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ALL / CARDIOLOGY
ACE inhibitors
Angiotensin-converting enzyme (ACE) inhibitors are now the established first-line treatment in
younger patients with hypertension and are also extensively used to treat heart failure. They are
known to be less effective in treating hypertensive Afro-Caribbean patients. ACE inhibitors are
also used to treat diabetic nephropathy and have a role in the secondary prevention of ischaemic
heart disease.
Mechanism of action:
inhibits the conversion angiotensin I to angiotensin II
→ decrease in angiotensin II levels → to vasodilation and reduced blood pressure
→ decrease in angiotensin II levels → reduced stimulation for aldosterone release →
decrease in sodium and water retention by the kidneys
renoprotective mechanism
angiotensin II constricts the efferent glomerular arterioles
ACE inhibitors therefore lead to dilation of the efferent arterioles → reduced glomerular
capillary pressure → decreased mechanical stress on the delicate filtration barriers of the
glomeruli
this is particularly important in diabetic nephropathy
ACE inhibitors are activated by phase 1 metabolism in the liver
Side-effects:
cough
occurs in around 15% of patients and may occur up to a year after starting treatment
thought to be due to increased bradykinin levels
angioedema: may occur up to a year after starting treatment
hyperkalaemia
first-dose hypotension: more common in patients taking diuretics
Cautions and contraindications
pregnancy and breastfeeding - avoid
renovascular disease - may result in renal impairment
aortic stenosis - may result in hypotension
hereditary of idiopathic angioedema
specialist advice should be sought before starting ACE inhibitors in patients with a potassium
>= 5.0 mmol/L
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patients receiving high-dose diuretic therapy (more than 80 mg of furosemide a day)
significantly increases the risk of hypotension
Monitoring
urea and electrolytes should be checked before treatment is initiated and after increasing the
dose
a rise in the creatinine and potassium may be expected after starting ACE inhibitors
acceptable changes are an increase in serum creatinine, up to 30% from baseline and an
increase in potassium up to 5.5 mmol/l.
significant renal impairment may occur in patients who have undiagnosed bilateral renal
artery stenosis
Examples of common ACE inhibitors
ramipril
enalapril
lisinopril
Flow chart showing the management of hypertension as per
current NICE guideliness
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LINKS
NICE 64 41
2014 Chronic kidney disease guidelines
BNF 62 39
ACE inhibitors
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ACE inhibitors: side-effects
Side-effects:
cough: occurs in around 15% of patients and may occur up to a year after starting treatment.
Thought to be due to increased bradykinin levels
angioedema: may occur up to a year after starting treatment
hyperkalaemia
first-dose hypotension: more common in patients taking diuretics
Cautions and contraindications
pregnancy and breastfeeding - avoid
renovascular disease - significant renal impairment may occur in patients who have
undiagnosed bilateral renal artery stenosis
aortic stenosis - may result in hypotension
patients receiving high-dose diuretic therapy (more than 80 mg of furosemide a day) -
significantly increases the risk of hypotension
hereditary or idiopathic angioedema
Monitoring
urea and electrolytes should be checked before treatment is initiated and after increasing the
dose
a rise in the creatinine and potassium may be expected after starting ACE inhibitors.
Acceptable changes are an increase in serum creatinine, up to 30%* from baseline and an
increase in potassium up to 5.5 mmol/l*.
*Renal Association UK quote 50% which seems rather high. SIGN advise that the fall in eGFR
should be less than 20%. The NICE CKD guidelines suggest that a decrease in eGFR of up to 25%
or a rise in creatinine of up to 30% is acceptable
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Acute coronary syndrome: a very basic introduction
Acute coronary syndrome (ACS) is an umbrella term covering a number of acute presentations of
ischaemic heart disease.
It covers a number of presentations, including
ST elevation myocardial infarction (STEMI)
non-ST elevation myocardial infarction (NSTEMI)
unstable angina
considered to be present in patients with ischaemic symptoms suggestive of an ACS and
no elevation in troponins, with or without electrocardiogram changes indicative of
ischaemia
however, as a rise in troponins may take some hours it may be indistinguishable for
NSTEMI initially and is therefore treated the same until the troponin result is known
Before we go into more detail into these presentations it's useful to take a step back and consider
how such conditions develop.
ACS generally develops in patients who have ischaemic heart disease, either known or previously
undetected. Ischaemic heart disease is a term synonymous with coronary heart disease and
coronary artery disease. It describes the gradually build up of fatty plaques within the walls of the
coronary arteries. This leads to two main problems:
1. Gradual narrowing, resulting in less blood and therefore oxygen reaching the myocardium
at times of increased demand. This results in angina, i.e. chest pain due to insufficient oxygen
reaching the myocardium during exertion
2. The risk of sudden plaque rupture. The fatty plaques which have built up in the
endothelium may rupture leading to sudden occlusion of the artery. This can result in no
blood/oxygen reaching the area of myocardium.
Remember that there are a large number of factors which can increase the chance of a patient
developing ischaemic heart disease:
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