You are on page 1of 26

Acute Coronary

Syndromes
dr. Murthado Sani Sp.Jp (K), FIHA
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
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.





Etiology
Key stages in the development of ACS

[1] Ischaemic cascade
[2] Plaque formation and rupture
[3] Coronary occlusion and MI
[4] Ventricular remodelling
[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

[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.
Plaque Rupture
Plaque Rupture & Thrombus
Formation
Plaque
Plaque
Rupture &
Thrombus
Formation
[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.
[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.
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.
Investigate ACS case
[1] Immediate assessment [ECG].

[2] Admission tests
Cardiac markers.
Chest x-ray.

[3] Urgent coronary angiography (if indicated and
available).
[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.

[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.

Cardiac Markers
[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.






[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
Coronary Angiography
Diagnostic Coronary Angiography with proceeding
Stent implantation into the proximal RCA
(Primary Angioplasty)
Occluded
Proximal
RCA
Stent implantation
& patent RCA
Diagnosis of STEMI
ECG ST segment elevation
New onset LBBB

Cardiac markers Troponin I
CK



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
blockers
Insulin/glucose regimen if plasma glucose 11 mmol/L
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.
Thrombolytic Agents
Available Thrombolytic Agents

[1] Streptokinase

[2] tissue Plasminogen Activator (tPA)
Reteplase
Tenecteplase
Alteplase





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).

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
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)