Acute coronary syndromes

1. Acute Coronary
Syndromes

Dr. Rafik Dr. Rafik
AnisAnis

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.

7. Plaque Rupture

8. Plaque Rupture & Thrombus
Formation
Plaque
Plaque
Rupture &
Thrombus
Formation

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.

12. Investigate ACS case
[1] Immediate assessment [ECG].
[2] Admission tests
• Cardiac markers.
• Chest x-ray.
[3] Urgent coronary angiography (if indicated and
available).

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.

15. Cardiac Markers

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 ­

20. Management of STEMI On
Admission
IV access
Oxygen
Aspirin 300 mg (and 75 mg daily thereafter)
Pain relief (opiate)
Sublingual GTN
Urgent Thrombolysis (unless contraindicated)
Primary Angioplasty
b blockers
Insulin/glucose regimen if plasma glucose >11 mmol/L

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.

22. Thrombolytic Agents
Available Thrombolytic Agents
[1] Streptokinase
[2] tissue Plasminogen Activator (tPA)
• Reteplase
• Tenecteplase
• Alteplase

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.

27. Primary Angioplasty
Severe Proximal
LAD stenosis
Stent Implantation
& restored LAD flow

28. Subsequent Management of STEMI
Continue aspirin + b 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
b blockers
Glycoprotein IIb/IIIa inhibitor if high risk

31. Subsequent Management of
NSTEMI/Unstable Angina
Continue aspirin + b 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

33. Early Complications of ACS
(first week)
Failed thrombolysis
Post-infarct angina
Rt. Ventricular infarction
Lt. Ventricular failure
Cardiogenic shock & Arrhythmia
Acute mitral regurgitation & VSD
Haemorrhage (treatment related)
Cardiac tamponade

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.

37. Thank Thank
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