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Heart failure

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Heart failure
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Heart failure (HF), often used to mean chronic heart failure (CHF), occurs when the heart is unable to pump sufficiently to maintain blood flow to meet the needs of the body.[1][2][3] The terms congestive heart failure (CHF) or congestive cardiac failure (CCF) are often used interchangeably with chronic heart failure.[4] Symptoms commonly include shortness of breath, excessive tiredness, and leg swelling.[5] The shortness of breath is usually worse with exercise, when lying down, and at night while sleeping.[5] There is often a limitation on the amount of exercise people can perform, even when well treated.[6]

Common causes of heart failure include coronary artery disease including a previous myocardial infarction (heart attack), high blood pressure, atrial fibrillation, valvular heart disease, and cardiomyopathy.[5][7] These cause heart failure by changing either the structure or the functioning of the heart.[5] There are two main types of heart failure: heart failure due to left ventricular dysfunction and heart failure with normal ejection fraction depending on if the ability of the left ventricle to contract is affected, or the heart's ability to relax.[5] The severity of disease is usually graded by how much the ability to exercise is decreased.[8] Heart failure is not the same as myocardial infarction (in which part of the heart muscle dies) or cardiac arrest (in which blood flow stops altogether).[9][10] Other diseases that may have symptoms similar to heart failure include: obesity, kidney problems, liver problems, anemia and thyroid disease among others.[8]

The condition is diagnosed based on the history of the symptoms and a physical examination with confirmation by echocardiography.[11] Blood tests, electrocardiography, and chest radiography may be useful to determine the underlying cause.[11] Treatment depends on the severity and cause of the disease.[11] In people with chronic disease already in a stable situation, treatment commonly consists of lifestyle measures such as stopping smoking,[12] physical exercise,[13] and dietary changes, as well as medications.[12] In those with heart failure due to left ventricular dysfunction, angiotensin converting enzyme inhibitors and beta blockers are recommended.[11] For those with severe disease, aldosterone antagonists, an angiotension receptor blocker or hydralazine with a nitrate may be used.[11] If there is a normal ejection fraction, associated health problems should be treated.[11] Diuretics are useful for preventing fluid retention and thus recommended.[12] Sometimes, depending on the cause, an implanted device such as a pacemaker or implantable cardiac defibrillator may be useful.[11] A ventricular assist device or occasionally a heart transplant may be recommended in those with severe disease despite all other measures.[12]

Heart failure is a common, costly, and potentially fatal condition.[7] In developed countries, around 2% of adults have heart failure and in those over the age of 65, this increases to 6–10%.[7][14] In the year after diagnosis the risk of death is about 35% after which it decreases to below 10% each year.[5] This is similar to the risks with a number of types of cancer.[5] In the United Kingdom the disease is the reason for 5% of emergent hospital admissions.[5] Heart failure has been known since ancient times with the Ebers papyrus commenting on it circa 1550 BCE.[6]

Terminology

Heart failure is a physiological state in which cardiac output is insufficient to meet the needs of the body and lungs. The termed "congestive heart failure" (CHF) is often used as one of the common symptoms is swelling or water retention.[15]

Heart failure is divided into two different types: heart failure due to reduced ejection fraction (HFREF) also known as heart failure due to left ventricular systolic dysfunction or systolic heart failure and heart failure with preserved ejection fraction (HFPEF) also known as diastolic heart failure or heart failure with normal ejection fraction (HFNEF).[5][13] Heart failure with reduced ejection fraction occurs when the ejection fraction is less than 40%.[16] In diastolic heart failure, the heart muscle contracts well but the ventricle does not fill with blood well in the relaxation phase.[5] Ejection fraction is the proportion of blood in the heart pumped out of the heart during a single contraction.[17] It is a percentage with normal being between 50 and 75%.[17]

The term "acute" is used to mean rapid onset, and "chronic" refers to long duration. Chronic heart failure is a long term situation, usually with stable treated symptomatology. Acute decompensated heart failure is worsening or decompensated heart failure, referring to episodes in which a person can be characterized as having a change in heart failure signs and symptoms resulting in a need for urgent therapy or hospitalization.[18] Heart failure may also occur in situations of "high output," (termed "high output cardiac failure") where the ventricular systolic function is normal but the heart cannot deal with an important augmentation of blood volume.[19]

Signs and symptoms

A man with congestive heart failure and marked jugular venous distension. External jugular vein marked by an arrow.

Heart failure symptoms are traditionally and somewhat arbitrarily divided into "left" and "right" sided, recognizing that the left and right ventricles of the heart supply different portions of the circulation. However, heart failure is not exclusively backward failure (in the part of the circulation which drains to the ventricle).

There are several other exceptions to a simple left-right division of heart failure symptoms. Left sided forward failure overlaps with right sided backward failure.[clarification needed] Additionally, the most common cause of right-sided heart failure is left-sided heart failure.[20] The result is that patients commonly present with both sets of signs and symptoms.

Left-sided failure

Common respiratory signs are increased rate of breathing and increased work of breathing (non-specific signs of respiratory distress). Rales or crackles, heard initially in the lung bases, and when severe, throughout the lung fields suggest the development of pulmonary edema (fluid in the alveoli). Cyanosis which suggests severe hypoxemia, is a late sign of extremely severe pulmonary edema.

Additional signs indicating left ventricular failure include a laterally displaced apex beat (which occurs if the heart is enlarged) and a gallop rhythm (additional heart sounds) may be heard as a marker of increased blood flow, or increased intra-cardiac pressure. Heart murmurs may indicate the presence of valvular heart disease, either as a cause (e.g. aortic stenosis) or as a result (e.g. mitral regurgitation) of the heart failure.

Backward failure of the left ventricle causes congestion of the pulmonary vasculature, and so the symptoms are predominantly respiratory in nature. Backward failure can be subdivided into failure of the left atrium, the left ventricle or both within the left circuit. The patient will have dyspnea (shortness of breath) on exertion and in severe cases, dyspnea at rest. Increasing breathlessness on lying flat, called orthopnea, occurs. It is often measured in the number of pillows required to lie comfortably, and in orthopnea, the patient may resort to sleeping while sitting up. Another symptom of heart failure is paroxysmal nocturnal dyspnea: a sudden nighttime attack of severe breathlessness, usually several hours after going to sleep. Easy fatigability and exercise intolerance are also common complaints related to respiratory compromise.

"Cardiac asthma" or wheezing may occur.

Compromise of left ventricular forward function may result in symptoms of poor systemic circulation such as dizziness, confusion and cool extremities at rest.

Right-sided failure

Physical examination may reveal pitting peripheral edema, ascites, and hepatomegaly. Jugular venous pressure is frequently assessed as a marker of fluid status, which can be accentuated by eliciting hepatojugular reflux. If the right ventricular pressure is increased, a parasternal heave may be present, signifying the compensatory increase in contraction strength.

Backward failure of the right ventricle leads to congestion of systemic capillaries. This generates excess fluid accumulation in the body. This causes swelling under the skin (termed peripheral edema or anasarca) and usually affects the dependent parts of the body first (causing foot and ankle swelling in people who are standing up, and sacral edema in people who are predominantly lying down). Nocturia (frequent nighttime urination) may occur when fluid from the legs is returned to the bloodstream while lying down at night. In progressively severe cases, ascites (fluid accumulation in the abdominal cavity causing swelling) and hepatomegaly (enlargement of the liver) may develop. Significant liver congestion may result in impaired liver function, and jaundice and even coagulopathy (problems of decreased blood clotting) may occur.

Biventricular failure

Dullness of the lung fields to finger percussion and reduced breath sounds at the bases of the lung may suggest the development of a pleural effusion (fluid collection in between the lung and the chest wall). Though it can occur in isolated left- or right-sided heart failure, it is more common in biventricular failure because pleural veins drain into both the systemic and pulmonary venous systems. When unilateral, effusions are often right sided.

Causes

Congestive heart failure

Heart failure may also occur in situations of "high output," (termed "high output cardiac failure") where the ventricular systolic function is normal but the heart can't deal with an important augmentation of blood volume.[19] This can occur in overload situation (blood or serum infusions), renal diseases, chronic severe anemia, beriberi (vitamin B1/thiamine deficiency), thyrotoxicosis, Paget's disease, arteriovenous fistulae, or arteriovenous malformations.

A study of healthy adults in the United States found the following risk factors:[21]

  1. Ischaemic heart disease 62%
  2. Cigarette smoking 16%
  3. Hypertension (high blood pressure) 10%
  4. Obesity 8%
  5. Diabetes 3%
  6. Valvular heart disease 2% (much higher in older populations)

Italians had the following underlying causes:[22]

  1. Ischaemic heart disease 40%
  2. Dilated cardiomyopathy 32%
  3. Valvular heart disease 12%
  4. Hypertension 11%
  5. Other 5%

Rarer causes of heart failure include:

Obstructive sleep apnea (a condition of sleep wherein disordered breathing overlaps with obesity, hypertension, and/or diabetes) is regarded as an independent cause of heart failure.

Acute decompensation

Main article: Acute decompensated heart failure

Chronic stable heart failure may easily decompensate. This most commonly results from an intercurrent illness (such as pneumonia), myocardial infarction (a heart attack), arrhythmias, uncontrolled hypertension, or a patient's failure to maintain a fluid restriction, diet, or medication.[23] Other well recognized factors that may worsen CHF include: anemia and hyperthyroidism which place additional strain on the heart muscle, excessive fluid or salt intake, and medication that causes fluid retention such as NSAIDs and thiazolidinediones.[24] NSAIDs in general increase the risk twofold.[25]

Pathophysiology

Heart failure is caused by any condition which reduces the efficiency of the myocardium, or heart muscle, through damage or overloading. As such, it can be caused by a wide number of conditions, including myocardial infarction (in which the heart muscle is starved of oxygen and dies), hypertension (which increases the force of contraction needed to pump blood) and amyloidosis (in which protein is deposited in the heart muscle, causing it to stiffen). Over time these increases in workload will produce changes to the heart itself:

  • Reduced force of contraction, due to overloading of the ventricle. In a healthy heart, increased filling of the ventricle results in increased force of contraction (by the Frank–Starling law of the heart) and thus a rise in cardiac output. In heart failure this mechanism fails, as the ventricle is loaded with blood to the point where heart muscle contraction becomes less efficient. This is due to reduced ability to cross-link actin and myosin filaments in over-stretched heart muscle.[26]
  • A reduced stroke volume, as a result of a failure of systole, diastole or both. Increased end systolic volume is usually caused by reduced contractility. Decreased end diastolic volume results from impaired ventricular filling – as occurs when the compliance of the ventricle falls (i.e. when the walls stiffen).
  • Reduced spare capacity. As the heart works harder to meet normal metabolic demands, the amount cardiac output can increase in times of increased oxygen demand (e.g. exercise) is reduced. This contributes to the exercise intolerance commonly seen in heart failure. This translates to the loss of one's cardiac reserve, or the ability of the heart to work harder during strenuous physical activity. Since the heart has to work harder to meet the normal metabolic demands, it is incapable of meeting the metabolic demands of the body during exercise.
  • Increased heart rate, stimulated by increased sympathetic activity[27] in order to maintain cardiac output. Initially, this helps compensate for heart failure by maintaining blood pressure and perfusion, but places further strain on the myocardium, increasing coronary perfusion requirements, which can lead to worsening of ischemic heart disease. Sympathetic activity may also cause potentially fatal arrhythmias.
  • Hypertrophy (an increase in physical size) of the myocardium, caused by the terminally differentiated heart muscle fibres increasing in size in an attempt to improve contractility. This may contribute to the increased stiffness and decreased ability to relax during diastole.
  • Enlargement of the ventricles, contributing to the enlargement and spherical shape of the failing heart. The increase in ventricular volume also causes a reduction in stroke volume due to mechanical and contractile inefficiency.[28]

The general effect is one of reduced cardiac output and increased strain on the heart. This increases the risk of cardiac arrest (specifically due to ventricular dysrhythmias), and reduces blood supply to the rest of the body. In chronic disease the reduced cardiac output causes a number of changes in the rest of the body, some of which are physiological compensations, some of which are part of the disease process:

  • Arterial blood pressure falls. This destimulates baroreceptors in the carotid sinus and aortic arch which link to the nucleus tractus solitarii. This center in the brain increases sympathetic activity, releasing catecholamines into the blood stream. Binding to alpha-1 receptors results in systemic arterial vasoconstriction. This helps restore blood pressure but also increases the total peripheral resistance, increasing the workload of the heart. Binding to beta-1 receptors in the myocardium increases the heart rate and make contractions more forceful, in an attempt to increase cardiac output. This also, however, increases the amount of work the heart has to perform.
  • Increased sympathetic stimulation also causes the posterior pituitary to secrete vasopressin (also known as antidiuretic hormone or ADH), which causes fluid retention at the kidneys. This increases the blood volume and blood pressure.
  • Reduced perfusion (blood flow) to the kidneys stimulates the release of renin – an enzyme which catalyses the production of the potent vasopressor angiotensin. Angiotensin and its metabolites cause further vasoconstriction, and stimulate increased secretion of the steroid aldosterone from the adrenal glands. This promotes salt and fluid retention at the kidneys.
  • The chronically high levels of circulating neuroendocrine hormones such as catecholamines, renin, angiotensin, and aldosterone affects the myocardium directly, causing structural remodelling of the heart over the long term. Many of these remodelling effects seem to be mediated by transforming growth factor beta (TGF-beta), which is a common downstream target of the signal transduction cascade. initiated by catecholamines[29] and angiotensin II,[30] and also by epidermal growth factor (EGF), which is a target of the signaling pathway activated by aldosterone[31]
  • Reduced perfusion of skeletal muscle causes atrophy of the muscle fibres. This can result in weakness, increased fatigueability and decreased peak strength – all contributing to exercise intolerance.[32]

The increased peripheral resistance and greater blood volume place further strain on the heart and accelerates the process of damage to the myocardium. Vasoconstriction and fluid retention produce an increased hydrostatic pressure in the capillaries. This shifts the balance of forces in favour of interstitial fluid formation as the increased pressure forces additional fluid out of the blood, into the tissue. This results in edema (fluid build-up) in the tissues. In right-sided heart failure this commonly starts in the ankles where venous pressure is high due to the effects of gravity (although if the patient is bed-ridden, fluid accumulation may begin in the sacral region.) It may also occur in the abdominal cavity, where the fluid build-up is called ascites. In left-sided heart failure edema can occur in the lungs – this is called cardiogenic pulmonary edema. This reduces spare capacity for ventilation, causes stiffening of the lungs and reduces the efficiency of gas exchange by increasing the distance between the air and the blood. The consequences of this are dyspnea (shortness of breath), orthopnea and paroxysmal nocturnal dyspnea.

The symptoms of heart failure are largely determined by which side of the heart fails. The left side pumps blood into the systemic circulation, whilst the right side pumps blood into the pulmonary circulation. Whilst left-sided heart failure will reduce cardiac output to the systemic circulation, the initial symptoms often manifest due to effects on the pulmonary circulation. In systolic dysfunction, the ejection fraction is decreased, leaving an abnormally elevated volume of blood in the left ventricle. In diastolic dysfunction, end-diastolic ventricular pressure will be high. This increase in volume or pressure backs up to the left atrium and then to the pulmonary veins. Increased volume or pressure in the pulmonary veins impairs the normal drainage of the alveoli and favors the flow of fluid from the capillaries to the lung parenchyma, causing pulmonary edema. This impairs gas exchange. Thus, left-sided heart failure often presents with respiratory symptoms: shortness of breath, orthopnea and paroxysmal nocturnal dyspnea.

In severe cardiomyopathy, the effects of decreased cardiac output and poor perfusion become more apparent, and patients will manifest with cold and clammy extremities, cyanosis, claudication, generalized weakness, dizziness, and syncope.

The resultant hypoxia caused by pulmonary edema causes vasoconstriction in the pulmonary circulation, which results in pulmonary hypertension. Since the right ventricle generates far lower pressures than the left ventricle (approximately 20 mmHg versus around 120 mmHg, respectively, in the healthy individual) but nonetheless generates cardiac output exactly equal to the left ventricle, this means that a small increase in pulmonary vascular resistance causes a large increase in amount of work the right ventricle must perform. However, the main mechanism by which left-sided heart failure causes right-sided heart failure is actually not well understood. Some theories invoke mechanisms that are mediated by neurohormonal activation.[33] Mechanical effects may also contribute. As the left ventricle distends, the intraventricular septum bows into the right ventricle, decreasing the capacity of the right ventricle.

Systolic dysfunction

Heart failure caused by systolic dysfunction is more readily recognized. It can be simplistically described as failure of the pump function of the heart. It is characterized by a decreased ejection fraction (less than 45%). The strength of ventricular contraction is attenuated and inadequate for creating an adequate stroke volume, resulting in inadequate cardiac output. In general, this is caused by dysfunction or destruction of cardiac myocytes or their molecular components. In congenital diseases such as Duchenne muscular dystrophy, the molecular structure of individual myocytes is affected. Myocytes and their components can be damaged by inflammation (such as in myocarditis) or by infiltration (such as in amyloidosis). Toxins and pharmacological agents (such as ethanol, cocaine, doxorubicin, and amphetamines) cause intracellular damage and oxidative stress. The most common mechanism of damage is ischemia causing infarction and scar formation. After myocardial infarction, dead myocytes are replaced by scar tissue, deleteriously affecting the function of the myocardium. On echocardiogram, this is manifest by abnormal wall motion (hypokinesia) or absent wall motion (akinesia).

Because the ventricle is inadequately emptied, ventricular end-diastolic pressure and volumes increase. This is transmitted to the atrium. On the left side of the heart, the increased pressure is transmitted to the pulmonary vasculature, and the resultant hydrostatic pressure favors extravasation of fluid into the lung parenchyma, causing pulmonary edema. On the right side of the heart, the increased pressure is transmitted to the systemic venous circulation and systemic capillary beds, favoring extravasation of fluid into the tissues of target organs and extremities, resulting in dependent peripheral edema.

Diastolic dysfunction

Heart failure caused by diastolic dysfunction is generally described as the failure of the ventricle to adequately relax and typically denotes a stiffer ventricular wall. This causes inadequate filling of the ventricle, and therefore results in an inadequate stroke volume. The failure of ventricular relaxation also results in elevated end-diastolic pressures, and the end result is identical to the case of systolic dysfunction (pulmonary edema in left heart failure, peripheral edema in right heart failure).

Diastolic dysfunction can be caused by processes similar to those that cause systolic dysfunction, particularly causes that affect cardiac remodeling.

Diastolic dysfunction may not manifest itself except in physiologic extremes if systolic function is preserved. The patient may be completely asymptomatic at rest. However, they are exquisitely sensitive to increases in heart rate, and sudden bouts of tachycardia (which can be caused simply by physiological responses to exertion, fever, or dehydration, or by pathological tachyarrhythmias such as atrial fibrillation with rapid ventricular response) may result in flash pulmonary edema. Adequate rate control (usually with a pharmacological agent that slows down AV conduction such as a calcium channel blocker or a beta-blocker) is therefore key to preventing decompensation.

Left ventricular diastolic function can be determined through echocardiography by measurement of various parameters such as the E/A ratio (early-to-atrial left ventricular filling ratio), the E (early left ventricular filling) deceleration time, and the isovolumic relaxation time.

Diagnosis

Acute pulmonary edema. Note enlarged heart size, apical vascular redistribution ( circle ), and small bilateral pleural effusions ( arrow ).

No system of diagnostic criteria has been agreed as the gold standard for heart failure. Commonly used systems are the "Framingham criteria"[34] (derived from the Framingham Heart Study), the "Boston criteria",[35] the "Duke criteria",[36] and (in the setting of acute myocardial infarction) the "Killip class".[37]

Imaging

Echocardiography is commonly used to support a clinical diagnosis of heart failure. This modality uses ultrasound to determine the stroke volume (SV, the amount of blood in the heart that exits the ventricles with each beat), the end-diastolic volume (EDV, the total amount of blood at the end of diastole), and the SV in proportion to the EDV, a value known as the ejection fraction (EF). In pediatrics, the shortening fraction is the preferred measure of systolic function. Normally, the EF should be between 50% and 70%; in systolic heart failure, it drops below 40%. Echocardiography can also identify valvular heart disease and assess the state of the pericardium (the connective tissue sac surrounding the heart). Echocardiography may also aid in deciding what treatments will help the patient, such as medication, insertion of an implantable cardioverter-defibrillator or cardiac resynchronization therapy. Echocardiography can also help determine if acute myocardial ischemia is the precipitating cause, and may manifest as regional wall motion abnormalities on echo.

Chest X-rays are frequently used to aid in the diagnosis of CHF. In the compensated patient, this may show cardiomegaly (visible enlargement of the heart), quantified as the cardiothoracic ratio (proportion of the heart size to the chest). In left ventricular failure, there may be evidence of vascular redistribution ("upper lobe blood diversion" or "cephalization"), Kerley lines, cuffing of the areas around the bronchi, and interstitial edema.

Electrophysiology

An electrocardiogram (ECG/EKG) may be used to identify arrhythmias, ischemic heart disease, right and left ventricular hypertrophy, and presence of conduction delay or abnormalities (e.g. left bundle branch block). Although these findings are not specific to the diagnosis of heart failure a normal ECG virtually excludes left ventricular systolic dysfunction.[38]

Blood tests

Blood tests routinely performed include electrolytes (sodium, potassium), measures of renal function, liver function tests, thyroid function tests, a complete blood count, and often C-reactive protein if infection is suspected. An elevated B-type natriuretic peptide (BNP) is a specific test indicative of heart failure. Additionally, BNP can be used to differentiate between causes of dyspnea due to heart failure from other causes of dyspnea. If myocardial infarction is suspected, various cardiac markers may be used.

According to a meta-analysis comparing BNP and N-terminal pro-BNP (NTproBNP) in the diagnosis of heart failure, BNP is a better indicator for heart failure and left ventricular systolic dysfunction. In groups of symptomatic patients, a diagnostic odds ratio of 27 for BNP compares with a sensitivity of 85% and specificity of 84% in detecting heart failure.[39]

Angiography

Heart failure may be the result of coronary artery disease, and its prognosis depends in part on the ability of the coronary arteries to supply blood to the myocardium (heart muscle). As a result, coronary catheterization may be used to identify possibilities for revascularisation through percutaneous coronary intervention or bypass surgery.

Monitoring

Various measures are often used to assess the progress of patients being treated for heart failure. These include fluid balance (calculation of fluid intake and excretion), monitoring body weight (which in the shorter term reflects fluid shifts).[40]

Classification

There are many different ways to categorize heart failure, including:

  • the side of the heart involved (left heart failure versus right heart failure). Right heart failure compromises pulmonary flow to the lungs. Left heart failure compromises aortic flow to the body and brain. Mixed presentations are common; left heart failure often leads to right heart failure in the longer term.
  • whether the abnormality is due to insufficient contraction (systolic dysfunction), or due to insufficient relaxation of the heart (diastolic dysfunction), or to both.
  • whether the problem is primarily increased venous back pressure (preload), or failure to supply adequate arterial perfusion (afterload).
  • whether the abnormality is due to low cardiac output with high systemic vascular resistance or high cardiac output with low vascular resistance (low-output heart failure vs. high-output heart failure).
  • the degree of functional impairment conferred by the abnormality (as reflected in the New York Heart Association Functional Classification[41])
  • the degree of coexisting illness: i.e. heart failure/systemic hypertension, heart failure/pulmonary hypertension, heart failure/diabetes, heart failure/renal failure, etc.

Functional classification generally relies on the New York Heart Association functional classification. The classes (I-IV) are:

  • Class I: no limitation is experienced in any activities; there are no symptoms from ordinary activities.
  • Class II: slight, mild limitation of activity; the patient is comfortable at rest or with mild exertion.
  • Class III: marked limitation of any activity; the patient is comfortable only at rest.
  • Class IV: any physical activity brings on discomfort and symptoms occur at rest.

This score documents severity of symptoms, and can be used to assess response to treatment. While its use is widespread, the NYHA score is not very reproducible and doesn't reliably predict the walking distance or exercise tolerance on formal testing.[42]

In its 2001 guidelines the American College of Cardiology/American Heart Association working group introduced four stages of heart failure:[43]

  • Stage A: Patients at high risk for developing HF in the future but no functional or structural heart disorder.
  • Stage B: a structural heart disorder but no symptoms at any stage.
  • Stage C: previous or current symptoms of heart failure in the context of an underlying structural heart problem, but managed with medical treatment.
  • Stage D: advanced disease requiring hospital-based support, a heart transplant or palliative care.

The ACC staging system is useful in that Stage A encompasses "pre-heart failure" – a stage where intervention with treatment can presumably prevent progression to overt symptoms. ACC Stage A does not have a corresponding NYHA class. ACC Stage B would correspond to NYHA Class I. ACC Stage C corresponds to NYHA Class II and III, while ACC Stage D overlaps with NYHA Class IV.

Algorithms

There are various algorithms for the diagnosis of heart failure. For example, the algorithm used by the Framingham Heart Study adds together criteria mainly from physical examination. In contrast, the more extensive algorithm by the European Society of Cardiology (ESC) weights the difference between supporting and opposing parameters from the medical history, physical examination, further medical tests as well as response to therapy.

Framingham criteria

By the Framingham criteria, diagnosis of congestive heart failure (heart failure with impaired pumping capability)[15] requires the simultaneous presence of at least 2 of the following major criteria or 1 major criterion in conjunction with 2 of the following minor criteria:

Major criteria include the following:[44]

Minor criteria include the following:[44]

Minor criteria are acceptable only if they can not be attributed to another medical condition such as pulmonary hypertension, chronic lung disease, cirrhosis, ascites, or the nephrotic syndrome.[44] The Framingham Heart Study criteria are 100% sensitive and 78% specific for identifying persons with definite congestive heart failure.[44]

ESC algorithm

The ESC algorithm weights the following parameters in establishing the diagnosis of heart failure:[46]

Diagnostic assessments supporting the presence of heart failure
Assessment Diagnosis of heart failure
Supports if present Opposes if normal or absent
Compatible symptoms ++ ++
Compatible signs ++ +
Cardiac dysfunction on echocardiography +++ +++
Response of symptoms or signs to therapy +++ ++
ECG
Normal ++
Abnormal ++ +
Dysrhythmia +++ +
Laboratory
Elevated BNP/NT-proBNP +++ +
Low/normal BNP/NT-proBNP + +++
Hyponatraemia + +
Renal dysfunction + +
Mild elevations of troponin + +
Chest X-ray
Pulmonary congestion +++ +
Reduced exercise capacity +++ ++
Abnormal pulmonary function tests + +
Abnormal haemodynamics at rest +++ ++
+ = some importance; ++ = intermediate importance; +++ = great importance.

Differential diagnosis

There are several terms which are closely related to heart failure, and may be the cause of heart failure, but should not be confused with it:

Management

Main article: Management of heart failure

Treatment focuses on improving the symptoms and preventing the progression of the disease. Reversible causes of the heart failure also need to be addressed (e.g. infection, alcohol ingestion, anemia, thyrotoxicosis, arrhythmia, hypertension). Treatments include lifestyle and pharmacological modalities, and occasionally various forms of device therapy and rarely cardiac transplantation.

Acute decompensation

Main article: Acute decompensated heart failure

In acute decompensated heart failure (ADHF), the immediate goal is to re-establish adequate perfusion and oxygen delivery to end organs. This entails ensuring that airway, breathing, and circulation are adequate. Immediate treatments usually involve some combination of vasodilators such as nitroglycerin, diuretics such as furosemide, and possibly non invasive positive pressure ventilation (NIPPV).

Chronic management

The goal is to prevent the development of acute decompensated heart failure, to counteract the deleterious effects of cardiac remodeling, and to minimize the symptoms. First-line therapy for all heart failure patients is angiotensin-converting enzyme (ACE) inhibition. ACE inhibitors (i.e., enalapril, captopril, lisinopril, ramipril) improve survival and quality of life in heart failure patients, and have been shown to reduce mortality in patients with left ventricular dysfunction in numerous randomized trials.[47][48] Diuretics have been a mainstay of treatment for treatment of fluid accumulation, and include classes of diuretics such as loop diuretics, thiazide-like diuretic, and potassium-sparing diuretic. Although widely used, evidence on their efficacy and safety is limited.[49] A recent Cochrane review found in a small studies, patients taking diuretics appeared to have improved mortality.[50] However, how well these results can be extrapolated to a general population is limited by the small number patients in the cited studies.[49] In addition to pharmacologic agents (oral loop diuretics, beta-blockers, ACE inhibitors or angiotensin receptor blockers, vasodilators, and in severe cardiomyopathy aldosterone receptor antagonists), behavioral modification should be pursued, specifically with regard to dietary guidelines regarding fluid intake. Exercise should be encouraged as tolerated, as sufficient conditioning can significantly improve quality-of-life.[citation needed]

Anaemia is an independent factor in mortality in people with chronic heart failure; treatment of anaemia significantly improves patient's quality of life, and has been shown to improve the classification of severity of heart failure.[51] Treatment of anaemia improves quality of life and decreases mortality rates.[52] Due to this increasing evidence, the latest European guidelines recommend screening for anaemia and treating with parenteral iron if anaemia is found.[53]

In people with severe cardiomyopathy (left ventricular ejection fraction below 35%), implantation of an automatic implantable cardioverter defibrillator (AICD) should be considered to reduce the risk of severe life-threatening arrhythmias. A select population (LVEF <35% and evidence of abnormal conduction on ECG or echocardiogram) will also probably benefit from ventricular resynchronization.[54] In select cases, cardiac transplantation can be considered. While this may resolve the problems associated with heart failure, the patient generally must remain on an immunosuppressive regimen to prevent rejection, which has its own significant downsides.[citation needed] Some patients may also be candidates for ventricular assist devices (VAD), which have commonly been used as a bridge to heart transplants, but are also now being used as treatments for very advanced heart failure in certain patients even if transplantation will not be offered.[55]

Home visits and heart failure clinic have been found to be beneficial with respect to need for hospitalization and life expectancy.[56]

Palliative care

People with CHF often have significant symptoms, such as shortness of breath and chest pain. Both palliative care and cardiology are trying to get palliative care involved earlier in the course of patients with heart failure, and some would argue any patient with NYHA class III CHF should have a palliative care referral. Palliative care can not only provide symptom management, but also assist with advanced care planning, goals of care in the case of a significant decline, and making sure the patient has a medical power of attorney and discussed his or her wishes with this individual.[57]

Without transplantation, heart failure may not be reversible and cardiac function typically deteriorates with time. The growing number of patients with Stage IV heart failure (intractable symptoms of fatigue, shortness of breath or chest pain at rest despite optimal medical therapy) should be considered for palliative care or hospice, according to American College of Cardiology/American Heart Association guidelines.[57]

Prognosis

Prognosis in heart failure can be assessed in multiple ways including clinical prediction rules and cardiopulmonary exercise testing. Clinical prediction rules use a composite of clinical factors such as lab tests and blood pressure to estimate prognosis. Among several clinical prediction rules for prognosing acute heart failure, the 'EFFECT rule' slightly outperformed other rules in stratifying patients and identifying those at low risk of death during hospitalization or within 30 days.[58] Easy methods for identifying low risk patients are:

  • ADHERE Tree rule indicates that patients with blood urea nitrogen < 43 mg/dl and systolic blood pressure at least 115 mm Hg have less than 10% chance of inpatient death or complications.
  • BWH rule indicates that patients with systolic blood pressure over 90 mm Hg, respiratory rate of 30 or less breaths per minute, serum sodium over 135 mmol/L, no new ST-T wave changes have less than 10% chance of inpatient death or complications.

A very important method for assessing prognosis in advanced heart failure patients is cardiopulmonary exercise testing (CPX testing). CPX testing is usually required prior to heart transplantation as an indicator of prognosis. Cardiopulmonary exercise testing involves measurement of exhaled oxygen and carbon dioxide during exercise. The peak oxygen consumption (VO2 max) is used as an indicator of prognosis. As a general rule, a VO2 max less than 12–14 cc/kg/min indicates a poor survival and suggests that the patient may be a candidate for a heart transplant. Patients with a VO2 max<10 cc/kg/min have clearly poorer prognosis. The most recent International Society for Heart and Lung Transplantation (ISHLT) guidelines[59] also suggest two other parameters that can be used for evaluation of prognosis in advanced heart failure, the heart failure survival score and the use of a criterion of VE/VCO2 slope > 35 from the CPX test. The heart failure survival score is a score calculated using a combination of clinical predictors and the VO2 max from the cardiopulmonary exercise test.

Heart failure is associated with significantly reduced physical and mental health, resulting in a markedly decreased quality of life.[60][61] With the exception of heart failure caused by reversible conditions, the condition usually worsens with time. Although some people survive many years, progressive disease is associated with an overall annual mortality rate of 10%.[62]

Epidemiology

Heart failure is associated with a high health expenditure, mostly because of the cost of hospitalizations; costs have been estimated to amount to 2% of the total budget of the National Health Service in the United Kingdom, and more than $35 billion in the United States.[63][64]

Heart failure is the leading cause of hospitalization in people older than 65.[65] In developed countries, the mean age of patients with heart failure is 75 years old. In developing countries, two to three percent of the population have heart failure, but in those 70 to 80 years old, it occurs in 20–30 percent.

More than 20 million people have heart failure worldwide.[66][67] The prevalence and incidence of heart failure are increasing, mostly because of increasing life span, but also because of increased prevalence of risk factors (hypertension, diabetes, dyslipidemia, and obesity) and improved survival rates from other types of cardiovascular disease (myocardial infarction, valvular disease, and arrhythmias).[67][68]

In the United States, heart failure affects 5.8 million people, and each year 550,000 new cases are diagnosed.[66] In 2011, congestive heart failure was the most common reason for hospitalization for adults aged 85 years and older, and the second most common for adults aged 65–84 years.[69] Heart failure is much higher in African Americans, Hispanics, Native Americans and recent immigrants from the eastern bloc countries like Russia. This high prevalence in these ethnic minority populations has been linked to high incidence of diabetes and hypertension. In many new immigrants to the U.S., the high prevalence of heart failure has largely been attributed to lack of preventive health care or substandard treatment.[70] Nearly one out of every four patients (24.7%) hospitalized in the U.S. with congestive heart failure are readmitted within 30 days.[71] Additionally, more than 50% of patients seek re-admission within 6 months after treatment and the average duration of hospital stay is 6 days.

In tropical countries, the most common cause of HF is valvular heart disease or some type of cardiomyopathy. As underdeveloped countries have become more affluent, there has also been an increase in the incidence of diabetes, hypertension and obesity, which have in turn raised the incidence of heart failure.[72]

Congestive heart failure is a leading cause of hospital readmissions in the U.S. In a study of 18 States, Medicare patients aged 65 and older were readmitted at a rate of 24.5 per 100 admissions in 2011. In the same year, Medicaid patients were readmitted at a rate of 30.4 per 100 admissions, and uninsured patients were readmitted at a rate of 16.8 per 100 admissions. These are the highest readmission rates for both patient categories. Notably, congestive heart failure was not among the top ten conditions with the most 30-day readmissions among the privately insured.[73]

Sex

Men have a higher incidence of heart failure, but the overall prevalence rate is similar in both sexes, since women survive longer after the onset of heart failure.[74] Women tend to be older when diagnosed with heart failure (after menopause), they are more likely than men to have diastolic dysfunction, and seem to experience a lower overall quality of life than men after diagnosis.[74]

Economics

In 2011, non-hypertensive congestive heart failure was one of the ten most expensive conditions seen during inpatient hospitalizations in the U.S., with aggregate inpatient hospital costs of more than $10.5 billion.[75]

Research

There is low quality evidence that stem cell therapy may help.[76] Although this evidence positively indicated benefit, the evidence was of lower quality than other evidence that does not indicate benefit.[77]

A previous claim, that a low salt diet increased the risk of death in those with congestive heart failure, has been withdrawn. The 2012 article[78] in the British Journal Heart that it was based on was retracted in 2013[79] because two of the studies cited contained duplicate data that could not be verified, and the data has since been lost.[80]

References

  1. ^ "heart failure" at Dorland's Medical Dictionary
  2. ^ "Heart failure". Health Information. Mayo Clinic. 23 December 2009. DS00061.
  3. ^ "Definition of Heart failure". Medical Dictionary. MedicineNet. 27 April 2011.
  4. ^ "Living Well With Chronic Heart Failure" (PDF). Heart Foundation. p. 18. Retrieved 25 May 2014.
  5. ^ a b c d e f g h i j "Chronic Heart Failure: National Clinical Guideline for Diagnosis and Management in Primary and Secondary Care: Partial Update". National Clinical Guideline Centre: 19–24. August 2010. PMID 22741186.
  6. ^ a b McDonagh, Theresa A. (2011). Oxford textbook of heart failure. Oxford: Oxford University Press. p. 3. ISBN 9780199577729.
  7. ^ a b c McMurray JJ, Pfeffer MA (2005). "Heart failure". Lancet. 365 (9474): 1877–89. doi:10.1016/S0140-6736(05)66621-4. PMID 15924986.
  8. ^ a b "Chronic Heart Failure: National Clinical Guideline for Diagnosis and Management in Primary and Secondary Care: Partial Update". National Clinical Guideline Centre: 38–70. August 2010. PMID 22741186.
  9. ^ Willard & Spackman's occupational therapy (12th ed. ed.). Philadelphia: Wolters Kluwer Health/Lippincott Williams & Wilkins. 2014. p. 1124. ISBN 9781451110807. {{cite book}}: |edition= has extra text (help)
  10. ^ Eyal Herzog (2012). The Cardiac Care Unit Survival Guide. Lippincott Williams & Wilkins. p. 98. ISBN 9781451177466.
  11. ^ a b c d e f g "Chronic Heart Failure: National Clinical Guideline for Diagnosis and Management in Primary and Secondary Care: Partial Update". National Clinical Guideline Centre: 34–47. August 2010. PMID 22741186.
  12. ^ a b c d "Chronic Heart Failure: National Clinical Guideline for Diagnosis and Management in Primary and Secondary Care: Partial Update". National Clinical Guideline Centre: 71–153. August 2010. PMID 22741186.
  13. ^ a b Taylor, RS; Sagar, VA; Davies, EJ; Briscoe, S; Coats, AJ; Dalal, H; Lough, F; Rees, K; Singh, S (27 April 2014). "Exercise-based rehabilitation for heart failure". The Cochrane database of systematic reviews. 4: CD003331. doi:10.1002/14651858.CD003331.pub4. PMID 24771460. {{cite journal}}: Unknown parameter |displayauthors= ignored (|display-authors= suggested) (help)
  14. ^ Dickstein K, Cohen-Solal A, Filippatos G; et al. (October 2008). "ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure 2008: the Task Force for the Diagnosis and Treatment of Acute and Chronic Heart Failure 2008 of the European Society of Cardiology. Developed in collaboration with the Heart Failure Association of the ESC (HFA) and endorsed by the European Society of Intensive Care Medicine (ESICM)". Eur. Heart J. 29 (19): 2388–442. doi:10.1093/eurheartj/ehn309. PMID 18799522. {{cite journal}}: Explicit use of et al. in: |author= (help)CS1 maint: multiple names: authors list (link)
  15. ^ a b "congestive heart failure" at Dorland's Medical Dictionary
  16. ^ "Ejection Fraction Heart Failure Measurement". American Heart Association. 11 February 2014. Retrieved 7 June 2014.
  17. ^ a b "Ejection Fraction". Heart Rhythm Society. Retrieved 7 June 2014.
  18. ^ Jessup M, Abraham WT, Casey DE; et al. (April 2009). "2009 focused update: ACCF/AHA Guidelines for the Diagnosis and Management of Heart Failure in Adults: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines: developed in collaboration with the International Society for Heart and Lung Transplantation". Circulation. 119 (14): 1977–2016. doi:10.1161/CIRCULATIONAHA.109.192064. PMID 19324967. {{cite journal}}: Explicit use of et al. in: |author= (help)CS1 maint: multiple names: authors list (link)
  19. ^ a b "high-output heart failure" at Dorland's Medical Dictionary
  20. ^ "Heart Failure: Signs and Symptoms". UCSF Medical Center.
  21. ^ He J; Ogden LG; Bazzano LA; Vupputuri S; et al. (2001). "Risk factors for congestive heart failure in US men and women: NHANES I epidemiologic follow-up study". Arch. Intern. Med. 161 (7): 996–1002. doi:10.1001/archinte.161.7.996. PMID 11295963. {{cite journal}}: Explicit use of et al. in: |author= (help)CS1 maint: multiple names: authors list (link)
  22. ^ Baldasseroni S; Opasich C; Gorini M; Lucci D; et al. (2002). "Left bundle-branch block is associated with increased 1-year sudden and total mortality rate in 5517 outpatients with congestive heart failure: a report from the Italian network on congestive heart failure". American Heart Journal. 143 (3): 398–405. doi:10.1067/mhj.2002.121264. PMID 11868043. {{cite journal}}: Explicit use of et al. in: |author= (help)CS1 maint: multiple names: authors list (link)
  23. ^ Fonarow GC, Abraham WT, Albert NM; et al. (April 2008). "Factors Identified as Precipitating Hospital Admissions for Heart Failure and Clinical Outcomes: Findings From OPTIMIZE-HF". Arch. Intern. Med. 168 (8): 847–854. doi:10.1001/archinte.168.8.847. PMID 18443260. {{cite journal}}: Explicit use of et al. in: |author= (help)CS1 maint: multiple names: authors list (link)
  24. ^ Nieminen MS, Böhm M, Cowie MR; et al. (February 2005). "Executive summary of the guidelines on the diagnosis and treatment of acute heart failure: the Task Force on Acute Heart Failure of the European Society of Cardiology". Eur. Heart J. 26 (4): 384–416. doi:10.1093/eurheartj/ehi044. PMID 15681577. {{cite journal}}: Explicit use of et al. in: |author= (help)CS1 maint: multiple names: authors list (link)
  25. ^ Coxib and traditional NSAID Trialists' (CNT), Collaboration (31 August 2013). "Vascular and upper gastrointestinal effects of non-steroidal anti-inflammatory drugs: meta-analyses of individual participant data from randomised trials". Lancet. 382 (9894): 769–79. doi:10.1016/S0140-6736(13)60900-9. PMC 3778977. PMID 23726390. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help)
  26. ^ Boron, Walter F.; Boulpaep, Emile L. (2005). Medical Physiology: A Cellular and Molecular Approach (Updated ed.). Saunders. p. 533. ISBN 0-7216-3256-4.
  27. ^ Rang HP (2003). Pharmacology. Edinburgh: Churchill Livingstone. p. 127. ISBN 0-443-07145-4.
  28. ^ "cardiac pathophysiology in heart failure". GPnotebook.
  29. ^ Shigeyama J, Yasumura Y, Sakamoto A; et al. (December 2005). "Increased gene expression of collagen Types I and III is inhibited by beta-receptor blockade in patients with dilated cardiomyopathy". Eur. Heart J. 26 (24): 2698–705. doi:10.1093/eurheartj/ehi492. PMID 16204268. {{cite journal}}: Explicit use of et al. in: |author= (help)CS1 maint: multiple names: authors list (link)
  30. ^ Tsutsui H, Matsushima S, Kinugawa S; et al. (May 2007). "Angiotensin II type 1 receptor blocker attenuates myocardial remodeling and preserves diastolic function in diabetic heart". Hypertens. Res. 30 (5): 439–49. doi:10.1291/hypres.30.439. PMID 17587756. {{cite journal}}: Explicit use of et al. in: |author= (help)CS1 maint: multiple names: authors list (link)
  31. ^ Krug AW, Grossmann C, Schuster C; et al. (October 2003). "Aldosterone stimulates epidermal growth factor receptor expression". J. Biol. Chem. 278 (44): 43060–6. doi:10.1074/jbc.M308134200. PMID 12939263. {{cite journal}}: Explicit use of et al. in: |author= (help)CS1 maint: multiple names: authors list (link) CS1 maint: unflagged free DOI (link)
  32. ^ "systemic pathophysiology in heart failure". GPnotebook.
  33. ^ Hunter JG, Boon NA, Davidson S, Colledge NR, Walker B (2006). Davidson's principles & practice of medicine. Elsevier/Churchill Livingstone. p. 544. ISBN 0-443-10057-8.{{cite book}}: CS1 maint: multiple names: authors list (link)
  34. ^ McKee PA, Castelli WP, McNamara PM, Kannel WB (1971). "The natural history of congestive heart failure: the Framingham study". N. Engl. J. Med. 285 (26): 1441–6. doi:10.1056/NEJM197112232852601. PMID 5122894.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  35. ^ Carlson KJ, Lee DC, Goroll AH, Leahy M, Johnson RA (1985). "An analysis of physicians' reasons for prescribing long-term digitalis therapy in outpatients". Journal of chronic diseases. 38 (9): 733–9. doi:10.1016/0021-9681(85)90115-8. PMID 4030999.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  36. ^ Harlan WR, oberman A, Grimm R, Rosati RA (1977). "Chronic congestive heart failure in coronary artery disease: clinical criteria". Annals of Internal Medicine. 86 (2): 133–8. doi:10.7326/0003-4819-86-2-133. PMID 835934.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  37. ^ Killip T, Kimball JT (1967). "Treatment of myocardial infarction in a coronary care unit. A two year experience with 250 patients". Am. J. Cardiol. 20 (4): 457–64. doi:10.1016/0002-9149(67)90023-9. PMID 6059183.
  38. ^ Loscalzo, Joseph; Fauci, Anthony S.; Braunwald, Eugene; Dennis L. Kasper; Hauser, Stephen L; Longo, Dan L. (2008). Harrison's Principles of Internal Medicine (17 ed.). McGraw-Hill Medical. p. 1447. ISBN 978-0-07-147693-5.{{cite book}}: CS1 maint: multiple names: authors list (link)
  39. ^ Ewald B, Ewald D, Thakkinstian A, Attia J (2008). "Meta-analysis of B type natriuretic peptide and N-terminal pro B natriuretic peptide in the diagnosis of clinical heart failure and population screening for left ventricular systolic dysfunction". Intern Med J. 38 (2): 101–13. doi:10.1111/j.1445-5994.2007.01454.x. PMID 18290826.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  40. ^ Yu, Cheuk-Man; Wang, Li; Chau, Elaine; Chan, Raymond Hon-Wah; Kong, Shun-Ling; Tang, Man-Oi (1 August 2005). "Correlation With Fluid Status and Feasibility of Early Warning Preceding Hospitalization". American Heart Association Journals. doi:10.1161/CIRCULATIONAHA.104.492207. Retrieved 8 July 2014.
  41. ^ Criteria Committee, New York Heart Association (1964). Diseases of the heart and blood vessels. Nomenclature and criteria for diagnosis (6th ed.). Boston: Little, Brown. p. 114.
  42. ^ Raphael C, Briscoe C, Davies J; et al. (2007). "Limitations of the New York Heart Association functional classification system and self‐reported walking distances in chronic heart failure". Heart. 93 (4): 476–82. doi:10.1136/hrt.2006.089656. PMC 1861501. PMID 17005715. {{cite journal}}: Explicit use of et al. in: |author= (help)CS1 maint: multiple names: authors list (link)
  43. ^ Hunt SA, Abraham WT, Chin MH; et al. (2005). "ACC/AHA 2005 Guideline Update for the Diagnosis and Management of Chronic Heart Failure in the Adult" (PDF). Circulation. 112 (12): e154–235. doi:10.1161/CIRCULATIONAHA.105.167586. PMID 16160202. {{cite journal}}: Explicit use of et al. in: |author= (help)CS1 maint: multiple names: authors list (link)
  44. ^ a b c d "Framingham Criteria for Congestive Heart Failure". MedicalCRITERIA.com. 2005. In turn citing: Framingham study 1971
  45. ^ Topic Review – Heart Failure By Osama Gusbi, MD. Albany Medical Review – January 2002
  46. ^ Dickstein K, Cohen-Solal A, Filippatos G; et al. (October 2008). "ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure 2008: the Task Force for the Diagnosis and Treatment of Acute and Chronic Heart Failure 2008 of the European Society of Cardiology. Developed in collaboration with the Heart Failure Association of the ESC (HFA) and endorsed by the European Society of Intensive Care Medicine (ESICM)". Eur. Heart J. 29 (19): 2388–442. doi:10.1093/eurheartj/ehn309. PMID 18799522. {{cite journal}}: Explicit use of et al. in: |author= (help)CS1 maint: multiple names: authors list (link) as PDF Also at doi:10.1016/j.ejheart.2008.08.005
  47. ^ The CONSENSUS Trial Study Group. (1987). "Effects of enalapril on mortality in severe congestive heart failure. Results of the Cooperative North Scandinavian Enalapril Survival Study (CONSENSUS)". N Engl J Med. 316 (23): 1429–35. doi:10.1056/NEJM198706043162301. PMID 2883575.
  48. ^ The SOLVD Investigators. (1991). "Effect of enalapril on survival in patients with reduced left ventricular ejection fractions and congestive heart failure". N Engl J Med. 325 (5): 293–302. doi:10.1056/NEJM199108013250501. PMID 2057034.
  49. ^ a b von Lueder, TG; Atar, D; Krum, H (October 2013). "Diuretic use in heart failure and outcomes". Clinical pharmacology and therapeutics. 94 (4): 490–8. doi:10.1038/clpt.2013.140. PMID 23852396.
  50. ^ Faris, RF; Flather, M; Purcell, H; Poole-Wilson, PA; Coats, AJ (15 February 2012). "Diuretics for heart failure". The Cochrane database of systematic reviews. 2: CD003838. doi:10.1002/14651858.CD003838.pub3. PMID 22336795.
  51. ^ He SW, Wang LX (2009). "The impact of anemia on the prognosis of chronic heart failure: a meta-analysis and systemic review". Congest Heart Fail. 15 (3): 123–30. doi:10.1111/j.1751-7133.2008.00030.x. PMID 19522961.
  52. ^ Peraira-Moral J. Roberto, Núñez-Gil Ivan J. (19 January 2012). "Anaemia in heart failure: intravenous iron therapy". E-journal of the ESC Council for Cardiology Practice. 10 (16).
  53. ^ ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure 2012 European Heart Journal (2012) 33, 1787–1847 doi:10.1093/eurheartj/ehs104
  54. ^ Yancy CW, Jessup M, Bozkurt B, Butler J, Casey DE; et al. (2013). "2013 ACCF/AHA Guideline for the Management of Heart Failure: A Report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines". Circulation. 128 (16): e240–e327. doi:10.1161/CIR.0b013e31829e8776. PMID 23741058. {{cite journal}}: Explicit use of et al. in: |author= (help)CS1 maint: multiple names: authors list (link)
  55. ^ Carrel, T; Englberger, L; Martinelli, MV; Takala, J; Boesch, C; Sigurdadottir, V; Gygax, E; Kadner, A; Mohacsi, P (18 October 2012). "Continuous flow left ventricular assist devices: a valid option for heart failure patients". Swiss medical weekly. 142: w13701. doi:10.4414/smw.2012.13701. PMID 23135811. {{cite journal}}: Unknown parameter |displayauthors= ignored (|display-authors= suggested) (help)
  56. ^ Feltner, C; Jones, CD; Cené, CW; Zheng, ZJ; Sueta, CA; Coker-Schwimmer, EJ; Arvanitis, M; Lohr, KN; Middleton, JC; Jonas, DE (3 June 2014). "Transitional care interventions to prevent readmissions for persons with heart failure: a systematic review and meta-analysis". Annals of internal medicine. 160 (11): 774–84. doi:10.7326/M14-0083. PMID 24862840.
  57. ^ a b Adler, Eric D.; Goldfinger, Judith Z.; Kalman, Jill; Park, Michelle E.; Meier, Diane E. "Palliative Care in the Treatment of Advanced Heart Failure". American Heart Association Journals. doi:10.1161/CIRCULATIONAHA.109.869123. Retrieved 8 July 2014.
  58. ^ Auble TE, Hsieh M, McCausland JB, Yealy DM (2007). "Comparison of four clinical prediction rules for estimating risk in heart failure". Annals of Emergency Medicine. 50 (2): 127–35, 135.e1–2. doi:10.1016/j.annemergmed.2007.02.017. PMID 17449141.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  59. ^ Mehra MR, Kobashigawa J, Starling R; et al. (September 2006). "Listing criteria for heart transplantation: International Society for Heart and Lung Transplantation guidelines for the care of cardiac transplant candidates–2006". J. Heart Lung Transplant. 25 (9): 1024–42. doi:10.1016/j.healun.2006.06.008. PMID 16962464. {{cite journal}}: Explicit use of et al. in: |author= (help)CS1 maint: multiple names: authors list (link)
  60. ^ Juenger J, Schellberg D, Kraemer S; et al. (March 2002). "Health related quality of life in patients with congestive heart failure: comparison with other chronic diseases and relation to functional variables". Heart. 87 (3): 235–41. doi:10.1136/heart.87.3.235. PMC 1767036. PMID 11847161. {{cite journal}}: Explicit use of et al. in: |author= (help)CS1 maint: multiple names: authors list (link)
  61. ^ Hobbs FD, Kenkre JE, Roalfe AK, Davis RC, Hare R, Davies MK (December 2002). "Impact of heart failure and left ventricular systolic dysfunction on quality of life: a cross-sectional study comparing common chronic cardiac and medical disorders and a representative adult population". Eur. Heart J. 23 (23): 1867–76. doi:10.1053/euhj.2002.3255. PMID 12445536.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  62. ^ Neubauer S (2007). "The failing heart – an engine out of fuel". N Engl J Med. 356 (11): 1140–51. doi:10.1056/NEJMra063052. PMID 17360992.
  63. ^ Stewart S, Jenkins A, Buchan S, McGuire A, Capewell S, McMurray JJ (June 2002). "The current cost of heart failure to the National Health Service in the UK". Eur. J. Heart Fail. 4 (3): 361–71. doi:10.1016/S1388-9842(01)00198-2. PMID 12034163.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  64. ^ Rosamond W, Flegal K, Furie K; et al. (January 2008). "Heart disease and stroke statistics--2008 update: a report from the American Heart Association Statistics Committee and Stroke Statistics Subcommittee". Circulation. 117 (4): e25–146. doi:10.1161/CIRCULATIONAHA.107.187998. PMID 18086926. {{cite journal}}: Explicit use of et al. in: |author= (help)CS1 maint: multiple names: authors list (link)
  65. ^ Krumholz HM, Chen YT, Wang Y, Vaccarino V, Radford MJ, Horwitz RI (2000). "Predictors of readmission among elderly survivors of admission with heart failure". Am. Heart J. 139 (1 Pt 1): 72–7. doi:10.1016/S0002-8703(00)90311-9. PMID 10618565.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  66. ^ a b Bui, AL; Horwich, TB; Fonarow, GC (January 2011). "Epidemiology and risk profile of heart failure". Nature Reviews Cardiology. 8 (1): 30–41. doi:10.1038/nrcardio.2010.165. PMC 3033496. PMID 21060326.
  67. ^ a b Mann DL, Chakinala M (2012). Harrison's principles of internal medicine: Chapter 234. Heart Failure and Cor Pulmonale (18th ed.). New York: McGraw-Hill. ISBN 978-0071748896.
  68. ^ Goldman, Lee (2011). Goldman's Cecil Medicine: Heart Failure (Ch 58, 59) (24th ed.). Philadelphia: Elsevier Saunders. pp. 295–317. ISBN 1437727883. {{cite book}}: Invalid |ref=harv (help)
  69. ^ Pfuntner A., Wier L.M., Stocks C. Most Frequent Conditions in U.S. Hospitals, 2011. HCUP Statistical Brief #162. September 2013. Agency for Healthcare Research and Quality, Rockville, MD. [1]
  70. ^ Heart Failure Information, Retrieved on 2010-01-21.
  71. ^ Elixhauser A, Steiner C. Readmissions to U.S. Hospitals by Diagnosis, 2010. HCUP Statistical Brief #153. Agency for Healthcare Research and Quality. April 2013. [2]
  72. ^ Melmed 2011, pp. 146
  73. ^ Hines AL, Barrett ML, Jiang HJ, and Steiner CA. (April 2014). "Conditions With the Largest Number of Adult Hospital Readmissions by Payer, 2011". HCUP Statistical Brief #172. Rockville, MD: Agency for Healthcare Research and Quality.{{cite web}}: CS1 maint: multiple names: authors list (link)
  74. ^ a b Strömberg A, Mårtensson J. (April 2003). "Gender differences in patients with heart failure". Eur. J. Cardiovasc. Nurs. 2 (1): 7–18. doi:10.1016/S1474-5151(03)00002-1. PMID 14622644.
  75. ^ Torio CM, Andrews RM. National Inpatient Hospital Costs: The Most Expensive Conditions by Payer, 2011. HCUP Statistical Brief #160. Agency for Healthcare Research and Quality, Rockville, MD. August 2013. [3]
  76. ^ Fisher, SA; Brunskill, SJ; Doree, C; Mathur, A; Taggart, DP; Martin-Rendon, E (29 April 2014). "Stem cell therapy for chronic ischaemic heart disease and congestive heart failure". The Cochrane database of systematic reviews. 4: CD007888. doi:10.1002/14651858.CD007888.pub2. PMID 24777540.
  77. ^ Nowbar, AN; Mielewczik, M; Karavassilis, M; Dehbi, HM; Shun-Shin, MJ; Jones, S; Howard, JP; Cole, GD; Francis, DP; DAMASCENE writing, group (28 April 2014). "Discrepancies in autologous bone marrow stem cell trials and enhancement of ejection fraction (DAMASCENE): weighted regression and meta-analysis". BMJ (Clinical research ed.). 348: g2688. doi:10.1136/bmj.g2688. PMC 4002982. PMID 24778175.
  78. ^ Dinicolantonio, JJ; Pasquale, PD; Taylor, RS; Hackam, DG (24 January 2013). "Low sodium versus normal sodium diets in systolic heart failure: systematic review and meta-analysis". Heart (British Cardiac Society). doi:10.1136/heartjnl-2012-302337. PMID 22914535.
  79. ^ no author given (June 2013). "Retraction. Low sodium versus normal sodium diets in systolic heart failure: systematic review and meta-analysis. Heart. Published Online First: 21 August 2012 doi:10.1136/heartjnl-2012-302337". Heart. 99 (11): 820. doi:10.1136/heartjnl-2011-301156.29ret. PMID 23640983. Retrieved 29 September 2013. {{cite journal}}: |last= has generic name (help)
  80. ^ amarcus41. "Heart pulls sodium meta-analysis over duplicated, and now missing, data". Retraction Watch. Retrieved 29 September 2013.{{cite web}}: CS1 maint: numeric names: authors list (link)
Wikimedia Commons has media related to Heart failure.
  • Heart failure, American Heart Association – information and resources for treating and living with heart failure
  • Heart Failure Matters – patient information website of the Heart Failure Association of the European Society of Cardiology
  • Heart failure in children by Great Ormond Street Hospital, London, UK

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