This document provides an overview of acute coronary syndrome (ACS). It defines ACS and describes the epidemiology in Malaysia. The pathophysiology, classification, clinical presentation and investigations are discussed for unstable angina/NSTEMI and STEMI. Management is outlined for both conditions, including medications, fibrinolytic therapy, percutaneous coronary intervention and complications. A clinical case of STEMI is then presented demonstrating diagnosis and management. The document concludes with references to Malaysian clinical practice guidelines for ACS.

1. Acute
Coronary
Syndrome
Dr Shaalina Nair

2. Subtopics covered
• Definition of ACS
• Epidemiology of ACS
• Pathophysiology of ACS (including signs and symptoms)
• Classification of ACS – UA, NSTEMI, STEMI
• Diagnosis of ACS
• Investigations
• Management of ACS
• Clinical case presentation

3. Definition
• Acute Coronary Syndrome refers to a spectrum of conditions compatible with
acute myocardial ischemia and/or infarction that are usually due to an
abrupt reduction in coronary blood flow*
*American College of Cardiology/American Heart Association Task Force on
Practice Guidelines 2014

4. Epidemiology
• According to the World Health Organization, CAD accounted for 98.9 deaths per
100,000 population in Malaysia in 2012, or 29,400 deaths (20.1% of all deaths); it is
the most common cause of deaths in the country
• The NCVD-ACS registry showed that Malaysians are having ACS at a younger age
compared to the developed countries, with a mean age of between 55.9 to 59.1 years
compared to mean ages of between 63.4 to 68 years in most developed countries
• CAD generally affects men more than women.
• Women on average were 5 years older than men at presentation and with higher
prevalence of risk factor (83 out of 936 female deaths were due to cardiac causes)
• Study by Ahmad and colleagues involving 525 patients with unstable angina or
NSTEMI in 17 tertiary hospitals between 2004-2005 and found 96.8% with at least
one established risk factor.
• Of the 525 patients, 66.1% of patients had hypertension, 38.9% diabetes mellitus
and 40.4% dyslipidaemia
*Data retrieved from ‘A Review of Coronary Artery Disease Research in Malaysia’- June 2016*

5. Pathophysiology of ACS

8. Clinical presentation
• Symptoms
1. Chest pain
 Intense substernal pressure sensation, often described as ‘crushing’ in nature
 Radiation to neck, jaw, arms or back, commonly to the left side
 Severe pain, not relieved by sublingual nitroglycerin
 Occurs at rest
 Atypical chest pain – dull in nature/epigastric pain : post-operative, diabetics, female and
elderly patients
2. Shortness of breath
3. Sweating
4. Weakness or fatigue
5. Nausea and vomiting
6. Syncope/dizziness
• Signs : pericardial friction rub, acute heart failure (raised JVP, bibasal crepts,
pitting edema, S3 heart sound)

9. Classification of ACS

10. Unstable Angina/Non-STEMI
• History includes typical chest pain at rest unresolved with
sublingual GTN, shortness of breath, nausea and vomiting, sweating
• Underlying co-morbids : HPT, DM, Dyslipidemia, anaemia,
thyrotoxicosis, severe aortic stenosis, hypertrophic cardiomyopathy
• Family history of CAD, premature death due to cardiac causes
• ECG criteria
 Dynamic ST/T changes
 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 (BBB)
 Sustained ventricular tachycardia.
 Evidence of previous infarctions such as Q waves may be present.

11. • Differentiating factor between unstable angina vs NSTEMI : elevation of cardiac
biomarkers (esp Trop I in NSTEMI)
• Troponin T or I are highly specific and sensitive for myocardial injury and/or
necrosis (infarction) and also provide important prognostic information
• The troponin level may not be elevated if the test is done early (<6 hours).
• To confidently exclude myocardial necrosis (infarction), a repeat test needs to be
done 6–12 hours after admission.
• Other causes of raised Trop I
 myocarditis,
 acute pulmonary embolism
 dissecting aortic aneurysm
 Heart failure
 Septic shock.
 Severe renal dysfunction
• CK and CK-MB are also indicators of myocardial necrosis (infarction),but are
less sensitive and specific compared to cardiac troponins.
• CK and CKMB have a shorter half life and hence are more useful to diagnose
reinfarction and a raised CK-MB with normal troponin levels have no prognostic
significance

13. Investigations for UA/NSTEMI
• Blood Ix
 Cardiac enzymes, FBC, RP, Electrolytes, Coag
• Imaging modalities
 CXR
 Echocardiography : Ejection fraction – LV systolic function, Transient
regional wall motion abnormalities (RWMA)

14. ECG – Unstable angina

15. Risk stratification for UA/NSTEMI
• TIMI risk score
Low risk (Score 0-2), Intermediate risk (Score 3-4), High risk (Score 5-7)

16. • HEART Score

17. Management of UA/NSTEMI
• The goals of management are:
 Immediate relief of ongoing ischemia and angina
 Prevention of recurrent ischemia and angina
 Prevention of serious adverse cardiac events
• Rapid assessment
 evaluation of patient’s clinical status:
 mental status
 comfort status
 respiration
 peripheral perfusion
 vital signs:
 blood pressure
 rate and volume of pulse
 respiratory rate
 history:
 presence and severity of chest pains
 past history of coronary and vascular events, interventions and surgery
 risk factors (hypertension, diabetes mellitus, dyslipidaemia, previous medications – eg anti-anginals,
antiplatelets, family history of premature CAD)
• Blood investigations
 cardiac biomarkers
 troponins
 CK-MB
• ECG, CXR

18. Initial management – General Measures
• Following risk stratification:
• Low risk patients may be treated as outpatient.
• High risk patients preferably should be admitted to CCU/HDU with continuous ECG monitoring.
• Supplemental oxygen should be given to maintain SpO2 >90%, in patients with left ventricular failure,
respiratory distress or having high risk features for hypoxemia.
• Pain relief, morphine (intravenous 2 mg to 5 mg) together with concomitant intravenous anti-emetic may be
given.
Specific management
1. Low risk patients
 Antiplatelet therapy : To give T.Aspirin 300 mg stat
 Nitrate therapy : Sublingual GTN 0.5 mg every 5 minutes for a total of 3 doses if persistent
chest pain
 Monitor symptoms and allow discharge with advice if patient is stable
 Risk stratify as outpatient and plan for non-invasive test for reversible ischemia as outpatient

20. 2. Intermediate/high risk patients
 Antiplatelet : T.Aspirin 300 mg stat and T.Clopidogrel 300 mg stat
 Nitrate therapy : Sublingual GTN 0.5 mg every 5 minutes for a total of 3 doses
if persistent chest pain
 Unfractionated heparin (Initial IV bolus : 60 IU/kg (max 4000 IU) followed by
infusion of 12IU/kg/hour (max 1000 IU/hour) adjusted to maintain aPTT 1.5-
2.0x normal) – if planning for PCI
Or
 Low molecular weight heparin (LMWH) – S/C Clexane 1mg/kg BD
Or
 Anti Factor Xa inhibitor – S/C Fondaparinux 2.5 mg OD
 Early referral to cardiology
 Monitoring in CCU/HDU
 Nitrates
 Beta-blockers
 ACEI/ARBs
 Statin therapy
 +/- CCB
 Revascularization
 Urgent coronary angiography/revascularization for patients with refractory or
recurrent angina associated with dynamic STdeviation, heart failure, life threatening
arrhythmias and/ orhemodynamic instability
 Early (<72 hours) coronary angiography/revascularization- in patients with high-risk
features as predicted by a positive biomarker assay, ST segment changes or a high risk
score
 according to the TIMI scale

22. STEMI
STEMI is diagnosed when there is:
• ST elevation of > 1 mm in 2 contiguous leads OR
• a new onset LBBB in the resting ECG in a patient with ischaemic
type chest pains of > 30 minutes AND
• accompanied by a rise and fall in cardiac biomarkers.

23. ECG changes

25. Types of MI

26. Management of STEMI

28. Fibrinolytic therapy
1. Streptokinase
 Dosage : 1.5 MU in 100 mls NS or 5% dextrose over 1 hour
 This is the most widely used agent but it is not fibrin specific
 The reduction in mortality is less than with fibrin specific agents
2. Tenecteplase (TNK-tPA)
 The benefit of using TNK-tPA is that it causes more rapid reperfusion of the occluded artery than streptokinase
and is given as a single bolus dose.
 This is a weight-based regimen and thus there is a risk of bleeding if the weight has been overestimated.
 Following administration of a fibrin specific agent, anticoagulant is recommended with:
 Heparin
 Enoxaparin
 Either one of these agents should be given immediately after the completion of fibrinolysis and continued for at
least 48 hours.

29. Contraindications to thrombolysis

30. • Side effects of streptokinase
1. Bleeding
Intracranial, gastrointestinal, genitourinary, gum bleeding
2. Allergic reaction (most common)
 fever and shivering
minor breathing difficulty to bronchospasm, periorbital swelling or
angioneurotic edema
urticaria, itching, flushing, nausea, headache and musculoskeletal pain
3. Hypotension
4. Cardiac arrhythmias
5. Respiratory depression
6. Transient elevation if serum transaminases

31. Percutaneous coronary intervention
(PCI)
• Primary PCI is the preferred reperfusion strategy in patients with ischaemic symptoms < 12 hours
when it can be performed in a timely manner and promptly by experienced operators in centres
performing a sufficient number of primary PCI procedures
• Indications for early PCI
 Failed reperfusion or re-occlusion after fibrinolytic therapy
 Cardiogenic shock or acute pulmonary oedema
 Stable patients within 3-24 hours post-fibrinolysis as part of a pharmaco-invasive strategy
 STEMI TIMI risk score of ≥ 6.0 at admission
 Spontaneous or easily provoked myocardial ischaemia such as recurrence of
chest pains and/or dynamic ECG changes
• Failed fibrinolytic therapy is manifested as one or more of the following:
 Ongoing chest pains.
 Persistent hyper-acute ECG changes (< 50% resolution of ST elevation in the lead showing the
greatest degree of ST elevation at presentation).
 Haemodynamic and electrical instability.
• Rescue PCI is initiated very early (1 to 2 hours) after failed fibrinolytic therapy.

32. Killip classification

33. Clinical case presentation
• Clinical history – RESUS patient on Thursday (21/5/2020)
• Mr R, 78 year old Indian gentleman, no known medical illness, no known drug or food allergy,
occasional smoker and h/o right TKR 6 years ago
• Presented with left sided chest pain radiating to left arm at 5 pm while watching TV
• The pain radiated to jaw, left arm and right arm, sudden in onset and given a pain score of 8/10
• Associated with profuse sweating and mild SOB
• Otherwise, no fever, no nausea/vomiting , no abdominal pain , no cough, no sorethroat , no hx of
contact with COVID-19 patient/ did not attend mass gatherings/family functions and no travel hx
prior to MCO

35. Physical examination
• Alert, Conscious, GCS 15/15, good pulse volume, CRT<2s, not
tachypneic, no radioradial delay
• CVS : S1, S2 heard, no murmur
• Lungs : clear
• Per abdomen : soft, non-tender
• No pedal edema

36. • Vital signs on arrival to RESUS
• BP : 154/95 mmHg, HR : 78 bpm, SpO2 : 100%
• The patient was alert and conscious, GCS 15/15, with reflo of 10.1 mmol/L

37. Right-sided ECG

38. Posterior ECG

39. Blood investigations

43. Chest x-ray

44. Bedside ECHO
• Good contractility
• Hypokinesia over inferior wall
• No thrombus
• No pericardial effusion
• Aortic root 2.5 cm

45. Diagnosis and Management
• Diagnosis : Acute inferior ST elevation myocardial infarction with no
right sided or posterior involvement, Killip class I
• He was given T.Aspirin 300 mg stat, T.Plavix 300 mg stat and S/C
Fondaparinux 2.5 mg stat
• Cardiologist oncall was consulted and patient was thrombolysed with IV
Streptokinase 1.5 MU in 100 mls normal saline over 1 hour
• Prior to thrombolysis, the absolute and relative contraindications were
ruled out and side effects of streptokinase was explained to the patient
• The patient was placed on cardiac monitoring throughout the
thrombolysis to detect any cardiac arrhythmias
• IV Morphine total of 4 mg was given to the patient for pain relief and
vital signs were monitored

46. • Vital signs were monitored every 5 mins for the first 15 mins then
every 10 mins for 30 mins

47. Post-streptokinase ECG
• There is no sensitive bedside clinical method to
reliably detect successful reperfusion.
 Some useful guides are:
 Resolution of chest pain (may be confounded
by the use of narcotic analgesics).
 Early return of ST segment elevation to
isoelectric line or a decrease in the height of
the ST elevation by 50% (in the lead that
records the highest ST elevation) within 60-
90 minutes of initiation of fibrinolytic
therapy
 Early peaking of CK and CK-MB levels.
 Restoration and/or maintenance of
haemodynamic and/or electrical stability.

48. Further management
• The patient was successfully thrombolysed and was planned for
pharmacoinvasive treatment the next day
• He was told to be fasted at 12 am the same day – he was able to
afford PCI
• He was then started on the following medications
 T.Aspirin 100 mg OD
T.Plavix 75 mg OD
S/C Arixtra 2.5 mg OD
T. Atorvastatin 40 mg ON
 T.Perindopril 2 mg OD

49. CPG Recommendations

50. Complications of STEMI
• Arrhythmias
 Tachyarrhythmias
 Pulseless Ventricular Tachycardia
 Ventricular fibrillation
 Ventricular tachycardia
 Ventricular premature contractions
 Atrial fibrillation
 Asystole and PEA
 Bradyarrythmias
Sinus bradycardia
Atrio-ventricular block
• LV dysfunction and cardiogenic shock.
• Mechanical complications.
 Free wall rupture - it is usually fatal and presents with sudden cardiovascular collapse and
haemopericardium.
 Ventricular septal rupture.
 Mitral regurgitation.
• RV infarction.
• Others e.g. pericarditis.

51. References
• CPG Unstable Angina/NSTEMI Malaysia 2011
• CPG STEMI Malaysia 2019