Heart Failure: Difference between revisions

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=== Pharmacological treatment ===
=== Pharmacological treatment ===
The treatment algorithm as proposed in the ESC guidelines 2008 are depicted in figure 2. Patients for whom the medication is indicated,  mode of action, contraindications of the medication, and possible side effects included in this algorithm are discussed below.
[[File:Treatment_algorithm_as_proposed_in_the_ESC_guidelines_2008.png|thumb|right|Treatment algorithm as proposed in the ESC guidelines 2008]]
The treatment algorithm as proposed in the ESC guidelines 2008 are depicted in Figure 2. Patients for whom the medication is indicated,  mode of action, contraindications of the medication, and possible side effects included in this algorithm are discussed below.


Angiotensin-converting enzyme (ACE) inhibitors  
Angiotensin-converting enzyme (ACE) inhibitors  
ACE inhibitors are indicated for every HF patient with an EF ≤ 40 %, irrespective of symptoms. (Class I recommendation, level of evidence A) Contraindications for the use of ACE inhibitors are:
ACE inhibitors are indicated for every HF patient with an EF ≤ 40 %, irrespective of symptoms. (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
Serum potassium concentration > 5.0 mmol/L
* Serum potassium concentration > 5.0 mmol/L
Serum creatine > 220 µmol/L
* Serum creatine > 220 µmol/L
Severe aortic stenosis
* Severe aortic stenosis
ACE inhibitors relieve the heart by decreasing the preload and afterload. This is achieved through two mechanisms. Firstly, conversion of angiotensin-I to angiotensin– II is inhibited, which reduces vasoconstriction and lowers BP. Secondly, production of aldosterone is decreased, as angiotensin II induces this production. Aldosterone increases blood volume and thus BP by stimulating sodium- and water retention.  
ACE inhibitors relieve the heart by decreasing the preload and afterload. This is achieved through two mechanisms. Firstly, conversion of angiotensin-I to angiotensin– II is inhibited, which reduces vasoconstriction and lowers BP. Secondly, production of aldosterone is decreased, as angiotensin II induces this production. Aldosterone increases blood volume and thus BP by stimulating sodium- and water retention.  
Possible side effects are symptomatic hypotension (dizziness), hyperkalaemia, worsening renal function and cough.   
Possible side effects are symptomatic hypotension (dizziness), hyperkalaemia, worsening renal function and cough.   
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==== Angiotensin receptor blockers (ARBs) ====
==== Angiotensin receptor blockers (ARBs) ====
In HF patients with a LVEF≤40% who remain symptomatic despite optimal ACEI en β-blocker treatment, use of ARBs is recommended. (Class I recommendation, level of evidence A). Contraindications are:
In HF patients with a LVEF≤40% who remain symptomatic despite optimal ACEI en β-blocker treatment, use of ARBs is recommended. (Class I recommendation, level of evidence A). Contraindications are:
Combination of an ACE inhibitor and an aldosterone antagonist
* Combination of an ACE inhibitor and an aldosterone antagonist
Bilateral renal artery stenosis
* Bilateral renal artery stenosis
Serum potassium concentration > 5.0 mmol/L
* Serum potassium concentration > 5.0 mmol/L
Serum creatine > 220 µmol/L
* Serum creatine > 220 µmol/L
Severe aortic stenosis
* Severe aortic stenosis
Possible side effects include symptomatic hypotension (dizziness), hyperkalaemia, and a worsening renal function.
Possible side effects include symptomatic hypotension (dizziness), hyperkalaemia, and a worsening renal function.


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