Slides on ACS Malaysia guidelines Hospital CME

1. ACUTE CORONARY SYNDROME
By : Dr Nawal Adibah Yahsah
Supervisor : Dr Vivian

2. INTRODUCTION
• Acute coronary syndrome is an important
cause of death in Malaysia
• 20-25% of death in public hospital
• TIME LOST IS MYOCARDIUM LOST

3. DEFINITION
• A set of signs and symptoms due to decreased
blood flow in the coronary arteries such that
part of the heart muscle unable to function
properly or dies
• Myocardial infarction is classified under this
syndrome which defined as myocardial cell
death due to prolonged ischemia

4. PRESENTATION
ECG
ACUTE CORONARY SYNDROME
STEMI
CARDIAC
BIOMARKERS
ELEVATED
NORMAL ELEVATED
NO ST ELEVATION
ISCHEMIC CHEST DISCOMFORT
ST ELEVATION
PROVISIONAL
DIAGNOSIS
UNSTABLE
ANGINA
NSTEMI
FINAL DIAGNOSIS
MI

5. TYPES OF MI

6. CLINICAL PRESENTATION

7. HISTORY AND EXAMINATION
• Risk factors and co morbidities

8. • Examination findings
- Left ventricular failure signs (hypotension,
respiratory crackles, S3 gallop)
- Arrhythmias
- Presence of carotid bruit and signs of
peripheral vascular disease indicate extensive
artherosclerosis and likelihood of concomitant
CAD

9. INVESTIGATIONS
• ECG
• Cardiac biomarkers
• Echocardiogram

10. ECG

11. ECG IN STEMI

12. DIAGNOSIS :
-Ischemic type chest pain >30 minutes accompanied by
-rise and fall in cardiac biomarkers with
-ST elevation >1mm in 2 contiguous lead or
-new onset of LBBB in resting ECG

14. ECG CHANGES IN STEMI (COURSE)

15. • The cut-off points for new or presumed new ST segment
elevation (in the absence of LVH and LBBB) is
-Presence of ≥ 0.1 mV ST segment elevation in all leads except leads V2-
V3
-In leads V2-V3, a cut-off point of ≥ 0.25 mV (in males < 40 years), ≥ 0.2
mV (in males ≥ 40 years) and ≥ 0.15 mV in females is used
• In the early stages of MI, the initial ECG may be normal,
equivocal or show hyperacute T-wave changes only.
-In these patients if the index of suspicion of STEMI is high, the ECG
should be repeated at close intervals of at least 15 minutes to look
for progressive ST changes.

16. ECG IN NSTEMI/UA

17. DIAGNOSIS :
• Ischemic type chest pain >30 minutes accompanied by
• rise cardiac biomarkers in NSTEMI and normal cardiac biomarkers in
UA
• ST depression > 0.5 mm in 2 or more contiguous leads
• T-wave inversion –deep symmetrical T-wave inversion
• Other ECG changes include new or presumed new onset bundle
branch block (aside from LBBB) and cardiac arrhythmias, especially

19. CARDIAC BIOMARKERS
• HISTORY and ECG is of paramount importance in
making the diagnosis of STEMI and determining
the reperfusion strategy.
• •One should NOT wait for the results of
biomarkers prior to initiating reperfusion therapy
• •Available cardiac biomarkers include
• •Cardiac troponin T and troponin I
• •Creatine Kinase-Myocardial Band (CK-MB)
• •Creatine Kinase

21. • In patients with clinical features and ECG diagnostic of
STEMI, the preferred cardiac biomarker is CK-MB. In this
situation, troponins are not necessary since there is already
ECG evidence of myocardial injury
• If the clinical features and ECG are suspicious but non-
diagnostic of MI, then the preferred biomarkers are
troponins -cTn(I or T). The absence of ST elevation on the
resting ECG and elevated troponin levels indicates NSTEMI
• Non coronary causes for elevated troponins are extremely
rare . It may occur in acute myocarditis, acute pulmonary
embolism, a dissecting aortic aneurysm, acute heart failure
and sometimes in septic shock. Severe renal

22. • Aspartate aminotransferase (AST) and lactate
dehydrogenase (LDH) levels are not sensitive
or specific for acute MI with frequent false
positive elevations.
• Total CK measurement is also not
recommended owingto its poor specificity and
large distribution in skeletal muscles

23. ECHOCARDIOGRAPHY
• Echocardiography is a particularly useful
bedside imaging technique. It is useful in
detecting:
• •New regional wall motion abnormalities in
difficult diagnostic situations.
• •Mechanical complications of acute MI e.g.
free wall rupture, acute ventricular septal
defect (VSD), mitral regurgitation.

24. MANAGEMENT
• Initial management
• Reperfusion theraphy
• Concomitant theraphy

25. • Always starts with ABC!
• •S/L GTN (avoids if SBP <90 mmHg)
• •Oral antiplatelet agents
• •T. aspirin 300mg
• •T. clopidogrel 300mg (other choice; T.
Ticagrelor 180mg)
• •Pain relief –e.g. IV morphine
• •Supplemental oxygen (if SpO2 < 95%)

26. -Two options; PCI or fibrinolytic therapy.
-If both choices are available, the reperfusion
strategy of choice is still primary PCI
-Things needed to be considered:
•Onset of symptoms
•Contraindications to fibrinolytic therapy
•High risk patients
•Primary PCI is preferred strategy in high risk
patients or contraindications to fibrinolytic
therapy

28. Early presentation (within 3 hours)
• Both PCI and fibrinolytic therapy is equally effective
• Except in cases below, PCI is preferred :
-Fibrinolytic therapy is contraindicated
-High-risks patients
-PCI time delay (DBT –DNT) is more than 60mins
Late presentation (3 to 12 hours)
• Primary PCI is preferred
• However if time delay to primary PCI is more than 2 hours, to
give fibrinolytic therapy and arrange for transfer
Very late presentation (after 12 hours)
• Both primary PCI and fibrinolytic therapy not routinely
recommended
• However, reperfusion therapy would still be beneficial in
patients with persistent ischaemic symptoms, haemodynamic
or electrical instability.

30. THROMBOLYTIC AGENTS
Streptokinase
• 1.5 mega units in 100cc NS or 5% dextrose over 1
hour
Tenecteplase
• Weight based regimen, given in a single IV bolus
• Dose reduced by 50% for patients >75 years old
• Causes more rapid perfusion of occluded artery
than streptokinase
• Higher risk of bleeding if weight has been
overestimated

31. SUCCESSFUL REPERFUSION
• Resolution of chest pain
• Early return of ST segment elevation or decrease
in the height of ST elevation by 50% within 60-90
mins
• Early peaking of CK and CK-MB levels
• Restoration and maintenance of haemodynamic
and electrical stability
FAILED? Persistent chest pain, ST segment elevation
and haemodynamic instability
• Treatment of choice –rescue PCI

32. CONCOMITANT THERAPHY
• ANTITHROMBOTIC

33. • ANTIPLATELETS
-Aspirin –low dose aspirin 75-100mg OD
indicated INDEFINITELY unless contraindicated
-Alternatives:
-Clopidogrel 75mg OD
-Ticlopidine 250mg BD
-DAPTs should be given at least one month post-
fibrinolytic therapy for secondary prevention

34. • ACE-INHIBITORS / ARB
-Indicated within first 24 hours especially (LV
dysfunction, DM or anterior infarct) and should
be continued indefinitely if no contraindications
-Choices
Perindopril
Captopril
Enalapril
ARB if unable to tolerate ACE-I(e.g. losartan,
valsartan)

35. • BETA BLOCKERS
-In the absence of contraindications, should be
started early
-Choices
Bisoprolol
Metoprolol
Atenolol

36. • STATINS
-Early initiation of statin therapy improves
outcome regardless of baseline cholesterol
-Early and intensive high dose statins in ACS
have been proven to produce superior
benefits in reduction of major adverse cardiac
events
-Examples
Atorvastatin
Simvastatin

37. • NITRATES
-IV nitrates can be considered in patients with
Persistent chest pain and/or ischemia
Presence of left ventricular failure
Concomitant hypertension
-Contraindication to nitrate therapy
Hypotension (SBP <90mmHg)
RV infarction
History of phospho-diesterase5 inhibitors
ingestion (depending on half-life)

38. • CALCIUM CHANNEL BLOCKERS
-In patients who cannot tolerate beta blockers, verapamil
or diltiazem may be used for secondary prevention
-May also be used as adjunctive therapy for patients with
HPT or recurring angina despite nitrates and beta
blockers
-Short acting dihydropyridine such as nifedipine should
be avoided
• ALDOSTERONE ANTAGONIST
-When added to beta blockers and ACE-I, have been
shown to reduce mortality when given to patients with
impaired LV function and heart failures
-Care should be taken in renal dysfunction and
hyperkalemia