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ACS syndromes

Unstable angina



Fissuring of an atheromatous plaque causes:

haemorrhage into plague-->swelling and restriction of the lumen of the artery

Contraction of the smooth muscle of the artery wall-further constricts

thrombus formation-->possible embolus

The underlying problem in acute coronary syndromes is coronary artery disease in which plaques filled with cholesterol build up in the lining of these arteries.

Acute coronary syndromes are caused by rupture of the inner surface of one of these plaques.

Blood then enters the plaque causing it to swell and protrude into the artery. Smooth muscle in the wall of the artery may constrict, causing further narrowing of the artery and further restriction of the blood supply to the heart muscle that it supplies. Finally, the chemical effect of the injury to the wall of the blood vessel stimulates thrombus formation and if this develops into a large clot, it may cause further narrowing of the artery or may block it completely.


Unstable Angina

1) Pain on exertion over a few days with increasing frequency and less and less exertion (crescendo angina)

2) Angina occurring recurrently and unpredictably without provocation by exercise. Often relieved spontaneously or GTN and then recur again

3) Pain without definitive ECG changes or lab evidence

In all of these situations, the ECG may be normal. However if the ECG shows ST segment depression, this suggests a high risk of progression to myocardial infarction and an increased risk of death.

In unstable angina there is no damage to the heart muscle, so blood tests will not detect any troponin release.


ECG changes in unstable Angina

T wave abnormalities

cardiac enzymes are usually normal

ST depression:
Likely low benefit from fibrinolysis
high risk of further coronary events, need immediate therapy (LMWH, aspirin, clopidogrel) prompt PCI or bypass surgery



Angina pain

ST segment depression or T wave inversion or normal ECG

Raised trop



Angina pain

ST elevation


usually due to complete occlusion of the coronary artery. Further damage is revealed by Q waves.

Treatment: emergency PCI or fibrinolytic therapy


Checking for aortic dissection

- Loss of pulse or pulse asymmetry in upper limbs
- Acute aortic regurgitation
- Signs of stroke from carotid artery
- marked hypotension without major ECG changes


RV infarction

Inferior or posterior STEMI with elevated JVP but no sign of pulmonary oedema

Kussmaul sign-elevated JVP on inspiration.


Anterior or anteroseptal infarction

Usually leads V1-4
Almost always due to Left Anterior Descending artery

Involvement V5-6 I and aVL indicates anterolateral infarct

Anterior MI has a worse prognosis, patients need repercussion therapy and early treatment with an ACEi


Inferior infarcts

II, III and aVF usually due to right coronary artery or less commonly circumflex artery


lateral infarction

V5-6 and/or i and aVL or aVL alone

Circumflex artery or diagonal branch of LAD artery


posterior MI

Reciprocal change in anterior chest leads

ST depression in ant chest leads reflects posteror ST elevation and development of dominant R waves reflects posterior Q wave development.

Posterior chest leads to confirm (V9 at left of spine, V8 halfway V7 and V9, V10 to right of the spine) V7 is at post axillary line.


Cardiac troponins other conditions raised e.g.

Aortic dissection

CK MB and echo can also be helpful


Immediate treatment

- Aspirin 300mg
- GTN unless patient is hypotensive or extensive RV infarction
- Oxygen 94-98% or 88-92%
- IV morphine/diamorphine


If STEMI treatment

Mechanical or pharmacological reperfusion is necessary

PCI or fibrinolytic therapy <12hrs


PCI indications

- ST eleation in 2 adjacent leads
- Dominant R waves and ST depression in V1-3 post infarction
- New onset LBBB

GLP IIb/IIIa inhib often injected

Call to balloon time 120mins

Aspirin and
-Clopidogrel 600mg loading dose
-prasugrel 60mg loading dose (not >75yrs, <60kg or history of bleeding)


Contraindications to fibrinolytic therapy

Prev haemorrhagic stroke
Ischaemic stroke in 6months
CNS tumour/damage
Recent surgery (<3weeks)
Active bleeding exc menses or GI bleeding
Known aortic dissection
known bleeding disorder


Contraindications to fibrinolytic therapy

Refractory hypertension (>180mmHg systolic)
TIA prev 6 months
Oral anticoag therapy
Preg or 1 week post partum
Active peptic ulcer
Advanced liver disease
infective endocarditis
prev reaction to fibrinolytics



Aspirin 300mg
Clopidogrel 600mg
Antithrombin therapy LMWH


Rescue angioplasty

20-30% undergoing fibrinolytic therapy reperfusion is not achieved

ECG 60-90mins post therapy

ST elevation to not reduce by 50%

Transfer to cath lab for PCI


Preventing further episode: Preventing thrombus

LMWH therapeutic doses

Aspirin 75mg/day post loading dose
clopidogrel 300mg (600mg before urgent angiography) then 75mg/day

Diabetic patients prasugrel

High risk patients glp2b3a if early PCI planned.


Preventing further episode: Reducing O2 demand

Start beta adrenoceptor blockade

If contra give diltiazem

Avoid dihydropyridine Ca blockers e.g. nifedipine

IV/buccal nitrate if angina persists

Early intro of ACEi


Must see

page 30


Subsequent management of patients ACS: Unstable angina-low risk

Exercise testing or non-invasive imaging


Subsequent management of patients ACS: High risk unstable angina and NSTEMI

High risk features

Invasive coronary angiography within 72hrs

May need PCI or CABG


Subsequent management of patients ACS: STEMI

Post fibrinolytic therapy PCI can stabilise stenosis or unstable plaque. Coronary angiography and if needed PCI undertaken.



After recovery low risk



higher risk of

Myocardial ischaemia therefore revascularization

No ischaemia risk of recurrent arrythmias need ICD


Other complications of ACS

Heart failure
(Loop diuretic, GTN, ACEi/ARB) if <40% ejection fraction consider aldosterone antagonist

Cardiogenic shock
Hypotension with poor peripheral perfusion often accompanied by pulmonary oedema, drowsiness or mental confusion. Early PCI, inotropic therapy e.g. dobutamine and possibly intra aortic balloon pumping


Secondary prevention

All patients: Aspirin 75mg for life
PLUS Clopidogrel 75mg or prasugrel 10mg in high risk patients and all undergoing PCI

Intolerant to aspirin clopidogrel alone.

If AF develops consider warfarin in addition or replacement for the above.

Consider all patients for ACEi post AMI

Beta blockade: Can prevent arrhythmias

Reduce cholesterol via statins

Avoid smoking



Unstable angina which is an acute coronary syndrome can present in one of three ways.

Firstly, the angina may still be provoked by exercise, but occurs with increasing frequency over a matter of hours or days and tends to be provoked by progressively less exertion as it progresses. This is sometimes referred to as crescendo angina.

Secondly, unstable angina can present with angina that occurs recurrently at rest but usually resolves after a few minutes on each occasion.

Thirdly, unstable angina can present as a single episode of prolonged chest pain (usually raising suspicion of myocardial infarction).

In all of these situations, the ECG may be normal. However if the ECG shows ST segment depression, this suggests a high risk of progression to myocardial infarction and an increased risk of death.

In unstable angina there is no damage to the heart muscle, so blood tests will not detect any troponin release.


Unstable angina and ACS

Although unstable angina is part of the spectrum of acute coronary syndromes, it is not myocardial infarction as there is no evidence of myocardial necrosis. Non-ST-elevation and ST-elevation MIs are acute coronary syndromes, presenting typically with chest pain and evidence of troponin release on blood testing. Troponin release indicates that there has been some myocardial cell death and is used to differentiate unstable angina from non-ST-elevation and ST-elevation myocardial infarctions. The differentiation between non-ST-elevation MI and ST-elevation MI is based on the ECG findings.



non-ST-elevation myocardial infarction typically presents with prolonged angina-like chest, throat or arm pain which may be associated with feeling clammy and nauseous. The pain usually lasts for 20 minutes or longer. Often there will be associated ECG changes such as ST depression or T wave inversion, but occasionally the ECG may be normal, at least in the early stages. However, there will be troponin release.

The diagnosis of non-ST-elevation infarction is made not purely from the ECG but from a typical history coupled with troponin release. The pattern of ECG abnormality simply serves to highlight that the patient is at risk and that they require prompt and effective treatment.



When an acute myocardial infarct is accompanied by ST segment elevation, this usually implies complete occlusion of the affected coronary artery. It is important to differentiate between non-ST-elevation MIs and ST-elevation MIs because the treatment options are different.

Both types of myocardial infarct usually present with typical symptoms as discussed and both are accompanied by troponin release. The difference with ST-elevation MIs is seen in the ECG. Acute elevation of the ST segments in the leads overlying the area of infarction is usually present at an early stage. This is likely to be followed by the development of pathological Q waves (representing myocardial death) within these leads.

Patients with an acute coronary syndrome presenting with new LBBB on their ECG fall into the same category as patients with ST-elevation myocardial infarction and should be treated similarly.

Recognition of ST-elevation MI and early effective treatment of it may limit the amount of myocardial damage and, by so doing, prevent the development of Q waves in the ECG and reduce the risk of complications including heart failure and death.


All patients who we suspect of having an acute coronary syndrome:

A loading dose of aspirin should be given to start to protect against new thrombus formation also, we should give sublingual GTN, in either spray or tablet form
we should consider giving oxygen unless there is a clear contra-indication and once it is started, the concentration should be adjusted on the basis of oxygen saturation
and, of course, it is important to provide effective pain relief using morphine or diamorphine


In most patients with unstable angina or a non-ST-elevation MI, the coronary artery that has caused the problem has not yet blocked. Therefore, we need to give drug treatment to prevent further thrombus formation that might block the artery.

In addition to aspirin we give clopidogrel or prasugrel tablets and we give injections of low molecular weight heparin or fondaparinux unless there are clear contra-indications such as active bleeding.

In very high risk patients we may also give a glycoprotein IIb/IIIa inhibitor (via an infusion) whilst preparing the patient for very urgent coronary angiography with a view to probable stent insertion.

As with all patients with acute coronary syndromes, it is important to relieve pain using nitrates which may be given sublingually or can be given over a longer period as an infusion. In addition the use of morphine or diamorphine is appropriate in any patient whose pain does not respond promptly to sublingual nitrate. Oxygen is given as we have already described.

In addition, in the absence of any contra-indication we should consider trying to provide myocardial protection by starting a beta blocking drug.



Coronary angiography with a view to possible percutaneous coronary intervention should be considered in all these patients during the same hospital admission. There will be a few in whom the potential benefit from invasive assessment and treatment is unlikely to outweigh the risk, but for most patients coronary angiography will be appropriate. However, this does not have to be done as an emergency unless the patient is exhibiting on-going high-risk behaviour.

In complete contrast is the patient with an ST-elevation myocardial infarction or new left bundle branch block due to acute myocardial infarction. The majority of patients who present with this condition have an occluded coronary artery and unless it is re-opened, achieving reperfusion of the heart muscle that it supplied, further muscle damage will occur. This puts the patient at an increased risk of cardiac arrest and death.


STEMI treatment

After initial assessment using the ABCDE approach and after administration of appropriate medical treatment (including aspirin, other anti-thrombotic agents, nitrate, oxygen and analgesia as required) the priority is to re-open the coronary artery that has caused and is continuing to cause myocardial damage.

The most reliable way of re-opening an occluded coronary artery in this situation is by percutaneous coronary intervention so this is currently the recommended approach in the majority of these patients.

When PCI is not available on an emergency basis in the locality, an alternative approach would be to use fibrinolytic therapy which will re-open the artery in a proportion of patients and then to transport the patient to a hospital where PCI can be performed later if necessary.

The important thing is to re-open the artery as quickly as possible. The greater the delay, the more myocardium will be damaged irreversibly.


PCI is the most reliable way of re-opening an occluded coronary artery

Another advantage of primary PCI over fibrinolytic therapy is that it is associated with a lower risk of major bleeding, and this list shows the absolute contra-indications to fibrinolytic therapy because of the risk of bleeding. If people with these problems present with an ST-elevation myocardial infarction, they will need careful assessment on an individual basis in order to plan their treatment and consider whether or not it is appropriate to transfer them immediately for primary PCI.


PCI VS drug treatments

For patients who have been treated for ST-elevation myocardial infarction we need to consider what on-going treatment they should receive to minimise future risk.

Having re-opened a blocked coronary artery, it is important to maintain anti-thrombotic therapy to keep it open.

There is good evidence that in the absence of any clear contra-indication such as asthma the use of a beta blocking drug will help to reduce the risk of further myocardial infarction and of death. In addition, the use of an ACE inhibitor will help to protect against deterioration in left ventricular function that in turn may place the patient at risk of heart failure and of sudden death.

We have already mentioned that for those patients who have not already undergone coronary angiography and primary PCI, an angiogram and the need for reperfusion would be appropriate in the majority of patients whose initial treatment was with fibrinolytic therapy.



We have considered the immediate treatments that (unless contra-indicated) should be given to all patients with acute coronary syndromes. In addition, for patients with ST-segment-elevation myocardial infarction we have emphasised the importance of re-opening the blocked coronary artery at the earliest possible moment as safely and effectively as possible. For most people this will mean primary percutaneous coronary intervention.

Finally, whilst many patients with acute coronary syndromes will undergo coronary angiography as part of their assessment at some stage, we have recognised that some high-risk features can be identified, such as persistent or recurrent pain and certain ECG features that will help to identify some patients who are at higher risk and who should therefore be considered for coronary angiography sooner rather than later.