CardiologysevereICD-10 · I50.9

Heart Failure.

Q: What is the life expectancy with heart failure?

Five-year all-cause mortality with clinically apparent heart failure is roughly 50%, but this varies dramatically by stage, ejection fraction, and treatment. Patients on guideline-directed quadruple therapy for HFrEF have substantially better survival than historical figures suggest, and selected stage D patients can receive transplant or LVAD that extends median survival to 5-10 years.

Q: What is the difference between HFrEF and HFpEF?

HFrEF means heart failure with reduced ejection fraction (LVEF ≤40%) — a problem of systolic pump function. HFpEF means heart failure with preserved ejection fraction (LVEF ≥50%) — a problem of diastolic relaxation despite a normal-looking pump. Treatment differs: HFrEF responds to quadruple therapy with mortality benefit, while HFpEF mainly responds to SGLT2 inhibitors and aggressive comorbidity control.

Q: What is congestive heart failure?

Congestive heart failure is an older term used when fluid backs up into the lungs, abdomen, or legs from a failing heart. Modern cardiology simply uses heart failure, with congestion described as a symptom. The signs are the same — breathlessness, swelling, weight gain, and reduced exercise tolerance.

Q: What is ejection fraction?

Ejection fraction is the percentage of blood the left ventricle pumps out with each beat. A normal LVEF is 55-70%. LVEF 41-49% is mildly reduced (HFmrEF); LVEF 40% or below is reduced (HFrEF); LVEF 50% or above with HF symptoms is preserved (HFpEF). Echocardiogram is the standard way to measure it.

Q: What causes heart failure?

The leading causes are coronary artery disease and prior heart attack, long-standing hypertension, valve disease, atrial fibrillation, cardiomyopathies, diabetes, obesity, and cardiotoxic drugs such as anthracycline chemotherapy. In many patients more than one cause is present.

Q: What are the early signs of heart failure?

Early signs include new breathlessness when walking up stairs, new orthopnea (using extra pillows), ankle swelling that returns each evening, weight gain of more than 1.4 kg over two days, and reduced exercise tolerance. Persistent dry cough that is worse at night can also be an early manifestation.

Q: Can heart failure be cured?

Heart failure is usually a chronic syndrome rather than a curable disease, but selected causes are fully reversible — tachycardia-mediated cardiomyopathy with rate control, alcoholic cardiomyopathy with abstinence, peripartum cardiomyopathy in many cases, and severe valve disease after surgical correction. For most patients with chronic HFrEF, optimized therapy improves ejection fraction and quality of life without permanent cure.

Q: What is the four-drug therapy for heart failure?

Modern quadruple therapy for HFrEF combines an ARNI (sacubitril-valsartan) or ACE inhibitor or ARB, an evidence-based beta-blocker (carvedilol, metoprolol succinate, or bisoprolol), a mineralocorticoid receptor antagonist (spironolactone or eplerenone), and an SGLT2 inhibitor (dapagliflozin or empagliflozin). Started together and titrated rapidly, this regimen cuts mortality by roughly 70% compared with placebo.

Q: Is heart failure the same as a heart attack?

No. A heart attack (myocardial infarction) is an acute event where a coronary artery blockage damages heart muscle. Heart failure is a chronic syndrome where the heart cannot pump effectively. A heart attack can cause heart failure by destroying muscle, but they are distinct diagnoses with different treatments.

Q: Can young people get heart failure?

Yes. Young adults can develop heart failure from genetic cardiomyopathies (dilated, hypertrophic), myocarditis after viral infection, peripartum cardiomyopathy in pregnancy, congenital heart disease, anthracycline chemotherapy in childhood cancer survivors, and stimulant or alcohol use. Genetic testing and cardiac MRI are increasingly important in this age group.

Heart failure is a clinical syndrome in which the heart cannot pump enough blood at the pressures the body needs, producing breathlessness, fatigue, and fluid retention. About 6.7 million US adults are affected and the lifetime risk after age 40 is roughly 1 in 4, driven mostly by hypertension and coronary artery disease.

Chest X-ray of congestive heart failure — enlarged cardiac silhouette and pulmonary congestion are typical findings. · Credit: CDC / Dr. Thomas Hooten — Wikimedia Commons · Public Domain

aliases · Heart Failure (congestive heart failure, CHF)· Dil Ki Kamzori· Hridayavakaranam Kuraiv· reviewed May 12, 2026

Reviewed by AIHealz Medical Editorial Board · CardiologyLast reviewed May 12, 2026

About our board →

§ 01

What it is

Heart failure (ICD-10: I50; I50.2 systolic, I50.3 diastolic, I50.4 combined, I50.9 unspecified) is a clinical syndrome defined by symptoms (dyspnea, fatigue, fluid retention) and signs (elevated jugular venous pressure, pulmonary crackles, peripheral edema) that result from a structural or functional cardiac abnormality which raises intracardiac pressures or reduces cardiac output at rest or during stress. The universal definition adopted by ACC/AHA/HFSA and ESC in 2021 also requires objective evidence of cardiac dysfunction — abnormal echocardiogram, elevated natriuretic peptides, or hemodynamic measurements. Heart failure is staged A through D: stage A is high-risk without structural disease; stage B is structural disease without symptoms; stage C is symptomatic disease; stage D is advanced disease requiring specialized interventions. The NYHA functional class (I-IV) describes symptom severity at the time of assessment.

key facts

Prevalence: ~6.7 million US adults; ~64 million people worldwide (AHA 2024 stats)
Demographics: Higher rates in Black adults and men; risk doubles each decade after age 50
Avg. age: Median age at first diagnosis 73; HFpEF skews older and more female
Global cases: ~64 million people; >1 million US hospitalizations per year for decompensation
Specialist: Cardiology
ICD-10: I50.9

§ 02

How you might notice it

Clinical photograph of severe bilateral lower extremity edema in advanced heart failure — Severe peripheral edema — a visible sign of decompensated heart failure when fluid overload progresses untreated. · Credit: Ryaninuk / Wikimedia Commons · CC BY-SA 4.0

01Shortness of breath with activity that worsens steadily over days to weeks; later, breathlessness occurs at rest and limits speech in long sentences.

02Orthopnea — breathlessness when lying flat, relieved by sitting up or sleeping on 2-3 pillows. A specific symptom that signals elevated left-sided filling pressures.

§ 03

How it’s diagnosed

Four-chamber echocardiogram showing the left atrium, left ventricle, right atrium, and right ventricle used to measure ejection fraction — Four-chamber echocardiogram — the cornerstone test that quantifies ejection fraction and classifies HFrEF, HFmrEF, or HFpEF. · Credit: Wikimedia Commons · Public Domain

diagnosis

Heart failure diagnosis is clinical, anchored by symptoms (Framingham major and minor criteria are still useful) and confirmed by objective testing. The workup begins with a focused history (effort tolerance, orthopnea, paroxysmal nocturnal dyspnea, recent weight change) and an examination for elevated jugular venous pressure, S3 gallop, displaced apical impulse, bibasilar crackles, hepatomegaly, and pitting edema. The single most useful blood test is BNP or NT-proBNP — a level below the rule-out threshold (NT-proBNP <125 pg/mL in chronic ambulatory, <300 pg/mL in acute presentation) makes heart failure unlikely; levels above the rule-in threshold support the diagnosis but are not specific. Twelve-lead ECG looks for prior MI, left ventricular hypertrophy, conduction disease, and arrhythmia; a completely normal ECG makes systolic HF less likely. The diagnostic linchpin is transthoracic echocardiogram, which yields left ventricular ejection fraction, chamber sizes, wall thickness, valvular function, and diastolic indices — and so determines whether the patient has HFrEF, HFmrEF, or HFpEF. Additional testing — coronary angiography or CT coronary angiography for suspected ischemic cause, cardiac MRI for suspected infiltrative disease, viability imaging before revascularization, right heart catheterization in selected cases — is targeted to the phenotype. Once heart failure is established, a search for the underlying cause is mandatory; reversible causes (tachycardia-mediated cardiomyopathy, alcoholic cardiomyopathy, peripartum cardiomyopathy, severe valve disease) change treatment trajectory.

Key tests

§ 04

Treatment & cost

medical treatments

✓Sacubitril-valsartan (24/26 mg twice daily; titrate to 97/103 mg twice daily)
✓Carvedilol, metoprolol succinate, or bisoprolol
✓Spironolactone (12.5-25 mg daily; up to 50 mg) or eplerenone (25-50 mg daily)
✓Dapagliflozin or empagliflozin (10 mg daily)

surgical options

Coronary revascularization (CABG or PCI)CABG reduces all-cause mortality by ~16% over 10 years versus medical therapy alone in STICH-eligible patients with ischemic HFrEF.

Valve repair or replacement (surgical or transcatheter)TAVR for severe AS in HF reduces mortality by 30-40% at 1 year vs medical therapy; COAPT showed 47% reduction in HF hospitalization with MitraClip in selected secondary MR.

Cardiac resynchronization therapy (CRT)~30% relative reduction in HF hospitalization and mortality in CARE-HF; ~70% are clinical responders.

Implantable cardioverter-defibrillator (ICD)23% relative reduction in mortality (SCD-HeFT) over 5 years in HFrEF on background medical therapy.

§ 05

Causes & risk factors

known causes

Coronary artery disease and prior myocardial infarction: Ischemic cardiomyopathy is the leading cause of HFrEF in high-income countries. Myocardial infarction destroys functioning muscle and triggers maladaptive remodeling. About two-thirds of HFrEF cases worldwide have an ischemic etiology.
Long-standing hypertension: Chronically elevated afterload produces left ventricular hypertrophy, diastolic stiffness, and ultimately systolic decline. Hypertension is the leading single risk factor for HFpEF and the second-leading for HFrEF after coronary disease.
Valvular heart disease: Severe aortic stenosis, aortic regurgitation, mitral regurgitation, and mitral stenosis all impose pressure or volume overload that culminates in heart failure. Valve surgery or transcatheter intervention can reverse the syndrome early in the course.
Cardiomyopathies (dilated, hypertrophic, restrictive): Genetic and acquired myocardial diseases produce systolic or diastolic dysfunction independent of coronary disease. Dilated cardiomyopathy is the most common HF cause in patients under 60; titin and lamin gene variants are increasingly identified.
Atrial fibrillation with rapid ventricular response: Sustained tachycardia (>110 bpm for weeks) causes tachycardia-induced cardiomyopathy in some patients. Rate or rhythm control can fully reverse HF in this subgroup.
Diabetes, obesity, and metabolic syndrome: Obesity and type 2 diabetes drive both HFrEF and especially HFpEF through microvascular disease, myocardial lipid accumulation, systemic inflammation, and AGE-mediated stiffening. They roughly double HF lifetime risk.
Cardiotoxic drugs and substances: Anthracycline chemotherapy (doxorubicin), trastuzumab, certain tyrosine kinase inhibitors, immune checkpoint inhibitors, methamphetamine, cocaine, and heavy chronic alcohol use cause cardiomyopathy. Risk is dose-related and often partially reversible if recognized early.

§ 06

Living with it

01Treat hypertension to a systolic target of <130 mmHg in most adults; intensive control lowers HF incidence by ~40% per SPRINT.

02Identify and treat coronary artery disease early — statins, antiplatelet therapy, and timely revascularization reduce post-MI HF risk substantially.

03Achieve and maintain a healthy weight; each 1 kg/m² lower BMI translates to ~5% lower HF risk.

04Use SGLT2 inhibitors in adults with type 2 diabetes who have atherosclerotic vascular disease or multiple cardiovascular risk factors.

05Limit alcohol to no more than 1 drink/day for women and 2 drinks/day for men; abstain entirely with any cardiomyopathy.

06Treat sleep apnea — moderate-to-severe untreated OSA roughly doubles HF risk and worsens existing HF.

recommended foods

•DASH-style eating: vegetables, fruit, whole grains, lean protein, low-fat dairy, nuts and seeds
•Mediterranean dietary pattern — associated with ~30% lower HF incidence in PREDIMED

§ 07

When to seek help

why see a cardiology

Refer to a cardiologist or heart-failure specialist at first diagnosis, after any hospitalization for decompensation, when starting or up-titrating quadruple therapy, when LVEF is below 35%, when ICD or CRT eligibility is being considered, when the cause is unclear, or for advanced therapies (LVAD, transplant). Stage D heart failure specifically warrants referral to a dedicated advanced HF program.

Find specialists →

01Acute decompensation — repeat hospitalizations carry a stepwise mortality penalty; 30-day readmission is a quality metric. Detect early via daily weights and symptom monitoring.

02Ventricular arrhythmia and sudden cardiac death — particularly in HFrEF with EF ≤35%. ICD is the principal preventive intervention.

03Atrial fibrillation — develops in 30-40% of HF, raises stroke risk, and worsens symptoms. Manage with anticoagulation and rate or rhythm control.

04Cardiorenal syndrome — progressive decline in renal function during diuresis or low-output states. Requires careful balance of decongestion, RAAS blockade, and SGLT2 inhibitors.

05Cardiac cachexia and sarcopenia — unintentional weight loss and muscle wasting in chronic advanced HF; associated with markedly worse prognosis. Detect with periodic weight and grip strength.

Related conditions

Coronary Artery DiseaseThe leading cause of HFrEF in high-income countries.Read →High Blood PressureThe leading single risk factor for HFpEF and a major contributor to HFrEF.Read →Atrial FibrillationCoexists with HF in 30-40% of patients; each worsens the other and requires integrated management.Read →Ischemic CardiomyopathyThe ischemic subtype of HFrEF, defined by underlying coronary artery disease.Read →Dilated CardiomyopathyThe most common non-ischemic cause of HFrEF in adults under 60; often genetic.Read →

Easily confused with

vs. Heart Failure

Coronary Artery DiseaseCoronary artery disease is the most common cause of HFrEF, but the two are distinct. CAD presents with angina or MI and is diagnosed by coronary imaging; HF is diagnosed by symptoms plus structural cardiac dysfunction on echo. A patient can have one without the other.Compare →

vs. Heart Failure

Atrial FibrillationAF causes palpitations and irregular pulse without necessarily impairing pump function. HF causes symptoms even in sinus rhythm. The two frequently coexist; rapid AF can trigger HF, and HF predisposes to AF.Compare →

vs. Heart Failure

High Blood PressureHypertension is a single risk factor; HF is a multi-organ clinical syndrome that hypertension causes over years. A patient can have severe hypertension with normal heart function or established HF after years of poorly controlled BP.Compare →

vs. Heart Failure

COPDBoth cause exertional breathlessness, but COPD primarily produces wheeze, prolonged expiration, and barrel chest; HF produces orthopnea, pedal edema, and an S3 gallop. The two coexist commonly; spirometry plus BNP and echo separate them.Compare →

vs. Heart Failure

Often appears alongside

High Blood Pressure →Coronary Artery Disease →Atrial Fibrillation →Type 2 Diabetes →

Types and stages

HFrEF — reduced ejection fraction (LVEF ≤40%)The classic systolic failure phenotype. Most often follows myocardial infarction, dilated cardiomyopathy, or long-standing hypertension. Strongest evidence base — quadruple therapy provides ~70% relative mortality benefit.

HFmrEF — mildly reduced ejection fraction (LVEF 41-49%)Intermediate phenotype. Recovers or progresses depending on cause and treatment response. Evidence supports the same disease-modifying therapy as HFrEF in many patients.

HFpEF — preserved ejection fraction (LVEF ≥50%)Diastolic dysfunction with normal pump function. Strongly tied to hypertension, obesity, diabetes, atrial fibrillation, and aging. SGLT2 inhibitors are the first class to reduce HFpEF hospitalization.

HFimpEF — improved ejection fractionPatients whose LVEF improves above 40% after treatment. Recurrence risk remains substantial if therapy is withdrawn; guidelines recommend continuing therapy indefinitely.

Right-sided heart failurePredominant right-ventricular failure, most often from pulmonary hypertension, left heart failure, or chronic lung disease. Presents with elevated JVP, hepatomegaly, ascites, and peripheral edema more than pulmonary congestion.

Acute decompensated heart failureSudden worsening of chronic HF or new-onset acute pulmonary edema. The most common reason for HF hospital admission and the highest-risk window — 30-day readmission rates exceed 20%.

Living with Heart Failure

Timeline

After an acute decompensation, congestion typically resolves over 3-7 days of inpatient diuresis and oral therapy is initiated or up-titrated during the same admission. Most patients reach a new functional baseline within 4-6 weeks. With rapid quadruple-therapy titration over 6 weeks per STRONG-HF, EF improvement (in HFrEF) is often visible at 3-6 months; full myocardial reverse remodeling can continue for 12 months or more. Cardiac rehabilitation across 8-12 weeks measurably improves exercise tolerance and quality of life.

Lifestyle

01Weigh daily on the same scale at the same time and report a 1.4 kg gain over 2 days or 2.3 kg gain over a week.
02Restrict sodium to under 2 g per day during decompensation; under 3 g per day in stable chronic HF.
03Limit fluid intake to 1.5-2.0 L per day if hyponatremia or severe congestion is present; loose restriction in mild HF.
04Perform structured aerobic exercise 30-45 minutes most days, ideally through a cardiac rehabilitation program.
05Take an annual influenza vaccine and the recommended pneumococcal and COVID-19 vaccines.
06Avoid NSAIDs — they retain sodium and water, raise blood pressure, and trigger decompensation.
07Sleep with the head of the bed elevated 20-30° if orthopnea is present, and seek evaluation for sleep apnea.
08

Complementary approaches

Cardiac rehabilitationSupervised exercise training plus risk-factor education for 8-12 weeks. Improves peak VO2, quality of life, and reduces HF readmission by ~25% (HF-ACTION subgroup analyses).

Choosing a doctor

For complex heart failure, choose a cardiologist who is board certified in cardiovascular disease and ideally fellowship trained in advanced heart failure and transplant cardiology. Look for affiliation with a heart-failure clinic offering rapid in-hospital titration (STRONG-HF protocol), device programs (ICD/CRT), and where applicable, LVAD and transplant capability. For HFpEF, expertise in evaluating diastolic function, exclusion of cardiac amyloidosis, and management of co-morbid hypertension, AF, and obesity is essential.

Patient support resources

American Heart Association — Heart Failure →Patient-facing overview, self-management tools, and links to support groups.

Heart Failure Society of America (HFSA) →Patient education from the specialty society; resources by stage and topic.

Mended Hearts →Peer-to-peer support network for adults with heart disease and their families.

British Heart Foundation — Heart Failure →Plain-English explanations of diagnosis, treatments, and recovery for UK readers.

§ 08

Frequently asked

What is the life expectancy with heart failure?

Five-year all-cause mortality with clinically apparent heart failure is roughly 50%, but this varies dramatically by stage, ejection fraction, and treatment. Patients on guideline-directed quadruple therapy for HFrEF have substantially better survival than historical figures suggest, and selected stage D patients can receive transplant or LVAD that extends median survival to 5-10 years.

What is the difference between HFrEF and HFpEF?

HFrEF means heart failure with reduced ejection fraction (LVEF ≤40%) — a problem of systolic pump function. HFpEF means heart failure with preserved ejection fraction (LVEF ≥50%) — a problem of diastolic relaxation despite a normal-looking pump. Treatment differs: HFrEF responds to quadruple therapy with mortality benefit, while HFpEF mainly responds to SGLT2 inhibitors and aggressive comorbidity control.

What is congestive heart failure?

Congestive heart failure is an older term used when fluid backs up into the lungs, abdomen, or legs from a failing heart. Modern cardiology simply uses heart failure, with congestion described as a symptom. The signs are the same — breathlessness, swelling, weight gain, and reduced exercise tolerance.

What is ejection fraction?

Ejection fraction is the percentage of blood the left ventricle pumps out with each beat. A normal LVEF is 55-70%. LVEF 41-49% is mildly reduced (HFmrEF); LVEF 40% or below is reduced (HFrEF); LVEF 50% or above with HF symptoms is preserved (HFpEF). Echocardiogram is the standard way to measure it.

What causes heart failure?

The leading causes are coronary artery disease and prior heart attack, long-standing hypertension, valve disease, atrial fibrillation, cardiomyopathies, diabetes, obesity, and cardiotoxic drugs such as anthracycline chemotherapy. In many patients more than one cause is present.

What are the early signs of heart failure?

Early signs include new breathlessness when walking up stairs, new orthopnea (using extra pillows), ankle swelling that returns each evening, weight gain of more than 1.4 kg over two days, and reduced exercise tolerance. Persistent dry cough that is worse at night can also be an early manifestation.

Can heart failure be cured?

Heart failure is usually a chronic syndrome rather than a curable disease, but selected causes are fully reversible — tachycardia-mediated cardiomyopathy with rate control, alcoholic cardiomyopathy with abstinence, peripartum cardiomyopathy in many cases, and severe valve disease after surgical correction. For most patients with chronic HFrEF, optimized therapy improves ejection fraction and quality of life without permanent cure.

What is the four-drug therapy for heart failure?

Modern quadruple therapy for HFrEF combines an ARNI (sacubitril-valsartan) or ACE inhibitor or ARB, an evidence-based beta-blocker (carvedilol, metoprolol succinate, or bisoprolol), a mineralocorticoid receptor antagonist (spironolactone or eplerenone), and an SGLT2 inhibitor (dapagliflozin or empagliflozin). Started together and titrated rapidly, this regimen cuts mortality by roughly 70% compared with placebo.

Is heart failure the same as a heart attack?

No. A heart attack (myocardial infarction) is an acute event where a coronary artery blockage damages heart muscle. Heart failure is a chronic syndrome where the heart cannot pump effectively. A heart attack can cause heart failure by destroying muscle, but they are distinct diagnoses with different treatments.

Can young people get heart failure?

Yes. Young adults can develop heart failure from genetic cardiomyopathies (dilated, hypertrophic), myocarditis after viral infection, peripartum cardiomyopathy in pregnancy, congenital heart disease, anthracycline chemotherapy in childhood cancer survivors, and stimulant or alcohol use. Genetic testing and cardiac MRI are increasingly important in this age group.

How much salt can I have with heart failure?

Most guidelines recommend keeping sodium under 2-3 grams per day for chronic heart failure, dropping to under 2 grams during decompensation. Processed and restaurant foods are usually the biggest sources. Read labels for sodium content rather than just avoiding the salt shaker.

Can I exercise with heart failure?

Yes, and most patients should. Structured aerobic exercise — 30-45 minutes most days at moderate intensity — improves quality of life, exercise tolerance, and reduces readmissions by roughly 25% in cardiac rehabilitation programs. Start in a supervised program if you have had a recent hospitalization or advanced disease.

What is BNP and what does it mean?

BNP (B-type natriuretic peptide) and NT-proBNP are hormones released by stretched cardiac muscle. Levels rise in heart failure and fall with successful treatment. NT-proBNP below 125 pg/mL in chronic ambulatory patients makes heart failure unlikely; markedly elevated levels support the diagnosis and indicate higher risk.

Why is daily weight important in heart failure?

Sudden weight gain reflects fluid retention before breathlessness or swelling become severe. A gain of 1.4 kg over two days or 2.3 kg over a week should prompt a call to the heart-failure clinic for diuretic adjustment, often preventing hospitalization. Weigh yourself the same time each morning after voiding.

Should I have an ICD for heart failure?

An implantable cardioverter-defibrillator is recommended for primary prevention in HFrEF with ejection fraction at or below 35% on optimized medical therapy for at least 3 months and an expected survival of more than one year. It is recommended for secondary prevention after sustained ventricular tachycardia or fibrillation. Your cardiologist will weigh benefit against age and comorbidities.

Can I drink alcohol with heart failure?

Avoid alcohol entirely if you have alcohol-related or any cause cardiomyopathy. Other patients may have one drink daily for women or two for men, but no more — alcohol triggers arrhythmias and raises blood pressure. Discuss specific recommendations with your cardiologist based on your cause and severity.

What is cardiac resynchronization therapy (CRT)?

CRT is a pacemaker with leads in both ventricles that resynchronizes contraction in patients with a wide QRS, especially left bundle branch block. It is recommended for symptomatic HFrEF with ejection fraction at or below 35% and QRS at or above 150 ms (or 130-149 ms with LBBB). It reduces hospitalization and mortality by about 30%.

What is a heart transplant evaluation?

Heart transplant evaluation is a multi-day workup of stage D heart failure patients who have failed optimal medical and device therapy. It includes cardiopulmonary exercise testing (peak VO2 below 14 mL/kg/min is a key threshold), right heart catheterization, cancer screening, and psychosocial assessment. Selected candidates are listed for donor matching.

Can heart failure affect the kidneys?

Yes. Cardiorenal syndrome describes the bidirectional relationship in which heart failure worsens kidney function and chronic kidney disease worsens heart failure. SGLT2 inhibitors benefit both organs simultaneously and are now recommended at any eGFR above 20 in HFrEF.

Are SGLT2 inhibitors safe if I do not have diabetes?

Yes. Dapagliflozin and empagliflozin reduce hospitalization and mortality in heart failure regardless of diabetes status. Side effects include occasional genital yeast infections and rare diabetic ketoacidosis in diabetics. The cardiovascular benefit is independent of glucose-lowering.

What is the difference between left and right heart failure?

Left-sided failure backs blood up into the lungs, causing breathlessness, orthopnea, and pulmonary edema. Right-sided failure backs blood up into the body, causing leg swelling, hepatic congestion, and ascites. The two often coexist because left heart failure is the leading cause of right heart failure.

§ 09