Heart failure (HF) is a clinical syndrome in which the heart is not able to meet the demands of the body, manifested by low cardiac output, elevated ventricular filling pressure, or both. Chronic heart failure refers to the long-term state of this clinical syndrome. Chronic heart failure may be compensated, indicating a relatively stable state that may or may not be symptomatic. When chronic heart failure involves an acute or subacute worsening of symptoms or hemodynamics, it becomes acute decompensated heart failure. Diagnosis is by examination, blood tests, and imaging. Treatment focuses on management of lifestyle and risk factors and guideline-directed medical therapy.
In addition to the 6.7 million people in the United States with heart failure, about one-third of the adult population is at risk for developing heart failure, and about 1 in 4 people will develop it at some point in their lifetime (1). The definition, pathophysiology, and causes of heart failure, including chronic heart failure, are reviewed in Overview of Heart Failure.
Chronic heart failure is staged as follows (2):
A: Risk of HF but no structural or functional cardiac abnormalities or symptoms
B: Structural or functional cardiac abnormalities but no symptoms
C: Structural heart disease with symptoms
D: Refractory HF requiring advanced therapies or palliative care
Patient functional status in stages B to D can be further classified based on symptoms using the New York Heart Association Functional Classification system. The type of heart failure can be further classified based on the left ventricular ejection fraction.
General references
1. Bozkurt B, Ahmad T, Alexander K, et al. HF STATS 2024: Heart Failure Epidemiology and Outcomes Statistics An Updated 2024 Report from the Heart Failure Society of America. J Card Fail. 2025;31(1):66-116. doi:10.1016/j.cardfail.2024.07.001
2. Bozkurt B, Coats AJ, Tsutsui H, et al. Universal Definition and Classification of Heart Failure: A Report of the Heart Failure Society of America, Heart Failure Association of the European Society of Cardiology, Japanese Heart Failure Society and Writing Committee of the Universal Definition of Heart Failure. J Card Fail. Published online March 1, 2021. doi:10.1016/j.cardfail.2021.01.022
Symptoms and Signs of Chronic Heart Failure
Common chronic heart failure symptoms include exertional dyspnea, exercise intolerance, and peripheral edema (particularly in the ankles and feet) (1). Other symptoms may include anorexia or early satiety, nausea, presyncope or syncope, and coughing or wheezing (part of cardiac asthma).
In earlier or milder stages, dyspnea occurs with varying degrees of exertion. As HF worsens, dyspnea can occur during rest and at night, sometimes causing nocturnal cough. Dyspnea occurring immediately or soon after lying flat and relieved promptly by sitting up (orthopnea) is common as heart failure advances. In paroxysmal nocturnal dyspnea,dyspnea awakens patients several hours after they lie down and is relieved only after they sit up for 15 to 20 minutes. In severe HF, periodic cycling of breathing (Cheyne-Stokes respiration—from a brief period of apnea, patients breathe progressively faster and deeper, then slower and shallower until they become apneic and repeat the cycle)—can occur during the day or night; the sudden hyperpneic phase may awaken the patient from sleep. Cheyne-Stokes breathing differs from paroxysmal nocturnal dyspnea in that the hyperpneic phase is short, lasting only 10 to 15 seconds, but the cycle recurs regularly, lasting 30 seconds to 2 minutes. Paroxysmal nocturnal dyspnea is associated with pulmonary congestion, and Cheyne-Stokes respiration with low cardiac output.
Severely reduced cerebral blood flow and hypoxemia can cause chronic irritability and impair mental performance.
Sleep-related breathing disorders, such as sleep apnea (central and obstructive), are common in HF and may both aggravate HF and be worsened by HF.
Physical signs specific to heart failure included jugular venous distention or elevated jugular venous pulsations, a third heart sound (S3) or summation gallop, displaced apical impulse due to cardiomegaly, and the hepatojugular reflex (1). Signs of pulmonary edema (crackles, hypoxemia), poor perfusion (cool extremities, delayed capillary refill), decreased stroke volume (narrow pulse pressure), or a compensatory response (tachycardia, hypertension) may also occur. Weight loss and cardiac cachexia may occur in advanced heart failure.
Symptoms and signs reference
1. Bozkurt B, Coats AJ, Tsutsui H, et al. Universal Definition and Classification of Heart Failure: A Report of the Heart Failure Society of America, Heart Failure Association of the European Society of Cardiology, Japanese Heart Failure Society and Writing Committee of the Universal Definition of Heart Failure. J Card Fail. Published online March 1, 2021. doi:10.1016/j.cardfail.2021.01.022
Diagnosis of Chronic Heart Failure
Diagnostic techniques in heart failure are discussed in detail under Acute Heart Failure. Attention to symptoms, weight, serial imaging (eg, echocardiography) and measurement of natriuretic peptides and other biomarkers can help guide treatment and identify acute decompensation.
Treatment of Chronic Heart Failure
Diet and lifestyle changes
Treatment of cause
Medication therapy
Multidisciplinary care
Sometimes device therapy (eg, implantable cardioverter-defibrillator, cardiac resynchronization therapy, mechanical circulatory support)
Sometimes cardiac transplantation
Treatment goals for chronic heart failure include correcting hypertension, preventing myocardial infarction and progression of atherosclerosis, improving cardiac function, reducing hospitalizations, improving quality of life, and lengthening survival.
Treatment involves dietary and lifestyle changes, medications, devices, and sometimes percutaneous coronary interventions or surgery.
Treatment is multidisciplinary and tailored to the patient, considering causes, symptoms, and response to medications, including adverse effects. There are several evidence-based therapies for chronic heart failure with reduced ejection fraction (HFrEF) (1, 2). There are fewer evidence-based treatments for chronic heart failure with preserved ejection fraction (HFpEF), chronic heart failure with mildly reduced ejection fraction and improved ejection fraction (HFmrEF and HRimpEF), and chronic right ventricular failure (3).
Medications
See Medications for Heart Failure for detailed information on specific medications and classes.
Guideline-directed medical therapy of heart failure with reduced ejection fraction (HFrEF)
Guideline-directed medical therapy consists of evidence-based medications that have been shown to improve clinical outcomes for patients with HF. Medical treatment of chronic HRrEF generally consists of 4 foundational classes of therapy for all patients, as all classes have been demonstrated to reduce mortality (1, 2, 4). These include:
Beta-blockers
Angiotensin receptor/neprilysin inhibitor (ARNI)
Mineralocorticoid receptor antagonist (MRA)
Sodium-glucose co-transporter 2 (SGLT2) inhibitor
Doses of medications in these pharmacologic classes are generally titrated to maximum tolerable doses to achieve optimal benefit.
Beta-blockers (eg, bisoprolol, carvedilol, metoprolol) reduce sympathetic nervous system tone and overall neurohormonal activation and have been a main stay of chronic heart failure therapy ((eg, bisoprolol, carvedilol, metoprolol) reduce sympathetic nervous system tone and overall neurohormonal activation and have been a main stay of chronic heart failure therapy (1, 2). Beta-blockers can also help to control arrhythmias associated with heart failure, in addition to being antianginal agents for patients with ischemic cardiomyopathy. Reduction of basal heart rate has been demonstrated to be an important marker of outcome. Because of their negative inotropic effects, beta-blockers are avoided in the acute decompensated phase of heart failure; they are initiated when a patient is stable and well compensated. Beta-blockers are the only foundational class of pharmacologic chronic heart failure agents that have demonstrated value only for patients with reduced ejection fraction, and not for patients with preserved left ventricular ejection fraction. For patients who are unable to tolerate beta-blockers or who achieve suboptimal resting heart rate reduction (> 77 beats/minute for those in sinus rhythm), ivabradine, a sinus node inhibitor, can be used to achieve heart rate reduction. ). Beta-blockers can also help to control arrhythmias associated with heart failure, in addition to being antianginal agents for patients with ischemic cardiomyopathy. Reduction of basal heart rate has been demonstrated to be an important marker of outcome. Because of their negative inotropic effects, beta-blockers are avoided in the acute decompensated phase of heart failure; they are initiated when a patient is stable and well compensated. Beta-blockers are the only foundational class of pharmacologic chronic heart failure agents that have demonstrated value only for patients with reduced ejection fraction, and not for patients with preserved left ventricular ejection fraction. For patients who are unable to tolerate beta-blockers or who achieve suboptimal resting heart rate reduction (> 77 beats/minute for those in sinus rhythm), ivabradine, a sinus node inhibitor, can be used to achieve heart rate reduction.
Treatment with an angiotensin receptor/neprilysin inhibitor (sacubitril/valsartan) is the standard for patients with chronic heart failure ((sacubitril/valsartan) is the standard for patients with chronic heart failure (1, 2, 5, 6, 7). This medication combination is a potent vasodilator and may induce symptomatic hypotension. Therefore, caution is recommended when initiating or uptitrating sacubitril/valsartan, especially for patients with a systolic blood pressure of less than 100 mm Hg. Sacubitril/valsartan has demonstrated superior mortality reduction, compared to angiotensin-converting enzyme-inhibitors or angiotensin II receptor blockers, although both classes of medication are still used routinely, particularly in patients who are intolerant of sacubitril/valsartan.
Spironolactone and eplerenone are Spironolactone and eplerenone aremineralocorticoid receptor antagonists used for the treatment of chronic heart failure (1, 2, 8). Agents, such as finerenone, are under investigation in different patient subpopulations, including those with significant diabetes and those with significant renal dysfunction. ). Agents, such as finerenone, are under investigation in different patient subpopulations, including those with significant diabetes and those with significant renal dysfunction.Spironolactone has a relatively weak diuretic effect, but is potassium sparing and can be associated with hyperkalemia. Potassium levels must be monitored in patients when initiating spironolactone or when increasing the dose. Spironolactone can also be associated with gynecomastia, and should be discontinued If this adverse effect develops. Eplerenone has a more favorable adverse effect profile, including less relative hyperkalemia and gynecomastia.
SGLT2 inhibitors (eg, dapagliflozin, empagliflozin) have demonstrated significant survival benefit for patients with heart failure, regardless of ejection fraction ((eg, dapagliflozin, empagliflozin) have demonstrated significant survival benefit for patients with heart failure, regardless of ejection fraction (1, 2, 9, 10). They are generally well tolerated and have a relatively weak diuretic effect. Originally developed as oral hypoglycemic agents, they can reduce blood glucose levels.
Other pharmacologic therapies are available for specific populations of patients with chronic heart failure, particularly those who remain symptomatic despite optimal doses of the foundational pharmacologic therapy classes (1, 2).
Digoxin can be used to reduce the risk of heart failure hospitalizations in patients with reduced ejection fraction. Digoxin can be used to reduce the risk of heart failure hospitalizations in patients with reduced ejection fraction.Digoxin is contraindicated in patients with moderate to severe chronic kidney disease due to the risk of toxicity.
Additional diuretic therapy, particularly loop diuretics, are frequently used in patients with ongoing symptoms of congestion, despite optimal medical therapy for chronic heart failure.
Ivabradine can be used to control resting heart rate in patients who are in sinus rhythm who are either poorly tolerant of beta-blockers or do not achieve satisfactory resting heart rate control with them. Ivabradine can be used to control resting heart rate in patients who are in sinus rhythm who are either poorly tolerant of beta-blockers or do not achieve satisfactory resting heart rate control with them.Ivabradine is recommended therapy for patients with HRrEF and an EF < 35% with a resting heart rate ≥ 70 beats per minute on beta blocker therapy (11).
Vericiguat is an oral, soluble guanylate cyclase agonist that has vasodilator effects. It can be added to other heart failure therapies in patients with heart failure with reduced ejection fraction with ongoing symptoms who have also had an acute decompensation within the last 6 months (Vericiguat is an oral, soluble guanylate cyclase agonist that has vasodilator effects. It can be added to other heart failure therapies in patients with heart failure with reduced ejection fraction with ongoing symptoms who have also had an acute decompensation within the last 6 months (12).
Vasodilators, as a combination of isosorbide dinitrate and hydralazine, can be used in patients with persistent symptoms of congestion, particularly those who are unable to tolerate ARNIs or when they are contraindicated due to poor kidney function. Vasodilators, as a combination of isosorbide dinitrate and hydralazine, can be used in patients with persistent symptoms of congestion, particularly those who are unable to tolerate ARNIs or when they are contraindicated due to poor kidney function.
Calcium channel blockers, nonsteroidal anti-inflammatory drugs, thiazolidinediones, and class 1C antiarrhythmic medications can worsen heart failure and should be avoided unless no alternative exists; patients who must take such medications should be followed closely.
Medical therapy of heart failure with mildly reduced or improved ejection fraction (HRmrEF and HRimpEF)
In general, the therapeutic approach for HRmrEF and HRimpEF is similar to that for HRrEF, although far less evidence exists to support specific medications or classes (1, 2). Diuretics are recommended for anti-congestive therapy. SGLT2 inhibitors may be beneficial in preventing hospitalization in HRmrEF. Data directly supporting beta blockade, angiotensin-renin system inhibition, and mineralocorticoid antagonists are lacking and recommendations are based on observational or post-hoc analyses.
Medical therapy of heart failure with preserved ejection fraction (HRpEF)
Recommended therapies for HRpEF include an SGLT2 inhibitor for all patients, diuretics for patients with congestion and symptoms, and mineralocorticoid antagonists and angiotensin-renin system inhibition for select patient groups (1, 2, 13). Cardiovascular comorbidities, including hypertension, atherosclerotic disease, and atrial fibrillation should be treated. As with HRmrEF, SGLT2 inhibitors, beta blockers, angiotensin-renin system inhibitors, and mineralocorticoid antagonists may be considered.
See Medications for Heart Failure for more detailed information on specific medication classes.
Disease management
General measures, especially patient and caregiver education and diet and lifestyle modifications, are important for all patients with heart failure (1).
Education
Sodium restriction
Appropriate weight and fitness levels
Correction of underlying conditions
Patient and caregiver education are critical to long-term success. The patient and family should be involved in treatment choices. They should be taught the importance of medication adherence, warning signs of an exacerbation, and how to link cause with effect (eg, increased salt in the diet with weight gain or symptoms).
Many centers (eg, specialized outpatient clinics) have integrated health care practitioners from different disciplines (eg, HF nurses, pharmacists, social workers, rehabilitation specialists) into multidisciplinary teams or outpatient heart failure management programs. These approaches can improve outcomes and reduce hospitalizations and are most effective in the sickest patients.
Dietary sodium restriction helps limit fluid retention. All patients should eliminate salt in cooking and at the table and avoid salted foods; the most severely ill should limit sodium to < 2 g/day by consuming only low-sodium foods (1, 2).
Monitoring daily morning weight helps detect sodium and water accumulation early (1, 2). If weight increases > 2 kg over a few days, patients may be able to adjust their diuretic dose themselves, but if weight gain continues or symptoms occur, patients should seek medical attention.
Intensive case management, particularly by monitoring medication adherence and frequency of unscheduled visits to the physician or emergency department and hospitalizations, can identify when intervention is needed (1, 2). Nurses who specialize in the care of patients with HF are valuable in education, follow-up, and dosage adjustment according to predefined protocols.
Patients with atherosclerosis or diabetes should strictly follow a diet appropriate for their disorder. Obesity may cause and always aggravates the symptoms of HF; patients should attain a body mass index (BMI) ≤ 30 kg/m2 (ideally 21 to 25 kg/m2).
Regular light activity (eg, walking), tailored to symptoms, is encouraged (1, 2). Activity prevents skeletal muscle deconditioning, which worsens functional status; however, activity does not appear to improve survival or decrease hospitalizations (1, 2). Rest is appropriate during acute exacerbations. Formal exercise through cardiac rehabilitation is useful for patients with chronic HFrEF and is likely helpful for patients with chronic HFpEF.
Patients should have annual influenza vaccination because influenza can precipitate HF exacerbations, particularly in institutionalized or older patients. Patients should be vaccinated against SARS-CoV-2.
If causes such as hypertension, persistent tachyarrhythmia, severe anemia, hemochromatosis, uncontrolled diabetes, thyrotoxicosis, beriberi, alcohol use disorder, or toxoplasmosis are successfully treated, patients may dramatically improve.
Anemia is common among patients with chronic heart failure and is frequently multifactorial. Anemia is associated with worse symptoms and outcomes in HF and so reversible causes should be sought and treated. Iron deficiency is among the most common causes of anemia in HF, and iron replacement therapy should be considered once treatable causes such as blood loss (gastrointestinal or other) have been excluded (2). Oral iron replacement is often less effective due to poor absorption and other reasons, thus intravenous iron replacement is preferred.
Management of extensive ventricular infiltration (eg, in amyloidosis) has improved considerably. Treatments for amyloidosis have markedly improved prognosis for many of these patients.
Device therapy
Use of an implantable cardioverter-defibrillator (ICD) or cardiac resynchronization therapy (CRT) is appropriate for some patients.
An implantable cardioverter-defibrillator is recommended for patients with an otherwise good life expectancy if they have symptomatic sustained ventricular tachycardia or ventricular fibrillation or if they remain symptomatic and have an left ventricular ejection fraction persistently < 35% while receiving guideline-directed medical therapy (2). The data for ICD use in HFrEF are stronger for ischemic cardiomyopathy than in nonischemic cardiomyopathy. A clinical trial that included patients with HFrEF with nonischemic cardiomyopathy demonstrated no mortality benefit from prophylactic (primary prevention) ICD placement (14).
Cardiac resynchronization therapy is a mode of pacing that synchronizes contraction of the left ventricle by simultaneously pacing its opposing wall, thereby improving stroke volume. CRT may relieve symptoms and reduce heart failure hospitalizations for patients who have HF, left ventricular ejection fraction < 35%, and a widened QRS complex with a left bundle branch block pattern (> 0.15 second—the wider the QRS, the greater potential benefit) (2). Many CRT devices also incorporate an ICD in their mechanism.
An implantable device that remotely monitors invasive hemodynamics (eg, pulmonary artery pressure) to guide therapy can help reduce frequency of heart failure exacerbation and hospitalization in selected patients (4, 15).
Durable or ambulatory LV assist devices (LVADs) are longer-term implantable pumps that augment LV output. They are commonly used to maintain patients with severe HF who are awaiting transplantation and are also used as "destination therapy" (ie, as a long-term or permanent solution) in some patients who are not candidates for transplant.
Surgery and percutaneous procedures
Surgery may be appropriate when certain underlying disorders are present. Surgery in patients with advanced HF should be done in a specialized center.
Surgical closure of congenital or acquired intracardiac shunts can be curative.
Coronary artery bypass grafting (CABG) for patients with LV systolic dysfunction secondary to coronary artery disease and evidence of myocardial viability may be beneficial (1, 2); however, those patients with prior myocardial infarction and non-viable myocardium are less likely to benefit from CABG. Thus, the decision to use revascularization in a patient with HF and multivessel coronary artery disease should be made on a case-by-case basis.
If HF is primarily due to a valvular disorder, valve repair or replacement should be considered (1, 2). Patients with primary mitral regurgitation are more likely to benefit than patients with mitral regurgitation secondary to LV dilation, in whom poor myocardial function is likely to continue postoperatively. Surgery is preferably done before myocardial dilation and damage become irreversible. Percutaneous mitral valve repair procedure (also called transcatheter end-to-end repair [TEER]), in which a clip is applied to approximate the anterior and posterior mitral leaflets, has been shown to reduce death and HF hospitalization in carefully selected patients with symptomatic HF despite optimal medical management and moderate to severe or severe mitral regurgitation with preserved LV size (end-systolic dimension ≤ 70 mm) (16).
Heart transplantation is the treatment of choice for patients < 70 years who have severe HF refractory to guideline-directed medical therapy (1, 2). Some older patients with otherwise good health are also considered if they meet other criteria for transplantation.
Treatment of persistent heart failure symptoms
Management may need to be adjusted when symptoms persist despite treatment. Reasons and appropriate actions include:
Persistence of an underlying disorder (eg, hypertension, ischemia or infarction, valvular disease) despite treatment: Optimize treatment of underlying disorder
Suboptimal treatment of heart failure: Escalate or optimize heart failure treatment regimen
Medication nonadherence: Adherence strategies
Excess intake of dietary sodium or alcohol: Reduction of sodium intake, alcohol intake, or both; refer to dietician or addiction specialist as necessary
Presence of an undiagnosed thyroid disorder, anemia, or supervening arrhythmia (eg, atrial fibrillation with rapid ventricular response, intermittent ventricular tachycardia): Test for and treat undiagnosed disorders
End-of-life care
All patients and family members should be taught about disease progression and the risk of sudden cardiac death. For some patients, improving quality of life is as important as increasing quantity of life. Thus, it is important to determine patients’ wishes about resuscitation (eg, endotracheal intubation, CPR [cardiopulmonary respiration]) if their condition deteriorates, especially when HF is already severe.
All patients should be reassured that symptoms will be relieved, and they should be encouraged to seek medical attention early if their symptoms change significantly. Involvement of pharmacists, nurses, social workers, and clergy (when desired), who may be part of an interdisciplinary team or disease management program already in place, is particularly important in end-of-life care.
Treatment references
1. McDonagh TA, Metra M, Adamo M, et al: 2021 ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure: Developed by the Task Force for the diagnosis and treatment of acute and chronic heart failure of the European Society of Cardiology (ESC) with the special contribution of the Heart Failure Association (HFA) of the ESC. Eur Heart J 42(36):3599-3726, 2021. doi: 10.1093/eurheartj/ehab368
2. Heidenreich PA, Bozkurt B, Aguilar D, et al: 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. Circulation 145:e895–e1032, 2022, doi: 10.1161/CIR.0000000000001063
3. Shah SJ, Kitzman D, Borlaug B, et al: Phenotype-specific treatment of heart failure with preserved ejection fraction: A multiorgan roadmap. Circulation 134(1):73–90, 2016. doi: 10.1161/CIRCULATIONAHA.116.021884
4. Maddox TM, Januzzi JL Jr, Allen LA, et al: 2024 ACC Expert Consensus Decision Pathway for Treatment of Heart Failure With Reduced Ejection Fraction: A Report of the American College of Cardiology Solution Set Oversight Committee. J Am Coll Cardiol 83(15):1444–1488, 2024. doi:10.1016/j.jacc.2023.12.024
5. McMurray JJ, Packer M, Desai AS, et al: Angiotensin-neprilysin inhibition versus enalapril in heart failure. N Engl J Med 371(11):993–1004, 2014. doi:10.1056/NEJMoa1409077
6. Solomon SD, McMurray JJ, Anand IS, et al: Angiotensin-neprilysin inhibition in heart failure with preserved ejection fraction. N Engl J Med 381:1609–1620, 2019. doi:10.1056/NEJMoa1908655
7. McMurray JJV, Jackson AM, Lam CSP, et al: Effects of Sacubitril-Valsartan Versus Valsartan in Women Compared With Men With Heart Failure and Preserved Ejection Fraction: Insights From PARAGON-HF. Circulation 141(5):338–351, 2020. doi:10.1161/CIRCULATIONAHA.119.044491
8. Pitt B, Pfeffer MA, Assmann SF, et al: Spironolactone for heart failure with preserved ejection fraction. N Engl J Med 370(15):1383–1392, 2014. doi:10.1056/NEJMoa1313731
9. McMurray JJV, Solomon SD, Inzucchi SE, et al: Dapagliflozin in Patients with Heart Failure and Reduced Ejection Fraction. N Engl J Med 381(21):1995–2008, 2019. doi:10.1056/NEJMoa191130
10. Anker SD, Butler J, Filippatos G, et al: Empagliflozin in Heart Failure with a Preserved Ejection Fraction. N Engl J Med 385(16):1451–1461, 2021. doi:10.1056/NEJMoa2107038
11. Swedberg K, Komajda M, Böhm M, et al: Ivabradine and outcomes in chronic heart failure (SHIFT): a randomised placebo-controlled study. Lancet 376(9744):875–885, 2010. doi:10.1016/S0140-6736(10)61198-1
12. Armstrong PW, Pieske B, Anstrom KJ, et al: Vericiguat in Patients with Heart Failure and Reduced Ejection Fraction. N Engl J Med 382(20):1883–1893, 2020. doi:10.1056/NEJMoa1915928
13. Kittleson MM, Panjrath GS, Amancherla K, et al: 2023 ACC Expert Consensus Decision Pathway on Management of Heart Failure With Preserved Ejection Fraction: A Report of the American College of Cardiology Solution Set Oversight Committee. J Am Coll Cardiol 81(18):1835–1878, 2023. doi:10.1016/j.jacc.2023.03.393
14. Kober L, Thune JJ, Nielsen JC, et al: Defibrillator implantation in patients with nonischemic systolic heart failure. N Engl J Med 375(13):1221–2130, 2016. doi: 10.1056/NEJMoa1608029
15. Clephas PRD, Radhoe SP, Boersma E, et al: Efficacy of pulmonary artery pressure monitoring in patients with chronic heart failure: a meta-analysis of three randomized controlled trials. Eur Heart J 44(37):3658–3668, 2023. doi:10.1093/eurheartj/ehad346
16. Stone GW, Lindenfield J, Abraham WT, et al: Transcatheter mitral-valve repair in patients with heart failure. N Engl J Med 379(24):2307–2318, 2018. doi: 10.1056/NEJMoa1806640
Prognosis for Chronic Heart Failure
HF usually involves gradual deterioration, interrupted by bouts of severe decompensation, and ultimately death, although the time course is being lengthened with modern therapies. However, death can also be sudden and unexpected, without prior worsening of symptoms. Overall 1-year mortality in patients with chronic HF is approximately 7 to 14% (1, 2, 3).
Specific factors that suggest a poor prognosis include older age at diagnosis, male gender, New York Heart Assocation class III or IV symptoms, ejection fraction < 30%, frequent or recent hospitalization, presence of chronic kidney, lung, or pulmonary disease, diabetes, lower measures of exercise tolerance (such as peak oxygen consumption or 6-minute walk distance), elevation of natriuretic peptide levels, and hyponatremia (4, 5, 6).
BNP, NTproBNP, and risk scores such as the Meta-Analysis Global Group in Chronic Heart Failure (MAGGIC) Risk Score and the Seattle Heart Failure model, are helpful to predict prognosis in HF patients as an overall group, although there is significant variation in survival among individual patients (7, 8).
Prognosis references
1. Crespo-Leiro MG, Anker SD, Maggioni AP, et al. European Society of Cardiology Heart Failure Long-Term Registry (ESC-HF-LT): 1-year follow-up outcomes and differences across regions [published correction appears in Eur J Heart Fail. 2017 Mar;19(3):438. doi: 10.1002/ejhf.772]. Eur J Heart Fail. 2016;18(6):613-625. doi:10.1002/ejhf.566
2. Jones NR, Roalfe AK, Adoki I, Hobbs FDR, Taylor CJ. Survival of patients with chronic heart failure in the community: a systematic review and meta-analysis. Eur J Heart Fail. 2019;21(11):1306-1325. doi:10.1002/ejhf.1594
3. Pongiglione B, Torbica A, Gale CP, Tavazzi L, Vardas P, Maggioni AP. Patient, hospital and country-level risk factors of all-cause mortality among patients with chronic heart failure: Prospective international cohort study. PLoS One. 2021;16(5):e0250931. Published 2021 May 10. doi:10.1371/journal.pone.0250931
4. Hollenberg SM, Warner Stevenson L, Ahmad T, 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 [published correction appears in J Am Coll Cardiol. 2020 Jan 7;75(1):132. doi: 10.1016/j.jacc.2019.11.020]. J Am Coll Cardiol. 2019;74(15):1966-2011. doi:10.1016/j.jacc.2019.08.001
5. Peura JL, Colvin-Adams M, Francis GS, et al. Recommendations for the use of mechanical circulatory support: device strategies and patient selection: a scientific statement from the American Heart Association. Circulation. 2012;126(22):2648-2667. doi:10.1161/CIR.0b013e3182769a54
6. Pocock SJ, Wang D, Pfeffer MA, et al. Predictors of mortality and morbidity in patients with chronic heart failure. Eur Heart J. 2006;27(1):65-75. doi:10.1093/eurheartj/ehi555
7. Rich JD, Burns J, Freed BH, Maurer MS, Burkhoff D, Shah SJ. Meta-Analysis Global Group in Chronic (MAGGIC) Heart Failure Risk Score: Validation of a Simple Tool for the Prediction of Morbidity and Mortality in Heart Failure With Preserved Ejection Fraction. J Am Heart Assoc. 2018;7(20):e009594. doi:10.1161/JAHA.118.009594
8. Levy WC, Mozaffarian D, Linker DT, et al. The Seattle Heart Failure Model: prediction of survival in heart failure. Circulation. 2006;113(11):1424-1433. doi:10.1161/CIRCULATIONAHA.105.584102
Key Points
Chronic heart failure affects over 6 million people in the United States.
Chronic heart failure is staged based on structural and functional abnormalities as well as the presence and degree of symptoms.
Pharmacologic treatment of chronic heart failure with reduced ejection fraction involves 4 key medication classes: beta-blockers, renin-angiotensin system-neprilysin antagonist, sodium-glucose co-transporter 2 (SGLT2) inhibitor, and mineralocorticoid receptor antagonist.
Multidisciplinary care and lifestyle changes are important elements for treatment of chronic heart failure.
Implantable cardioverter-defibrillators and cardiac resynchronization therapy are used in select patients.
Drugs Mentioned In This Article
