2. Introduction
The term of ACS has been developed to describe
the collection of ischaemic conditions which occur
through Coronary Plaque Rupture
ACS includes:
[1] STEMI
[2] NSTEMI & Unstable angina
3. NSTEMI & Unstable Angina
UA/NSTEMI defines a syndrome in which the symptoms of CAD and
ISHD increase in frequency, occur with less physical activity (later at
rest), last longer or become more severe.
Clinically, it is difficult to distinguish between UA and NSTEMI
based on symptoms alone. The differentiating feature is that patients
with NSTEMI have abnormal blood enzymes (Troponin) proving
that a heart attack has occurred. For many patients, it takes 6-12 hours
to complete a series of blood enzyme tests to make this determination.
It is not necessary for an artery to be severely blocked in order for
unstable angina to occur.
4. Aetiology
Key stages in the development of ACS
[1] Ischaemic cascade
[2] Plaque formation and rupture
[3] Coronary occlusion and MI
[4] Ventricular remodelling
5. [1] Ischaemic Cascade
A cascade of ischaemic events is triggered as shown in
the diagram
Perfusion Deficit Diastolic Dysfunction
Systolic Dysfunction TIME
ECG Changes
MI Unstable Angina
6. [2] Plaque Formation and Rupture
Plaques composed of fibrous and fatty tissues formed
within the arterial wall.
The atheromatous plaques usually grow slowly as they
have a Fibrous Cap on their luminal surface.
Sometimes, the cap is breached and the softer plaque
tissues become exposed to the thrombotic factors in the
blood.
The plaque suddenly increase in size, causing a critical
reduction in myocardial blood flow.
9. [3] Coronary Artery Occlusion and MI
Sudden Plaque Rupture and thrombus
formation to the extent where the coronary
artery becomes totally occluded causing MI.
If blood flow is not restored rapidly (within 6
hr.), the muscle dies and becomes scar tissue.
10. [4] Ventricular Remodelling
Once an area of the heart becomes scar tissue, the
myocardium becomes this, fibrosed and functionless
The remaining healthy myocardium hypertrophies and
becomes hyperdynamic in function in an attempt to
compensate for the dead area.
This increased activity ultimately leads to worsening
cardiac function and development of a dilated poorly
functioning ventricle.
11. Clinical Features
Central chest pain
Dyspnoea
Nausea/vomiting
Sweating
Beware of Atypical Presentation without classic
chest pain (pulmonary oedema, acute confusion)
in diabetics and elderly patients.
13. [1] Immediate Assessment (ECG)
12-lead ECG is the most urgent investigation in a
patient with a suspected ACS.
ECG changes and in particular ST elevation or
new onset LBBB mandates immediate action.
14. [2] Admission Tests
1- Cardiac Markers
Cardiac markers are measured at an appropriate time interval.
Commonly measured markers of myocardial damage include:
Troponin I
Creatine kinase (CK)
Lactate dehydrogenase (LDH)
Aspartate transaminase (AST)
Cardiac markers are of no value in making a decision regarding
thrombolysis, as even the earliest markers may be undetectable for the
first 6-12 hours after the infarction.
16. [2] Admission Tests
2- Chest x-ray
Chest x-ray is often normal in patients with ACS.
However it may show evidence of:
• Aortic Dissection
• Cardiomegaly
• Pulmonary oedema
In case of STEMI, thrombolysis should not be
delayed while awaiting a CXR unless an Aortic
Dissection is suspected.
17. [3] Urgent Coronary Angiography
Cardiac catheterisation allows invasive assessment
of:
• Coronary arteries. • Left ventricle.
• Cardiac output. • Oxygen saturations.
• Aorta. • Bypass grafts.
• Intracardiac pressures.
With coronary angiography there is a possibility
to proceed into Primary Angioplasty
18. Coronary Angiography
Diagnostic Coronary Angiography with proceeding
Stent implantation into the proximal RCA
(Primary Angioplasty)
Occluded
Proximal
RCA
Stent implantation
& patent RCA
19. Diagnosis of STEMI
ECG … ST segment elevation
New onset LBBB
Cardiac markers … Troponin I ↑
CK ↑
21. Thrombolysis
The decision to consider thrombolysis depends upon:
• A Good Clinical History for MI with an onset
within the last 12 hours.
• ECG that shows evidence of acute STEMI or
new onset LBBB.
Where thrombolysis is indicated, aim to initiate treatment
within 20 min of presentation to hospital.
23. Tissue Plasminogen Activator (tPA)
Indications for tPA Administration
(1) Streptokinase allergy
(2) Previous streptokinase treatment (5 days to 2 years)
(3) Hypotension
(4) Large anterior wall damage.
(5) New thrombus after streptokinase therapy (in 10 to 15%
of patients, usually within a few hours to days after
thrombolysis).
24. Contraindications to Thrombolysis
Recent stroke (2 months)
Previous haemorrhagic stroke (ever)
Recent head trauma (4 weeks)
Recent surgery – including dental extraction (2 weeks)
Lumbar puncture (within 4 weeks)
Active peptic ulceration or other GI blood loss
Concurrent anticoagulation (unless INR <2.0)
Cont…
25. Contraindications to Thrombolysis (Cont.)
Severe liver disease or clotting disorder
Pregnancy or <18 weeks postnatal
Acute pancreatitis
Aortic dissection
Active pulmonary disease with cavitation
Oesophageal varices
Cerebral neoplasm
Uncontrolled hypertension (BP >200/120)
26. Primary Angioplasty
According to the Current Guidelines, primary angioplasty is considered
for high risk patients with:
(1) Extensive infarction + contraindication to thrombolysis.
(2) Extensive anterior infarction.
(3) Inferior infarction with significant right ventricular involvement.
(4) Acute heart failure.
(5) Cardiogenic shock.
The results of angioplasty carried out after pharmacological reperfusion
therapy are not as good as those of a primary angioplasty.
After implantation of a stent, the Antithrombotic agent to be used is
Aspirin, which should be combined with Clopidogrel for 3 to 6 months to
prevent thrombosis and restenosis.
28. Subsequent Management of STEMI
Continue aspirin + β blockers.
Initiate statin (where indicated).
Initiate ACE inhibitors.
Subcutaneous insulin if diabetic.
Will need Echocardiogram and Treadmill test
before or shortly after discharge.
Cardiac rehabilitation programme.
29. Diagnosis of
NSTEMI / Unstable angina
ECG … ischaemic changes or normal.
Cardiac markers:
NSTEMI … Troponin I ↑
Unstable angina … all normal.
30. Management of
NSTEMI/Unstable Angina
on Admission
IV access
Oxygen
Aspirin 300 mg (and 75 mg daily thereafter)
Pain relief (opiate)
Sublingual GTN
LMW heparin
β blockers
Glycoprotein IIb/IIIa inhibitor if high risk
31. Subsequent Management of
NSTEMI/Unstable Angina
Continue aspirin + β blockers.
Initiate statin (where indicated).
Initiate ACE inhibitors (where indicated).
If high risk, may need inpatient Coronary
Angiography
32. ACS In Brief
Acute Coronary Syndrome
Chest Pain Chest Pain
ST depression / T inversion ST elevation / new onset LBBB
Troponin – ve Troponin +ve Troponin +ve
Unstable Angina NSTEMI STEMI
LMW heparin ± glycoprotein IIb/IIIa inhibitor Thrombolysis
Primary PCI
34. Late Complications of ACS
[1] Dressler’s syndrome:
• Pericarditis several weeks after MI (can occur as
late as 1 year after MI, it is immune mediated).
• Characterized clinically by pericardial chest pain +
fever + pericardial effusion.
[2] Lt. Ventricular aneurysm.
[3] Heart failure.
35. Cardiac Rehabilitation & Follow-up
It is an important process for patients with any
cardiac disease.
It consists of:
(1) Patient education.
(2) Risk factor assessment.
(3) Advice on lifestyle changes.
(4) Forum for meeting similar patients.
(5) Structured exercise programme.
(6) Long term care and follow-up.
36. Prevention
Primary: in those individuals who may have risk
factors for vascular disease but have not yet
developed clinical evidence of vascular disease.
Secondary: in those who have developed clinical
evidence of vascular disease
• CVD (angina, MI)
• CVA (stroke, TIA)
• PVD.
![Introduction
The term of ACS has been developed to describe
the collection of ischaemic conditions which occur
through Coronary Plaque Rupture
ACS includes:
[1] STEMI
[2] NSTEMI & Unstable angina](data:image/gif;base64,R0lGODlhAQABAIAAAAAAAP///yH5BAEAAAAALAAAAAABAAEAAAIBRAA7)