Based on Malaysian CPG

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