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==Introduction==
==Introduction==
[[File:Foxglove_(digitalis).png|thumb|150px|right|Figure 1: Foxglove (digitalis), used as a medicine for heart failure.]]
[[File:Foxglove_(digitalis).png|thumb|150px|right|Foxglove (digitalis), used as a medicine for heart failure.]]


===History===
===History===
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{| class="wikitable" border="0" cellpadding="0" cellspacing="0" width="600px"
{| class="wikitable" border="0" cellpadding="0" cellspacing="0" width="600px"
|-
|-
!Table 1 Definition of heart failure
!Table 1. Definition of heart failure
|-
|-
|'''''Heart failure is a clinical syndrome in which patients have the following features:'''''
|'''''Heart failure is a clinical syndrome in which patients have the following features:'''''
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|-
|-
|'''''And'''''
|'''''And'''''
|-
|
*'''Signs typical of heart failure'''
*'''Signs typical of heart failure'''
**Elevated jugular venous pressure **Hepatomegaly
**Elevated jugular venous pressure  
**Hepatomegaly
**Third heart sound
**Third heart sound
**Pulmonary rales
**Pulmonary rales
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|-
|-
|'''''And'''''
|'''''And'''''
|-
|
*'''Objective evidence of a structural or functional abnormality of the heart at rest'''
*'''Objective evidence of a structural or functional abnormality of the heart at rest'''
**Abnormal echocardiogram
**Abnormal echocardiogram
**Abnormal pump function on nuclear imaging or on MRI)
**Abnormal pump function on nuclear imaging or on MRI
|}
|}


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===Pathophysiology of heart failure===
===Pathophysiology of heart failure===
[[Image:frank_starling.svg|thumb|right|400px|Figure 1. Frank-Starling curve]]
[[Image:frank_starling.svg|thumb|right|400px|'''Figure 1.''' Frank-Starling curve]]
[[Image:pressure_volume_curve.svg|thumb|400px|''Figure 2. Effects of decreased afterload. Red arrows indicate aortic valve opening, which occurs later and at higher LV systolic pressure when the diastolic aortic pressure is higher. Blue arrows indicate closing of the aortic valve. Bidirectional arrows represent stroke volume. When aortic pressure is decreased, stroke volume increases as a result of a lower aortic pressure during closure of the aortic valve.]]
[[Image:pressure_volume_curve.svg|thumb|400px|'''Figure 2.''' Effects of decreased afterload. Red arrows indicate aortic valve opening, which occurs later and at higher LV systolic pressure when the diastolic aortic pressure is higher. Blue arrows indicate closing of the aortic valve. Bidirectional arrows represent stroke volume. When aortic pressure is decreased, stroke volume increases as a result of a lower aortic pressure during closure of the aortic valve.]]
[[Image:management_outline.svg|thumb|400px|Figure 3 management in heart failure.]]
[[Image:management_outline.svg|thumb|400px|'''Figure 3.''' Management in heart failure.]]


HF is caused by a loss of cardiac pump function, which can be due to a structural abnormality of the heart muscle (e.g. myocardial infarction) or a change in the heart function (and often structure) in response to an abnormal load (e.g. aortic valve stenosis). The relationship between loading the ventricle (by filling it) and its output was described by Frank and Starling in 1918 and has become the cornerstone in understanding heart failure and how to treat it. The relationship states that as a result of loading the heart (increasing its filling or its pressure), the output increases (Figure 1). A heart that has a lower output can be improved by increasing its volume and its loading pressure. This is what naturally happens (LV dilatation and increased filling pressure) when the heart does not pump out enough volume, and, in the first phase of disease, compensates for the loss of contractility. It takes more energy from the heart to work at an increased loading, but the heart has a reasonable energy reserve. In a chronic situation, remodeling of the heart progresses (by hypertrophy of the myocytes and dilatation by increasing myocyte length and matrix changes), which, in the long term, leads to a further loss in function. The result of this dysfunction is further increased loading pressures in the heart and, by communicating the diastolic loading pressures to the left atrium and pulmonary veins, the pulmonary capillaries may become overloaded and leak water into the lungs. This is the practical restriction of further filling the heart as a tool to improve its function; even poor left ventricles may be filled more to increase their output <cite>6</cite> but the patients’ pulmonary capillaries cannot tolerate these hydrostatic pressures and start to leak water.     
HF is caused by a loss of cardiac pump function, which can be due to a structural abnormality of the heart muscle (e.g. myocardial infarction) or a change in the heart function (and often structure) in response to an abnormal load (e.g. aortic valve stenosis). The relationship between loading the ventricle (by filling it) and its output was described by Frank and Starling in 1918 and has become the cornerstone in understanding heart failure and how to treat it. The relationship states that as a result of loading the heart (increasing its filling or its pressure), the output increases (Figure 1). A heart that has a lower output can be improved by increasing its volume and its loading pressure. This is what naturally happens (LV dilatation and increased filling pressure) when the heart does not pump out enough volume, and, in the first phase of disease, compensates for the loss of contractility. It takes more energy from the heart to work at an increased loading, but the heart has a reasonable energy reserve. In a chronic situation, remodeling of the heart progresses (by hypertrophy of the myocytes and dilatation by increasing myocyte length and matrix changes), which, in the long term, leads to a further loss in function. The result of this dysfunction is further increased loading pressures in the heart and, by communicating the diastolic loading pressures to the left atrium and pulmonary veins, the pulmonary capillaries may become overloaded and leak water into the lungs. This is the practical restriction of further filling the heart as a tool to improve its function; even poor left ventricles may be filled more to increase their output <cite>6</cite> but the patients’ pulmonary capillaries cannot tolerate these hydrostatic pressures and start to leak water.     
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{| class="wikitable" border="0" cellspacing="0" cellpadding="0"  width="600px"
{| class="wikitable" border="0" cellspacing="0" cellpadding="0"  width="600px"
|-
|-
!colspan="2"|Table 2 NYHA functional classification
!colspan="2"|Table 2. NYHA functional classification
|-
|-
|colspan="2"|'''''Severity based on symptoms and physical activity'''''
|colspan="2"|'''''Severity based on symptoms and physical activity'''''
|-
|-
|width="20%"|'''Class I'''
|width="20%"|'''Class I'''
|No limitation of physical activity. Ordinary physical activity does not cause undue fatigue, palpitation, or dyspnoea.
|No limitation of physical activity.  
 
Ordinary physical activity does not cause undue fatigue, palpitation, or dyspnoea.
|-
|-
|'''Class II'''
|'''Class II'''
|Slight limitation of physical activity. Comfortable at rest, but ordinary physical activity results in fatigue, palpitation, or dyspnoea.
|Slight limitation of physical activity.  
 
Comfortable at rest, but ordinary physical activity results in fatigue, palpitation, or dyspnoea.
|-
|-
|'''Class III'''
|'''Class III'''
|Marked limitation of physical activity. Comfortable at rest,  but less than ordinary activity results in fatigue, palpitation, or dyspnoea.
|Marked limitation of physical activity.  
 
Comfortable at rest,  but less than ordinary activity results in fatigue, palpitation, or dyspnoea.
|-
|-
|'''Class IV'''
|'''Class IV'''
|Unable to carry on any physical activity without discomfort. Symptoms at rest. If any physical activity is undertaken, discomfort is increased.  
|Unable to carry on any physical activity without discomfort.  
 
Symptoms at rest.  
 
If any physical activity is undertaken, discomfort is increased.  
|}
|}


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===Laboratory tests===
===Laboratory tests===
[[Image:suspected_heart_failure.svg|thumb|400px|'''Figure 4.''' Flowchart suspected heart failure <cite>3</cite>]]
A standard blood assessment includes a complete blood count, electrolytes, renal function, glucose and liver function. Furthermore, urinalysis and other tests, depending on the clinical condition of the patient, complete the laboratory assessment.  For example, cardiac troponins must be sampled if an ACS is in the differential diagnosis. In patients suspected of HF, values of natriuretic peptides (such as B-type natriuretic peptide (BNP) and N-terminal pro-BNP (NT-proBNP)) can provide important information regarding the diagnosis, management and prognosis of HF. Natriuretic peptides are enzymes, secreted by the atria or ventricles in response to myocardial wall stress. The most commonly used tests are BNP and NT-proBNP measurements, which despite their different half-lives in the plasma, do not differ substantially in terms of diagnostic ability. Cut-off values are different in acute settings with acute dyspnea compared to chronic settings. Normal values are almost 100% specific, and exclude heart failure in patients >18 year old. Abnormal values do not have a 100% predictive value, and objective evidence for heart failure is still needed. The values for BNP and NTproBNP are also used to evaluate the prognosis in patients with known HF, in whom higher values carry a worse prognosis.  
A standard blood assessment includes a complete blood count, electrolytes, renal function, glucose and liver function. Furthermore, urinalysis and other tests, depending on the clinical condition of the patient, complete the laboratory assessment.  For example, cardiac troponins must be sampled if an ACS is in the differential diagnosis. In patients suspected of HF, values of natriuretic peptides (such as B-type natriuretic peptide (BNP) and N-terminal pro-BNP (NT-proBNP)) can provide important information regarding the diagnosis, management and prognosis of HF. Natriuretic peptides are enzymes, secreted by the atria or ventricles in response to myocardial wall stress. The most commonly used tests are BNP and NT-proBNP measurements, which despite their different half-lives in the plasma, do not differ substantially in terms of diagnostic ability. Cut-off values are different in acute settings with acute dyspnea compared to chronic settings. Normal values are almost 100% specific, and exclude heart failure in patients >18 year old. Abnormal values do not have a 100% predictive value, and objective evidence for heart failure is still needed. The values for BNP and NTproBNP are also used to evaluate the prognosis in patients with known HF, in whom higher values carry a worse prognosis.  
[[Image:suspected_heart_failure.svg|thumb|400px|Figure 4 flowchart suspected heart failure <cite>3</cite>]]


===Exercise test===
===Exercise test===
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===Heart catheterization===
===Heart catheterization===
Heart catheterization is not always part of the routine diagnosis and work-up of patients with HF.  It should be considered however to exclude coronary heart disease (Class of recommendation IIa, level of evidence C, see Table 4). Coronary angiography is recommended in patients at high risk of coronary artery disease  (Class of recommendation I, level of evidence C) and in HF patients with significant valvular disease (Class of recommendation IIa, level of evidence C).
Heart catheterization is not always part of the routine diagnosis and work-up of patients with HF.  It should be considered however to exclude coronary heart disease (Class of recommendation IIa, level of evidence C, see [[Heart_Failure_Table_4|Table 4]]). Coronary angiography is recommended in patients at high risk of coronary artery disease  (Class of recommendation I, level of evidence C) and in HF patients with significant valvular disease (Class of recommendation IIa, level of evidence C).


{| class="wikitable" border="0" cellpadding="0" cellspacing="0" width="600px"
{| class="wikitable" border="0" cellpadding="0" cellspacing="0" width="650px"
|-  
|-  
!colspan="3"|Table 3 Common echocardiographic abnormalities in heart failure
!colspan="3"|Table 3. Common echocardiographic abnormalities in heart failure
|-
|-
!Measurement
!Measurement
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|Myocardial infarction/ischaemia,  
|Myocardial infarction/ischaemia,  


cardiomyopathy,  
Cardiomyopathy,  


myocarditis
Myocarditis
|-
|-
|Left ventricular end-diastolic diameter
|Left ventricular end-diastolic diameter
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|Increased filling pressures,  
|Increased filling pressures,  


mitral valve dysfunction
Mitral valve dysfunction
|-
|-
|Left ventricular thickness
|Left ventricular thickness
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|Hypertention,  
|Hypertention,  


aortic stenosis,  
Aortic stenosis,  


hypertrophic cardiomyopathy
Hypertrophic cardiomyopathy
|-
|-
|Valvular structure and function
|Valvular structure and function
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|Effusion,  
|Effusion,  


haemopericardium,  
Haemopericardium,  


calcification
Calcification
|Consider tamponade,  
|Consider tamponade,  


malignancy,  
Malignancy,  


systemic disease,  
Systemic disease,  


acute or chronic pericarditis,  
Acute or chronic pericarditis,  


constrictive pericarditis
Constrictive pericarditis
|-
|-
|Aortic outflow velocity time integral
|Aortic outflow velocity time integral
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|Increased right atrial pressures,  
|Increased right atrial pressures,  


right ventricular dysfunction,  
Right ventricular dysfunction,  


volume overload Pulmonary hypertention possible
Volume overload Pulmonary hypertention possible
|}
|}


{| class="wikitable" border="0" cellpadding="0" cellspacing="0" width="600px"
|-
!colspan="5"|Table 4 Size of treatment effect
|-
|
|'''Class I'''
Benefit >>> Risk
|'''Class IIa'''
Benefit >> Risk
Additional studies with focused objectives needed
|'''Class IIb'''
Benefit≥Risk
Additional studies with broad objectives needed; additional registry data would be helpful
|'''Class III'''
Benefit≥Risk
No additional studies needed
|-
|
|Procedure/treatment should be performed/administered
|It is reasonable to perform/administer treatment
|Procedure/treatment may be considered
|Procedure/treatment should not be performed/administered since it is not helpful and may be harmful
|-
|'''Level A'''
Multiple (3-5) population risk strata evaluated
|
*Recommendation that procedure or treatment is useful/effective
*Sufficient evidence from multiple randomized trials or non-randomized trials
|
*Recommendation in favor of treatment or procedure being useful/effective
*Some conflicting evidence from multiple randomized trials or meta-analyses
|
*Recommendation’s usefulness/efficacy less well established
*Greater conflicting evidence from multiple randomized trials or meta-analyses
|
*Recommendation that procedure or treatment not useful/effective and may be harmful
*Sufficient evidence from multiple randomized trials or meta-analyses
|-
|'''Level B'''
Limited (2-3) population risk strata evaluated
|
*Recommendation that procedure or treatment is useful/effective
*Limited evidence from single randomized trial or non-randomized studies
|
*Recommendation in favor of treatment or procedure being useful/effective
*Some conflicting evidence from single randomized trial or non-randomized studies |
|
*Recommendation’s usefulness/efficacy less well established
*Greater conflicting evidence from single randomized trial or non-randomized studies |
|
*Recommendation that procedure or treatment not useful/effective and may be harmful
*Limited evidence from single randomized trial or non-randomized studies
|-
|'''Level C'''
Very limited (1-2) population risk strata evaluated
|
*Recommendation that procedure or treatment is useful/effective
*Only experts opinion, case studies, or standard-of-care
|
*Recommendation in favor of treatment or procedure being useful/effective
*Only diverging expert opinion case studies, or standard-of-care
|
*Recommendation’s usefulness/efficacy less well established
*Only diverging expert opinion case studies, or standard-of-care
|
*Recommendation that procedure or treatment not useful/effective and may be harmful
*Only expert opinion case studies, or standard-of-care
|}
==Etiology of heart failure==
==Etiology of heart failure==
===Coronary heart disease===  
===Coronary heart disease===  
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Deficiency of thiamine, selenium, or camitine, in states of severe cachexia.
Deficiency of thiamine, selenium, or camitine, in states of severe cachexia.


Infiltrative and storage disorders
===Infiltrative and storage disorders===
*Sarcoidosis
*[[Sarcoidosis]]
*Amyloidosis
*[[Amyloidosis]]
*Haemochromatosis  
*[[Haemochromatosis]]
*Connective tissue disease
*Connective tissue disease


===Infectious disease===
===Infectious disease===
*Chagas’ disease
*[[Chagas’ disease]]
*HIV infection
*[[HIV infection]]
*Viral, bacterial or protozoal diseases causing myocarditis.
*Viral, bacterial or protozoal diseases causing myocarditis.


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A flowchart for the treatment of patients presenting with systolic HF is depicted in Figure 5. Medications with a class I indication in patients with systolic heart failure are summarized in Table 5. Indications, mode of action, contraindications of the medication, and possible side effects of drugs included in this algorithm are discussed below.
A flowchart for the treatment of patients presenting with systolic HF is depicted in Figure 5. Medications with a class I indication in patients with systolic heart failure are summarized in Table 5. Indications, mode of action, contraindications of the medication, and possible side effects of drugs included in this algorithm are discussed below.
   
   
[[Image:management_chronic_systolic_hf.svg|thumb|400px|Figure 5. Treatment options for patients with chronic systolic HF]]
[[Image:management_chronic_systolic_hf.svg|thumb|400px|'''Figure 5.''' Treatment options for patients with chronic systolic HF]]


{| class="wikitable" border="1" cellpadding="1" cellspacing="1" width="600px"
{| class="wikitable" border="1" cellpadding="1" cellspacing="1" width="600px"
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|bgcolor="99FFCC" align="center"|'''Aldosteron antagonist'''
|bgcolor="99FFCC" align="center"|'''Aldosteron antagonist'''
|bgcolor="99FFCC"|
|bgcolor="99FFCC"|
|bgcolor="9ACD32" align="center"|'''EF = 35%'''
|bgcolor="9ACD32" align="center"|'''EF < 35%'''
|bgcolor="9ACD32" align="center"|'''EF = 35%'''
|bgcolor="9ACD32" align="center"|'''EF < 35%'''
|bgcolor="9ACD32" align="center"|'''EF = 35%'''
|bgcolor="9ACD32" align="center"|'''EF < 35%'''
|-
|-
|bgcolor="99FFCC" align="center"|'''Nitrate / Hydralazine'''
|bgcolor="99FFCC" align="center"|'''Nitrate / Hydralazine'''
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|bgcolor="9ACD32" align="center"|'''Afro-American'''
|bgcolor="9ACD32" align="center"|'''Afro-American'''
|bgcolor="9ACD32" align="center"|'''Afro-American'''
|bgcolor="9ACD32" align="center"|'''Afro-American'''
|-
|bgcolor="99FFCC" align="center"|'''Ivabradine'''
|bgcolor="99FFCC"|
|bgcolor="9ACD32" align="center"|'''SR>75/min & EF<35%'''
|bgcolor="9ACD32" align="center"|'''SR>75/min & EF<35%'''
|bgcolor="9ACD32" align="center"|'''SR>75/min & EF<35%'''
|-
|-
|bgcolor="99FFCC" align="center"|'''Digoxin'''
|bgcolor="99FFCC" align="center"|'''Digoxin'''
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|bgcolor="9ACD32"|
|bgcolor="9ACD32"|
|-
|-
|colspan="5"|Table 5 Medication with a class I indication in patients with systolic heart failure. Note that AT-II antagonists are alternative medicine for ACE inhibitors in case of intolerance (coughing, allergy). Nitrates and Hydralazine are added therapy for patients of Afro-American descent, and alternative therapy for patients that cannot tolerate ACE-inhibitors and AT-II antagonists). Digoxin can also be seen as symptomatic (instead of added preventive) treatment, not always necessary in NYHA III or even IV.
|colspan="5"|'''Table 5.''' Medication with a class I indication in patients with systolic heart failure. Note that AT-II antagonists are alternative medicine for ACE inhibitors in case of intolerance (coughing, allergy). Nitrates and Hydralazine are added therapy for patients of Afro-American descent, and alternative therapy for patients that cannot tolerate ACE-inhibitors and AT-II antagonists). Digoxin can also be seen as symptomatic (instead of added preventive) treatment, not always necessary in NYHA III or even IV.
|}
|}


===Angiotensin-converting enzyme (ACE) inhibitors===  
===Angiotensin-converting enzyme (ACE) inhibitors===  
An ACE inhibitor (in addition to beta blocker) is indicated for every patient with symptomatic systolic HF and an EF ≤40 % (NYHA class II-IV). (Class I recommendation, level of evidence A) Contraindications for the use of ACE inhibitors are:
An ACE inhibitor is indicated for every patient with symptomatic systolic HF and an EF ≤40 % (NYHA class II-IV). (Class I recommendation, level of evidence A) Contraindications for the use of ACE inhibitors are:
*History of angioedema
*History of angioedema
*Bilateral renal artery stenosis
*Bilateral renal artery stenosis
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===Diuretics (Loop of Henle diuretics, Thiazides, Aldosterone antagonists)===
===Diuretics (Loop of Henle diuretics, Thiazides, Aldosterone antagonists)===
[[Image:Henle_loop.svg|thumb|400px|'''Figure 6.''' Diuretics and site of action in the nephron.]]
Diuretics reduce preload by venous vasodilatation and by increasing diuresis. As a result, filling pressures of the heart and the lung vasculature decrease. Although the effects of diuretics on mortality and morbidity have not been studied in patients with HF (irrespective of EF), it is recommended in patients with signs and symptoms of congestion as diuretics relieve dyspnea and edema. Figure 6 depicts the nephron and the sites where different diuretics work.
Diuretics reduce preload by venous vasodilatation and by increasing diuresis. As a result, filling pressures of the heart and the lung vasculature decrease. Although the effects of diuretics on mortality and morbidity have not been studied in patients with HF (irrespective of EF), it is recommended in patients with signs and symptoms of congestion as diuretics relieve dyspnea and edema. Figure 6 depicts the nephron and the sites where different diuretics work.


===Loop of Henle diuretics===
====Loop of Henle diuretics====
Loop of Henle diuretics act on the ascending loop of Henle in the kidney tubules to inhibit sodium and chloride (and indirectly calcium and magnesium) reabsorption. This will ultimately result in increased urine production of sodium and water. Compared to thiazides, loop diuretics produce a more intense and shorter diuresis.
Loop of Henle diuretics act on the ascending loop of Henle in the kidney tubules to inhibit sodium and chloride (and indirectly calcium and magnesium) reabsorption. This will ultimately result in increased urine production of sodium and water. Compared to thiazides, loop diuretics produce a more intense and shorter diuresis.


===Thiazides===
====Thiazides====
Thiazide increases urine production by decreasing reabsorption of sodium in the distal tubule. This type of diuretic is often used in combination with loop diuretics to enhance their effects, but may be less effective in patients with a severely reduced kidney function.  
Thiazide increases urine production by decreasing reabsorption of sodium in the distal tubule. This type of diuretic is often used in combination with loop diuretics to enhance their effects, but may be less effective in patients with a severely reduced kidney function.  


===Aldosterone antagonists===
====Aldosterone antagonists====
Adding this drug is suggested for patients with moderate to severe symptomatic HF (NYHA class II to IV, refer to Table 2) and an LVEF < 35%. (Class I recommendation, level of evidence A) Contraindications:
Adding this drug is suggested for patients with moderate to severe symptomatic HF (NYHA class II to IV, refer to Table 2) and an LVEF < 35%. (Class I recommendation, level of evidence A) Contraindications:


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Possible side effects include hyperkalemia, hyponatremia, worsening renal function, and breast tenderness and/or enlargement. Eplerenon has less mastopathy side effects and is an alternative to spironolacton. In patients with severe heart failure, spironolactone in addition to standard therapy, reduces morbidity and mortality. <cite>20</cite>
Possible side effects include hyperkalemia, hyponatremia, worsening renal function, and breast tenderness and/or enlargement. Eplerenon has less mastopathy side effects and is an alternative to spironolacton. In patients with severe heart failure, spironolactone in addition to standard therapy, reduces morbidity and mortality. <cite>20</cite>


[[Image:Henle_loop.svg|thumb|400px|Figure 6. Diuretics and site of action in the nephron.]]
====Choice and combination of diuretics====
 
===Choice and combination of diuretics===
Patients with heart failure may be treated with a thiazide diuretic, which should be switched to a loop diuretic if a suboptimal response occurs. In patients with a decreased renal function, a loop diuretic is the mainstay of treatment. Addition of a thiazide diuretic to a loop diuretic can be considered in case of a suboptimal response of loop diuretic alone, when given in sufficient doses (furosemide 250 mg twice daily), suggesting that diuretic resistance is due to distal tubular increased activity of retaining sodium. In all patients with NYHA II or more, except in those with a creatinine clearance < 20 ml/min (creatinine > 220 micromol/L), addition of an aldosterone antagonist should be considered. In special cases in which hypercapnia plays a role, metabolic alkalosis can result from diuretics, and acetazolamide, a reversible carbonic anhydrase inhibitor, is then prescribed as an alternative diuretic.  
Patients with heart failure may be treated with a thiazide diuretic, which should be switched to a loop diuretic if a suboptimal response occurs. In patients with a decreased renal function, a loop diuretic is the mainstay of treatment. Addition of a thiazide diuretic to a loop diuretic can be considered in case of a suboptimal response of loop diuretic alone, when given in sufficient doses (furosemide 250 mg twice daily), suggesting that diuretic resistance is due to distal tubular increased activity of retaining sodium. In all patients with NYHA II or more, except in those with a creatinine clearance < 20 ml/min (creatinine > 220 micromol/L), addition of an aldosterone antagonist should be considered. In special cases in which hypercapnia plays a role, metabolic alkalosis can result from diuretics, and acetazolamide, a reversible carbonic anhydrase inhibitor, is then prescribed as an alternative diuretic.  


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The H-ISDN combination acts by decreasing peripheral vascular resistance.  
The H-ISDN combination acts by decreasing peripheral vascular resistance.  
Possible side effects include symptomatic hypotension or drug-induced lupus-like syndrome.
Possible side effects include symptomatic hypotension or drug-induced lupus-like syndrome.


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==Therapy of acute heart failure==
==Therapy of acute heart failure==
[[Image:acute_hf_flowchart.svg|400px|thumb|'''Figure 7.''' Flowchart acute HF.]]
When severe symptoms of heart failure quickly develop over time, it is termed acute heart failure. In Table 6, common acute HF medications and their recommended doses are summarized. In Figure 7, a flowchart for the treatment of acute HF is depicted. The mainstay of acute heart failure therapy includes diuretics, vasodilators, inotropics and vasopressors. Moreover, oxygen and morphine can be added.  
When severe symptoms of heart failure quickly develop over time, it is termed acute heart failure. In Table 6, common acute HF medications and their recommended doses are summarized. In Figure 7, a flowchart for the treatment of acute HF is depicted. The mainstay of acute heart failure therapy includes diuretics, vasodilators, inotropics and vasopressors. Moreover, oxygen and morphine can be added.  


[[Image:acute_hf_flowchart.svg|400px|thumb|Figure 7. Flowchart acute HF.]]
{| class="wikitable" border="0" cellpadding="0" cellspacing="0" width="630px"
 
{| class="wikitable" border="0" cellpadding="0" cellspacing="0" width="600px"
|-
|-
!colspan="3"|Table 6 Medication in acute heart failure
!colspan="3"|Table 6. Medication in acute heart failure
|-
|-
!Medication
!Medication
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|-
|-
|'''Diuretics'''
|'''Diuretics'''
|Adequate blood pressure and signs of overfilling
|colspan="2"|Adequate blood pressure and signs of overfilling
|
|-
|-
|
|
*Furosemide i.v.
*Furosemide i.v.
|
|valign="bottom"|
|40 mg
Renal failure
|-
|40 mg
|
125 mg – max 1000 mg  
|Renal failure
|80 mg – max 200 mg  
|-
|-
|
|
*Bumetanide i.v.
*Bumetanide i.v.
|
|valign="bottom"|
Renal failure
|1 mg
|1 mg
3 mg – max 25 mg
|-
|-
|
|'''Vasodilators'''
|Renal failure
|colspan="2"|Adequate blood pressure and signs of severe overfilling
|2 mg – max 5 mg
|-
|-
|'''Vasodilators'''
|Adequate blood pressure and signs of severe overfilling
|
|
*Nitroglycerine i.v.
*Nitroglycerine i.v.
|-
|
|
|20 µg/min – max 200 µg/min (guided by blood pressure)  
|20 µg/min – max 200 µg/min (guided by blood pressure)  
|-
|
|
*Nitroprusside i.v.
*Nitroprusside i.v.
|-
||Hypertensive crisis or in combination with inotropic in case of a cardiogenic shock
|
|Hypertensive crisis or in combination with inotropic in case of a cardiogenic shock
|0.3 µg/kg/min – max 5 µg/kg/min (guided by blood pressure)  
|0.3 µg/kg/min – max 5 µg/kg/min (guided by blood pressure)  
|-
|-
|'''Inotropes'''
|colspan="3"|'''Inotropes'''
|
|
|-
|-
|
|
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|If beta-blockade is thought to be contributing to hypoperfusion
|If beta-blockade is thought to be contributing to hypoperfusion
|0.1 µg/kg/min,
|0.1 µg/kg/min,
can be decreased to
can be decreased to 0.05 or increased to 0.2 µg/kg/min
0.05 or increased to
0.2 µg/kg/min
|-
|-
|'''Vasopressors'''
|colspan="3"|'''Vasopressors'''
|
|
|-
|-
|
|
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Patient presents at first aid or emergency room with signs of acute HF.
Patient presents at first aid or emergency room with signs of acute HF.


{| class="wikitable" border="0" cellpadding="0" cellspacing="0" width="600px"
{| class="wikitable" border="0" cellpadding="0" cellspacing="0" width="630px"
|-
|-
!colspan="3"|Table 7. Medication in chronic heart failure
!colspan="3"|Table 7. Medication in chronic heart failure
Line 697: Line 618:
|
|
|-
|-
|
|valign="top"|
*Furosemide
*Furosemide
|
|valign="bottom"|
Renal failure
|40 mg  
|40 mg  
80 mg – max 1000 mg
|-
|-
|
|valign="top"|
|Renal failure
|80 mg – max 1000 mg
|-
|  
*Bumetanide
*Bumetanide
|
|valign="bottom"|
Renal failure
|1 mg
|1 mg
2 mg – max 25 mg
|-
|-
|
|bgcolor="#F0F0F0" colspan="3"|'''ACE inhibitors'''
|Renal failure
|2 mg – max 25 mg
|-
|-
|'''ACE inhibitors'''
|valign="top"|
|
*Captopril
|
|
|-
|Start 6.25mg
|
 
*Captopril
1<sup>st</sup> week 6.25mg three times daily.
|Start:::6.25mg
 
3-5 weeks 12.5mg three times daily.
 
>7 weeks 25mg three times daily.
|-
|-
|valign="top"|
*Lisinopril
|
|
|
|Start 2.5-5mg
|1<sup>st</sup> week:::6.25mg three times daily.
 
1<sup>st</sup> week 2.5-5mg twice daily.
 
3-5 weeks 5-10mg twice daily.
 
>7 weeks 10-20mg twice daily.
|-
|-
|
|bgcolor="#F0F0F0 " colspan="3"|'''Beta blockers'''
|
|3-5 weeks:::12.5mg three times daily.
|-
|
|
|>7 weeks:::25mg three times daily.
|-
|-
|
|valign="top"|
*Lisinopril
|
|Start:::2.5-5mg
|-
|
|
|1<sup>st</sup> week:::5-10mg once daily.
|-
|
|
|5-7 weeks:::25mg three times daily.
|-
|
|
|>7 weeks:::50 mg three times daily.
|-
|
*Enalapril/quinalapril
|
|Start:::2.5-5mg
|-
|
|
|1<sup>st</sup> week:::2.5-5mg twice daily.
|-
|
|
|3-5 weeks:::5-10mg twice daily.
|-
|
|
|>7 weeks:::10-20mg twice daily.
|-
|'''Beta blockers'''
|
|
|-
|
*Metoprolol zoc (succinate)
*Metoprolol zoc (succinate)
|EF >30-45% and NYHA II-III
|valign="top"|EF >30-45% and NYHA II-III
|Start:::25mg
|Start 25mg
 
1<sup>st</sup> week 50mg once daily.
 
3-5 weeks 100mg once daily.
 
>7 weeks 100-200mg once daily.
|-
|-
|
|
|
|valign="top"|EF <30% and NYHA IV
|1<sup>st</sup> week:::50mg once daily.
|Start 12.5mg
 
1<sup>st</sup> week 25mg once daily.
 
3-5 weeks 50mg once daily.
 
>7 weeks 100-200mg once daily.
|-
|-
|
|valign="top"|
|
*Bisoprolol
|3-5 weeks:::100mg once daily.
|valign="top"|EF >30-45% and NYHA II-III
|Start 2.5mg
 
1<sup>st</sup> week 3.75mg once daily.
 
3-5 weeks 5mg once daily.
 
>7 weeks 7.5-10mg once daily.
|-
|-
|
|
|
|valign="top"|EF <30% and NYHA IV
|>7 weeks:::100-200mg once daily.
|Start 1.25mg
 
1<sup>st</sup> week 2.5mg once daily.
 
3-5 weeks 3.75mg once daily.
 
>7 weeks 5-7.5-10mg once daily.
|-
|-
|
|valign="top"|
|EF <30% and NYHA IV
*Carvedilol
|Start:::12.5mg
|valign="top"|EF >30-45% and NYHA II-III
|Start 6.25mg
 
1<sup>st</sup> week 6.25mg twice daily.
 
3-5 weeks 12.5mg twice daily.
 
>7 weeks 25mg twice daily.
|-
|-
|
|
|
|valign="top"|EF <30% and NYHA IV
|1<sup>st</sup> week:::25mg once daily.
|Start 3.125mg
 
1<sup>st</sup> week 3.125mg twice daily.
 
3-5 weeks 6.25mg twice daily.
 
>7 weeks 12.5-25mg twice daily.
|-
|-
|
|valign="top"|
|
*Nebivolol
|3-5 weeks:::50mg once daily.
|valign="top"|EF >30-45% and NYHA II-III
|Start 1.25mg
 
1<sup>st</sup> week 2.5mg once daily.
 
3-5 weeks 5mg once daily.
 
>7 weeks 10mg once daily.
|-
|-
|
|
|
|valign="top"|EF <30% and NYHA IV
|>7 weeks:::100-200mg once daily.
|Start 1.25mg
 
1<sup>st</sup> week 2.5mg once daily.
 
3-5 weeks 5mg once daily.
 
>7 weeks 10mg once daily.
|-
|-
|
|bgcolor="#F0F0F0 " colspan="3"|'''Aldosterone antagonist'''
*'''Bisoprolol'''
|EF >30-45% and NYHA II-III
|Start:::2.5mg
|-
|-
|valign="top"|
*Spironolactone/eplerenone
|
|
|
|Start 25mg s.i.d.
|1<sup>st</sup> week:::3.75mg once daily.
 
1<sup>st</sup> week potassium <5.0: 25mg once daily.
 
potassium 5.0-5.5: 12.5mg once daily.
 
potassium >5.5: stop
 
3rd week potassium <5.0: 25mg once daily.
 
potassium 5.0-5.5: 12.5mg once daily.
 
potassium >5.5: stop
|-
|-
|valign="top"|
*Digoxin
|
|
|
|Start 0.5mg, 0.25mg and 0,25 mg, each with 6 hours in between
|3-5 weeks:::5mg once daily.
 
Continue with 0.25mg once daily.
 
Half dose with age above 70 or creatinin above 110 or with amiodarone use
|-
|-
|
|bgcolor="#F0F0F0 " colspan="3"|'''AT II blockers'''
|
|>7 weeks:::7.5-10mg once daily.
|-
|-
|valign="top"|
*Candesartan
|
|
|EF <30% and NYHA IV
|Start 4mg
|Start:::1.25mg
 
3-5 weeks 8mg once daily.
 
>7 weeks 16mg once daily.
|-
|-
|valign="top"|
*Valsartan
|
|
|
|Start 40mg twice daily
|1<sup>st</sup> week:::2.5mg once daily.
 
3-5 weeks 80mg twice daily.
 
>7 weeks 160mg twice daily.
|-
|-
|
|colspan="3" bgcolor="#F0F0F0 "|'''Hydralazine and isosorbide dinitrate (H-ISDN)'''
|
|3-5 weeks:::3.75mg once daily.
|-
|-
|valign="top"|
*Hydralazine
|
|
|
|Start 25mg three times daily.
|>7 weeks:::5-7.5-10mg once daily.
 
3-5 weeks 50mg three times daily.
 
>7 weeks 75-100mg three times daily.
|-
|-
|valign="top"|
*ISDN
|
|
*'''Carvedilol'''
|Start 20mg twice daily
|EF >30-45% and NYHA II-III
 
|Start:::6.25mg
3-5 weeks 40mg twice daily
|-
 
|
>7 weeks 80mg twice daily
|
|1<sup>st</sup> week:::6.25mg twice daily.
|-
|
|
|3-5 weeks:::12.5mg twice daily.
|-
|
|
|>7 weeks:::25mg twice daily.
|-
|
|EF <30% and NYHA IV
|Start:::3.125mg
|-
|
|
|1<sup>st</sup> week:::3.125mg twice daily.
|-
|
|
|3-5 weeks:::6.25mg twice daily.
|-
|
|
|>7 weeks:::12.5-25mg twice daily.
|-
|
*'''Nebivolol'''
|EF >30-45% and NYHA II-III
|Start:::1.25mg
|-
|
|
|1<sup>st</sup> week:::2.5mg once daily.
|-
|
|
|3-5 weeks:::5mg once daily.
|-
|
|
|>7 weeks:::10mg once daily.
|-
|
|EF <30% and NYHA IV
|Start:::1.25mg
|-
|
|
|1<sup>st</sup> week:::2.5mg once daily.
|-
|
|
|3-5 weeks:::5mg once daily.
|-
|
|
|>7 weeks:::10mg once daily.
|-
|'''Aldosterone antagonist'''
|
|
|-
|
*'''Spironolactone/eplerenone'''
|
|Start:::25mg s.i.d.
|-
|
|
|1<sup>st</sup> week:::potassium <5.0: 25mg once daily.
|-
|
|
|potassium 5.0-5.5: 12.5mg once daily.
|-
|
|
|potassium >5.5: stop
|-
|
|
|3rd week:::potassium <5.0: 25mg once daily.
|-
|
|
|potassium 5.0-5.5: 12.5mg once daily.
|-
|
|
|potassium >5.5: stop
|-
|'''Digoxin'''
|
|Start:::0.5mg, 0.25mg and 0,25 mg, each with 6 hours in between
|-
|
|
|Continue with 0.25mg once daily.
|-
|
|
|Half dose with age above 70 or creatinin above 110 or with amiodarone use
|-
|'''AT II blockers'''
|
|
|-
|
*'''Candesartan'''
|
|Start:::4mg
|-
|
|
|3-5 weeks:::8mg once daily.
|-
|
|
|>7 weeks:::16mg once daily.
|-
|
*'''Valsartan'''
|
|Start:::80mg
|-
|
|
|3-5 weeks:::160mg once daily.
|-
|
|
|>7 weeks:::320mg once daily.
|-
|'''Hydralazine and isosorbide dinitrate (H-ISDN)'''
|
|
|-
|
*'''Hydralazine'''
|
|Start:::25mg three times daily.
|-
|
|
|3-5 weeks:::50mg three times daily.
|-
|
|
|>7 weeks:::75-100mg three times daily.
|-
|
*'''ISDN'''
|
|Start:::20mg twice daily
|-
|
|
|3-5 weeks:::40mg twice daily
|-
|
|
|>7 weeks:::80mg twice daily
|}
|}


==Management of HF beyond medication==
==Management of HF beyond medication==
[[Image:CRT_flowchart.svg|thumb|400px|Figure 8. flowchart CRT]]
[[Image:CRT_flowchart.svg|thumb|400px|'''Figure 8.''' flowchart CRT]]
[[Image:HF_prognosis_trials.svg|thumb|right|400px|Figure 9. Two-year mortality in landmark contemporary clinical heart failure trials (from Cleland et al)]]
===Device treatment===
===Device treatment===
Prevention of sudden death is an important goal in HF because approximately half of the deaths occur suddenly, and many of these are related to ventricular arrhythmias.  Implantable cardioverter-defibrillator (ICD) therapy is recommended in survivors of cardiac arrest , irrespective of EF, when life expectancy is >1 year. (Class I recommendation, level of evidence A).  
Prevention of sudden death is an important goal in HF because approximately half of the deaths occur suddenly, and many of these are related to ventricular arrhythmias.  Implantable cardioverter-defibrillator (ICD) therapy is recommended in survivors of cardiac arrest , irrespective of EF, when life expectancy is >1 year. (Class I recommendation, level of evidence A).  
Line 1,025: Line 826:
   
   
===Heart transplantation and Left Ventricular Assist Devices===
===Heart transplantation and Left Ventricular Assist Devices===
When a patient has severe and progressive HF, his or her prognosis is grim. Considering the paucity of donor hearts, the waiting list for heart transplantation may be long and early consideration of heart transplantation is part of the treatment strategy in HF. Average 2-year survival rates after cardiac transplantation are approximately 80%. A patient in NYHA class III should be evaluated with an exercise test for maximal oxygen uptake, in order to consider further steps. Indication for heart transplantation includes a VO<sub>2max</sub> < 14 ml/min/kg.<cite>17</cite> Exclusion criteria are pulmonary hypertension (risk of immediate RV donor failure), severe comorbidity, and diabetes mellitus with organ damage.  Left Ventricular Assist Devices are more commonly used as a bridge to transplantation, when the patient in on a waiting list. They have evolved from pulsatile to continuous flow pumps, with less complications and a longer durability.  Often Left Ventricular Assist Devices become destination therapy.  
When a patient has severe and progressive HF, his or her prognosis is grim. Considering the paucity of donor hearts, the waiting list for heart transplantation may be long and early consideration of heart transplantation is part of the treatment strategy in HF. Average 2-year survival rates after cardiac transplantation are approximately 80%. A patient in NYHA class III should be evaluated with an exercise test for maximal oxygen uptake, in order to consider further steps. Indication for heart transplantation includes a VO<sub>2max</sub> < 14 ml/min/kg.<cite>17</cite>  
[[Image:HF_prognosis_trials.svg|thumb|right|400px|'''Figure 9.''' Two-year mortality in landmark contemporary clinical heart failure trials (from Cleland et al)]]
Exclusion criteria are pulmonary hypertension (risk of immediate RV donor failure), severe comorbidity, and diabetes mellitus with organ damage.  Left Ventricular Assist Devices are more commonly used as a bridge to transplantation, when the patient in on a waiting list. They have evolved from pulsatile to continuous flow pumps, with less complications and a longer durability.  Often Left Ventricular Assist Devices become destination therapy.  


===Management of HF patients with preserved LVEF (HFPEF)===
===Management of HF patients with preserved LVEF (HFPEF)===
Line 1,031: Line 834:


===Prognosis===
===Prognosis===
The life expectancy of a patient with heart failure is determined by age, NYHA class, LVEF, normal level of sodium, systolic blood pressure, use of medication and use of ICD or CRT-D (Seattle Heart failure score). The mean yearly annual mortality is approximately 10%, varying from <6% per year when a normal LVEF is identified, to > 14% per year with an EF of < 15%.  
The life expectancy of a patient with heart failure is determined by age, NYHA class, LVEF, normal level of sodium, systolic blood pressure, use of medication and use of ICD or CRT-D ([http://depts.washington.edu/shfm/app.php Seattle Heart failure score]). The mean yearly annual mortality is approximately 10%, varying from <6% per year when a normal LVEF is identified, to > 14% per year with an EF of <15%.  
Trials with medication illustrate that the (short term) benefit of medication is highest when the NYHA class is higher (Figure 9).<cite>11</cite>
Trials with medication illustrate that the (short term) benefit of medication is highest when the NYHA class is higher (Figure 9).<cite>11</cite>
 
==References==
==References==
<biblio>
<biblio>
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