doxorubicin), or either (eg, secondary to cyclophosphamide) r10c52c53c54
        • Cardiotoxic cancer chemotherapies, particularly anthracyclines, can cause structural changes c55
          • Other therapies that are also cardiotoxic include trastuzumab (especially with concomitant anthracyclines), high-dose cyclophosphamide, taxoids, mitomycin C, fluorouracil, and the interferons
        • Long-term alcohol or cocaine use may cause dilated cardiomyopathy c56c57
        • Cardiomyopathy may be caused by other drugs, many with misuse potential (eg, ephedra, anabolic steroids, amphetamines, methylphenidate)
      • Inflammatory cardiomyopathy c58
        • Immune-mediated inflammatory myocarditis c59
          • Hypersensitivity to medication (eg, sulfonamides, penicillin, methyldopa, amphotericin B, streptomycin, phenytoin, isoniazid, tetanus toxoid, hydrochlorothiazide, dobutamine, chlorthalidone) c60c61c62c63c64c65c66c67c68
          • Autoimmune disorders (eg, systemic lupus erythematosus, scleroderma, sarcoidosis) c69c70c71c72
        • Infective inflammatory myocarditis c73
          • Most commonly of viral origin but also can be caused by other pathogens
          • Commonly occurs in patients with HIV infection
      • Metabolic/endocrine cardiomyopathy c74c75
        • Includes cardiomyopathy caused by obesity, diabetes, hyperthyroidism, acromegaly, growth hormone imbalances, hypophosphatemia, hypocalcemia, and pheochromocytoma
        • Also includes cardiomyopathy caused by nutritional deficiencies (eg, thiamine deficiency, selenium deficiency), which may be seen in patients with chronic alcohol use disorder and anorexia nervosa c76c77c78
      • Infiltration cardiomyopathy c79
        • Caused by malignancy or amyloidosis
      • Iron overload cardiomyopathy c80
        • Caused by increased iron deposition in heart. Associated with common genetic disorders (eg, primary hemochromatosis) and disorders that require lifetime transfusions (eg, thalassemia major)
      • Peripartum cardiomyopathy c81
        • Left ventricular dysfunction occurs typically in third trimester of pregnancy or in immediate postpartum period
        • Incidence varies from 0.2% to 3% of live births worldwide, depending on region r11
        • Prognosis is directly related to degree of recovery to near baseline left ventricular function; if cardiomegaly lasts for more than 6 months, the 6-year mortality rate is 50% r2
      • Tachycardia-related cardiomyopathy c82
        • Left ventricular myocardial dysfunction correlates with duration of tachycardia and magnitude of increased ventricular rate
        • Generally reversible with rate control
      • Stress cardiomyopathy (takotsubo cardiomyopathy) c83c84
        • Acute reversible left ventricular dysfunction in the absence of significant coronary artery disease; triggered by acute emotional or physical stress
        • Characteristic apical ballooning is present
        • Often affects postmenopausal women

Risk factors and/or associations

Age
  • Incidence increases with age, from approximately 20 cases per 1000 person-years among those aged 65 to 69 years to more than 80 cases per 1000 person-years among those aged 85 years or older r2r12c85c86
  • Prevalence is 10% or more in patients aged 70 years or older r6
Sex
  • Higher incidence in men than women by approximately 10 cases per 1000 person-years r12c87c88
Genetics
  • Genetic loci with multiple genes and alleles with multiple mutations are involved in familial cardiomyopathies leading to heart failure r13c89
    • Underlying genetic causes include mutations in more than 30 genes encoding the sarcomere, components of the cytoskeleton, ion channels, and other elements r13
Ethnicity/race
  • Compared with White Americans, Black Americans have a higher incidence of, and higher 5-year mortality from, heart failure r2r12c90c91c92c93
    • Approximately 3% of Black adults in the United States have heart failure r6
Other risk factors/associations
  • Atherosclerotic disease c94
  • Diabetes mellitus c95
    • Risk factor independent of age, hypertension, obesity, hypercholesterolemia, or coronary artery disease r2
  • Metabolic syndrome c96
  • Smoking r14c97
  • Alcohol use disorder r15c98
    • Significant negative correlation between ejection fraction and lifetime alcohol intake
    • Positive correlation between left ventricular mass and lifetime alcohol consumption
  • Exposure to drugs or toxins associated with cardiotoxicity, including cancer chemotherapies (eg, anthracyclines, trastuzumab), drugs of abuse (eg, cocaine, amphetamines, anabolic steroids), and others r2r10c99c100c101c102c103c104c105c106

Diagnostic Procedures

Primary diagnostic tools

  • Diagnosis is suspected based on thorough history and physical examination r2r6r8c107
  • Obtain chest radiograph in acutely dyspneic patients to identify pulmonary edema. In nonacute diagnostic settings, chest radiograph is also recommended to detect or exclude alternative causes of symptoms r2r6r8
  • Obtain ECG as part of initial evaluation in all patients r2r5r8c108
  • Obtain laboratory testing
    • All patients r2r6r8
      • Electrolyte levels, BUN and creatinine levels, and urinalysis (important for treatment decisions) c109c110c111
      • Liver function tests
      • Fasting lipid levels and fasting glucose level to assess cardiovascular risk factors
      • CBC and TSH level to exclude anemia and thyroid disease (as a cause or exacerbating factor of heart failure) c112c113
      • B-type natriuretic peptide or N-terminal pro–B-type natriuretic peptide c114
        • Obtain for all patients with symptoms suggesting acute heart failure
          • American College of Cardiology Foundation, American Heart Association, and Heart Failure Society of America guidelines recommend measuring B-type natriuretic peptide or N-terminal pro–B-type natriuretic peptide level to support clinical decision making, especially in the setting of clinical uncertainty (in both ambulatory and hospitalized patients) r6r16r17
        • When making an initial diagnosis
          • Negative predictive value exceeds positive predictive value. Negative predictive value is best used to rule-out rather than rule-in the diagnosis on initial evaluation
          • European Society of Cardiology guideline recommends obtaining these measurements to help establish an initial working diagnosis, identifying those who require further cardiac investigation. If values are below the cut point, echocardiography is not needed r3
        • During hospitalization for heart failure, measure predischarge natriuretic peptide level to help establish a postdischarge prognosis r17
    • Patients with acute decompensated heart failure:
      • On admission to hospital, measure baseline levels of natriuretic peptide biomarkers and/or cardiac troponin to help establish a prognosis r17
  • Obtain transthoracic 2-dimensional echocardiogram with Doppler flow studies for all patients with suspected heart failure, per 2013 American College of Cardiology Foundation/American Heart Association guideline for management of heart failure and the 2017 comprehensive update of the Canadian Cardiovascular Society guidelines for the management of heart failure r2r5
    • 2016 European Society of Cardiology guidelines recommend transthoracic echocardiogram as part of the initial diagnostic evaluation only if B-type natriuretic peptide or N-terminal pro–B-type natriuretic peptide are elevated r3
  • Consider cardiac MRI if echocardiographic images are inadequate r3
  • Noninvasive (myocardial perfusion/ischemia imaging) and/or invasive (coronary angiography) cardiac evaluation is not routine, but it is recommended for new-onset heart failure in the setting of known or suspected coronary artery disease or ischemic symptoms r6r8r18
  • Hemodynamic monitoring via pulmonary artery catheter (right-sided heart catheterization) is not routine, but it may be indicated in critically ill patients and in some noncritically ill patients to obtain additional information r2

Laboratory

  • Routine laboratory tests r2r6r8
    • Obtain on presentation to assist in determining causes of heart failure, identifying risk factors, and assessing baseline kidney function
      • Comprehensive metabolic panel c115
        • Electrolyte, magnesium, calcium, BUN, and creatinine levels c116c117c118c119c120
        • Elevated liver enzyme levels may be due to hepatic congestion or dysfunction c121
      • Fasting blood glucose level c122
        • Diabetes is a common comorbidity and risk factor for heart failure
      • Fasting lipid profile c123
        • To assess risk for coronary artery disease and metabolic syndrome
      • TSH level c124
        • Thyroid disease may mimic, aggravate, or cause heart failure
      • CBC c125
        • Anemia may cause or exacerbate heart failure
      • Urinalysis c126
  • Cardiac biomarker tests r19
    • Natriuretic peptide levels c127c128
      • Hormones secreted by cardiomyocytes with myocardial stretch
      • Elevated B-type natriuretic peptide or N-terminal pro–B-type natriuretic peptide levels support the diagnosis of heart failure in cases of diagnostic uncertainty (eg, if echocardiography is nondiagnostic) or if echocardiography is not available r8r16
        • B-type natriuretic peptide level of 100 pg/mL or more for acute onset or 35 pg/mL or more for nonacute onset suggests heart failure
        • N-terminal pro–B-type natriuretic peptide level of 300 pg/mL or more for acute onset or 125 pg/mL or more for nonacute onset suggests heart failure
      • High degree of sensitivity but low degree of specificity for heart failure; natriuretic peptide levels may be elevated owing to other cardiac and noncardiac causes r20
      • Note that obese patients may have falsely low natriuretic peptide levels
    • Cardiac troponin T or I levels c129c130c131c132
      • Elevated levels:
        • May reflect acute coronary syndrome
        • Are often associated with severe heart failure without an obvious acute ischemic process
      • Decreasing cardiac troponin levels over time suggest improving heart failure and are associated with better prognosis

Imaging

  • Chest radiography r2r6r8c133
    • Indicated for suspected new-onset heart failure and acute decompensated heart failure
    • Posteroanterior and lateral chest views are recommended; supine chest radiography has limited value
    • Has low sensitivity and specificity for heart failure; useful in identifying an alternative pulmonary process causing a patient's symptoms and signs
    • Cardiomegaly and/or pulmonary venous congestion are suggestive of heart failure
      • Characteristic findings are cardiac chamber enlargement, increased pulmonary venous pressure, interstitial or alveolar edema, and valvular or pericardial calcification
      • Increased pulmonary venous pressure may be seen as:
        • Redistribution of blood flow from base of lung to apex
        • Linear densities reflecting interstitial edema
        • Bilateral perihilar haziness in a butterfly pattern

Functional testing

  • ECG r2r7r8c134
    • Perform 12-lead ECG initially on all patients presenting with symptoms of heart failure
    • Less than 2% of patients who have heart failure with systolic dysfunction will have a completely normal ECG result. If results are normal, consider other causes of symptoms. Routine ECG primarily is performed to identify those patients and to detect other abnormalities that may need investigation or treatment r8
    • No particular ECG feature is specific to heart failure
      • Left ventricular hypertrophy may be evident on ECG
      • Q waves indicate myocardium loss due to previous infarction
      • Atrial and ventricular arrhythmias are common
  • 2-dimensional echocardiography with Doppler flow imaging r21r22c135
    • 2-dimensional echocardiography displays cross-sectional view of beating heart, including chambers of heart, valves, and major blood vessels; Doppler flow imaging evaluates blood flow
      • Provides essential information on chamber volumes, wall thickness, wall motion abnormalities, and valve structure
      • Left ventricular ejection fraction and cardiac output can be estimated
      • Diastolic and systolic function of heart can be assessed
      • Pulmonary capillary wedge pressure can be estimated
      • Transthoracic echocardiography is the preferred method
        • Transesophageal echocardiography is an alternative if transthoracic route is nondiagnostic owing to inadequate transthoracic window, which may occur in patients who are obese, have chronic lung disease, and require mechanical ventilation
    • Interpretation r7r8
      • Heart failure with reduced ejection fraction (left ventricular systolic dysfunction) is suggested by:
        • Ejection fraction less than 50%
        • Hypokinesis, akinesis, or dyskinesis
        • Increased left ventricular diameter and volume
        • Decreased outflow velocity
      • Heart failure with preserved ejection fraction (left ventricular diastolic dysfunction) is suggested by: r23
        • Normal or near normal ejection fraction (50% or higher)
        • Abnormal mitral inflow
        • Increased atrial volume
        • Increased left ventricular mass
  • Cardiac MRI r2r7r8c136
    • Alternative to echocardiography for assessing left ventricular volume and ejection fraction; may be used if echocardiography is not diagnostic
    • Provides additional information on myocardial perfusion, viability, and fibrosis
    • Can identify inflammatory and infiltrative causes and provide prognostic information
    • Less accurate than echocardiography with high heart rates
    • Limitations include:
      • Lack of availability
      • Cost
      • Contraindications, including metal implants or severe kidney disease, which precludes use of contrast solution

Procedures

Cardiac catheterization with coronary angiography r2r24c137c138c139c140
General explanation
  • Catheters are placed percutaneously in peripheral blood vessels and advanced into central circulation
  • Measures intravascular pressure, oxygen saturation in heart and great vessels, and cardiac contractility and function
  • Angiography delineates anatomic structures and coronary artery patency
  • Usually performed under light sedation
Indication
  • Patients who have heart failure with anginal symptoms r2
  • May be useful for patients with new-onset heart failure but no anginal symptoms r2
  • Perform in accordance with American College of Cardiology Foundation/American Heart Association guidelines on coronary artery bypass graft and percutaneous coronary intervention, only in patients who are potentially eligible for revascularization r2
Contraindications
  • Severe comorbidities that would preclude revascularization (eg, renal, hepatic, or pulmonary failure or malignancy)
  • Contrast medium allergy
  • Severe anemia
  • Uncontrolled coagulopathy
  • Hemodynamic instability
  • Acute stroke
  • Active infection, sepsis
  • Pregnancy
  • Uncooperative patient
Interpretation of results
  • Can identify ischemic causes for systolic or diastolic dysfunction
Complications
  • Uncommon
    • Stroke
    • Myocardial infarction
    • Bleeding/hematoma
    • Thromboembolism
    • Arrhythmia
    • Allergic reaction to contrast medium
    • Blood vessel perforation
    • Death

Differential Diagnosis

Most common

  • Conditions that cause dyspnea r25
    • Chronic obstructive pulmonary disease r26c141d1
      • Group of chronic and progressive pulmonary diseases (emphysema and chronic bronchitis) that limit airflow; occur nearly exclusively in smokers
      • Similar feature: chronic dyspnea
      • Differing features: great variation of dyspnea from day to day, productive cough, rhonchi and/or expiratory wheezing on auscultation, hyperinflation (barrel chest), and hyperresonant chest sounds
      • Diagnosed by: spirometry shows decreased pulmonary function; chest radiography may show diaphragm flattening, increased retrosternal air space, and/or bronchovascular markings
      • Chronic obstructive pulmonary disease may coexist with heart failure
    • Asthma c142d2
      • Chronic inflammatory condition of airways that produces edema and bronchoconstriction; episodes are often caused by triggers (eg, allergens, exercise, infection)
      • Similar features: wheezing and dyspnea
      • Differing features: typically earlier age of onset; episodic and reversible symptoms of airflow obstruction, often after triggers; and chest tightness
      • Diagnosed by: spirometry with postbronchodilator response; chest radiography may show hyperinflation
    • Pulmonary embolism r27c143d3
      • Pulmonary artery or branch artery is suddenly occluded, most often because of a dislodged thrombus
      • Similar features: dyspnea, tachypnea, and tachycardia
      • Differing features: abrupt onset of chest pain, which may be pleuritic; hypoxia; and sometimes hemoptysis
      • Diagnosed by: CT angiography detects pulmonary emboli; D-dimer levels are elevated
    • Myocardial infarction r28c144d4
      • Myocardial necrosis resulting from occlusion of a coronary artery
      • Similar features: dyspnea and fatigue
      • Differing features: retrosternal chest pain and/or pressure (radiating to neck, jaw, shoulder, and/or arm) is typical; atypical presentation without chest pain may occur in women, elderly people, and those with diabetes
      • Diagnosed by: ECG shows ST elevation, ST depression, or T-wave inversion; cardiac troponin levels are elevated
    • Pneumonia c145
      • Acute inflammation of lung tissue caused by infection
      • Similar features: tachypnea, tachycardia, rales, and wheezing
      • Differing features: productive cough, fever and rigors, rhonchi, and hypoxia
      • Diagnosed by: chest radiography shows lobar or lobular consolidation; viral or atypical bacterial pneumonias often appear as interstitial infiltrates
    • Acute respiratory distress syndrome c146d5
      • Severe and often fatal acute respiratory failure; characterized by diffuse inflammatory lung injury rapidly progressing to increased pulmonary vascular permeability, increased lung weight, and hypoxemia
      • Similar features: dyspnea, cough, tachypnea, tachycardia, and pulmonary edema
        • Cardiogenic and noncardiogenic pulmonary edema can coexist
      • Differing features: cardiac biomarker levels are less likely to be elevated; echocardiographic findings are more likely to be within reference range
      • Diagnosed by: history, physical examination, arterial blood gas levels, and chest radiography or CT
        • Criteria include timing of symptoms (within 1 week of a known clinical insult such as pneumonia, sepsis, or trauma), hypoxemia (as shown by blood gas levels), bilateral opacities not otherwise explained and not cardiogenic in nature, and respiratory failure or pulmonary edema not fully explained by heart failure or fluid overload
  • Conditions that cause edema r25
    • Cirrhosis c147d6
      • Irreversible liver disease caused by long-term excessive alcohol intake or viral hepatitis
      • Similar features: peripheral edema and ascites; dyspnea may be present because of ascites
      • Differing features: stigmata of liver disease are usually present; liver function test results are outside reference range
      • Diagnosed by: abdominal sonography or other abdominal imaging shows liver nodularity and features of portal hypertension; definitive diagnosis is by liver biopsy
    • Nephrotic syndrome c148
      • Renal disease affecting kidney basement membrane, resulting in heavy proteinuria and hypoalbuminuria
      • Similar features: peripheral edema (including edema of face/eyes) and ascites
      • Differing features: dyspnea may occur but is usually exertional only and associated with pleural effusion and very low protein levels
      • Diagnosed by: high random urine protein to creatinine ratio is suggestive; protein excretion of 3.5 g or more per 24 hours confirms. Renal biopsy confirms renal pathology

Treatment

Goals

  • For acute decompensated heart failure or de novo heart failure: r2r8
    • Identify and reverse precipitating factors
    • Maintain oxygenation and hemodynamic stability
    • Relieve symptoms
  • For chronic stable heart failure, goals depend on disease stage (American College of Cardiology Foundation/American Heart Association) and classification (New York Heart Association) and generally include the following: relieve symptoms, prevent hospitalizations, improve quality of life and functional capacity, and reduce mortality r2r8
    • For patients in stage A, goal is risk factor modification to prevent disease
    • For patients in stage B or class I, goal is to prevent symptoms and progressive cardiac remodeling
    • For patients in stage C or class II and class III, goals are to control symptoms, improve quality of life, prevent hospitalization, and prevent mortality
    • For patients in stage D or class IV, goals are to control symptoms, improve quality of life, reduce hospital readmissions, and explore alternative treatments (eg, mechanical circulatory support, heart transplant)
    • There is no evidence of benefit from antiplatelet drugs (including aspirin) in patients with chronic stable heart failure unless concomitant coronary artery disease is present. Likewise, oral anticoagulants are not recommended unless atrial fibrillation or known cardiac thrombus is present r3

Disposition

Admission criteria r2

Patients with de novo acute heart failure or acute decompensated heart failure: admit for appropriate laboratory tests, imaging, and start of treatment

Specific heart failure admission indications include:

  • Evidence or suspicion of acute myocardial ischemia or infarction
  • Respiratory distress and/or pulmonary edema
  • Significant arrhythmias
  • Syncope or symptomatic hypotension
  • Significant electrolyte abnormalities
  • Anasarca
  • Thromboembolic complications requiring inpatient treatment
  • Severe comorbidities
Criteria for ICU admission r2r29
  • Respiratory failure needing advanced respiratory support including endotracheal intubation and noninvasive positive pressure ventilation
  • Hemodynamic instability needing pharmacologic or mechanical support

Recommendations for specialist referral

  • Cardiologist for diagnostic evaluation of heart failure causes and optimization of medical management
  • Cardiothoracic surgeon for coronary revascularization surgery and/or ventricular assist device
  • Electrophysiologist for implantation of cardiac defibrillator and/or cardiac resynchronization therapy
  • Transplant specialist for heart transplant and management of immunosuppressant therapy
  • Nephrologist for associated kidney disease and treatment with ultrafiltration
  • Geriatrician for critical decisions on elderly patients with multiple comorbidities
  • Palliative care specialist for end-of-life decisions

Treatment Options

Management of acute heart failure (either decompensated or de novo)

  • Obtain IV access and begin supplemental oxygen via noninvasive positive pressure ventilation (either CPAP or bilevel positive airway pressure) r30
  • Identify and manage immediate life-threatening conditions, if present (eg, unstable arrhythmia, acute coronary syndrome) r2
    • May require advanced cardiac life support (eg, endotracheal intubation, cardioversion, cardiac pacing) depending on organ system dysfunction
    • May require cardiac catheterization and percutaneous coronary intervention
  • Identify and manage other potential precipitating causes of decompensation r2
    • Uncorrected high blood pressure, atrial fibrillation and other arrhythmias, acute or worsening valvular disease, medication nonadherence, recent addition of negative inotropic drugs, dietary sodium indiscretion, acute kidney injury or worsening chronic kidney disease, anemia, acute infection, thyroid disorders, excessive alcohol intake or illicit drugs, and others r31
  • Alleviate symptoms
    • Provide loop diuretics and monitor urine output for all patients with evidence of fluid overload r2
      • If patient is already using outpatient loop diuretic therapy, give an initial IV dose that equals or exceeds the long-term oral daily dose
      • Short-term infusion of inotropic agents, in addition to loop diuretic, may improve diuresis in patients with hypotension and evidence of hypoperfusion (cardiogenic shock)
      • May consider a vasopressor for patients who have persistent evidence of cardiogenic shock despite inotrope use
      • Consider ultrafiltration if diuretic strategies are unsuccessful
    • In patients hospitalized with volume overload and severe hyponatremia, consider vasopressin antagonists r2
    • If patient is not hypotensive and diuresis is inadequate, consider adjuvant therapy with a vasodilator (eg, IV nitroglycerin, nitroprusside) r2
      • Use vasodilators with caution in patients with preserved ejection fraction who are typically more volume sensitive r2
      • Nesiritide (recombinant human B-type natriuretic peptide) is no longer routinely used for treatment of acute decompensated heart failure in the United States r32
    • Invasive hemodynamic monitoring with pulmonary artery catheter is not routine but may help guide therapeutic decision-making if persistent symptoms or volume status is uncertain r2
    • Continue usual goal-directed outpatient medical therapy for patients who have chronic heart failure with reduced ejection fraction except in cases of hemodynamic instability r2
    • Begin β-blocker therapy at low dose after optimization of volume status and discontinuation of IV agents r2

Management of stable chronic heart failure depends on disease stage r2

  • Stage A (at high risk for heart failure without structural heart disease or symptoms, based on risk factors of hypertension, dyslipidemia, diabetes, and obesity)
    • Manage comorbid hypertension, lipid disorders, diabetes, and obesity according to relevant guidelines r2
    • Counsel and assist patient with smoking cessation, alcohol restriction or discontinuation, and cardiotoxic agent avoidance r2
  • Stage B (structural heart disease, such as ventricular remodeling, left ventricular hypertrophy, or ventricular dilation, without signs and symptoms of heart failure) r2
    • All recommendations for patients with stage A heart failure also apply to those with stage B heart failure; in addition, the following apply: r2
      • Pharmacologic therapy
        • ACE inhibitor r2
          • Indicated for all patients with reduced ejection fraction; angiotensin receptor blocker is an alternative if ACE inhibitors are not tolerated
          • Prevents symptoms and reduces mortality in New York Heart Association class I heart failure by inhibiting the renin-angiotensin-aldosterone system; decreases cardiac remodeling
        • β-blocker r2
          • Indicated for all patients with reduced ejection fraction (in conjunction with an ACE inhibitor), unless specific contraindications exist
          • Consider for patients with history of myocardial infarction even if ejection fraction is not reduced r3
          • Prevents symptoms and reduces mortality by blocking catecholamines and slowing the heart rate, which allow for improved ventricular filling; improves ejection fraction
        • Statin r2r3
          • Indicated for all patients with history of myocardial infarction or at high risk of coronary artery disease; otherwise, not recommended strictly for heart failure
    • Device therapy
      • Implantable cardioverter-defibrillator for primary prevention of sudden death is reasonable in selected patients with history of myocardial infarction and asymptomatic ischemic cardiomyopathy r2
  • Stage C (structural heart disease with prior or current symptoms of heart failure)
    • All recommendations for patients with stage A also apply to those with stage C heart failure; in addition, the following apply: r2
      • Reduced ejection fraction r2
        • Pharmacologic therapy
          • Inhibition of the renin-angiotensin-aldosterone system with an ACE inhibitor or with an angiotensin receptor blocker or with an angiotensin receptor–neprilysin inhibitor—in conjunction with evidence-based β-blockers and aldosterone antagonists in selected patients—is recommended for patients with chronic heart failure with reduced ejection fraction r17
            • Use an ACE inhibitor for patients with current or prior symptoms of chronic heart failure with reduced ejection fraction; confers morbidity and mortality benefit r17
              • No superior morbidity or mortality benefit is associated with any specific ACE inhibitor r33
            • Use an angiotensin receptor blocker for patients with prior or current symptoms of chronic heart failure with reduced ejection fraction who are intolerant to ACE inhibitors owing to cough or angioedema. This medication also confers morbidity and mortality benefit r17
            • In patients with chronic symptomatic heart failure with reduced ejection fraction (New York Heart Association class II or III) who tolerate an ACE inhibitor or angiotensin receptor blocker, it is recommended to replace these medications with an angiotensin receptor–neprilysin inhibitor to further reduce morbidity and mortality r17
              • Do not give angiotensin receptor–neprilysin inhibitor concomitantly with ACE inhibitors or within 36 hours of the last dose of an ACE inhibitor (unacceptable risk of angioedema) r17
              • Do not give angiotensin receptor–neprilysin inhibitor to patients with history of angioedema r17
              • Increases risk of hypotension r33
          • Use β-blocker in all patients (ie, 1 of the 3 β-blockers proven to reduce mortality: long-acting metoprolol, bisoprolol, and carvedilol) r17
          • Use aldosterone receptor antagonists (mineralocorticoid receptor antagonists) in selected patients: r17
            • New York Heart Association class II to IV heart failure with left ventricular ejection fraction of 35% or less, to reduce morbidity and mortality r2
              • Patients with class II heart failure should have a history of prior cardiovascular hospitalization or elevated plasma natriuretic peptide levels to be considered for aldosterone receptor antagonists r2
            • After acute myocardial infarction in patients with left ventricular ejection fraction of 40% or less who develop symptoms of heart failure or who have history of diabetes mellitus r2
            • Creatinine level should be 2.5 mg/dL or less in men and 2 mg/dL or less in women (or estimated GFR more than 30 mL/minute/1.73 m²), and potassium level should be less than 5 mEq/L r2
          • Ivabradine can help reduce hospitalization for selected patients (approved in the United States in 2015; reduces heart rate by selective inhibition of alternative sinoatrial node current) r17
            • Symptomatic (New York Heart Association class II or Ill) stable chronic heart failure with reduced ejection fraction in which left ventricular ejection fraction is 35% or less, andr33
            • Already receiving maximally tolerated β-blocker, ACE inhibitor, angiotensin receptor blocker, or angiotensin receptor–neprilysin inhibitor and mineralocorticoid receptor antagonist, andr33
            • In sinus rhythm with heart rate of 70 or more beats per minute at rest r33
          • Use diuretics in all patients with evidence of fluid retention, unless contraindicated, to improve symptoms r2
            • Loop diuretics are preferred unless patient is hypertensive and has only mild fluid retention, in which case thiazide diuretics may be reasonable
              • No differences between specific loop diuretics in their effects on symptoms or survival
          • Consider hydralazine plus isosorbide dinitrate for persistently symptomatic Black patients (New York Heart Association class III or IV) despite concomitant use of ACE inhibitors, β-blockers, and aldosterone receptor antagonists r2
          • Can consider digoxin (unless contraindicated) for additional symptom relief; use caution in patients taking other drugs that can depress sinus or atrioventricular nodal function or affect digoxin levels (eg, amiodarone, β-blocker) r2
          • Manage atrial fibrillation, if present, according to current guidelines, including anticoagulation r2d7
          • Increasing evidence suggests a class of oral hypoglycemic agent, sodium glucose cotransporter-2 inhibitors, may have a place in therapy for heart failure with reduced ejection fraction, even in patients without type 2 diabetes r34
            • Dapagliflozin reduces symptoms, hospitalizations, and cardiac mortality in patients both with and without diabetes r35
            • Sodium glucose cotransporter-2 inhibitors may play role in patients refractory to standard guideline-directed therapy r36
        • Device therapy
          • Implantable cardioverter-defibrillator therapy is indicated for primary prevention of sudden cardiac death in selected patients who are expected to live more than 1 year r2
          • Cardiac resynchronization therapy (biventricular pacing) is indicated for selected patients r2
      • Preserved ejection fraction
        • These treatments are also recommended for patients with borderline (mid-range) ejection fraction, as these patients have generally been included in trials of heart failure with preserved ejection fraction r3
        • Pharmacologic therapy
          • No convincing evidence of morbidity or mortality benefit r3
          • Recommended therapies for heart failure with preserved ejection fraction are symptom-directed or for management of comorbidities r17
            • Systolic and diastolic blood pressure control is particularly important; β-blockers, ACE inhibitors, and angiotensin receptor blockers are reasonable choices r17
            • Manage atrial fibrillation, if present, according to current guidelines, including anticoagulation r17
            • Use diuretics for symptom relief r17
            • Can consider angiotensin receptor blockers to decrease hospitalizations r17
            • Consider aldosterone receptor antagonists to decrease hospitalizations in patients who meet all of the following criteria: r17
              • Ejection fraction 45% or higher
              • Elevated B-type natriuretic peptide levels or heart failure admission within 1 year
              • Estimated GFR higher than 30 mL/minute
              • Creatinine level lower than 2.5 mg/dL
              • Potassium level lower than 5 mEq/L
          • Refer for coronary revascularization patients with angina or demonstrable cardiac ischemia despite medical management of heart failure r17
  • Stage D (symptoms refractory to optimal goal-directed medical therapy; also known as advanced heart failure or end-stage heart failure)
    • Carefully reconsider diagnosis to ensure that there are no remedial or alternative causes for symptoms before labeling the condition refractory heart failurer2
    • Treatment of advanced heart failure is often palliative; reevaluate quality of indicators to avoid prolongation of futile efforts
    • Pharmacologic therapy r2
      • Use IV inotropic support with dopamine (also promotes renal blood flow at low doses), dobutamine, or milrinone to maintain systemic perfusion and preserve end-organ performance r2
        • As short-term therapy (until resolution of acute precipitating event)
        • As bridge therapy (for patients waiting for mechanical circulatory support or heart transplant)
        • As long-term palliative/destination therapy (for patients ineligible for mechanical circulatory support or heart transplant)
    • Mechanical circulatory support r2
      • Temporary ventricular assist devices (percutaneous and extracorporeal) are indicated as bridge therapy, allowing time for either improvement or clinical decision making for carefully selected patients with reduced ejection fraction and marked hemodynamic compromise
      • Durable mechanical circulatory support can prolong survival for carefully selected patients with severe heart failure with reduced ejection fraction (destination therapy)
    • Heart transplant r2
      • Indicated for carefully selected patients with stage D heart failure despite optimal medical therapy, device therapy, and surgical management
      • Donated hearts are scarce; bridge therapy must maintain patient during wait for transplant

Drug therapy c149c150

  • ACE inhibitors r8c151
    • Enalapril c152
      • Enalapril Maleate Oral tablet; Adults: Initially, 2.5 mg PO twice daily. Reduce initial dose to 2.5 mg PO once daily in patients with hyponatremia. Increase dose as tolerated, adjusting to clinical response of patient up to Max: 10 to 20 mg PO twice daily.
    • Lisinopril c153
      • Lisinopril Oral tablet; Adults: Initially, 2.5 to 5 mg PO once daily. Increase dose as tolerated, adjusting to clinical response of patient up to Max: 20 to 40 mg/day.
    • Captopril c154
      • Captopril Oral tablet; Adults: Initially, 6.25 mg PO 3 times daily. Increase dose as tolerated, adjusting to clinical response of patient up to Max: 50 mg PO 3 times daily.
  • Angiotensin receptor blockers r8c155
    • Candesartan c156
      • Candesartan Cilexetil Oral tablet; Adults: Initially, 4 to 8 mg PO once daily. Increase dose as tolerated, adjusting to clinical response of patient up to Max: 32 mg/day.
    • Losartan c157
      • Losartan Potassium Oral tablet; Adults: Initially, 25 to 50 mg PO once daily. Increase dose as tolerated, adjusting to clinical response of patient up to Max: 50 to 150 mg/day.
    • Valsartan c158c159
      • Valsartan Oral tablet; Adults: Initially, 20 to 40 mg PO twice daily. Increase dose as tolerated, adjusting to clinical response of patient up to up to Max: 160 mg PO twice daily.
  • Angiotensin receptor–neprilysin inhibitor r8
    • Sacubitril-valsartan c160
      • Sacubitril, Valsartan Oral tablet; Adults: 24 mg sacubitril; 26 mg valsartan PO twice daily in patients not taking or on a low dose of an ACE inhibitor or ARB. 49 mg sacubitril; 51 mg valsartan PO twice daily in patients taking a high dose of an ACE inhibitor or ARB. Double the dose every 2 to 4 weeks as tolerated to a target dose of 97 mg sacubitril; 103 mg valsartan PO twice daily.
  • β-blockers r8c161c162
    • Bisoprolol c163c164
      • Bisoprolol Fumarate Oral tablet; Adults: Initially, 1.25 mg PO once daily for 48 hours, then 2.5 mg PO once daily for first month, then 5 mg PO once daily. Max: 10 mg PO once daily.
    • Carvedilol c165c166
      • Carvedilol Oral tablet; Adults: Initially, 3.125 mg PO twice daily for 2 weeks. Increase dosage to 6.25, 12.5, and then 25 mg PO twice daily over intervals of at least 2 weeks as tolerated. Max: 50 mg PO twice daily. Reduce dose for bradycardia.
    • Metoprolol succinate c167c168
      • Metoprolol Succinate Oral tablet, extended-release; Adults: Initially, 25 mg PO once daily in patients with NYHA class II heart failure or 12.5 mg PO once daily in patients with more severe heart failure. Double the dose every 2 weeks as tolerated, up to target dosage of 200 mg PO once daily.
  • Aldosterone receptor antagonists r8c169
    • Eplerenone c170
      • Eplerenone Oral tablet; Adults: Initially, 25 mg PO once daily. Increase dosage to 50 mg PO once daily as tolerated within 4 weeks. Coadministration of certain drugs may need to be avoided or dosage adjustments may be necessary; review drug interactions. Monitor serum potassium at baseline, within first week, and at 1 month after dosage initiation or adjustments; monitor more frequently in at-risk patients. If serum potassium 5.5 mEq/L or more, decrease dosage. Hold if serum potassium 6 mEq/L or more; may restart at 25 mg PO every other day once serum potassium less than 5.5 mEq/L.
    • Spironolactone c171
      • Spironolactone Oral tablet; Adults: Initially, 12.5 to 25 mg PO once daily. May reduce dosage to 25 mg PO every other day if hyperkalemia occurs with 25 mg PO once daily. May increase dosage to 50 mg/day, if clinically indicated and lower dose tolerated.
  • Loop diuretics r8c172
    • Furosemide c173
      • Furosemide Oral tablet; Adults: Initially, 20 to 80 mg PO as a single dose; may repeat dose in 6 to 8 hours. Usual dose: 40 to 120 mg/day. Max: 600 mg/day.
      • Furosemide Solution for injection; Adults: Initially, 40 mg IV injected slowly. May give 80 mg injected slowly in 2 hours if needed.
    • Bumetanide c174c175
      • Bumetanide Oral tablet; Adults: 0.5 to 1 mg PO daily initially. Multiple daily doses may be given at 4 to 5 hour intervals if the initial diuretic response is not adequate. Max: 10 mg/day.
      • Bumetanide Solution for injection; Adults: 0.5 to 1 mg IV or IM initially. If the desired response is not achieved, administer a second or third dose at 2 to 3 hour intervals. Max: 10 mg/day.
    • Torsemide
      • Torsemide Oral tablet; Adults: Initially, 10 to 20 mg PO once daily. If needed, titrate by doubling the dose up to a maximum of 200 mg.
  • Thiazide diuretics r8c176
    • Hydrochlorothiazide c177
      • Hydrochlorothiazide Oral tablet; Adults: 25 to 100 mg/day PO given in single or divided doses. Many patients respond to intermittent therapy (e.g., every other day or 3 to 5 days each week).
    • Indapamide c178c179
      • Indapamide Oral tablet; Adults: Initially, 2.5 mg PO once daily. May increase dosage up to 5 mg PO once daily after 1 week if response is inadequate. Doses greater than 5 mg have not appeared to provide additional benefits and are associated with greater degree of hypokalemia.
    • Metolazone c180
      • Metolazone Oral tablet; Adults: 5 to 20 mg PO once daily.
  • Vasodilators r8c181
    • Hydralazine c182
      • Hydralazine Hydrochloride Oral tablet; Adults: Initially, 25 to 50 mg PO 3 to 4 times daily. Dosage may be increased weekly (e.g., by 25 mg/dose) to Max: 100 mg PO 3 times daily.
    • Isosorbide dinitrate c183
      • Isosorbide Dinitrate Oral tablet; Adults: Initially, 20 to 30 mg PO 3 to 4 times daily. Titrate dose at weekly intervals up to Max: 40 mg PO 3 times daily.
    • Nitroglycerin c184
      • Nitroglycerin Solution for injection; Adults: Initially, 5 mcg/minute continuous IV infusion. Titrate by 5 mcg/minute IV every 3 to 5 minutes until clinical response, or to a dose of 20 mcg/minute IV. May further increase dosage in increments of 10 mcg/minute, and if desired effect still not achieved, may increase in increments of 20 mcg/minute. Max titration: 20 mcg/minute every 3 to 5 minutes. Usual dose: 5 to 100 mcg/minute. Max: 200 mcg/minute.
    • Nitroprusside c185
      • Sodium Nitroprusside Solution for injection; Adults: 0.3 to 0.5 mcg/kg/minute continuous IV infusion, initially. Titrate by 0.5 mcg/kg/minute every 5 minutes until desired effect or blood pressure cannot be further reduced without compromising organ perfusion. Max: 10 mcg/kg/minute for 10 minutes.
    • Nesiritide c186
      • No longer routinely used for acute decompensated heart failure in the United States
      • Should not be used before traditional nitrates except by intensive care cardiologists familiar with potentially adverse hemodynamic effects
      • Nesiritide (E. coli) Solution for injection; Adults: 2 mcg/kg IV followed by 0.01 mcg/kg/minute continuous IV infusion. May titrate up no more frequently than every 3 hours. Max: 0.03 mcg/kg/minute. Loading dose may not be appropriate for patients with low systolic blood pressure or patients recently treated with afterload reducers. If hypotension occurs, reduce dose or discontinue nesiritide. May restart at a dose that is reduced by 30% (with no bolus administration) after stabilization of hemodynamics. Limited experience with use for longer than 96 hours.
  • Hyperpolarization-activated cyclic nucleotide–gated channel blocker r8c187c188
    • Ivabradine c189
      • Ivabradine Oral tablet; Adults: 5 mg PO twice daily initially. Start at 2.5 mg PO twice daily in patients with conduction defects or in those whom bradycardia could lead to hemodynamic compromise. After 2 weeks, adjust dose to achieve resting heart rate of 50 to 60 bpm. For resting heart rate more than 60 bpm, increase dose by 2.5 mg PO twice daily. For resting heart rate of 50 to 60 bpm, maintain current dose. For a resting heart rate less than 50 bpm or symptomatic bradycardia, decrease dose by 2.5 mg PO twice daily; if current dose is 2.5 mg PO twice daily, discontinue therapy. After that, adjust dose as needed based on resting heart rate and tolerability. Max: 7.5 mg PO twice daily.
  • Digitalis glycoside r8c190
    • Digoxin c191
      • Digoxin Oral tablet; Adults, Adolescents, and Children older than 10 years: Initially, 3.4 to 5.1 mcg/kg/day PO given once daily. Usual daily maintenance dose requirements for the treatment of congestive heart failure are based on corrected CrCl (mL/minute per 70 kg or mL/minute/1.73m2) and lean body weight (LBW). Doses are rounded to the nearest whole/half tablet. According to the Beers Criteria, digoxin should be avoided as first-line therapy for atrial fibrillation or heart failure; if use is necessary, the drug should not be prescribed in daily doses greater than 0.125 mg.
  • Inotropic agents r8c192
    • Dopamine c193
      • Dopamine Hydrochloride Solution for injection; Adults: 2 to 5 mcg/kg/minute continuous IV infusion, initially. Titrate by 5 to 10 mcg/kg/minute until goal hemodynamic and/or renal response is attained. Usual dose: 5 to 15 mcg/kg/minute. Max: 50 mcg/kg/minute
    • Dobutamine c194
      • Dobutamine Hydrochloride Solution for injection; Adults: 0.5 to 1 mcg/kg/minute continuous IV infusion; titrate to clinical response. Usual dosage range: 2 to 20 mcg/kg/minute. Max: 40 mcg/kg/minute.
    • Milrinone c195
      • Milrinone Lactate Solution for injection; Adults: 50 mcg/kg IV load, then 0.125 to 0.75 mcg/kg/minute continuous IV infusion.

Nondrug and supportive care

Dietary recommendations

  • At least 1 session of nutritional evaluation and counseling is recommended for patients with heart failure r37
    • Ensure adequate intake of macro and micronutrients
    • Recommend DASH (dietary approaches to stop hypertension) or Mediterranean style diet of patients of normal weight r38
    • Recommend weight loss of 5% to 10% for patients with BMI 35 kg/m² or higher
    • Aim for protein intake of at least 1.1g/kg/day for patients with malnutrition or cachexia (develops in 10%-20% of patients with heart failure)
  • American College of Cardiology Foundation/American Heart Association guideline recommends: r2c196c197
    • Restrict sodium to 1500 mg/day or less for patients with stage A and B heart failure
    • Consider some degree of sodium restriction (eg, less than 3 g/day) for patients with stage C and D heart failure, while noting that evidence is lacking for this recommendation
  • American Heart Association recommends 1 to 2 meals of seafood per week be included to reduce risk of congestive heart failure, coronary heart disease, ischemic stroke, and sudden cardiac death r39
    • Marine omega-3 supplementation of 1 g/day is recommended for primary prevention for individuals who do not consume at least 1.5 fish or seafood meals per week r40
    • High-dose marine omega-3 supplements are recommended for patients with congestive heart disease who are taking statins who and have elevated triglycerides r40

Exercise

  • For adults with congestive heart failure and heart failure with reduced ejection fraction, recommend exercise interventions (eg, cardiac rehabilitation), stressing full adherence to recommended regimens r38
  • In adults with chronic heart failure with reduced ejection fraction, evidence suggests that exercise training (eg, cardiac rehabilitation) reduces all-cause hospitalizations, reduces hospitalizations due to heart failure in the short term, improves quality of life, and reduces long-term mortality. r17r41

General recommendations

  • Order careful intake and output measurements in acute care setting c198
  • Order daily weight monitoring on inpatient and outpatient basis; have patient or caregiver notify physician for overnight gain of 0.9 kg or more or gain in 1 week of 2.3 kg or more c199
  • Advise and assist with moderation or elimination of alcohol intake, owing to its negative effect on ventricular systolic function c200
  • Advise and assist with smoking cessation c201d8
    • Smoking increases myocardial oxygen consumption (via increased heart rate and blood pressure) and decreases myocardial oxygen supply
  • Vaccinations
    • Pneumococcal vaccine and annual influenza vaccine are recommended unless contraindicated c202c203

Provide patients and caregivers with comprehensive education about heart failure, medication regimens, and lifestyle modifications r2r8c204c205

Procedures
Implantable cardioverter-defibrillator therapy r2c206
General explanation
  • Cardioverter-defibrillator is implanted to perform cardioversion, defibrillation, and pacing of heart and thereby reduce sudden death from cardiac arrhythmias
  • Decision to implant cardioverter-defibrillator is made by cardiologist or electrophysiologist
Indication
  • Primary prevention of sudden death in selected patients who have heart failure with reduced ejection fraction (European guidelines differ slightly) r2r3
    • Left ventricular ejection fraction of 35% or less caused by prior myocardial infarction, with New York Heart Association class II or III symptoms on optimal medication therapy
    • Left ventricular ejection fraction of 30% or less caused by prior myocardial infarction, with New York Heart Association class I symptoms on optimal medication therapy
    • Left ventricular ejection fraction of 40% or less with sustained ventricular tachycardia or inducible ventricular fibrillation on electrophysiology study
    • Left ventricular ejection fraction of 35% or less with nonischemic dilated cardiomyopathy
  • Secondary prevention of sudden death in selected patients with heart failure
    • Prior cardiac arrest
    • Sustained ventricular arrhythmias
Contraindications
  • Less than 40 days after myocardial infarction
    • Less than 90 days after revascularization
  • Life expectancy of less than 1 year of meaningful survival
Interpretation of results
  • Decrease in mortality from sudden cardiac death associated with arrhythmias r2
Complications r42
  • Bleeding or pneumothorax related to procedural access
  • Infection
  • Lead malfunction, including oversensing (delivery of inappropriate shocks) and undersensing (not delivering a shock when indicated)
  • Generator malfunction
Cardiac resynchronization therapy r2c207
General explanation
  • Biventricular pacemaker is implanted to pace both right and left ventricles of the heart simultaneously in order to improve ventricular contractility and function, reverse ventricular remodeling, and diminish secondary mitral regurgitation
Indication
  • Patients who have left ventricular ejection fraction of 35% or less with sinus rhythm, left bundle branch block with QRS interval of 150 milliseconds or more, and New York Heart Association class II, class III, or ambulatory class IV symptoms on optimal medication therapy r2
  • May also be useful in: r2
    • Patients who, despite optimal medication therapy, have left ventricular ejection fraction of 35% or less with sinus rhythm; non–left bundle branch block with QRS interval of 150 milliseconds or more; and class III or ambulatory class IV symptoms
    • Patients who, despite optimal medication therapy, have left ventricular ejection fraction of 35% or less with sinus rhythm; left bundle branch block with QRS interval of 120 to 149 milliseconds; and class II, class III, or ambulatory class IV symptoms
    • Patients with atrial fibrillation who, despite optimal medication therapy, have left ventricular ejection fraction of 35% or less, and
      • Ventricular pacing is required, or
      • Patient meets other cardiac resynchronization therapy requirements and rate control medication or atrioventricular nodal ablation allows virtually 100% ventricular pacing with cardiac resynchronization therapy
    • Patients who, despite optimal medication therapy, have left ventricular ejection fraction of 35% or less and are undergoing new or replacement device implantation for ventricular pacing of more than 40%
Contraindications
  • Functional status or life expectancy reduced by noncardiac chronic comorbidities
Interpretation of results
  • Decrease in mortality and functional improvements in oxygen consumption, exercise tolerance, and quality of life r2
Complications
  • Bleeding or pneumothorax related to procedural access
  • Infection
  • Lead failure
  • Generator failure
Ultrafiltration r2r43c208
General explanation
  • Renal replacement therapy to mechanically remove fluid from body by using hydrostatic pressure across a semipermeable membrane to separate isotonic plasma water from blood r44
Indication
  • Used for selected patients with advanced heart failure, diuretic resistance, and worsening renal function
Contraindications
  • Inability to take required anticoagulants
Interpretation of results
  • Weight loss and improvement of symptoms (eg, improved dyspnea) are positive results
Complications
  • Bleeding
  • Infection
  • Hypotension
Mechanical circulatory support r2r6c209
General explanation
  • Ventricular assist device provides hemodynamic support in patients with end-stage heart failure refractory to medical therapy by restoring cardiac output, improving end-organ function, and promoting physiologic recovery
  • May be extracorporeal (temporary) or implanted (permanent); may use left ventricular or biventricular modes
Indication
  • Patients who have end-stage heart failure with reduced left ventricular ejection fraction refractory to optimal medication therapy
  • May be considered a bridge to transplant (temporary) or a destination therapy (permanent) in patients who are not transplant candidates
Contraindications
  • Complex, include lack of family support system
Interpretation of results
  • Prolonged survival; 6-month survival while supported on a device has been measured as approximately 75% r45
  • In 1 study, the 1-year survival rate for those on a left ventricular assist device with medical therapy was 52%, versus 25% for those on medical therapy alone r6
Complications
  • Vary depending on type of device
Heart transplant r2r6c210
General explanation
  • Surgical procedure in which failing heart is removed and replaced with healthy donor heart; curative of refractory end-stage heart failure
Indication
  • Patients with end-stage heart failure with functional limitations refractory to optimal medication therapy
Contraindications
  • Advanced age
  • Obesity
  • Diabetes mellitus with widespread microvascular complications
  • Irreversible pulmonary disease or acute pulmonary emboli
  • Irreversible chronic kidney disease
  • Infection
  • Malignancy
  • Smoking
  • Polysubstance abuse
  • Other psychosocial comorbidities that would limit survival
Interpretation of results
  • 1-year transplant survival rate is 88%; 5-year survival rate is 72% r2r6
Complications
  • Perioperative complications including bleeding and infection
  • Organ rejection
  • Increased risk of infection, hypertension, and diabetes due to immunosuppressive drugs
  • Death

Comorbidities

  • Hypertension c211c212
    • In the Framingham study, 91% of patients with incident heart failure had underlying hypertension r46
    • Control of hypertension is important for all patients with heart failure and is the primary management strategy for those with preserved ejection fraction r2
    • Treatment goals r47
      • In patients at increased risk for heart failure (stage A heart failure), optimal blood pressure in those with hypertension is lower than 130/80 mm Hg as a novel strategy to prevent progression to symptomatic heart failure r17
      • For patients who have heart failure with reduced ejection fraction and hypertension, prescribe guideline-directed management and titrate therapy to attain systolic blood pressure lower than 130 mm Hg r17
        • This is a threshold now associated with improved clinical outcomes but not yet proven by randomized clinical trials in a population with heart failure
      • For patients who have heart failure with preserved ejection fraction and persistent hypertension after management of volume overload, prescribe guideline-directed management and titrate therapy to attain systolic blood pressure lower than 130 mm Hg r17
    • For patients in all stages of heart failure with reduced ejection fraction, antihypertensive therapy with a diuretic (if required for volume overload), an ACE inhibitor/angiotensin II receptor blockers or angiotensin receptor-neprilysin inhibitor, and a β-blocker is recommended based on high-quality, randomized controlled data r17r48
      • Second line agents (mineralocorticoid receptor antagonists or hydralazine) are added as required
      • Avoid nondihydropyridine calcium channel blockers and α-blockers r31
    • For patients who have heart failure with preserved ejection fraction, β-blockers, ACE inhibitor, angiotensin II receptor blockers, and possibly angiotensin receptor-neprilysin inhibitors are reasonable choices to manage blood pressure r17
  • Diabetes mellitus r2r8c213c214
    • Risk factor for, and common comorbidity of, heart failure
      • Each condition independently increases risk for the other
      • Patients with diabetes mellitus without symptomatic heart failure often have subclinical abnormalities of cardiac structure and function and therefore may be American College of Cardiology/American Heart Association stage B
      • Among patients with heart failure, 46% of those aged 65 years or older have diabetes mellitus; this percentage is even higher in younger patients with heart failure r2
    • Having both conditions is associated with worse clinical outcomes
      • Health-related quality of life is worse than for patients with heart failure alone r49r50
      • Higher risk of hospitalization (up to 50% higher)r51 and rehospitalizationr52 with diabetes mellitus
      • Diabetes mellitus increases mortality risk in both ambulatory and hospitalized patients with heart failure r53
        • Overall mortality risk is similar risk for both heart failure with reduced ejection fraction and heart failure with preserved ejection fraction
        • Cardiovascular mortality risk is higher for patients with diabetes mellitus and heart failure with preserved ejection fraction as compared to heart failure with reduced ejection fraction r54r55
    • Management of heart failure in diabetes mellitus
      • Based on benefit in patients who have heart failure with reduced ejection fraction (regardless of diabetes mellitus status), these therapies should routinely be implemented in patients with diabetes mellitus and heart failure with reduced ejection fraction who meet guideline indications: r53
        • RAAS inhibitors
        • Angiotensin receptor-neprilysin inhibitors
        • β-blockers
        • Ivabradine
        • Implantable cardioverter-defibrillators and cardiac resynchronization therapy
    • Management of diabetes mellitus in heart failure
      • Consider glycemic goals, and the impact of heart failure medications on glycemic control
        • Moderate, rather than intensive, glycemic control may be optimal for patients with diabetes mellitus and heart failure
          • U-shaped relationship between mortality and hemoglobin A1C in patients with heart failure (lowest risk of death with modest glucose control and hemoglobin A1C of 7.1%-7.8%) r56
          • Recommend target hemoglobin A1C of 7% to 8% for most patients with heart failure and diabetes r53
          • Less stringent goals may be appropriate for patients with advanced, stage D heart failure not pursuing mechanical circulatory support or transplantation r53
        • ACE inhibitors, angiotensin II receptor blockers, and angiotensin receptor-neprilysin inhibitors have favorable effects on the development of diabetes mellitus and glycemic control in patients with heart failure with reduced ejection fraction r53
        • Spironolactone may modestly worsen glycemic control in patients with diabetes mellitus and heart failure with reduced ejection fraction r53
        • Carvedilol may be preferable to metoprolol succinate and bisoprolol for patients with heart failure with reduced ejection fraction and diabetes mellitus with poor glycemic control r53
      • Management of type 1 diabetes mellitus in patients with heart failure is same as for patients without heart failure
      • In patients with type 2 diabetes mellitus, consider the effect of specific glucose-lowering pharmacotherapies on cardiovascular outcomes r57r58
        • In patients at high risk for heart failure and those with established heart failure, metformin and sodium glucose cotransporter type 2 inhibitors are preferable to use over sulfonylurea drugs r53
          • Metformin
            • First line treatment for most patients with type 2 diabetes mellitus r59r60
            • Reduced mortality and a small reduction in all-cause hospitalization in patients with heart failure compared with control subjects
            • Lower risk of heart failure hospitalization than with sulfonylurea drugs
          • Sodium glucose cotransporter type 2 inhibitors
            • First class of glucose-lowering agents demonstrated to reduce heart failure symptoms, risk of heart failure hospitalization, and death in patients with diabetes mellitus, with and without established diagnosis of heart failure at baseline r61r62r63
            • Empagliflozin, canagliflozin, and dapagliflozin are recommended for treatment of type 2 diabetes in patients with known atherosclerotic cardiovascular disease, patients older than 50 years with additional risk factors for atherosclerotic heart disease, and those with mild-moderate heart failure with reduced ejection fraction r35r62r64r65r66r67
              • Also recommended in patients without type 2 diabetes who have mild to moderate heart failure with reduced ejection fraction as associated with reduced symptoms, hospitalizations, and cardiac mortality r35r62r68
            • Cardiovascular benefit must be balanced with potential risks, including genital candidiasis and other, rare potential complications (ie, euglycemic diabetic ketoacidosis; lower-limb amputation and fractures associated with canagliflozin)
        • Insulin may be considered; should be used with caution and close monitoring only if adequate glycemic control cannot be achieved with metformin and sodium glucose cotransporter type 2 inhibitors; associated with weight gain and increased risk of hypoglycemia r53r58
        • Glucagon-like peptide 1 receptor agonists and dipeptidyl peptidase-4 inhibitors sitagliptin and linagliptin have a neutral effect on heart failure r58
          • Use glucagon-like peptide 1 receptor agonists with caution in patients who have heart failure with reduced ejection fraction and recent decompensation. There are no data to guide use of these medications in heart failure with preserved ejection fraction r53
        • Thiazolidinediones are not recommended for patients with established heart failure; both rosiglitazone and pioglitazone are associated with fluid retention and heart failure events r53r58
        • Do not use dipeptidyl peptidase-4 inhibitor saxagliptin in patients with established heart failure or those at high risk for heart failure r53r58
  • Atrial fibrillation r2r8c215c216
    • Heart failure and atrial fibrillation have a bidirectional association, share many of the same risk factors, and frequently complicate each other
    • Heart failure with atrial fibrillation is associated with worse outcomes, including increase in stroke severity and all-cause mortality. Women have worse outcomes than men r69
    • Best treatment strategies for patients with heart failure and atrial fibrillation are unclear r70
      • Approach (rate control versus restoration of sinus rhythm) may be individualized depending on whether atrial fibrillation is resulting from or contributing to progression of underlying cardiac failure r71
      • Rate control is typically accomplished with β-blockers in patients with heart failure
        • Non-dihydropyridine calcium-channel blockers are contraindicated in patients with left ventricle systolic dysfunction but are reasonable when systolic function is preserved r72
        • Digoxin has been associated with an increase mortality risk in patients with atrial fibrillation and patients with heart failure r73
      • The Atrial Fibrillation and Congestive Heart Failure Trial showed that pharmacological rhythm control is not superior to a rate control strategy for preventing cardiac death. Consider a rhythm control strategy for patients who remain symptomatic despite rate control alone r74
        • Pharmacologic rhythm control options are limited to amiodarone and dofetilide in heart failure with reduced ejection fraction r72
      • Catheter ablation (pulmonary vein isolation) may be superior to both pharmacological rate and rhythm control in patients with both heart failure and atrial fibrillation
        • CASTLE-AF trial showed that, for patients with heart failure with reduced ejection fraction, atrial fibrillation catheter ablation was associated with a significantly lower rate of a composite end point of death from any cause or hospitalization for worsening heart failure r75
        • Catheter ablation appears to be similarly effective for atrial fibrillation (freedom from recurrent atrial arrhythmia; improvements in New York Heart Association functional class; symptom severity) in both heart failure with reduced ejection fraction and heart failure with preserved ejection fraction r76
        • For the overall population, results from CABANA trialr77r78 do not show improved survival with catheter ablation; detailed analysis of the heart failure subgroup in the trial is ongoing and will add additional information r70
      • Atrioventricular nodal ablation and cardiac resynchronization device placement can be useful if other methods fail r2
    • Anticoagulation is typically indicated for the prevention of thromboembolic complications based on the CHA₂DS₂-VASc scoring system r31
  • Coronary artery disease r2r8c217
    • Present in approximately two-thirds of patients with heart failure r2
    • Evaluate patients with heart failure with reduced ejection fraction for coronary artery disease and treat accordingly
    • β-blockers, nitrates, and ACE inhibitors are used to treat both heart failure and ischemic heart disease r79
    • Revascularization may be considered r31
  • Anemia r2r8c218
    • Present in 25% to 40% of patients with heart failure r2
    • Often normocytic and accompanied by an abnormally low reticulocyte count r22
    • Associated with an increased risk of hospitalization and mortality and decreased exercise capacity and quality of life
    • Correct any specific underlying cause (eg, iron, vitamin B₁₂, folate deficiency)
    • In patients with New York Heart Association class II and III heart failure and iron deficiency (ferritin lower than 100 ng/mL or 100-300 ng/mL if transferrin saturation is less than 20%), consider IV iron replacement to improve functional status and quality of life r17r80
    • Patients with heart failure and symptomatic anemia may require RBC transfusion; in patients without symptoms due to anemia, a restrictive transfusion strategy (at hemoglobin levels of 7-8 g/dL) is recommended r81
      • Care must be taken to monitor volume status and avoid overload when transfusion is administered
    • Do not use erythropoietin-stimulating agents to improve morbidity and mortality in patients with anemia and heart failure r17r81
  • Chronic kidney disease r2r8r59c219c220
    • Complex interplay between heart and kidney whereby dysfunction in 1 organ can induce or worsen dysfunction in the other r59
      • Chronic heart failure resulting in chronic kidney disease is described as chronic cardiorenal syndrome
      • Chronic kidney disease resulting in chronic heart failure is described as chronic renocardiac syndrome
    • GFR is reduced in most patients with advanced heart failure
    • Reduced renal function is strongly prognostic of poor outcome
    • Avoid treatment with nephrotoxic agents r31
  • Chronic obstructive pulmonary disease r2r8c221
    • Present in approximately one-third of patients with heart failure r2
    • Associated with poorer functional status and prognosis
    • β-blockers may exacerbate bronchospasm; oral corticosteroids can lead to sodium and fluid retention and thus worsen congestive symptoms
  • Depression r2c222c223
    • Prevalence of 24% to 42%
    • Major depression is common in patients with heart failure during hospitalization and is often not recognized
    • Associated with nonadherence to heart failure therapy and worse prognosis r82
    • Avoid tricyclic antidepressants in patients with heart failure, owing to association with cardiovascular adverse effects; selective serotonin reuptake inhibitors are a safer alternative for these patients r8
  • Hyperlipidemia r2r8c224
    • Most patients with heart failure also have hyperlipidemia
    • Statin therapy has not been shown to improve symptoms of heart failure r83
    • Statin therapy is recommended according to current guidelinesr84 for prevention of atherosclerotic cardiovascular disease; not recommended routinely for heart failure in the absence of other indications r38
  • Sleep disturbances r2r8c225
    • Common owing to orthopnea, paroxysmal nocturnal dyspnea, and nocturnal diuresis associated with diuretic use
    • In addition, obstructive sleep apnea has been noted in about one-third of patients with chronic heart failure r85
    • In patients with New York Heart Association class II through IV heart failure who are suspected to have sleep disordered breathing or excessive daytime sleepiness, consider a formal sleep assessment r17
    • In patients with cardiovascular disease and obstructive sleep apnea, consider CPAP to improve sleep quality and alleviate daytime sleepiness r17
      • However, it is important to differentiate central sleep apnea from obstructive sleep apnea as adaptive servo-ventilation for central sleep apnea may cause harm in patients with systolic heart failure r17

Special populations

  • Women
    • In general, women with heart failure have a survival advantage compared with men r71
      • Women are more likely to have nonischemic heart failure than men
    • Digoxin is associated with increased risk for death in women compared with men, presumably owing to increased serum digoxin levels related to decreased lean body mass and renal function
    • Benefits of treatment with ACE inhibitors, angiotensin II receptor blockers and β-blockers are observed at lower dosages than required by men r86
  • Black populations
    • Age of onset of heart failure is significantly younger in Black populations compared with White populations r6
    • Heart failure in Black populations is less likely due to ischemia and more likely due to hypertension compared with White populations r6
    • Morbidity and mortality are higher in Black populations than in White populations r2
    • ACE inhibitors are less effective and carry increased risk of angioedemar2 in black patients with heart failure compared with white patients with heart failure
    • Use hydralazine and isosorbide dinitrate in addition to, or in place of, ACE inhibitors for Black patients with disease of New York Heart Association class II or higher r2
  • Elderly people
    • Heart failure is associated with increased morbidity and mortality in elderly people; median survival is 2.5 years after hospitalization for heart failure, with a 1-year mortality rate of 25% r6
    • During treatment with ACE inhibitors, β-blockers, and diuretics, it is imperative to monitor volume status, postural hypotension, and cerebrovascular symptoms

Monitoring

  • At each outpatient encounter, assess:
    • Symptoms, activity level, and functional capacity r6
    • Vital signs and volume status (ie, weight change, estimate of jugular venous pressure, presence of peripheral edema or orthopnea) r2
    • Adherence to recommended treatment and therapeutic efficacy r6
  • Monitor electrolyte levels and renal function test results c226c227
    • At least every 6 months in clinically stable patients r6
      • Monitor more frequently if aldosterone antagonists or high-dose diuretics are used, if drug therapies are changed, or if clinical status declines r6
  • American College of Cardiology Foundation/American Heart Association 2017 update to the Heart Failure guidelines states that there is insufficient data to guide recommendation for serial measurement of B-type natriuretic peptide or N-terminal pro–B-type natriuretic peptide level l for guiding optimal therapy in patients with heart failure r2r17
    • Usefulness of routine serial measurement is not established r2r17
    • Measurement of levels at the time of admission for the purpose of diagnosis and prognosis or to determine disease severity at the time of hospital admission has been established r17
  • Serial echocardiograms to monitor ejection fraction and severity of structural remodeling are not routinely recommended, but they may be useful in select patients: r2
    • In those with change in clinical status (significant improvement or worsening)
    • In those with change in treatment
    • In a patient who may be a candidate for device therapy

Complications and Prognosis

Complications

  • Premature death due to pump failure r6r87c228
  • Malignant ventricular arrhythmias r87c229
    • Sustained ventricular tachycardia occurs in up to 10% of patients with advanced heart failure r87c230
    • Electrolyte disturbances, prolonged QT interval, digoxin toxicity, and myocardial ischemia are often the precipitating factors for ventricular arrhythmias
  • Atrial fibrillation r87c231
    • Considered both a cause and a consequence of heart failure; present in about one-third of patients with heart failure r87
    • Mitral valve disease, thyroid disease, sinus node disease, and myocardial infarction are predisposing factors for atrial fibrillation; atrial fibrillation after myocardial infarction with severe left ventricular dysfunction carries a poor prognosis
    • Concurrent heart failure and atrial fibrillation place the patient at high risk for thromboembolic events (eg, transient ischemic attack, stroke, deep vein thrombosis)
  • Thromboembolic events r87c232
    • Annual incidence in patients with heart failure is 2% r87
    • Caused by blood stasis in the dilated cardiac chamber, wall motion abnormalities, atrial fibrillation, and immobility
    • Risk of stroke in patients with severe heart failure is 4%, compared with less than 0.5% in those without heart failure r87

Prognosis

  • For acute decompensated heart failure
    • Prognosis of patients hospitalized with heart failure, and especially those with serial readmissions, is poor
    • Best single predictor for mortality in acute decompensated heart failure is high BUN level (43 mg/dL or more) at admission, followed by low systolic blood pressure (less than 115 mm Hg) and then by high level of serum creatinine (2.75 mg/dL or more) r88
    • Predictive multivariable models have been developed to improve prediction of individual prognosis
      • ADHERE classification, based on ADHERE registry data (Acute Decompensated Heart Failure National Registry) r88
      • American Heart Association Get With the Guidelines score r89
      • EFFECT risk score, based on data from the EFFECT study (Enhanced Feedback for Effective Cardiac Treatment) r90
  • For chronic heart failure
    • Mortality rate for patients with heart failure is approximately 50% within 5 years of diagnosis r2
    • For patients with advanced heart failure, the 1-year survival rate is 50% r1
    • Although chronic heart failure is usually a progressively worsening condition, patients may remain stable or have improvements in ventricular remodeling with appropriate therapy r6
    • Predictive multivariable models have been developed to improve prediction of individual prognosis
      • Seattle Heart Failure Model r91
      • Heart Failure Survival Score r92
      • CHARM risk score, based on data from the CHARM trials (Candesartan in Heart Failure: Assessment of Reduction in Mortality and Morbidity) r93
      • I-PRESERVE score (for heart failure with preserved ejection fraction only), based on data from the I-PRESERVE trial (Irbesartan in Heart Failure With Preserved Systolic Function) r94

Screening and Prevention

Screening c233

Prevention

  • All adults are recommended to follow American College of Cardiology Foundation/American Heart Association guidelines for primary prevention of cardiovascular disease r95
    • Consume a healthy diet and engage in regular physical activity
    • Smoking cessation
    • Weight loss if overweight or obese
    • Interventions (nonpharmacologic or pharmacologic) to reduce blood pressure if elevated
    • Statin therapy in patients with elevated LDL cholesterol, diabetes, or aged 40 to 75 years with elevated risk of atherosclerotic cardiovascular disease
  • American College of Cardiology Foundation/American Heart Association guideline recommends that patients at high risk for developing heart failure (stage A) control specific modifiable risk factors r2
    • Control hypertension with diuretics, ACE inhibitors, angiotensin receptor blockers, and/or β-blockers c234
    • Control dyslipidemia with statins c235
    • For patients with diabetes mellitus, control hyperglycemia c236
    • For obese patients, advise and assist with weight loss c237c238
    • For tobacco users, advise and assist with cessation c239
    • For alcohol users, advise and assist with moderation or cessation c240
    • Avoid known cardiotoxic agents (eg, cocaine, antineoplastic drugs, ephedra, cobalt, anabolic steroids, chloroquine, clozapine, amphetamines, methylphenidate, catecholamines) c241
Yang J et al: Heart failure: advanced development in genetics and epigenetics. Biomed Res Int. 2015:352734, 201525949994Yancy CW 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. J Am Coll Cardiol. 62(16):e147-239, 201323747642Ponikowski P 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. 18(8):891-975, 201627207191Udelson JE: Heart failure with preserved ejection fraction. Circulation. 124(21):e540-3, 201122105201Ezekowitz JA et al: 2017 comprehensive update of the Canadian Cardiovascular Society guidelines for the management of heart failure. Can J Cardiol. 33(11):1342-433, 201729111106Heart Failure Society of America et al: HFSA 2010 comprehensive heart failure practice guideline. J Card Fail. 16(6):e1-194, 201020610207Shamsham F et al: Essentials of the diagnosis of heart failure. Am Fam Physician. 61(5):1319-28, 200010735340McMurray JJ et al: ESC guidelines for the diagnosis and treatment of acute and chronic heart failure 2012: the Task Force for the Diagnosis and Treatment of Acute and Chronic Heart Failure 2012 of the European Society of Cardiology. Developed in collaboration with the Heart Failure Association (HFA) of the ESC. Eur J Heart Fail. 14(8):803-69, 201222828712Boudoulas H et al: Valvular heart disease: the influence of changing etiology on nosology. J Heart Valve Dis. 3(5):516-26, 19948000586Feenstra J et al: Drug-induced heart failure. J Am Coll Cardiol. 33(5):1152-62, 199910193711Cemin R et al: Peripartum cardiomyopathy: moving towards a more central role of genetics. Curr Cardiol Rev. 9(3):179-84, 201323909634Curtis LH et al: Incidence and prevalence of heart failure in elderly persons, 1994-2003. Arch Intern Med. 168:418-24, 200818299498Sturm AC: Genetic testing in the contemporary diagnosis of cardiomyopathy. Curr Heart Fail Rep. 10(1):63-72, 201323135967Leone A: Toxics of tobacco smoke and cardiovascular system: from functional to cellular damage. Curr Pharm Des. 21(30):4370-9, 201526234797Urbano-Marquez A et al: The effects of alcoholism on skeletal and cardiac muscle. N Engl J Med. 320(7):409-15, 19892913506Chow SL et al: Role of biomarkers for the prevention, assessment, and management of heart failure: a scientific statement from the American Heart Association. Circulation. 135(22):e1054-91, 201728446515Yancy CW et al: 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. J Am Coll Cardiol. 136(6):e137-61, 201728455343Harjola VP et al: Acute coronary syndromes and acute heart failure: a diagnostic dilemma and high-risk combination. A statement from the Acute Heart Failure Committee of the Heart Failure Association of the European Society of Cardiology. Eur J Heart Fail. 22(8):1298-314, 202032347648Drexler B et al: Quantifying cardiac hemodynamic stress and cardiomyocyte damage in ischemic and nonischemic acute heart failure. Circ Heart Fail. 5(1):17-24, 201221976469McKie PM et al: B-type natriuretic peptide as a biomarker beyond heart failure: speculations and opportunities. Mayo Clin Proc. 80(8):1029-36, 200516092582Anagnostopoulos C et al: Non-invasive investigations. Br Med Bull. 59:29-44, 200111756202Cheitlin MD et al: ACC/AHA/ASE 2003 guideline update for the clinical application of echocardiography: summary article. A report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (ACC/AHA/ASE Committee to Update the 1997 Guidelines for the Clinical Application of Echocardiography). J Am Soc Echocardiogr. 16(10):1091-110, 200314566308Nagueh SF et al: Recommendations for the evaluation of left ventricular diastolic function by echocardiography: an update from the American Society of Echocardiography and the European Association of Cardiovascular Imaging. J Am Soc Echocardiogr. 29(4):277-314, 201627037982Amsterdam EA et al: 2014 AHA/ACC guideline for the management of patients with non-ST-elevation acute coronary syndromes: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. Circulation. 130(25):e344-426, 201425249585Teichman SL et al: Challenges in acute heart failure clinical management: optimizing care despite incomplete evidence and imperfect drugs. Crit Pathw Cardiol. 14(1):12-24, 201525679083Poon CS et al: Submissive hypercapnia: why COPD patients are more prone to CO₂ retention than heart failure patients. Respir Physiol Neurobiol. 216:86-93, 201525891787van der Hulle T et al: Recent developments in the diagnosis and treatment of pulmonary embolism. J Intern Med. 279(1):16-29, 201626286356Stillman AE et al: Assessment of acute myocardial infarction: current status and recommendations from the North American Society for Cardiovascular Imaging and the European Society of Cardiac Radiology. Int J Cardiovasc Imaging. 27(1):7-24, 201120972835Smith G et al: ABC of intensive care: criteria for admission. BMJ. 318(7197):1544-7, 199910356016Scott MC et al: Congestive heart failure. Emerg Med Clin North Am. 33(3):553-62, 201526226866Hollenberg SM et al: 2019 ACC expert consensus decision pathway on risk assessment, management, and clinical trajectory of patients hospitalized with heart failure: a report of the American College of Cardiology Solution Set Oversight Committee. J Am Coll Cardiol. 74(15):1966-2011, 201931526538O'Connor CM et al: Effect of nesiritide in patients with acute decompensated heart failure. N Engl J Med. 365(1):32-43, 201121732835Yancy CW et al: 2016 ACC/AHA/HFSA focused update on new pharmacological therapy for heart failure: an 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. J Am Coll Cardiol. 22(9):659-69, 201627216111Nakagawa Y et al: Sodium-glucose cotransporter-2 inhibitors are potential therapeutic agents for treatment of non-diabetic heart failure patients. J Cardiol. 76(2):123-31, 202032340780McMurray JJV et al: Dapagliflozin in patients with heart failure and reduced ejection fraction. N Engl J Med. 381(21):1995-2008, 201931535829Bassi NS et al: Association of optimal implementation of sodium-glucose cotransporter 2 inhibitor therapy with outcome for patients with heart failure. JAMA Cardiol. 5(8):1-5, 202032374344Vest AR et al: Nutrition, obesity, and cachexia in patients with heart failure: a consensus statement from the Heart Failure Society of America Scientific Statements Committee. J Card Fail. 25(5):380-400, 201930877038Bozkurt B et al: Contributory risk and management of comorbidities of hypertension, obesity, diabetes mellitus, hyperlipidemia, and metabolic syndrome in chronic heart failure: a scientific statement from the American Heart Association. Circulation. 134(23):e535-78, 201627799274Rimm EB et al: Seafood long-chain n-3 polyunsaturated fatty acids and cardiovascular disease: a science advisory from the American Heart Association. Circulation. 138(1):e35-e47, 201829773586O'Keefe EL et al: Sea change for marine omega-3s: randomized trials show fish oil reduces cardiovascular events. Mayo Clin Proc. 94(12):2524-33, 201931627938Long L et al: Exercise-based cardiac rehabilitation for adults with heart failure. Cochrane Database Syst Rev. 1:CD003331, 201930695817Ezzat VA et al: A systematic review of ICD complications in randomised controlled trials versus registries: is our "real-world" data an underestimation? Open Heart. 2(1):e000198, 201525745566Fiaccadori E et al: Ultrafiltration in heart failure. Am Heart J. 161(3):439-49, 201121392597Zafar MR et al: Pharmacological and non-pharmacological strategies for volume overload in acute decompensated congestive heart failure: a review article. Cureus. 12(2):e6952, 202032190502Kirklin JK et al: Mechanical circulatory support: registering a therapy in evolution. Circ Heart Fail. 1(3):200-5, 200819808290Levy D et al: The progression from hypertension to congestive heart failure. JAMA. 275(20):1557-62, 19968622246Whelton PK et al: 2017 ACC/AHA/AAPA/ABC/ACPM/AGS/APhA/ASH/ASPC/NMA/PCNA guideline for the prevention, detection, evaluation, and management of high blood pressure in adults: executive summary: a report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines. Circulation. 138(17):e426-83, 201830354655Slivnick J et al: Hypertension and heart failure. Heart Fail Clin. 15(4):531-41, 201931472888Fotos NV et al: Health-related quality of life of patients with severe heart failure. A cross-sectional multicentre study. Scand J Caring Sci. 27(3):686-94, 201323004008Allen LA et al: Identifying patients hospitalized with heart failure at risk for unfavorable future quality of life. Circ Cardiovasc Qual Outcomes. 4(4):389-98, 201121693723Dunlay SM et al: Hospitalizations after heart failure diagnosis a community perspective. J Am Coll Cardiol. 54(18):1695-702, 200919850209Arora S et al: Etiologies, trends, and predictors of 30-day readmission in patients with heart failure. Am J Cardiol. 119(5):760-9, 201728109560Dunlay SM et al: Type 2 diabetes mellitus and heart failure: a scientific statement From the American Heart Association and the Heart Failure Society of America: this statement does not represent an update of the 2017 ACC/AHA/HFSA heart failure guideline update. Circulation. 140(7):e294-e324, 201931167558Kristensen SL et al: Clinical and echocardiographic characteristics and cardiovascular outcomes according to diabetes status in patients with heart failure and preserved ejection fraction: a report from the I-Preserve Trial (Irbesartan in Heart Failure With Preserved Ejection Fraction). Circulation. 135(8):724-35, 201728052977MacDonald MR et al: Impact of diabetes on outcomes in patients with low and preserved ejection fraction heart failure: an analysis of the Candesartan in Heart failure: Assessment of Reduction in Mortality and morbidity (CHARM) programme. Eur Heart J. 29(11):1377-85, 200818413309Aguilar D et al: Relationship of hemoglobin A1C and mortality in heart failure patients with diabetes. J Am Coll Cardiol. 54(5):422-8, 200919628117Davies MJ et al: Management of hyperglycemia in type 2 diabetes, 2018. A consensus report by the American Diabetes Association (ADA) and the European Association for the Study of Diabetes (EASD). Diabetes Care. 41(12):2669-701, 201830291106Cosentino F et al: 2019 ESC guidelines on diabetes, pre-diabetes, and cardiovascular diseases developed in collaboration with the EASD. Eur Heart J. 41(2):255-323, 202031497854Rangaswami J et al: Cardiorenal syndrome: classification, pathophysiology, diagnosis, and treatment strategies: a scientific statement from the American Heart Association. Circulation. 139(16):e840-78, 201930852913Das SR et al: 2018 ACC expert consensus decision pathway on novel therapies for cardiovascular risk reduction in patients with type 2 diabetes and atherosclerotic cardiovascular disease: a report of the American College of Cardiology Task Force on Expert Consensus Decision Pathways. J Am Coll Cardiol. 72(24):3200-23, 201830497881Nassif ME et al: Dapagliflozin effects on biomarkers, symptoms, and functional status in patients with heart failure with reduced ejection fraction: the DEFINE-HF trial. Circulation. 140(18):1463-76, 201931524498O'Meara E et al: CCS/CHFS heart failure guidelines: clinical trial update on functional mitral regurgitation, SGLT2 inhibitors, ARNI in HFpEF, and tafamidis in amyloidosis. Can J Cardiol. 36(2):159-69, 202032036861Nassif ME et al: A review of cardiovascular outcomes trials of glucose-lowering therapies and their effects on heart failure outcomes. Am J Cardiol. 124 Suppl 1:S12-9, 201931741435Kosiborod MN et al: Effects of dapagliflozin on symptoms, function, and quality of life in patients with heart failure and reduced ejection fraction: results from the DAPA-HF Trial. Circulation. 141(2):90-9, 202031736335Fitchett D et al: Effects of empagliflozin on risk for cardiovascular death and heart failure hospitalization across the spectrum of heart failure risk in the EMPA-REG OUTCOME® trial. Eur Heart J. 39(5):363-370, 201829020355Rådholm K et al: Canagliflozin and heart failure in type 2 diabetes mellitus: results from the CANVAS program. Circulation. 138(5):458-68, 201829526832Fitchett D et al: Heart failure outcomes with empagliflozin in patients with type 2 diabetes at high cardiovascular risk: results of the EMPA-REG OUTCOME trial. Eur Heart J. 37(19):1526-34, 201626819227Petrie MC et al: Effect of dapagliflozin on worsening heart failure and cardiovascular death in patients with heart failure with and without diabetes. JAMA. 323(14):1353-68, 202032219386Madan N et al: Atrial fibrillation and heart failure in women. Heart Fail Clin. 15(1):55-64, 201930449380Carlisle MA et al: Heart failure and atrial fibrillation, like fire and fury. JACC Heart Fail. 7(6):447-56, 201931146871Cleland JGF et al: The year in cardiology: heart failure. Eur Heart J. 41(12):1232-48, 202031901936January CT et al: 2014 AHA/ACC/HRS guideline for the management of patients with atrial fibrillation: executive summary: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines and the Heart Rhythm Society. Circulation. 130(23):2071-104, 201424682348Vamos M et al: Digoxin-associated mortality: a systematic review and meta-analysis of the literature. Eur Heart J. 36(28):1831-8, 201525939649Roy D et al: Rhythm control versus rate control for atrial fibrillation and heart failure. N Engl J Med. 358(25):2667-77, 200818565859Marrouche NF et al: Catheter ablation for atrial fibrillation with heart failure. N Engl J Med. 378(5):417-27, 201829385358Black-Maier E et al: Catheter ablation of atrial fibrillation in patients with heart failure and preserved ejection fraction. Heart Rhythm. 15(5):651-7, 201829222043Packer DL et al: Effect of catheter ablation vs antiarrhythmic drug therapy on mortality, stroke, bleeding, and cardiac arrest among patients with atrial fibrillation: the CABANA randomized clinical trial. JAMA. 321(13):1261-74, 201930874766Mark DB et al: Effect of catheter ablation vs medical therapy on quality of life among patients with atrial fibrillation: the CABANA randomized clinical trial. JAMA. 321(13):1275-85, 201930874716Pepine CJ et al: How do we best treat patients with ischemic heart disease? Circulation. 98(19):1985-6, 19989808592Anand IS et al: Anemia and iron deficiency in heart failure: current concepts and emerging therapies. Circulation. 138(1):80-98, 201829967232Qaseem A et al: Treatment of anemia in patients with heart disease: a clinical practice guideline from the American College of Physicians. Ann Intern Med. 159(11):770-9, 201324297193Carney RM et al: Depression and coronary heart disease: a review for cardiologists. Clin Cardiol. 20(3):196-200, 19979068903van der Harst P et al: Statins in the treatment of heart failure. Circ Heart Fail. 3(3):462-4, 201020484198Grundy SM et al: 2018 AHA/ACC/AACVPR/AAPA/ABC/ACPM/ADA/AGS/APhA/ASPC/NLA/PCNA guideline on the management of blood cholesterol: executive summary: a report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines. Circulation. 139(25):e1046-81, 201930565953MacDonald M et al: The current prevalence of sleep disordered breathing in congestive heart failure patients treated with beta-blockers. J Clin Sleep Med. 4(1):38-42, 200818350960Santema BT et al: Identifying optimal doses of heart failure medications in men compared with women: a prospective, observational, cohort study. Lancet. 394(10205):1254-63, 201931447116Watson RD et al: ABC of heart failure: clinical features and complications. BMJ. 320(7229):236-9, 200010642237Fonarow GC et al: Risk stratification for in-hospital mortality in acutely decompensated heart failure: classification and regression tree analysis. JAMA. 293(5):572-80, 200515687312American Heart Association: Predictors of In-Hospital Mortality in Patients Hospitalized With Heart Failure. AHA website. Accessed January 20, 2021. http://www.heart.org/idc/groups/heart-public/@wcm/@hcm/@gwtg/documents/downloadable/ucm_309103.pdfhttp://www.heart.org/idc/groups/heart-public/@wcm/@hcm/@gwtg/documents/downloadable/ucm_309103.pdfCanadian Cardiovascular Outcomes Research Team: EFFECT Heart Failure Mortality Prediction. CCORT website. Accessed January 20, 2021. http://www.ccort.ca/Research/CHFRiskModel.aspxhttp://www.ccort.ca/Research/CHFRiskModel.aspxUniversity of Washington: Seattle Heart Failure Model. University of Washington website. Accessed January 20, 2021. http://depts.washington.edu/shfm/http://depts.washington.edu/shfm/Aaronson KD et al: Development and prospective validation of a clinical index to predict survival in ambulatory patients referred for cardiac transplant evaluation. Circulation. 95(12):2660-7, 19979193435Pocock SJ et al: Predictors of mortality and morbidity in patients with chronic heart failure. Eur Heart J. 27(1):65-75, 200616219658Komajda M et al: Factors associated with outcome in heart failure with preserved ejection fraction: findings from the Irbesartan in Heart Failure with Preserved Ejection Fraction Study (I-PRESERVE). Circ Heart Fail. 4(1):27-35, 201121068341Arnett DK et al: 2019 ACC/AHA guideline on the primary prevention of cardiovascular disease: Executive Summary: a report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines. J Am Coll Cardiol. 74(10):1376-414, 201930894319
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