Chronic congestive heart failure is a complex clinical syndrome that can result from any structural or functional cardiac disorder that impairs the ability of the ventricle to fill with or eject blood.
It is a major and growing public health problem. It is the only cardiovascular disease that is increasing in incidence and prevalence, partly because the population is aging, but also because of improved cardiovascular interventions for disease processes that reduce early mortality but may result in cardiac changes that lead to heart failure.
The key manifestations are dyspnea and fatigue, which may limit exercise tolerance, and fluid retention, which may lead to pulmonary congestion and peripheral edema.
Diagnosis is largely clinical; a thorough history and physical examination should be obtained to identify cardiac and noncardiac disorders or behaviors that might cause congestive heart failure or accelerate progression.
The single most useful diagnostic test in the evaluation of patients is the comprehensive 2-dimensional echocardiogram coupled with Doppler flow studies. Measurement of B-type natriuretic peptide can be useful in the evaluation of patients at initial presentation.
Interventions that have a proven beneficial impact on patient survival include ACE inhibitors, angiotensin receptor blockers, beta-blockers, aldosterone antagonists, hydralazine and nitrates, cardiac resynchronization therapy, and implantable cardioverter-defibrillators.
Heart failure is a condition in which the heart is unable to generate a cardiac output sufficient to meet the demands of the body without increasing diastolic pressure. It can result from any cardiac disease that compromises ventricular systolic or diastolic function or both. The term "congestive heart failure" (CHF) is reserved for patients with breathlessness and abnormal sodium and water retention, resulting in edema.
Heart failure comprises a wide range of clinical scenarios, from patients with normal left ventricular ejection fraction (LVEF) >50% to those with reduced myocardial contractility (LVEF <40%).
Based on LVEF, heart failure is defined as follows.
1. Heart failure with reduced ejection fraction (HFrEF): symptoms and signs with LVEF <40%.
2. Heart failure with mid-range ejection fraction (HFmrEF): symptoms and signs with LVEF 40% to 49%. Other features include elevated natriuretic peptides (B-type natriuretic peptide [BNP] >35 picograms/mL or N-terminal pro-brain natriuretic peptide [NT-pro-BNP] >125 picograms/mL) and at least one additional criterion: (a) relevant structural heart disease (e.g., left ventricular hypertrophy [LVH] or left atrial enlargement), (b) diastolic dysfunction.
3. Heart failure with preserved ejection fraction (HFpEF): symptoms and signs with LVEF >50%. Other features include elevated natriuretic peptides (BNP >35 picograms/mL or NT-pro-BNP >125 picograms/mL) and at least one additional criteria: (a) relevant structural heart disease (e.g., LVH or left atrial enlargement), (b) diastolic dysfunction. See our topic "Heart failure with preserved ejection fraction" for more information on this subtype.
History and exam
- myocardial infarction (MI)
- diabetes mellitus
- old age
- low socioeconomic status
- tobacco consumption
- excess alcohol consumption
- excess sodium intake
- excess coffee consumption
- exposure to cardiotoxic agents
- left ventricular dysfunction
- left ventricular hypertrophy
- renal insufficiency
- valvular heart disease
- sleep apnea
- elevated homocysteine
- cocaine abuse
- family history of heart failure
- atrial fibrillation
- thyroid disorders
- elevated tumor necrosis factor-alfa (TNF-alfa) and interleukin-6 (IL-6)
- elevated C-reactive protein (CRP)
- decreased insulin-like growth factor-1 (IGF-1)
- elevated natriuretic peptides
- dilation of the left ventricle
- increased left ventricular mass
- abnormal left ventricular diastolic filling
- transthoracic echocardiogram
- B-type natriuretic peptide (BNP)/N-terminal pro-brain natriuretic peptide (NT-pro-BNP) levels
- serum electrolytes (including calcium and magnesium)
- serum creatinine, BUN
- blood glucose
- thyroid function tests (especially thyroid-stimulating hormone [TSH])
- blood lipids
- serum ferritin
- transferrin saturation
- noninvasive stress imaging (cardiovascular MRI, stress echocardiogram, SPECT, PET)
- standard exercise stress testing (bicycle or treadmill)
- coronary angiogram
- cardiac CT angiography
- cardiopulmonary exercise testing with VO₂ max
- 6-minute walking test exercise
- right heart catheterization
- endomyocardial biopsy
- serum HIV enzyme-linked immunosorbent assay
- cardiac MRI
- multi-slice computed tomography (MSCT)
Syed Wamique Yusuf, FACC, FRCPI
Professor of Medicine
Department of Cardiology
University of Texas MD Anderson Cancer Center
SWY declares that he has no competing interests.
Dr Syed Wamique Yusuf would like to gratefully acknowledge Dr Andrew R.J. Mitchell, Dr Grigorios Giamouzis, Dr Sonjoy Raja Laskar, and Dr Javed Butler, the previous contributors to this topic. ARJM, GG, SRL, and JB declare that they have no competing interests.
David Leaf, MD, MPH
Professor of Medicine
VA Greater Los Angeles Healthcare System
UCLA School of Medicine
DL declares that he has no competing interests.
Brian Griffin, MD
Cardiovascular Training Program
BG declares that he has no competing interests.
Abdallah Al-Mohammad, MD, FRCP(Edin.), FRCP(Lond.)
Consultant Cardiologist and Heart Failure Lead
Sheffield Teaching Hospitals NHS Foundation Trust (Northern General Hospital)
AAM has accepted hospitality by NOVARTIS in 2008 to attend the American College of Cardiology meeting in Chicago, and had received honoraria for delivering educational talks before 2008. AAM is the co-author of the NICE chronic heart failure partial update of the guideline in 2010, and of several related articles.
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