Top 10 Take-Home Messages:
- Guideline-directed medical therapy (GDMT) for heart failure (HF) with reduced ejection fraction (HFrEF) now includes 4 medication classes which include sodium-glucose cotransporter-2 inhibitors (SGLT2i).
- SGLT2 inhibitors have a 2a recommendation in heart failure with mildly reduced ejection fraction (HFmrEF). Weaker recommendations (2b) are made for ARNi, ACEi, ARB, MRA and beta blockers in this population.
- New recommendations for HFpEF are made for SGLT2 inhibitors (2a), MRAs (2b) and ARNi (2b). Several prior recommendations have been renewed including treatment of hypertension (1), treatment of atrial fibrillation (2a), use of ARBs (2b) avoidance of routine use of nitrates or phosphodiesterase-5 inhibitors (3-no benefit).
- Improved LVEF is used to refer to those patients with a previous HFrEF who now have an LVEF >40%. These patients should continue their HFrEF treatment.
- Value statements were created for select recommendations where high-quality cost-effectiveness studies of the intervention have been published.
- Amyloid heart disease has new recommendations for treatment including screening for serum and urine monoclonal light chains, bone scintigraphy, genetic sequencing, tetramer stabilizer therapy, and anticoagulation.
- Evidence supporting increased filling pressures is important for the diagnosis of HF if the LVEF is >40%. Evidence for increased filling pressures can be obtained from non-invasive (e.g., natriuretic peptide, diastolic function on imaging) or invasive testing (e.g., hemodynamic measurement).
- Patients with advanced HF who wish to prolong survival should be referred to a team specializing in HF. A heart failure specialty team reviews HF management, assesses suitability for advanced HF therapies and uses palliative care including palliative inotropes where consistent with the patient’s goals of care.
- Primary prevention is important for those at risk for HF (Stage A) or pre-HF (Stage B). Stages of HF were revised to emphasize the new terminologies of “at risk” for HF for Stage A and Pre-HF for Stage B.
- Recommendations are provided for select patients with HF and iron deficiency, anemia, hypertension, sleep disorders, diabetes type 2, atrial fibrillation, coronary artery disease and malignancy.
Table 3. Stages of HF
|Stages||Definition and Criteria|
|Stage A: |
At Risk for HF
|At risk for HF but without symptoms, structural heart disease, or cardiac biomarkers of stretch or injury (e.g., patients with hypertension, atherosclerotic CVD, diabetes, metabolic syndrome and obesity, exposure to cardiotoxic agents, genetic variant for cardiomyopathy, or positive family history of cardiomyopathy).|
|Stage B: Pre-HF||No symptoms or signs of HF and evidence of 1 of the following:|
|Structural heart disease* |
|Evidence for increased filling pressures* |
By invasive hemodynamic measurements
By noninvasive imaging suggesting elevated filling pressures (e.g., Doppler echocardiography)
|Patients with risk factors and |
|Stage C: |
|Structural heart disease with current or previous symptoms of HF.|
|Stage D: |
|Marked HF symptoms that interfere with daily life and with recurrent hospitalizations despite attempts to optimize GDMT.|
Colors in tables and figures correspond to Class of Recommendations and Level of Evidence tables on pages 78–79.
Figure 1. ACC/AHA Stages of HF
Figure 2. Trajectory of Class C HF
Table 4. Classification of HF by LVEF
|Type of HF According to LVEF||Criteria|
(HF with reduced EF)
(HF with improved EF)
|Previous LVEF ≤40% and a follow-up measurement of LVEF >40%|
(HF with mildly reduced EF)
(HF with preserved EF)
Figure 3. Classification and Trajectories of HF Based on LVEF
Figure 4. Diagnostic Algorithm for HF and EF-Based Classification
3. Epidemiology and Causes of HF
- Beginning in 2012, the age-adjusted death rate per capita for HF increased for the first time in the United States. A recent U.S. evaluation found total deaths caused by HF have increased from 275,000 in 2009 to 310,000 in 2014.
- Death rate per capita by race and ethnicity:
- Non-Hispanic Black – 92/100,000
- Non-Hispanic White – 87/100,000
- Hispanic – 53/100,000
- Causes of heart failure:
- Risk Factors (in the United States):
- 115 million have hypertension
- 100 million are obese
- 92 million have prediabetes
- 26 million have diabetes
- 125 million have atherosclerotic CVD
- Other common causes:
- ischemic heart disease and myocardial infarction (MI)
- valvular heart disease (VHD)
- familial or genetic cardiomyopathies
- cardiotoxicity with cancer or other treatments
- substance abuse such as alcohol, cocaine, or methamphetamine
- right ventricular (RV) pacing or stress-induced cardiomyopathies
- peripartum cardiomyopathy
- autoimmune causes
- iron overload including hemochromatosis
- thyroid disease
- other endocrine metabolic and nutritional causes
- Risk Factors (in the United States):
4. Initial and Serial Evaluation
4.1. Clinical Assessment: History and Physical Examination
Table 5. Other Potential Nonischemic Causes of HF
- Chemotherapy and other cardiotoxic medications
- Rheumatologic or autoimmune
- Endocrine or metabolic (thyroid, acromegaly, pheochromocytoma, diabetes, obesity)
- Familial cardiomyopathy or inherited and genetic heart disease
- Heart rhythm–related (e.g., tachycardia-mediated, PVCs, RV pacing)
- Infiltrative cardiac disease (e.g., amyloid, sarcoid, hemochromatosis)
- Myocarditis (infectious, toxin or medication, immunological, hypersensitivity)
- Peripartum cardiomyopathy
- Stress cardiomyopathy (Takotsubo)
- Substance abuse (e.g., alcohol, cocaine, methamphetamine)
4.1.1. Initial Laboratory and Electrocardiographic Testing
4.2. Use of Biomarkers for Prevention, Initial Diagnosis, and Risk Stratification
Table 6. Selected Potential Causes of Elevated Natriuretic Peptide Levels
4.3. Genetic Evaluation and Testing
Table 7. Examples of Factors Implicating Possible Genetic Cardiomyopathy
|Phenotypic Category||Patient or Family Member Phenotypic Finding*||Ask Specifically About Family Members* With|
|Cardiac morphology||Marked LV hypertrophy||Any mention of cardiomyopathy, enlarged or weak heart, HF. |
Document even if attributed to other causes, such as alcohol or peripartum cardiomyopathy
|Ventricular thinning or fatty replacement on imaging or biopsy|
|Findings on 12-lead ECG||Abnormal high or low voltage or conduction, and repolarization, altered RV forces||Recurrent syncope, long QT or Brugada syndrome|
|Dysrhythmias||Frequent NSVT or very frequent PVCs||ICD |
Sudden death attributed to “massive heart attack” without known CAD
Unexplained fatal event such as drowning or single-vehicle crash
|Sustained ventricular tachycardia or fibrillation|
|Early onset AF||“Lone” AF before age 65 years|
|Early onset conduction disease||Pacemaker before age 65 years|
|Extracardiac features|| ||Any known skeletal muscle disease, including mention of Duchenne and Becker’s, Emory-Dreifuss limb-girdle dystrophy |
4.4. Evaluation With Cardiac Imaging
4.5. Invasive Evaluation
4.6. Wearables and Remote Monitoring (Including Telemonitoring and Device Monitoring)
4.7. Exercise and Functional Capacity Testing
4.8. Initial and Serial Evaluation: Clinical Assessment: HF Risk Scoring
5. Stage A (Patients at Risk for HF)
5.1. Patients at Risk for HF (Stage A: Primary Prevention)
Figure 5. Recommendations (Class 1 and 2a) for Patients at Risk of HF (Stage A) and Those With Pre-HF (Stage B)
6. Stage B (Patients With Pre-HF)
6.1. Management of Stage B: Preventing the Syndrome of Clinical HF in Patients With Pre-HF
7. Stage “C” HF
7.1.1. Nonpharmacological Interventions: Self-Care Support in HF
7.1.2. Dietary Sodium Restriction
7.1.3. Management of Stage C HF: Activity, Exercise Prescription, and Cardiac Rehabilitation.
Table 11. Potential Barriers to Effective HF Self-Care and Example Interventions
|Potential Barrier||Example Screening Tools||Example Interventions|
|Cognitive impairment|| || |
|Depression|| || |
|Substance use disorders|| || |
|Frailty|| || |
|Financial burden of HF treatments|| || |
|Food insecurity|| || |
|Homelessness or housing insecurity|| || |
|Intimate partner violence or elder abuse|| || |
|Limited English proficiency or other language barriers|| || |
|Low health literacy|| || |
|Social isolation or low social support|| || |
|Transport limitations|| || |
7.2. Diuretics and Decongestion Strategies in Patients With HF
Table 12. Commonly Used Oral Diuretics in Treatment of Congestion for Chronic HF
|Drug||Initial Daily Dose||Maximum Total Daily Dose||Duration of Action|
|Bumetanide||0.5–1.0 mg once or twice||10 mg||4–6 h|
|Furosemide||20–40 mg once or twice||600 mg||6–8 h|
|Torsemide||10–20 mg once||200 mg||12–16 h|
|Chlorthiazide||250–500 mg once or twice||1000 mg||6–12 h|
|Chlorthalidone||12.5–25 mg once||100 mg||24–72 h|
|Hydrochlorothiazide||25 mg once or twice||200 mg||6–12 h|
|Indapamide||2.5 mg once||5 mg||36 h|
|Metolazone||2.5 mg once||20 mg||12–24 h|
7.3. Pharmacological Treatment* for HFrEF
7.3.1. Renin-Angiotensin System Inhibition With ACEi or ARB or ARNi
7.3.2. Beta Blockers
7.3.3. Mineralocorticoid Receptor Antagonists (MRAs)
7.3.4. Sodium-Glucose Cotransporter 2 Inhibitors
7.3.5. Hydralazine and Isosorbide Dinitrate
7.3.6. Other Drug Treatment
7.3.7. Drugs of Unproven Value or That May Worsen HF
Figure 6. Treatment of HFrEF Stages C and D
Table 13. Selected Prescription Medications That May Cause or Exacerbate HF
|Drug or Therapeutic Class||[Associated With HF] Causes Direct Myocardial Toxicity||[Associated With HF] Exacerbates Underlying Myocardial Dysfunction||Magnitude of HF Induction or Precipitation||Level of Evidence for HF Induction or Precipitation||Possible Mechanism(s)||Onset|
|COX, nonselective inhibitors (NSAIDs)||X||Major||B||Prostaglandin inhibition leading to sodium and water retention, increased systemic vascular resistance, and blunted response to diuretics||Immediate|
|COX, selective inhibitors (COX-2 inhibitors)||X||Major||B||Prostaglandin inhibition leading to sodium and water retention, increased systemic vascular resistance, and blunted response to diuretics||Immediate|
|Thiazolidinediones||X||Major||A||Possible calcium channel blockade||Intermediate|
|Saxagliptin||X||Major||A||Unknown||Intermediate to delayed|
|Alogliptin||X||Major||A||Unknown||Intermediate to delayed|
|Flecainide||X||Major||A||Negative inotrope, proarrhythmic effects||Immediate to intermediate|
|Disopyramide||X||Major||B||Negative inotrope, proarrhythmic effects||Immediate to intermediate|
|Sotalol||X||Major||A||Proarrhythmic properties, beta blockade||Immediate to intermediate|
|Dronedarone||X||Major||A||Negative inotrope||Immediate to intermediate|
|Doxazosin||X||Moderate||B||Beta-1-receptor stimulation with increases in renin and aldosterone||Intermediate to delayed|
|Diltiazem||X||Major||B||Negative inotrope||Immediate to intermediate|
|Verapamil||X||Major||B||Negative inotrope||Immediate to intermediate|
|Nifedipine||X||Moderate||C||Negative inotrope||Immediate to intermediate|
7.3.8. GDMT Dosing: Sequencing and Uptitration
Table 14. Drugs Commonly Used for HFrEF (Stage C HF)
|Drug||Initial Daily Dose(s)||Target Dose(s)||Mean Doses Achieved in Clinical Trials|
|Captopril||6.25 mg 3 times daily||50 mg 3 times daily||122.7 mg total daily|
|Enalapril||2.5 mg twice daily||10–20 mg twice daily||16.6 mg total daily|
|Fosinopril||5–10 mg once daily||40 mg once daily||NA|
|Lisinopril||2.5–5 mg once daily||20–40 mg once daily||32.5–35.0 mg total daily|
|Perindopril||2 mg once daily||8–16 mg once daily||NA|
|Quinapril||5 mg twice daily||20 mg twice daily||NA|
|Ramipril||1.25–2.5 mg once daily||10 mg once daily||NA|
|Trandolapril||1 mg once daily||4 mg once daily||NA|
|Candesartan||4–8 mg once daily||32 mg once daily||24 mg total daily|
|Losartan||25–50 mg once daily||50–150 mg once daily||129 mg total daily|
|Valsartan||20–40 mg once daily||160 mg twice daily||254 mg total daily|
|Sacubitril-valsartan||49 mg sacubitril and 51 mg valsartan twice daily (therapy may be initiated at 24 mg sacubitril and 26 mg valsartan twice daily)||97 mg sacubitril and 103 mg valsartan twice daily||182 mg sacubitril and 193 mg valsartan total daily|
|Bisoprolol||1.25 mg once daily||10 mg once daily||8.6 mg total daily|
|Carvedilol||3.125 mg twice daily||25–50 mg twice daily||37 mg total daily|
|Carvedilol CR||10 mg once daily||80 mg once daily||NA|
|Metoprolol succinate extended release (metoprolol CR/XL)||12.5–25 mg once daily||200 mg once daily||159 mg total daily|
|Mineralocorticoid receptor antagonists|
|Spironolactone||12.5–25 mg once daily||25–50 mg once daily||26 mg total daily|
|Eplerenone||25 mg once daily||50 mg once daily||42.6 mg total daily|
|Dapagliflozin||10 mg once daily||10 mg once daily||9.8 mg total daily|
|Empagliflozin||10 mg once daily||10 mg once daily||NR|
|Isosorbide dinitrate and hydralazine|
|Fixed dose combination||20 mg isosorbide dinitrate and 37.5 mg hydralazine 3 times daily||40 mg isosorbide dinitrate and 75 mg hydralazine 3 times daily||90 mg isosorbide dinitrate and ~175 mg hydralazine total daily|
|Isosorbide dinitrate and hydralazine||20–30 mg isosorbide dinitrate and 25–50 mg hydralazine 3–4 times daily||120 mg isosorbide dinitrate total daily in divided doses and 300 mg hydralazine total daily in divided doses||NA|
|If Channel inhibitor|
|Ivabradine||5 mg twice daily||7.5 mg twice daily||12.8 total daily|
|Soluble guanylate cyclase stimulator|
|Vericiguat||2.5 mg once daily||10 mg once daily||9.2 mg total daily|
|Digoxin||0.125–0.25 mg daily (modified according to monogram)||Individualized variable dose to achieve serum digoxin concentration 0.5–<0.9 ng/mL||NA|
Table 15. Benefits of Evidence-Based Therapies for Patients With HFrEF
|Evidence-Based Therapy||Relative Risk Reduction in All-Cause Mortality in Pivotal RCTs, %||NNT to Prevent All-Cause Mortality Over Time*||NNT for All-Cause Mortality (Standardized to 12 mo)||NNT for All-Cause Mortality (Standardized to 36 mo)|
|ACEi or ARB||17||22 over 42 mo||77||26|
|ARNi†||16||36 over 27 mo||80||27|
|Beta blocker||34||28 over 12 mo||28||9|
|Mineralocorticoid receptor antagonist||30||9 over 24 mo||18||6|
|SGLT2i||17||43 over 18 mo||63||22|
|Hydralazine or nitrate‡||43||25 over 10 mo||21||7|
|CRT||36||12 over 24 mo||24||8|
|ICD||23||14 over 60 mo||70||23|
† Benefit of ARNi therapy incremental to that achieved with ACEi therapy. For the other medications shown, the benefits are based on comparisons to placebo control.
‡ Benefit of hydralazine-nitrate therapy was limited to African American patients in this trial.
7.3.9. Additional Medical Therapies
184.108.40.206. Management of Stage C HF: Ivabradine
220.127.116.11. Pharmacological Treatment for Stage C HFrEF (Digoxin)
18.104.22.168. Pharmacological Treatment for Stage C HFrEF: Soluble Guanylyl Cyclase Stimulators
Figure 7. Additional Medical Therapies for Patients With HFrEF
7.4. Device and Interventional Therapies for HFrEF
7.4.1. ICDs and CRTs
Figure 8. Algorithm for CRT Indications in Patients With Cardiomyopathy or HFrEF
7.4.3. Revascularization for CAD
Figure 9. Additional Device Therapies
7.5. Valvular Heart Disease
Figure 10. Treatment Approach in Secondary Mitral Regurgitation
7.6. Mildly Reduced EF (HFmrEF) and Improved EF (HFimpHF)
7.6.1. HF With Mildly Reduced Ejection Fraction
Figure 11. Recommendations for Patients With Mildly Reduced LVEF (41%– 49%)
7.6.2. HF With Improved Ejection Fraction
7.7. Preserved EF (HFpEF)
7.7.1. HF With Preserved Ejection Fraction*
Figure 12. Recommendations for Patients With Preserved LVEF (≥50%)
* Greater benefit in patients with LVEF closer to 50%.
7.8. Cardiac Amyloidosis
7.8.1. Diagnosis of Cardiac Amyloidosis
7.8.2. Treatment of Cardiac Amyloidosis
Figure 13. Diagnostic and Treatment of Transthyretin Cardiac Amyloidosis Algorithm
8. Stage D (Advanced) HF
8.1. Specialty Referral for Advanced HF
Table 16. ESC Definition of Advanced HF
|All of these criteria must be present despite optimal guideline-directed treatment:|
|1. Severe and persistent symptoms of HF (NYHA class III [advanced] or IV)|
|2. Severe cardiac dysfunction defined by ≥1 of these:|
|3. Hospitalizations or unplanned visits in the past 12 mo for episodes of:|
|4. Severe impairment of exercise capacity with inability to exercise or low 6-minute walk test distance (<300 m) or peak VO2 (<12–14 mL/kg/min) estimated to be of cardiac origin.|
|Criteria 1 and 4 can be met in patients with cardiac dysfunction (as described in criterion 2) but who also have substantial limitations as a result of other conditions (e.g., severe pulmonary disease, noncardiac cirrhosis, renal disease). The therapeutic options for these patients may be more limited.|
Table 17. INTERMACS Profiles
|1||Critical cardiogenic shock||Life-threatening hypotension and rapidly escalating inotropic/pressor support, with critical organ hypoperfusion often confirmed by worsening acidosis and lactate levels.|
|2||Progressive decline||“Dependent” on inotropic support but nonetheless shows signs of continuing deterioration in nutrition, renal function, fluid retention, or other major status indicator. Can also apply to a patient with refractory volume overload, perhaps with evidence of impaired perfusion, in whom inotropic infusions cannot be maintained because of tachyarrhythmias, clinical ischemia, or other intolerance.|
|3||Stable but inotrope dependent||Clinically stable on mild-moderate doses of intravenous inotropes (or has a temporary circulatory support device) after repeated documentation of failure to wean without symptomatic hypotension, worsening symptoms, or progressive organ dysfunction (usually renal).|
|4||Resting symptoms on oral therapy at home||Patient who is at home on oral therapy but frequently has symptoms of congestion at rest or with activities of daily living (dressing or bathing). He or she may have orthopnea, shortness of breath during dressing or bathing, gastrointestinal symptoms (abdominal discomfort, nausea, poor appetite), disabling ascites, or severe lower extremity edema.|
|5||Exertion intolerant||Patient who is comfortable at rest but unable to engage in any activity, living predominantly within the house or housebound.|
|6||Exertion limited||Patient who is comfortable at rest without evidence of fluid overload but who is able to do some mild activity. Activities of daily living are comfortable, and minor activities outside the home such as visiting friends or going to a restaurant can be performed, but fatigue results within a few minutes or with any meaningful physical exertion.|
|7||Advanced NYHA class III||Patient who is clinically stable with a reasonable level of comfortable activity, despite a history of previous decompensation that is not recent. This patient is usually able to walk more than a block. Any decompensation requiring intravenous diuretics or hospitalization within the previous month should make this person a Patient Profile 6 or lower|
Table 18. Clinical Indicators of Advanced HF
- Repeated hospitalizations or emergency department visits for HF in the past 12 mo.
- Need for intravenous inotropic therapy.
- Persistent NYHA functional class III to IV symptoms despite therapy.
- Severely reduced exercise capacity (peak VO2, <14 mL/kg/min or <50% predicted, 6-minute walk test distance <300 m, or inability to walk 1 block on level ground because of dyspnea or fatigue).
- Intolerance to RAAS inhibitors because of hypotension or worsening renal function.
- Intolerance to beta blockers as a result of worsening HF or hypotension.
- Recent need to escalate diuretics to maintain volume status, often reaching daily furosemide equivalent dose >160 mg/d or use of supplemental metolazone therapy.
- Refractory clinical congestion.
- Progressive deterioration in renal or hepatic function.
- Worsening right HF or secondary pulmonary hypertension.
- Frequent SBP ≤90 mm Hg.
- Cardiac cachexia.
- Persistent hyponatremia (serum sodium, <134 mEq/L).
- Refractory or recurrent ventricular arrhythmias; frequent ICD shocks.
- Increased predicted 1-year mortality (e.g., >20%) according to HF survival models (e.g., MAGGIC, SHFM).
8.2. Nonpharmacological Management: Advanced HF
Table 19. Indications and Contraindications to Durable Mechanical Support
|Indications (combination of these):|
8.3. Inotropic Support
8.4. Mechanical Circulatory Support
8.5. Cardiac Transplantation
Table 20. Intravenous Inotropic Agents Used in the Management of HF
|Inotropic Agent||Dose (mcg/kg)||Drug Kinetics and Metabolism||Effects||Adverse Effects||Special Considerations|
|Dopamine||NA||5–10||t1/2: 2–20 min||↑||↑||↔||↔||T, HA, N, tissue necrosis||Caution: MAO-I|
|NA||10–15||R, H, P||↑||↑||↑||↔|
|Dobutamine||NA||2.5–20||t1/2: 2–3 min H||↑||↑||↔||↔||↑/↓BP, HA, T, N, F, hypersensitivity||Caution: MAO-I; CI: sulfite allergy|
|PDE 3 inhibitor|
|Milrinone||NR||0.125–0.75||t1/2: 2.5 h H||↑||↑||↓||↓||T, ↓BP||Accumulation may occur in setting of renal failure; monitor kidney function and LFTs|
|Epinephrine||NR||5–15 mcg/min||t1/2: 2–3 min||↑||↑||↑(↓)||↔||HA, T||Caution: MAO-I|
|15–20 mcg/min||t1/2: 2–3 min||↑||↑↑||↑↑||↔||HA, T||Caution: MAO-I|
|Norepinephrine||NR||0.5–30 mcg/min||t1/2: 2.5 min||↔||↑||↑↑||↔||↓ HR, tissue necrosis||Caution: MAO-I|
9. Patients Hospitalized With Acute Decompensated HF
9.1. Assessment of Patients Hospitalized With Decompensated HF
Goals for Optimization and Continuation of GDMT
Table 21. Common Factors Precipitating HF Hospitalization With Acute Decompensated HF
- Uncontrolled hypertension
- AF and other arrhythmias
- Additional cardiac disease (e.g., endocarditis)
- Acute infections (e.g., pneumonia, urinary tract)
- Nonadherence with medication regimen or dietary intake
- Hyper- or hypothyroidism
- Medications that increase sodium retention (e.g., NSAID)
- Medications with negative inotropic effect (e.g., verapamil)
9.2. Maintenance or Optimization of GDMT During Hospitalization
9.3. Diuretics in Hospitalized Patients: Decongestion Strategy
- higher doses of intravenous loop diuretics; or
- addition of a second diuretic.
9.4a. Parenteral Vasodilation Therapy in Patients Hospitalized With HF
9.4b. VTE Prophylaxis in Hospitalized Patients
9.5. Evaluation and Management of Cardiogenic Shock
Table 22. Suggested Shock Clinical Criteria*
|SBP <90 mm Hg for >30 min:|
|Hypoperfusion defined by:|
Table 23. Suggested Shock Hemodynamic Criteria*
- SBP <90 mm Hg or mean BP <60 mm Hg
- Cardiac index <2.2 L/min/m2
- Pulmonary capillary wedge pressure >15 mm Hg
- Other hemodynamic considerations
- Cardiac power output ([CO x MAP]/451) <0.6 W
- Shock index (HR/systolic BP) >1.0
- RV shock
- Pulmonary artery pulse index [(PASP-PADP)/CVP] <1.0
- CVP >15 mm Hg
- CVP-PCW >0.6
Table 24. Society for Cardiovascular Angiography and Interventions (SCAI) Cardiogenic Shock Criteria
|Stage||Bedside Findings||Selected Laboratory Markers||Hemodynamics|
|A: At risk || || || |
|B: Beginning shock (“pre-shock”) || || || |
|C: Classic cardiogenic shock || || || |
|D: Deteriorating || || || |
|E: Extremis || || || |
9.6 Integration of Care: Transitions and Team-Based Approaches
Table 25. Important Components of a Transitional Care Plan
|A transitional care plan, communicated with the patient and their outpatient clinicians before hospital discharge, should clearly outline plans for:|
10. Comorbidities in Patients With HF
10.1. Management of Comorbidities in Patients With HF
Management of Anemia or Iron Deficiency
Management of Hypertension
Management of Sleep Disorders
Management of Diabetes
Table 26. Most Common Co-Occurring Chronic Conditions Among Medicare Beneficiaries With HF (N=4,947,918), 2011
|Beneficiaries Age ≥65 y||Beneficiaries Age <65 y|
|Ischemic heart disease||3,145,718||71.9||Ischemic heart disease||365,889||64.0|
|Alzheimer’s disease or dementia||1,207,704||27.6||Asthma||88,816||15.5|
† Mean No. of conditions is 5.5; median is 5.
Figure 14. Recommendations for Treatment of Patients With HF and Selected Comorbidities
* Patients with chronic HF with permanent-persistent-paroxysmal AF and a CHA2DS2-VASc score of ≥2 (for men) and ≥3 (for women).
10.2. Management of AF in HF
11. Special Populations
11.1. Disparities and Vulnerable Populations*
Table 27. Risk of HF and Outcomes in Special Populations
|Vulnerable Population||Risk of HF||HF Outcomes|
|Women||The lifetime risk of HF is equivalent between sexes, but HFpEF risk is higher in women—in FHS participants with new-onset HF, odds of HfpEF (EF >45%) are 2.8-fold higher in women than in men. |
Sex-specific differences in the predictive value of cardiac biomarkers for incident HF.
Nontraditional cardiovascular risk factors, including anxiety, depression, caregiver stress, and low household income may contribute more toward incident heart disease in women than men.
|Overall, more favorable survival with HF than men. In the OPTIMIZE-HF registry, women with acute HF had a lower 1-y mortality (HR, 0.93; 95% CI, 0.89–0.97), although women are more likely not to receive optimal GDMT. |
Lower patient-reported quality of life for women with HFrEF, compared with men.
Greater transplant waitlist mortality for women but equivalent survival after heart transplantation or LVAD implantation.
|Older adults||Per FHS, at 40 y of age, the lifetime risk of incident HF is 20% for both sexes; at 80 y of age, the risk remains 20% for men and women despite the shorter life expectancy. |
LVEF is preserved in at least two-thirds of older adults with the diagnosis of HF.
|Among 1233 patients with HF aged ≥80 y, 40% mortality during mean 27-mo follow-up; survival associated with prescription of GDMT.|
|Lower socioeconomic status populations||Among 27,078 White and Black adults of low income (70% earned <$15,000/y) participating from 2002–2009 in the Southern Community Cohort Study, a 1 interquartile increase in neighborhood deprivation index was associated with a 12% increase in risk of HF (adjusted HR, 1.12; 95% CI, 1.07–1.18).||Age-adjusted 1999–2018 HF mortality (deaths/100,000; mean and 95% CI) was higher with increasing quartiles of ADI, which is based on 17 indicators of employment, poverty, and education: |
Quartile 1, 20.0 (19.4–20.5);
Quartile 2, 23.3 (22.6–24.0);
Quartile 3, 26.4 (25.5–27.3);
Quartile 4, 33.1 (31.8–34.4)
|Black populations||In MESA, patients of Black race had highest risk of incident HF (4.6/1000 person-years) and highest proportion of nonischemic incident HF. |
Higher prevalence of HF risk factors including hypertension, obesity, and diabetes, compared with White populations.
|CDC data show race-based differences in HF mortality over time: Black men had a 1.16-fold versus 1.43-fold higher age-adjusted HF-related CVD death rate compared with White men in 1999 versus 2017; Black women had a 1.35-fold versus 1.54-fold higher age-adjusted HF-related CVD death rate compared with White women in 1999 versus 2017. |
Gap in outcomes is more pronounced among younger adults (35–64 y of age) versus older adults (65–84 y of age); age-adjusted HF-related CVD death rates were 2.60-fold and 2.97-fold higher in young Black versus White men and women, respectively.
Higher rates of hospitalization and mortality among patients with HFpEF.
Lower 5-year survival after heart transplant.
|Hispanic populations||MESA study showed higher HF incidence in Hispanic compared with non-Hispanic White groups (3.5 versus 2.4 per 1000 person-years) but lower than for African Americans (4.6/1000 person-years).||Despite higher rates of hospitalization for HF compared with non-Hispanic Whites, Hispanic patients with HF have shown lower short-term mortality rates. |
In GWTG, Hispanic patients with HfpEF had lower mortality (OR, 0.50; 95% CI, 0.31–0.81) than non-Hispanic Whites, but this was not the case for Hispanic patients with HFrEF (OR, 0.94; 95% CI, 0.62–1.43).
Lower risk of developing AF in the setting of HF, compared with White patients.
|Asian and Pacific Islander populations||Limited population-specific data for Asian and pacific Islander subgroups in the United States.||High rates of preventable HF hospitalization observed in some Asian and Pacific Islander populations. |
Lower mortality rates from HF for Asian subgroups when listed as the primary cause of death, compared with non-Hispanic White groups.
|Native American and Alaskan Native populations||Limited population-specific data, with cardiovascular risk factor trends best characterized by the Strong Heart Study and Strong Heart Family Study, demonstrating high rates of hypertension and diabetes.||Limited data suggest HF mortality rates in American Indians and Alaska Natives are similar to those in White populations.|
Table 28. Cancer Therapies Known to Be Associated With Cardiomyopathy
|Cardiac Function Monitoring Often Performed in Clinical Practice|
|Alkylating agents||Cyclophosphamide, ifosfamide, melphalan||×|
|Antimetabolites||Fluorouracil, capecitabine, fludarabine, decitabine|
|Anti-HER2 agents||Trastuzumab, pertuzumab||×||×|
|Tyrosine-kinase inhibitors||Dabrafenib, dasatinib, lapatinib, pazopanib, ponatinib, sorafenib, trametinib, sunitinib, vandetanib, imatinib, vandetanib|
|Immune checkpoint inhibitors||Nivolumab, ipilimumab, pembrolizumab|
|Protease inhibitors||Bortezomib, carfilzomib|
|Endocrine therapy||Goserelin, leuprolide, flutamide, bicalutamide, nilutamide|
|Chimeric antigen receptor T-cell therapy||Tisagenlecleucel, axicabtageneciloleucel||×|
|Hematopoietic stem cell transplantation||Hematopoietic stem cell transplantation||×|
Table 29. Risk Factors for Cancer Therapy–Related Cardiomyopathy
- Age ≥60 y
- Black race
- Preexisting cardiomyopathy
- Previous exposure to anthracyclines
- Previous chest radiation
- Elevated troponin pretherapy
Table 30. HF Management Strategies Across the Pregnancy Continuum
|Nonpharmacological strategies||Preconception genetic counseling and testing for potentially heritable cardiac conditions. |
Use of pregnancy cardiovascular risk tools, and echocardiography for myocardial structure and function assessment, to provide information that facilitates informed counseling.
For women planning a pregnancy, provide personalized counseling that promotes the autonomy and goals of the patient (and her partner, as applicable), the patient’s ability for self-care and risk awareness, and ensures adequate psychosocial support for decision-making.
For women not currently planning a pregnancy but who might conceive, discuss HF-specific considerations regarding pregnancy and refer to gynecology or primary care for contraceptive counseling.
|Close maternal monitoring for HF signs or symptoms or other cardiovascular instability by cardiology and obstetric and maternal-fetal medicine teams; close fetal monitoring by the obstetric and maternal-fetal medicine teams. |
Consideration of routine echocardiographic screening in the third trimester for reassessment of myocardial structure and function before labor; echocardiography for any significant changes in HF symptoms or signs during pregnancy, or if HF medications are reduced or discontinued.
BNP or NT-proBNP monitoring during pregnancy may have some value for prediction of cardiovascular events.
Close maternal monitoring by obstetrics and maternal-fetal medicine teams for preeclampsia, which has shared risk factors and pathogenesis with PPCM.
For women presenting with decompensated HF or cardiogenic shock, hemodynamic monitoring and MCS, as appropriate, within a multidisciplinary collaborative approach that supports prompt decision-making about the timing and mechanism of delivery.
|Multidisciplinary recommendations from obstetrics and neonatology and pediatrics teams and shared decision-making regarding the maternal and neonatal risks and benefits of breastfeeding. |
For women presenting with decompensated HF or cardiogenic shock, HF management should include hemodynamic monitoring and mechanical circulatory support as appropriate
|Pharmacological strategies||Review of all current medications. |
For women planning pregnancy imminently, modification of HF pharmacotherapy including. discontinuation of any ACEi, ARB, ARNi, MRA, or SGLT2i or ivabradine medications; within a construct of multidisciplinary shared decision-making, continuation of a beta blocker (most commonly metoprolol), hydralazine, and nitrates; adjustment of diuretic dosing to minimize the risk of placental hypoperfusion.
Ideally, repeat echocardiography approximately 3 mo after preconception HF medication adjustments to ensure stability of myocardial structure and function before conception.
|Close monitoring of maternal blood pressure, heart rate, and volume status, with adjustment of the modified HF regimen as appropriate to avoid hypotension (systemic vasodilation peaks in the second trimester) and placental hypoperfusion. |
For women with HF or cardiomyopathy presenting during pregnancy without preconception counseling and assessment, urgent discontinuation of any GDMT pharmacotherapies with fetal toxicities; within a construct of multidisciplinary shared decision-making, continuation of a beta blocker (most commonly metoprolol succinate), hydralazine, and nitrates; adjustment of diuretic dosing to minimize the risk of placental hypoperfusion.
|For women with acute HF caused by PPCM and LVEF <30%, consideration of anticoagulation until 6–8 wk postpartum, although the efficacy and safety remain uncertain at this time. |
For postpartum women with severe acute HF caused by PPCM and LVEF <35%, in GDMT pharmacotherapy and prophylactic anticoagulation, to improve LVEF recovery; the efficacy and safety of bromocriptine for acute PPCM treatment remains uncertain at this time, particularly in the setting of contemporary HF GDMT and cardiogenic shock management.*
For women who choose to breastfeed, review medications with neonatology and pediatrics teams for neonatal safety during lactation, ideally with pharmacist consultation if available.
Within a construct of multidisciplinary shared decision-making, medications that may be appropriate during breastfeeding include ACEi (enalapril or captopril preferred, monitor neonatal weight), beta blockers (metoprolol preferred, monitor neonatal heart rate).
Diuretics can suppress lactation, but with neonatal follow-up the use of furosemide may be appropriate.
|Multidisciplinary care beyond the cardiology team||Consultation with genetics, gynecology, and maternal-fetal medicine teams, as appropriate to the outcome of shared decision-making.||Multidisciplinary management with obstetrics and maternal-fetal medicine teams during pregnancy. |
For women with decompensated HF or evidence of hemodynamic instability antepartum, delivery planning will include obstetrics and maternal-fetal medicine, anesthesia, and neonatology teams.
|Multidisciplinary management with obstetrics, maternal-fetal medicine, neonatology, and pediatrics teams, especially for multidisciplinary recommendations regarding lactation. |
Consultation with gynecology team for ongoing contraceptive planning.
11.3. HF and Pregnancy
12. Quality Metrics and Reporting
12.1. Performance Measurement
13. Goals of Care
13.1. Palliative and Supportive Care, Shared Decision-Making, and End-of-Life
Table 32. Palliative and Supportive Care Domains to Improve Processes of Care and Patient Outcomes
|Palliative and Supportive Domains of Care||What Palliative Care Adds to Overall HF Management|
|High-quality communication||Central to palliative care approaches are communication and patient-caregiver engagement techniques.|
|Conveyance of prognosis||Palliative care specifically addresses patient and caregiver understanding of disease, treatment, and prognosis. Research suggests that patients tend to overestimate their survival and overestimate the potential benefits of treatment. Objective risk models can calibrate expectations, but discussion of uncertainty should accompany prognostic conversations, often summarized as “hope for the best, plan for the worst.”|
|Clarifying goals of care||Management of patients with HF as their disease becomes end-stage and death seems near includes decisions about when to discontinue treatments designed primarily to prolong life (e.g., ICD, hospitalization, tube feeding), decisions on when to initiate treatments to reduce pain and suffering that may hasten death (e.g., narcotics), and decisions about the location of death, home services, and hospice care. Exploring patients’ expressed preferences, values, needs, concerns, means and desires through clinician-led discussion can clarify values-treatment concordance and improve medical decision-making.|
|Shared decision-making||Shared decision-making is a process by which patients and clinicians work together to make optimal health care decisions from medically reasonable options that align with what matters most to patients. Shared decision-making requires: unbiased medical evidence about the risks, benefits, and burdens of each alternative, including no intervention; clinician expertise in communication and tailoring that evidence for individual patients; and patient goals and informed preferences.|
|Symptom management||Dyspnea, fatigue, pain, nausea, depression, anxiety, and other symptoms of HF refractory to cardiovascular therapies can be partially remediated through palliative and supportive approaches in addition to GDMT.|
|Caregiver support||Care of the patient with heart failure should extend to their loved ones, including beyond their death, to offer support to families and help them cope with loss.|
Figure 15. A Depiction of the Clinical Course of HF With Associated Types and Intensities of Available Therapies Over Time
- 99mTc-PYP: Technetium Pyrophosphate
- AF: Atrial Fibrillation
- AL-CM: Immunoglobulin Light Chain Amyloid Cardiomyopathy
- ATTR-CM: Transthyretin Amyloid Cardiomyopathy
- ATTRv: Variant Transthyretin Amyloidosis
- ATTRwt: Wild-type Transthyretin Amyloidosis
- BNP: B-type Natriuretic Peptide
- CABG: Coronary Artery Bypass Graft
- CAD: Coronary Artery Disease
- CCM: Cardiac Contractility Modulation
- CHA2DS2-VASc: Congestive Heart Failure, Hypertension, Age 75+, Diabetes Mellitus, Prior Stroke, Transient Ischemic Attack Or Thromboembolic Event, Vascular Disease, Age 65-74, Sex Category
- CHF: Congestive Heart Failure
- CKD: Chronic Kidney Disease
- CMR: Cardiovascular Magnetic Resonance
- COVID-19: Coronavirus Disease 2019
- CPET: Cardiopulmonary Exercise Test
- CRT: Cardiac Resynchronization Therapy
- CRT-D: Cardiac Resynchronization Therapy With Defibrillator
- CRT-P: Cardiac Resynchronization Therapy With Pacemaker
- CT: Computed Tomography
- CVD: Cardiovascular Disease
- CVP: Central Venous Pressure
- DOAC: Direct-acting Oral Anticoagulants
- DPP-4: Dipeptidyl Peptidase-4
- ECG: Electrocardiogram
- EF: Ejection Fraction
- ERO: Effective Regurgitant Orifice
- FDA: U.S. Food And Drug Administration
- FLC: Free Light Chain
- GDMT: Guideline-directed Medical Therapy
- HF: Heart Failure
- HFimpEF: Heart Failure With Improved Ejection Fraction
- HFmrEF: Heart Failure With Mildly Reduced Ejection Fraction
- HFpEF: Heart Failure With Preserved Ejection Fraction
- HFrEF: Heart Failure With Reduced Ejection Fraction
- ICD: Implantable Cardioverter Defibrillator
- IFE: Immunofixation Electrophoresis
- LBBB: Left Bundle Branch Block
- LV: Left Ventricular
- LVAD: Left Ventricular Assist Device
- LVEDE: Left Ventricular End-diastolic Volume
- LVEF: Left Ventricular Ejection Fraction
- LVESD: Left Ventricular End-systolic Diameter
- LVH: Left Ventricular Hypertrophy
- MCS: Mechanical Circulatory Support
- MI: Myocardial Infarction
- MR: Mitral Regurgitation
- MRA: Mineralocorticoid Receptor Antagonist
- MRI: Magnetic Resonance Imaging
- MV: Mitral Valve
- NSAID: Nonsteroidal Anti-inflammatory Drug
- NSVT: Nonsustained Ventricular Tachycardia
- NT-proBNP: N-terminal Prohormone Of B-type Natriuretic Peptide
- NYHA: New York Heart Association
- PA: Pulmonary Artery
- PASP: Pulmonary Artery Systolic Pressure
- PCWP: Pulmonary Capillary Wedge Pressure
- PET: Positron Emission Tomography
- PPAR-γ: Peroxisome Proliferator-activated Receptor Gamma
- PUFA: Polyunsaturated Fatty Acid
- QALY: Quality-adjusted Life-year
- QOL: Quality Of Life
- RA: Right Atrial
- RAASi: Renin-angiotensin-aldosterone System Inhibitor
- RCT: Randomized Controlled Trial
- RF: Radiofrequency
- RV: Right Ventricular
- RVol: Regurgitant Volume
- Rx: Prescription
- SCD: Sudden Cardiac Death
- SGLT2i: Sodium-glucose Cotransporter-2 Inhibitors
- SPECT: Single Photon Emission CT
- TEE: Transesophageal Echocardiogram
- TEER: Transcatheter Mitral Edge-to-edge Repair
- TIA: Transient Ischemic Attack
- TTE: Transthoracic Echocardiogram
- VA: Ventricular Arrhythmia(s)
- VF: Ventricular Fibrillation
- VHD: Valvular Heart Disease
- VO2: Oxygen Consumption
- VT: Ventricular Tachycardia
- eGFR: Estimated Glomerular Filtration Rate
Heidenreich PA, Bozkurt B, Aguilar D, Allen LA, Byun JJ, Colvin MM, Deswal A, Drazner MH, Dunlay SM, Evers LR, Fang JC, Fedson SE, Fonarow GC, Hayek SS, Hernandez AF, Khazanie P, Kittleson MM, Lee CS, Link MS, Milano CA, Nnacheta LC, Sandhu AT, Stevenson LW, Vardeny O, Vest AR, Yancy CW. 2022 AHA/ACC/HFSA guideline for the management of heart failure: a report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines. J Am Coll Cardiol. 2022; https://doi.org/10.1016/j.jacc.2021.12.012.
Copublished in Circulation. 2022; https://www.ahajournals.org/doi/10.1161/CIR.0000000000001063.