Summary presentation on ACS definition, diagnosis and management. Focuses on myocardial infarction (STEMI/NSTEMI), low-risk chest pain, accelerated diagnostic protocols (ADP's) and objective testing.

1. Acute Coronary
Syndrome
Dr Andrew Crofton
Emergency Registrar

2. Epidemiology
• >30% of all deaths in developed countries
• 3-6% of those thought to have an alternative cause for chest pain ultimately have short-term
adverse cardiac events
• Reserve diagnoses of non-cardiac chest pain to those with a very low likelihood of coronary artery
disease (<1%) and clear evidence of alternative diagnoses only
• 1-6% of patients with a normal ECG will ultimately be diagnosed as NSTEMI + another
4% will have unstable angina
• Dynamic ECG changes confer
• 84% risk of CAD with classical anginal symptoms
• 85% risk of CAD with non-classic anginal symptoms

3. Definitions
• Rise and/or fall of troponin, with at least one value >99th centile + one of:
• Symptoms of myocardial ischaemia
• New (or presumably new) ST/T wave changes or LBBB
• Development of pathological Q waves (>40ms wide, >2mm deep (sometimes normal
in III, aVR), >25% of QRS, leads V1-3 (always pathological)
• New loss of viable myocardium or regional wall motion abnormality
• Identification of coronary thrombus by angiography or autopsy

4. Rise and or fall?
• European Society of Cardiology
• >99th centile
• >20% change = AMI
• <99th centile
• Rises to above 99th centile and by >=50% = AMI
• Remains <99th centile = AMI ruled out

5. Definitions
• Unstable angina
• <4% of patients have normal biomarkers and ECG with altered pattern of previously stable angina
• New onset angina is considered unstable at first presentation
• Types of MI
• Type I – Spontaneous due to plaque disruption
• Type 2 – Imbalance O2 delivery/demand
• Type 3 – MI resulting in death in absence of biomarkers
• Type 4 – PCI–related MI
• Type 5 – CABG-related MI

6. Unstable angina
• Rest angina
• Angina at rest that is usually >20 min duration (most common presentation of NSTEMI)
• New-onset angina
• New-onset angina that markedly limits normal physical activity such as walking 1-2 blocks or
climbing 1 flight of stairs or lighter activity
• Increasing angina
• Previously diagnosed angina that has become more frequent, of longer duration or is lower in
threshold, limiting ability to walk 1-2 blocks, climb 1 flight of stairs or perform lighter activity

7. Short-term risk of death or non-fatal MI in
patients with unstable angina (AHA)
• High-likelihood
• Accelerating tempo of ischaemic symptoms over last 48 hours
• Prolonged, ongoing rest pain >20 min
• Pulmonary oedema
• New or worsening MR
• S3 or new/worsening rales
• Hypotension, bradycardia, tachycardia
• Age >75
• Angina at rest with transient ST segment changes >0.5mm
• New BBB
• Sustained VT
• Elevated TnT >0.1ng/mL

8. Short-term risk of death or non-fatal MI in
patients with unstable angina (AHA)
• Intermediate likelihood
• Prior MI, PVD, cerebrovascular disease, CABG or aspirin use
• Prolonged >20 min rest angina (now resolved), with moderate-high likelihood of CAD
• Rest angina >20 min or relieved with rest or S/L GTN
• Nocturnal nagina
• New-onset or progresive angina in past 2 weeks without prolonged (>20min) rest pain but with intermediate or high risk of
CAD
• Age >70
• T waves changes, pathological Q waves or resting ST depression <1mm in multiple lead groups
• TnT 0.01-0.1ng/mL

9. Short-term risk of death or non-fatal MI in
patients with unstable angina (AHA)
• Low likelihood
• Increased angina frequency, severity or duration not meeting high or intermediate
criteria
• Angina provoked at lower threshold
• New-onset angina 2 weeks to 2 months before presentation
• Chest discomfort reproduced by palpation
• Normal or unchanged ECG
• Normal Tn

10. Risk factors
- Predict CAD over time not likelihood at specific point in
time
• DM
• HTN
• Lipids
• FHx <50
• Male
• Obesity
• Previous MI
• Hormone replacement therapy
• Inactivity

11. Universal Classification
• Type 1 – Spontaneous MI related to plaque rupture or dissection
• Type 2 – MI secondary to ischaemic imbalance
• Type 3 – MI resulting in death without available biomarkers
• Type 4a – MI related to PCI
• Type 4b – MI related to stent thrombosis
• Type 5 – MI related to CABG

12. NYHA Angina Classification
• Class 1 – Cardiac disease without limitation of activity
• Class 2 – Cardiac disease with slight limitation of activity
• Class 3 – Cardiac disease with marked limitation of activity
• Class 4 – Symptoms at rest or with any activity whatsoever

13. Risk stratification of possible ACS
• High risk (25% risk of MI)
• Persistent or dynamic ST/T wave changes
• ST depression >0.5mm
• New TWI >2.0mm in 2 or more contiguous leads
• Transient ST elevation > 0.5mm in 2 or more contiguous leads
• ECG changes consistent with Wellen’s/LMCA/DeWinter’s
• Haemodynamic compromise
• Ongoing or recurrent pain
• Sustained VT
• Syncope
• Elevated troponin
• LVEF <40%
• Previous PCI/CABG/MI in last 6 months

14. Risk stratification for possible ACS
• Intermediate risk
• No high or low risk factors
• Transient ECG changes that do not meet above criteria
• Low risk
• AGE <40
• Atypical symptoms
• Remain symptom free
• Absence of known CAD
• Normal troponin levels
• Normal ECG (including no transient changes)

15. Risk stratification of confirmed ACS
• Very high risk
• Haemodynamic instability
• Life-threatening arrhythmia or cardiac arrest
• Recurrent or ongoing ischaemia or recurrent dynamic ST/T wave changes, especially:
• Intermittent ST elevation
• DeWinter’s T waves
• Wellen’s syndrome
• LMCA syndrome
• Widespread ST elevation in 2 or more coronary territories

16. Risk stratification of confirmed ACS
• High risk
• Rise and/or fall in troponin consistent with MI
• Persistent or dynamic ST segment and/or T wave changes with or without symptoms
• GRACE score >140

17. Risk stratification of confirmed ACS
• Intermediate risk
• DM
• Renal insufficiency
• LVEF <40%
• Prior CABG/PCI
• GRACE 109-140

18. Risk stratification of confirmed ACS
• Low risk
• No recurrent symptoms
• No risk criteria

19. Likelihood that presentation due to CAD
(Tintinalli)
• High likelihood
• Chest or left arm pain as chief symptom with documented prior angina
• Known history of CAD
• Transient MR, hypotension, diaphoresis, pulmonary oedema or rales
• New or presumed new transient ST deviation >=1mm or TWI in multiple praecordial
leads
• Elevated Tn

20. Likelihood that presentation due to CAD
(Tintinalli)
• Intermediate
• Chest or left arm pain as chief symptom
• Age >70
• Male
• DM
• Extracardiac vascular disease
• Fixed Q waves
• St depression 0.5-1mm or TWI >1mm
• Normal Tn

21. Likelihood that presentation due to CAD
(Tintinalli)
• Low likelihood
• Probable ischaemic symptoms in absence of intermediate or high risk factors
• Recent cocaine use
• Chest discomfort reproducible with palpation
• T wave flatenning or inversion <1mm in leads with dominant R waves OR normal
ECG
• Normal Tn

22. Assessment of bleeding risk
• Important pre-thrombolysis
• CRUSADE score
• HR
• SBP
• Haematocrit
• Creatinine clearance
• Sex
• Signs of CCF
• Hx of vascular disease
• Hx of DM

23. TIMI score for possible NSTEMI
• Age >= 65
• >= 3 CAD risk factors (FHx of premature CVD, HTN, Dyslipidaemia/low HDL
<40mg/dL/, DM or current smoker)
• Premature CVD = male first-degree relative under 55yo or female first-degree relative under 65
• Known CAD (>= 50% stenosis)
• Aspirin use in last 7 days
• 2 or more episodes of angina in last 24 hours
• Elevated troponin
• ST deviation >= 0.5mm in contiguous leads

24. TIMI score interpretation
• % risk at 14 days of: All-cause mortality, new or recurrent MI or severe
recurrent ischaemia requiring urgent revascularisation
• 0-1= 4.7% risk
• 2 = 8.3% risk
• 3 = 13.2% risk
• 4 = 19.9% risk
• 5 = 26.2% risk
• 6-7 = >40.9% risk

25. GRACE score
• Age
• HR
• Systolic BP
• Creatinine
• Cardiac arrest at admission
• ST segment deviation
• Elevated troponin
• Killip class

26. GRACE score interpretation
• % risk at 6 months for all-cause mortality
• 60-100 – 3% risk
• 100-140 = 8% risk
• 140-180 = 20% risk
• >180 = >40% risk

27. HEART score
• History
• Slightly suspicious – 0
• Moderately suspicious +1
• Highly suspicious +2
• ECK
• Normal 0
• Non-specific repolarisation abnormality +1
• Significant ST elevation (if >1mm do not use score)/depression not due to LVH/LBBB/digoxin +2
• Age
• <45 - 0
• 45-64 + 1
• >=65 +2

28. HEART score
• Risk factors
• NO known risk factors – 0
• 1-2 risk factors +1
• >=3 risk factors or history of atherosclerotic disease +2
• HTN, dyslipidaemia, DM, obesity, smoking (current or within 3mo), FHx (first-degree before age 65), atherosclerotic disease (prior
MI;PCI;CABG;CVA;TIA;PAD)
• Initial troponin
• Normal 0
• 1-3x ULN +1
• >3x ULN +2

29. HEART score interpretation
• Score 0-3 = 0.9-1.7% risk of adverse cardiac event (all-cause mortality, MI,
intervention)
• Score 4-6 = 12-16.6% risk
• Score 7 or more = 50-65% risk

30. Commentary on scores and
ADP (accelerated diagnostic pathway)
• ADAPT (sensitive Tn), modified-ADAPT (hs-Tn) and HEART pathways all
have validated consistent NPV >99% for MACE within 30 days

31. NHFA sensitive Tn Pathway
ADAPT
• If high or very high-risk possible ACS
• Refer for admission and 6 hour troponin
• If no high risk features
• TIMI score = 0
• Repeat troponin and ECG testing at 2 hours from symptom onset (I use 6 hours from symptom onset for all
generally as troponin should be elevated by 4-6 hours, peaks at 10-24 hours and declines over 10 days)
• TIMI > 0
• Repeat troponin and ECG testing at 6 hours from symptom onset
• If any further symptoms, dynamic ECG changes or elevated troponin treat as high risk
• If troponin and ECG both remain normal = Low risk for AMI
• Consider need for objective testing

32. NHFA Pathway hsTn
Modified ADAPT
• If any high risk features – refer for admission and repeat troponin and ECG
at 3 hours
• If no high risk features
• TIMI 0 or 1 – Repeat troponin and ECG at 2 hours
• TIMI 2 or more – Repeat troponin and ECG at 3 hours

33. ASPECT
• 2 hour point-of-care relatively insensitive Tn with ECG and TIMI
• ADP identified 9.8% of patients as low risk and suitable for discharge with
early follow-up
• Sensitivity of 99.3% for 30 day MACE

34. ADAPT Trial
• Than et al. 2012
• TIMI, ECG and 0- and 2-hour sensitive Tn
• Brisbane and Christchurch
• Low risk = TIMI 0, normal ECG and both Tn below cut-off
• 1975 patients
• 15% primary outcome events (MI mostly)
• 20% of patients identified as low risk
• 1 patient in low risk group had MACE
• If TIMI 0 or 1 utilized as low-risk, resulted in 38.4% of patients designated low risk but reduced sensitivity to 97% and NPV to 98.8%
• 316 of 392 patients in low-risk group had stress testing within 30 days, 88% of which were done in index admission
• Therapeutic and procedural interventions were then performed in 2% of ADP negative patients
• Did not include atypical presentations and predominantly Caucasian group

35. Modified ADAPT
• Cullen et al. 2013
• TIMI <= 1 + hsTn allowed ~40% of patients to be classified as low-risk
with <1% risk of MACE at 30 days
• 77% rate of further testing for ADAPT cohort + ~25% rate of further
testing in APACE cohort
• Not clear why such different proportions and no detail on whether this testing altered
management in any way (majority stress ECG)
• 2 patients in ADAPT cohort and 1 patient in APACE cohort had a 30-day
MACE (all NSTEMI)

36. HEART Pathway
• HEART score <4 = low risk
• Serial Tn (sensitive or hsTn) testing at 3 hours
• Negative – Early discharge (0.4% 30 day MACE risk)
• Positive – Cardiology Consult and admission
• HEART score >=4 = High risk
• Serial Tn (sensitive or hsTn) testing at 3 hours
• Negative – Admission to Observation Unit/Inpatient for stress testing or imaging
• Positive – Cardiology Consult and admission for stress testing or imaging

37. HEART Pathway
• Mahler et al. 2015 introduced concept of Heart Pathway with 0 and 3 hour
conventional Tn assays
• Mahler et al. in 2017 compared conventional sensitive Tn assay to hsTn assay
at 0 and 3 hours and confirmed equally sensitive and specific
• Low risk with dual negative Tn discharged with referral to GP for ongoing
clinical assessment and consideration of provocative/stress testing

38. Previously evaluated
• Dunn
• Generally no provocative testing required for:
• Negative stress ECG test in last 6 months
• Negative stress cardiac MRI, CTCA, stress echo or MPS in last 12 months
• No significant coronary stenosis >50% in last 5 years
• CABG >6 weeks and <3 years ago (<5 years in UpToDate)
• Stenting >4 weeks and <2 years previously who are compliant with antiplatelets
• <1% rate of in-stent stenosis within 1 year of uncomplicated insertion

39. Previously evaluated
• Tintinalli
• Truly negative angiogram report confers very low risk of AMI for 2 years
• Prior negative stress test of any sort provides very little reassurance that a current chest pain
event is benign
• Patients with recent negative evaluation for ACS including objective testing (mostly stress ECG testing)
have 6 month incidence of AMI as high as 14%
• UpToDate
• Negative angiogram or CTCA strongly negatively predictive (up to 10 years in some series)
• Negative stress test not useful to rule out ACS if active chest pain in ED

40. NICE guideline
• Divides patients into acute chest pain and stable chest pain
• Acute chest pain is assessed for AMI + alternative Dx
• If no diagnosis of MI can be made then consideration is given to whether pain is stable angina or not
• Most people diagnosed with non-anginal chest pain need no further diagnostic testing
• If have risk factors for cardiovascular disease – refer to primary carer for risk factor modification
• However, atypical presentations are common and have worse outcomes (UpToDate, Dunn)
• If stable typical or atypical angina suspected:
• CTCA is first-line
• Non-invasive functional testing is then indicated if non-diagnostic (stress echo, MPS, MR NOT exercise ECG)
• Invasive angiography is third-line if non-invasive testing is non-diagnostic

41. NICE guideline
• Positive CTCA =
• >70% stenosis (or >50% in LMCA)
• If 50-70% stenosed, consider if anaemic, proximal, long lesion, LVH as may still be
symptomatic

42. NICE Guideline
• Three features = Typical
• 2/3 features = Atypical
• 0/3 or 1/3 features = Non-anginal chest pain  NICE advice to exclude diagnosis of stable angina in
this group and consider alternative diagnoses + no provocative testing
• Features
• Constricting discomfort in front of chest, or neck/shoulders/jaw/arms
• Precipitated by physical exertion
• Relieved by rest or GTN within about 5 minutes (although NICE guide says NOT to use response to GTN in
diagnostic consideration)

43. Atypical chest pain
• 1/3 of MI’s have NO CHEST PAIN
• Often present with dyspnea alone or weakness, N&V, epigastric discomfort,
palpitations, syncope or cardiac arrest
• Often diabetic, female, elderly

44. DeWinter’s T waves
• Tall, prominent, symmetric T waves in praecordial leads
• Upsloping ST segment depression >1mm in praecordial leads
• Absence of ST elevation in praecordial leads
• ST segment elevation 0.5-1mm in aVR
• Highly predictive of LAD occlusion

45. DeWinter’s T waves

46. Wellen’s syndrome
• Deeply inverted or biphasic T waves in V2-3 (may extend to V1-6)
• Minimal STE
• No praecordial Q waves
• Recent history of angina
• ECG pattern evident when pain free
• Normal or slightly elevated troponin
• Critical stenosis of LAD

47. Wellen’s syndrome
Type A Type B

48. Left main coronary artery syndrome
• Widespread horizontal ST depression, most prominent in I, II and V4-6
• ST elevation in aVR >1mm
• Also seen in proximal LAD, triple vessel, diffuse subendocardial ischaemia (i.e. following resuscitation from
cardiac arrest – mismatch)
• Predicts the need for CABG
• >0.5mm = 4-fold increase in mortality
• >1mm = 6-7 fold increase in mortality
• >1.5mm = Mortality of 20-75%
• ST elevation in aVR > V1
• Differentiates LMCA from proximal LAD occlusion

49. Left main coronary artery syndrome

50. New or presumed new LBBB
• <10% have AMI but early studies of fibrinolytic therapy found increased
mortality in this group and benefit from fibrinolysis
• Counts as STEMI in Heart Foundation guideline

51. Reciprocal ECG changes
• Due to subendocardial ischaemia and denote:
• Larger area of injury risk
• Increased severity of underlying CAD
• More severe pump failure
• Higher likelihood of cardiovascular complications
• Increased mortality

52. ST elevation
• In general, the higher the ST elevation and the more ST segments that are
elevated, the more extensive the injury
• New ST elevation >= 1mm in two contiguous chest leads is seen in 50% of
acute MI with PPV of 90%
• 50% of acute MI have normal or non-diagnostic ECG

53. Who needs further stress testing?
• Normal serial ECGs and troponins reduce likelihood of AMI but do not exclude unstable angina or
coronary disease, both of which carry risk of future adverse cardiac events
• Non-invasive objective testing is recommended for intermediate-risk patient with normal serial Tn and ECG
testing and who remain symptom free
• Patients in whom no further testing is required are those defined as low risk by a validated assessment
pathway (NHF)
• Age <40
• Atypical symptoms
• No known CAD
• Normal Tn and ECG
• Symptom free

54. Timing of testing
• High-risk: During index admission
• Intermediate-risk: Early inpatient or outpatient within 7 (or up to 14) days
• Investigate prior to discharge if high risk of FTA (higher risk of MACE)
• Low risk: Either none or within 30 days if warranted i.e. typical crescendo
angina or >40yo

55. Functional vs. Anatomical
• Based on:
• Patient criteria (ECG interpretable, ability to exercise)
• Diagnostic accuracy
• Local expertise/availability
• Risks and costs

56. Decision Tree
• Can perform EST if physically able and none of:
• LBBB
• LVH
• Pre-excitation
• >=1mm ST deviation at rest
• ECG changes of digoxin
• Ventricular paced rhythm

57. Decision Tree
• If imaging required:
• CTCA if no iodine allergy, sinus rhythm and GFR >45
• Otherwise MPS

58. EST Contraindications
• Left main stenosis
• Hypotension <=90
• HTN >=170/110
• Ongoing ACS symptoms
• MI within 2 days
• PCI within 2 weeks
• CABG within 6 weeks
• Tachyarrhythmia
• 2nd degree or higher AV block
• Decompensated CCF
• Active endocarditis
• Acute pericarditis/myocarditis
• Suspected/confirmed PE
• Moderate/severe stenotic valvular disease
• K <=3

59. MPS Contraindications
• Vasodilator (e.g. adenosine)
• Severe bronchospastic airway disease
• Hypotension
• Sick sinus
• 2nd degree or higher AV block
• Caffeine within 12 hours
• Oral dipyramidole within 72 hours
• Theophylline within 48 hours

60. MPS Contraindications
• Dobutamine (LBBB ok)
• Beta-blocker (cease >24 hours prior)
• Unstable angina
Ventricular arrhythmias
• Recent MI
• Haemodynamically LV obstruction
• Known or suspected aortic disease

61. CT angiogram (CTCA) relative
contraindications
• Irregular heart rate (Frequent ectopic, AF/flutter)
• Iodine allergy
• CI to beta-blocker
• Severe heart failure
• Severe aortic stenosis

62. Functional vs. anatomical
• ECG exercise testing
• Utility in prognostication is well understood, cheap, timely
• Prior to Tn testing had NPV of 97-99% for AMI or death
• Not suitable if: Cannot exercise, LBBB, LVH, Digoxin, severe valvular disease, pre-
excitation, cardiomyopathy, pacemaker, women <50yo, anaemia, electrolyte abnormality,
beta-blocker therapy
• Some benefit to stress echo or CTCA but incremental benefit over ECG
stress testing is unknown and of limited accessibility

63. Which stress testing is warranted?
• Exercise stress testing in most if ambulatory
• Chemical stress testing if non-ambulatory
• Myocardial perfusion scanning
• Stress echocardiography
• CTCA
• Cardiac MRI
• Angiogram

64. Which stress testing is warranted?
• Absolute contraindications
• Acute MI including Wellen’s syndrome
• High risk unstable angina
• Symptomatic severe AS
• Uncontrolled arrhythmia
• Unstable HF
• Acute PE
• Acute aortic dissection

65. Which stress testing is warranted?
• Relative contraindications
• Left main coronary artery disease
• Severe arterial hypertension
• Electrolyte abnormalities
• HOCM
• Uncontrolled arrhythmia

66. Which stress testing is warranted?
• Exercise stress test
• In very low pre-test probability, get lots of false positives and in very high pre-test probability get lots of false-negatives
• Therefore recommended for low to moderate risk patients but NOT very low risk or high risk patients
• Requires adequate workload ambulation
• Hyperventilation and tachycardia can reduce quality
• Lower diagnostic accuracy in women
• Positive = >=1mm ST horizontal or downsloping elevation or depression for at least 60-80ms
• Unable to interpret if LBBB, paced ventricular rhythm, pre-excitation syndrome or >1mm ST depression (e.g. LVH or digitalis effect)
• Sensitivity 68% and specificity 70-77% (worst of all with significant risk of false negative)
• Duke score – Low risk <1% per year cardiovascular mortality
• High risk >5% per year cardiovascular mortality

67. What stress testing is warranted?
• Stress echo
• Sensitivity 80-85%; Specificity 84-86%
• False negatives in single vessel/circumflex territory ischaemia
• Requires exercise or dobutamine
• No radiation exposure or environmental impact
• Exercise or chemical stress testing performed
• May see transient focal wall motion abnormality with stress suggesting inducible ischaemia
• Contrast (bubble) scanning improves contrast of endocardial border
• 0.4-0.9% per year cardiovascular event risk (like asymptomatic population) if normal study
• NPV 98.4% for MI and cardiac death at 33 months

68. What stress testing is warranted?
• Stress echo continued
• Limited use in obesity and those with prior MI as scarred tissue has resting focal wall motion
abnormality making interpretation difficult
• Operator-dependent
• Cannot distinguish between acute MI and ischaemia, cannot reliably detect subendocardial
ischaemia and can be falsely positive in conduction disturbances, volume overload, heart
surgery or trauma
• Must be timely with symptoms or stress as wall motion abnormalities can resolve within
minutes of an ischaemic episode
• A normal resting echo in ED does not exclude ACS but makes it less likely

69. What stress testing is warranted?
• Myocardial perfusion scanning
• Sensitivity 85-90%; Specificity 80-90%
• Radiation exposure
• Risk of false positives due to very high sensitivity
• Images captured at rest and with stress (either exercise or chemical)
• Can identify reversible inducible ischaemia
• In low risk group, has NPV approaching 100% for myocardial infarction and cardiac death at 36 months
• Normal scan = 0.7% per year CV all-cause mortality/MI/cardiac death (approaching asymptomatic
population)
• Limitations: Radiation (>angiography) and availability of nuclear tracers and experienced staff

70. Which stress test?
• MPS
• 201 Thallium
• Ischaemic cells lack take-up of thallium (K analogue) = cold spots
• Irreversible cold spots = infarct
• Higher radiation dose than sestamibi
• With exercise or dipyramidole single injection, scan 15min later then again 2-4 hours later
• Tc 99 sestamibi
• First injection at rest, imaging performed 30-60 min later, second injection later that day (2-3x higher
with stress) and repeat imaging 60-90 min later
• Acute scans (with chest pain) are highly sensitive for significant IHD

71. Which stress testing is warranted?
• CTCA
• Less clinically useful in high risk patients as often need to go onto traditional angiography anyway
• Very high negative predictive value in low-intermediate risk patients
• Radiation exposure significant (although much improved since prospective gated scanning), approximately the
same as traditional angiography and less then myocardial perfusion scanning
• Functional effect of stenosis remains unknown
• No data to suggest this is useful for asymptomatic patients

72. Which stress test?
• Electron beam CT
• New technology with lower radiation than helical CT
• Provides coronary calcium score
• Probably most useful in patients <60yo who present with ischaemic sounding chest
pain and normal ECG/biomarkers
• 80-90% sensitive and 40-50% specific

73. Which stress testing is warranted?
• Cardiac MRI
• No radiation or iodinated contrast
• Provides information on RV, LV function (volume, EF, wall motion abnormalities), myocardial oedema to suggest
acute injury, perfusion at rest and with stress and detects infarction size and transmurality with delayed enhancement
imaging
• No other technology can perform all of this in one study
• Real value is in diagnosing true ACS, as manifest by changes in function, perfusion, delayed enhancement and
myocardial oedema
• May also be able to diagnose unstable angina from myocardial infarction
• Limitations include patient contraindications (i.e. metallic implants), claustrophobia, availability of MRI and skilled
reporting, inability to visualise entire coronary tree (unlike CTCA or angiography) and may be undesirable to have
patients in scanner with ongoing chest pain

74. Stress ECG
• If known CAD and prior revasc – Stress ECG + stress MPS/echo to
localize ischaemia and determine its extent
• If known angiographic CAD of uncertain significance – Stress ECG +
imaging allow evaluation of functional significance
• Known CAD and prior MI – Stress ECG not very useful
• Intermediate or high pre-test probability – Addition of imaging has higher
sensitivity and specificity for diagnosis of obstructive CAD

75. UpToDate Stress Testing
• Exercise stress ECG is first line if can exercise and interpret ECG
• Insufficient evidence to recommend imaging for all patients
• Sensitivity of pharmacological stress ECG alone is not sufficient – need
imaging as well

76. SCOT-HEART
• CT coronary angiography in patients with suspected angina due to CAD
• Lancet 2015. All patients referred from primary clinics to Cardiology for Ix
• Standard care vs. Standard care + Calcium score and CTCA for patients
referred to Cardiology clinic for investigation of chest pain
• Primary endpoint – Certainty of diagnosis of angina secondary to CAD at 6
weeks
• Clarified diagnosis, enabled targeted interventions and non-significant
reduction of MI risk

77. SCOT-HEART
• At 6 weeks CTCA + coronary calcium score
• Increased certainty of coronary artery disease RR 2.56 and angina due to coronary
artery disease RR 1.79
• Increased frequency of coronary artery disease RR 1.09 but reduced frequency of
angina due to coronary artery disease RR 0.93
• Diagnosis changed in CTCA group of coronary artery disease in 27% of
participants vs. 1% of standard care group
• Diagnosis changed in CTCA group of angina due to coronary artery disease
in 23% vs 1% of standard care group

78. SCOT-HEART
• Changed in planned investigations in 15% of CTCA group vs. 1% of
standard care group
• Use of CTCA resulted in cancellation of 121 functional tests and 29 invasive
coronary angiograms
• CTCA associated with 94 further invasive coronary angiograms however
• These changes resulted in changes in recommendations for preventative
therapies (18% vs. 4%)

79. SCOT-HEART 5 years
• Coronary CT angiography and 5-year risk of Myocardial infarction
• NEJM 2018
• 4146 patients with stable chest pain
• Standard care vs. Standard care + CTCA
• Primary endpoint – Death from CAD or non-fatal MI at 5 years

80. SCOT-HEART 5 years
• 5-year rate of MI or death from CAD
• 2.3% vs. 3.9% standard care
• Rates of invasive coronary angiography and revascularization higher in CTCA group in
first few months but equal at 5 years
• May have driven reduced event rate overall however given earlier intervention
• More preventative therapies (statin/aspirin) in CTCA group vs. standard group (19%
vs. 14%) as it was protocolled that positive CTCA was prescribed this vs. standard
group positive stress tests not mandated to be started on medications

81. PROMISE
• Outcomes of anatomical versus Functional testing for CAD
• NEJM 2015
• 10 000 symptomatic patients to CTCA vs. functional testing
• Composite primary endpoint = Death, MI, Unstable angina or major
complication
• Secondary endpoints = Invasive angiography that did not show obstructive
CAD and radiation exposure

82. PROMISE
• Overall composite primary endpoint over 25 months
• 3.3% in CTA group vs. 3.0% in functional group
• CTA associated with fewer negative invasive caths (3.4% vs 4.3%)
• CTA associated with more caths overall within 90 days (12.2% vs. 8.1%)
• CTA associated with more revascularization (6.2 vs. 3.2%) but this was not a
trial endpoint
• Median cumulative radiation exposure per patient less in CTA group but
overall radiation exposure higher in CTA group

83. PROMISE
• Overall, test groups and ~53% risk of coronary artery disease pre-test
(intermediate risk) but in the end had relatively low levels of disease
• Suggests our pre-test risk calculations are relatively inaccurate and that there
is scope for improved selection of patients for noninvasive testing

84. Angiography
• >95% sensitivity/specificity
• Sensitivity improved by endovascular USS
• Normal angiogram rules out atherosclerosis
• Coronary artery spasm or slow flow can still precipitate symptoms
• Complications
• Arterial access – Haematoma, fistula, pseudoaneurysm
• Major bleeding in 5%
• Stroke 0.01%, ICH 0.05%
• Nephropathy in 2%
• VF in 4%
• Re-stenosis (1%)
• Dissection 1/1000

85. Angiography
• Results
• Severity of lesions and size of distal vessels can be underestimated
• 75% reduction in cross-section = 50% diameter reduction
• 90% reduction in cross-section = 67% diameter reduction
• Severity
• 50% stenosis likely to cause exertional pain
• >70% stenosis likely to cause functional impairment
• 90% stenosis likely to cause rest pain
• >95% stenosis likely to completely occlude within days/weeks
• Ulcerated lesions more likely to be thrombogenic
• The larger the area supplied by the artery, the more significant the lesion

86. Troponin
• Normal level = <99th percentile
• Elevated by 4-6 hours from symptom onset; declines over 10 days
• Peaks at 16-24 hours
• Accelerated protocols have been validated for hsTn only at 2 hours for low
risk patients
• Normal protocol is 6 hr troponin in Metro South

87. 99th centile and Delta
• Beckman Coulter Access hsTni
• Females = 11.6ng/L
• Males = 19.8ng/L

88. Delta
• >=3ng/nL
• Baseline to 1-3 hours: Sens 76%, Spec 95%
• Baseline to 3-6 hours: Sens 87%, Spec 92%
• >=5ng/L
• Baseline to 1-3 hours: Sens 71%, Spec 97%
• Baseline to 3-6 hours: Sens 78%, Spec 95%
• Need to ascertain suitable cutoff for specific ED
• Increase the absolute delta = more specific, less sensitive

89. Delta troponin
• Absolute changes in hsTn have better diagnostic accuracy than relative
changes
• If high clinical suspicion of ACS
• Tn value below or close to 99th centile, changes of >2-3 SD should prompt additional
testing as unlikely to reflect physiological variability

90. Can I ever do a single troponin?
• Never been validated
• Theoretically, even if pain was >6 hours ago and had resolved, the resultant
single troponin could be declining and thus the significant rise and/or fall of
the troponin is what is important
• Many clinicians will use a single troponin at 6 hours post-symptom onset in
low risk patients as shown in studies to confer very low risk of
mortality/cardiovascular event in following months

91. Single troponin
• AHF guideline
• Symptom-free for 12 hours prior to assessment
• Present >3 hours after symptom onset with value less than the limit of detection using
hsTn assay

92. STEMI criteria
• 2 or more contiguous leads
• >2.5mm STE in V2/3 in males <40
• >2.0mm STE in V2/3 in males >40
• >1.5mm STE in V2/3 in females
• >1.0mm STE in all other leads
• New LBBB considered STEMI equivalent and treated similarly (but not as predictive as once thought)
• Cameron suggests >2mm in any 2 contiguous praecordial leads and >1mm in any 2 contiguous limb
leads

93. Original Sgarbossa
• Concordant STE >1mm (5)
• Concordant ST depression >1mm in V1-3 (3)
• Discordant ST elevation >5mm (2)
• >= 3 = 90% specific for MI

94. Modified Sgarbossa
• Concordant STE >1mm
• Concordant ST depression >1mm in V1-3
• Discordant ST elevation >25% of preceding S wave amplitude
• If meet any of above criteria = activate cath lab (99% specific)
• Only 80% sensitive (therefore cannot rule out acute coronary occlusion)

95. Territories
• Anterior MI is most common
• Anteroseptal = V1-4 = LAD
• Anterolateral = V3-6, aVL, I = LCx
• Posterior = ST depression V1-4 = Cx or PDA (off RCA)
• + tall/wide R waves V1/2, R/S ratio >1 in V1/2 without right axis deviation, upright T
waves in V1/V2
• Inferior = II, III, aVF = RCA

96. STEMI management
• Target SpO2 >93%
• Analgesia
• Antiemetic
• GTN (S/L, tab or infusion)
• Antiplatelet
• Aspirin 300mg
• PCI
• Clopidogrel 600mg then 150mg daily
• Ticagrelor 180mg load (unless immediate CABG possibility) preferred if diabetic, stent thrombosis, recurrent events on clopidogrel or high burden of disease on angiography
• Ticagrelor should not be used if previous haemorrhage stroke or liver disease
• Fibrinolysis
• Clopidogrel 300mg
• CABG
• Nothing unless planned for a weeks time when ciagrelor preferred

97. STEMI management
• Anticoagulation
• If undergoing PCI
• Heparin bolus 60U/kg (max 4000IU) then heparin infusion 12U/kg/hr (max 1000IU/hr) or
Enoxaparin 1mg/kg SC BD
• If undergoing fibrinolysis
• Enoxaparin 30mg IV bolus if under 75 THEN 1mg/kg (max 100mg) beginning 15 minutes
after bolus) or 0.75mg/kg if over 75 yo
• Glycoprotein IIb/IIIa inhibitors
• At time of PCI

98. STEMI management
• TRITON-TIMI 38
– Prasugrel reduced composite (CV death, non-fatal MI or stroke) in clopidogrel-naïve patients undergoing PCI
– Prasugrel contraindicated in prior stroke/TIA, age >75 or <60kg
• PLATO trial
– Ticagrelor reduced composite (CV death, non-fatal MI and stroke) and reduced CV mortality in clopidogrel
naïve with STEMI or moderate-high risk NSTEMI
– Increased non-CABG-related bleeding risk vs. clopidogrel
– Ticagrelor associated with dyspnoea (no harm) and asymptomatic bradycardia in first week of therapy
• Both CI in coagulopathy or liver disease
• Clopidogrel never been compared to placebo in setting of primary PCI but high-dose superior to low-dose in
OASIS trial

99. STEMI Management
• UFH vs. Enoxaparin
• ATOLL trial
• Enoxaparin had no increased risk of bleeding
• Primary endpoint unchanged
• Secondary composite endpoint improved with enoxaparin (death, recurrent MI, ACS)
as well as cardiac arrest or complication of MI
• Enoxaparin may be preferred
• Should receive full-dose anticoagulants for at least 48 hours

100. STEMI management
• Timing of PCI
– If clinical presentation of STEMI within 12 hours of symptom onset and persistent ST elevation
or new/presumed new LBBB, immediate PCI
– Consider if clinical/ECG evidence of ischaemia, even if symptoms started >12 hours ago
– Unclear if immediate PCI warranted if >12 hours and no ongoing symptoms or ECG signs of
ischaemia
• Small RCT showed myocardial salvage and improved 4 year survival in this group
• Larger meta-analysis of late re-canalisation of occluded infarct culprit artery showed no
benefit
• Current ECS guideline states consider if 12-24 hrs and not recommended if >24 hours

101. STEMI management
• Reperfusion
• Consider all patients presenting within 12 hours of symptom onset
• Can even be considered if >12 hours duration if ongoing symptoms or instability (PCI
preferred at this stage)
• Primary PCI preferred if possible within 90 minutes of first medical contact (or 120 minutes
if at non-PCI centre) otherwise fibrinolysis preferred
• Tenecteplase
• See next page
• If >75yo: Can consider administering half the usual dose to reduce ICH risk

102. STEMI Management
• PCI clearly superior to thrombolysis if:
• Thrombolysis CI
• Cardiogenic shock
• Angiography required to confirmd diagnosis
• PCI generally preferred if:
• Door-to-balloon time <90 min
• (Door-to-baloon) – (Door -to-needle) is <1 hour
• High risk from STEMI: Age >75, extensive anterior, high bleeding risk, previous MI/CABG or Killip Class
>=3
• Symptom onset >3 hours ago

103. STEMI Management
• Fibrinolysis generally preferred if:
• <3 hour from symptom onset
• PCI not available
• Prolonged transport predicted
• (Door-to-balloon) – (Door-to-needle) >1 hour
• Door-to-balloon >90 minutes

104. STEMI management
• Tenecteplase dosing guide
Body weight IU mg
<60 6000 30
60-70 7000 35
70-80 8000 40
80-90 9000 45
>90 10000 50

105. STEMI management
• Absolute contraindications for thrombolysis
• Active bleeding or bleeding diathesis (excluding menses)
• Suspected aortic dissection
• Significant closed head or facial trauma within 3 months
• Any prior ICH
• Ischaemic stroke within 3 months
• Known cerebral vascular lesion
• Known malignant intracranial neoplasm
• ? Chest pain with new neurology

106. STEMI management
• Relative contraindications to thrombolysis
• Current anticoagulation
• Non-compressible vascular puncture
• Recent major surgery <3 weeks
• Traumatic or prolonged CPR >10 min
• Recent internal bleeding (<4 weeks) or active peptic ulcer disease
• Suspected pericarditis
• Advanced liver disease or metastatic cancer
• Hx of chronic, severe, poorly controlled HTN
• Severe uncontrolled HTN on presentation (SBP >180; DBP >110)
• Ischaemic stroke >3 months ago/known intracranial abnormality/Dementia
• Pregnancy or within 1 week postpartum

107. STEMI management
• ‘Failed’ thrombolysis
• Only judged definitively with angiography
• All patients should be transferred to PCI facility after thrombolysis within 24 hours
• If <50% ST recovery at 60-90 minutes or haemodynamic instability – t/f immediately
• If failure of relief of chest pain/haemodynamic/electrical compromise – t/f immediately
• Minor infarctions (esp. inferior) and severe comorbidities, especially if risk factors
for intracranial haemorrhage (age >75, female, smaller patients, prior stroke of any
kind, SBP >160mmHg) should not be thrombolysed
• Less effective for inferior STEMI (NNT 10-120)

108. Non-STEMI management
• O2 if necessary
• Analgesia
• Antiemetic
• GTN
• Aspirin 300mg
• Withold P2Y12 receptor inhibitors if going for CABG
• Ticagrelor 180mg or clopidogrel 300mg if intermediate or high risk
• Leave decision up to treating cardiologist as need to weigh bleeding risk with risk of recurrent ischaemia
• Clexane (or UFH if clexane CI) if intermediate or high risk
• 1mg/kg SC BD (0.75mg/kg SC BD if elderly or renal impairment)
• 60IU/kg load then 12IU/kg/hr infusion targeting APTT 45-70

109. Non-STEMI management
• GPIIb/IIIa inhibitors at time of PCI
• PCI
• For confirmed NSTEACS with intermediate/high and very high risk
• Very high risk within 2 hours
• High risk within 24 hours
• Intermediate risk within 72 hours
• Low risk – Selective invasive strategy guided by provocative testing
• Invasive approach within 24-48 hours reduces composite of death, MI or recurrent ACS by 19% in women and 27% in men
• More aggressive and earlier PCI in these patients is of no proven benefit

110. Non-STEMI management
• Statin within 24 hours
• Atorvastatin 40-80mg or Rosuvastatin 20-40mg
• Beta-blocker within 24 hours
• ACEi/ARB within 24 hours

111. Drug-eluting stents
• Decreased early vessel closure but increased delayed closure, particularly
once antiplatelet agents (i.e. clopidogrel) is stopped

112. PCI vs. fibrinolysis
• PCI reduces cardiovascular complication rate
• The longer the duration of symptoms, the greater the benefit of primary
PCI over fibrinolysis
• PCI more effective at establishing TIMI flow and reducing reocclusion
• PCI associated with decreased incidence of short- and long-term death, non-
fatal reinfarction and ICH

113. Fibrinolysis
• Indicated for STEMI if time to treatment is <6 hours to 12 hours from symptom onset and
ECG has at least 1mm of STE in two or more contiguous leads
• More beneficial if given earlier and for larger infarction
• More benefit for anterior than inferior or smaller infarctions
• 0.5-1% risk of ICH
• Fibrinolysis inherently exposes thrombin (potent platelet activator), which may explain
limited benefit of thrombolysis and benefit of potent antiplatelet and antithrombin therapy
given concurrently

114. Tenectaplase vs. alteplase
• Alteplase is recombinant tPA
• Tenectaplase is a variant of tPA with prolonged half-life (20 min), resistant to
endogenous plasminogen-activator inhibitor 1 inactivation and has high
fibrin specificity and binding with minimal systemic fibrinogen depletion
• Single bolus administration and weight-based dosing

115. Pharmacoinvasive therapy
• TRANSFER-AMI trial showed benefit of transfer to PCI-capable centre
after fibrinolysis within 6 hours
• 6.2% absolute risk reduction in composite endpoint of death, reinfarction, recurrent
ischaemia, new or worsening HF or cardiogenic shock at 30 days

116. Facilitated PCI
• Planned initial fibrinolysis followed by PCI not recommended
• ASSENT-4 trial showed no benefit and higher incidence of death, CCF or
shock at 90 days

117. Antiplatelets
• GpIIb/IIIa inhibitors are more potent than aspirin as interrupt platelet
activation regardless of stimulating agonist
• Aspirin only inhibits platelet aggregation stimulated through the
thromboxane A2 pathway

118. Aspirin
• Inhibition lasts 8-12 day life of platelet as they cannot produce new
cycloxygenase
• Relative reduction in mortality of 23% in STEMI alone
• NNT – 41 and NNH – 167 (non-dangerous bleeding)
• Do not withold from those with vague allergy, history of remote peptic ulcer
or GI bleeding as benefit is massive
• Clopidogrel is a viable alternative if truly contraindicated

119. Ticagrelor
• Reversible P2Y12 receptor antagonist
• Effect lasts 3 days
• PLATO study compared ticagrelor to clopidogrel in all ACS patients
• 1.9% absolute RR of composite endpoint
• No increase in bleeding risk
• In those with STEMI undergoing PCI, increased risk of stroke 1.7 vs 1%

120. Clopidogrel
• Addition to aspirin and antithrombin therapy in those undergoing fibrinolysis improves cardiovascular outcomes as shown in
CLARITY-TIMI 28 trial and COMMIT trial
• Improves hospital and 30-day outcomes
• NSTEMI/unstable angina
• Addition to aspirin reduces composite outcome of death, AMI and stroke
• CURE trial showed 20% reduction in death, AMI or stroke between 3 and 12 months
• Did increase bleeding risk but was reduced in patients receiving lower dose aspirin
• For those undergoing urgent PCI, 600mg is preferred to 300mg to prevent post-procedure MI but does increase bleeding risk
• Consider alternatives in:
• Patients on omeprazole have 50% reduction in antiplatelet effect
• Patient with CYP2C19 variant gene have reduced ability to active prodrug and increased risk of stent thromboses and
recurrent ischaemia

121. GPIIb/IIIa inhibitors
• Abciximab chimeric antibody binds irreversibly
• Eptifibatide binds reversibly
• Tirofiban binds reversibly
• All require IV infusion for sustained benefit
• Initiation prior to PCI has not shown benefit as compared to delivery at time of PCI
• 40% reduced risk of death or AMI in 30 days (13% over 3 years)
• Very minimal benefit in unstable angina/NSTEMI (especially if not undergoing early PCI)

122. UFH
• Reduces risk of AMI and death in unstable angina when combined with
aspirin by 56%
• Enoxaparin preferred as more reliable clinical effect (unless primary PCI for
STEMI, in which case heparin preferred)
• 0.9% reduction in death or recurrent AMI vs. UFH
• SYNERGY trial showed consistent therapy with a single antithrombin agent
had improved outcomes and less bleeding

123. Fondaparinux
• Binds to antithrombin III to form an antithrombin complex very specific for
Factor Xa inhibition
• Similar efficacy to UFH in STEMI
• Recommended to be used with UFH or bivalirudin before PCI
• Recommended by European Socitety of Cardiology over enoxaparin for
unstable angina/NSTEMI if conservative management regime employed

124. Bivalirudin
• Direct thrombin inhibitor
• Reduces short-term risk of post-ischaemic complications relative to UFH in
patients undergoing PCI
• Safe and effective for intermediate-to-high risk NSTEMI/unstable angina
patients undergoing PCI
• Reduced bleeding for STEMI going for primary PCI than UFH +
GPIIb/IIIa inhibitors

125. Nitrates
• Also inhibit platelet aggregation
• When used in patients not treated with thrombolytics they reduce infarct size, improves regional function and
decreases rate of cardiovascular complications
• 35% reduction in mortality
• In most studies, IV GTN used to reduce MAP by 10% (in normotensive patients) or 30% in hypertensive
patients rather than titrated to symptom resolution = THIS IS WHAT YOU AIM FOR
• Data is confounded in those receiving thrombolytics
• IV GTN recommended for STEMI with recurrent ischaemia, CCF or hypertension for 24-48 hours
• IV GTN recommended for NSTEMI if not responsive to S/L GTN
• Avoid use for 24 hours after sildenafil and 48 hours of tadalafil

126. Beta-blockers
• No benefit from early use (<24 hours) in recent trials
• Recommendation is to start PO beta-blockers within 24 hours if none of the
following:
• Signs of HF
• Evidence of low CO state
• Increased risk of cardiogenic shock: Age >70, SBP <120, sinus tachycardia >110 or
bradycardia <60 and longer duratino of STEMI symptoms before diagnosis and
treatment
• PR >0.24 seconds, 2nd/3rd degree AV block, active asthma, reactive airways disease

127. ACEi
• Reduce LV dysfunction and LV dilatation and slow development of CHF after AMI
• Oral ACEi lower mortality after AMI
• STEMI or heart failure patients should receive ACEi within 24 hours
• NSTEMI/unstable angina patients should receive ACEi within 24 hours if pulmonary
congestion or LVEF <40% in the absence of hypotension or contraindications
• Contraindications include hypotension, bilateral RAS, renal failure or history of
cough/angioedema from ACEi

128. Magnesium
• Correct documented hypomagnesaemia and give for torsades-type VT with
prolonged QT interval
• No clear evidence outside of torsades

129. CCB
• Do not reduce mortality after AMI and may be harmful
• Verapamil and diltiazem may have a role in ongoing ischaemia or AF with
RVR if no CCF, LV dysfunction, AV block and beta-blockers are
contraindicated

130. Complications of ACS
• Dysrhythmias seen in 72-100% of AMI patients admitted to CCU
• Consequences include reduced haemodynamic performance, compromised myocardial
viability, increased myocardial demand and predisposition to more serious arrhythmias due
to reduced VF threshold
• Loss of atrial kick in healthy heart reduces SV by 10-20% and up to 35% in those with
reduced LV compliance
• Pump failure may lead to sympathetically driven sinus tachycardia, AF/flutter and SVT
• Cardiogenic shock seen in 6-7% of AMI with 80% mortality

131. Early dysrhythmias
• Bradydysrhythmias
• Sinus brady 35-40%
• 1st degree block 4-15%
• Type 1 second-degree 4-10%
• Type 2 second-degree 0.5-1%
• 3rd degree 5-8%
• Asystole 1-5%

132. Early dysrhythmias
• Tachydysrhythmias
• Sinus tachy 30-35%
• Atrial premature contractions 50%
• SVT 2-9%
• AF 4-10%
• A flutter 1-2%
• Ventricular premature beats 99%
• Accelerated idioventricular rhythm 50-70%
• Non-sustained VT 60-69%
• Sustained VT 2-6%
• VF 4-7%

133. Dysrhythmias
• Sinus tachy
• Prominent in anterior MI and associated with a poor prognosis due to increased O2 demand
• Seek cause (anxiety, pain, LV failure, fever, pericarditis, hypovolaemia, atrial infarction, PE or
medications) and treat if possible
• AF
• Mostly in first 24 hours and usually transient
• Warrants anticoagulation
• Treatment depends on clinical status and previous anticoagulation

134. Dysrhythmias
• Sinus bradycardia
• If no hypotension, does not carry mortality risk
• Atropine indicated if hypotensive, ischaemia or ventricular escape rhythms OR treatment of AV nodal block (e.g. type 1
second-degree)
• In the setting of AMI, atropine may induce infarct extension, VF and excessive myocardial O2 demand so use with caution
• Complete heart block
• Seen in anterior and inferior MI as AV conduction system receives blood supply from AV branch of RCA and septal
perforating branch of LAD
• In absence of RV involvement, mortality is 15%. In the setting of RV involvement, mortality is >30%
• Complete heart block in anterior MI portends a grave prognosis
• Mortality in heart block in AMI is related to extensive infarction rather than heart block itself and as such, pacing does not confer a
mortality benefit but is still recommended to prevent/treat hypotension, acute ischaemia or ventricular dysrhythmias

135. Indications for temporary pacing
• Transcutaneous
• Unresponsive symptomatic bradycardia
• Mobitz II or higher AV blocks
• New LBBB and bifascicular blocks
• RBBB or LBBB with first-degree block
• Stable bradycardia and new or presumed new BBB (sometimes)
• Transvenous
• Asystole
• Unresponsive symptomatic bradycardia
• Mobitz II or higher AV bocks
• New or presumed-new LBBB
• Alternating BBB
• RBBB or LBBB with first-degree block
• Consider in RBBB with LAFB or LPFB
• Overdrive pacing in unresponsive VT
• Unresponsive recurrent sinus pauses (>3s)

136. Other dysrhythmias
• Accelerated idioventricular rhythms in those with AMI do not affect
prognosis or require treatment
• Primary VT (soon after symptom onset) does not confer poor prognosis
• Late VT is usually associated with transmural infarction and LV dysfunction, induces
haemodynamic deterioration and is associated with a mortality of around 50%
• Primary VF (soon after symptom onset) does not have a large effect on
mortality and prognosis, as long as it is quickly treated
• Delayed or secondary VF during hospitalisation is associated with severe ventricular
dysfunction and carries 75% in-hospital mortality

137. Other dysrhythmias
• New RBBB
• Seen in 2% of AMI (mostly anteroseptal MI)
• Associated with increased mortality and complete HB
• New LBBB
• <10% of patients with AMI and associated with higher mortality
• Left posterior fascicle is larger than anterior and subsequently left posterior hemifascicular block
carries higher mortality as represents larger area of infarction
• Bifascicular block (RBBB + LAFP/LPFB) has increased likelihood of progression to complete
heart block and represents a large infarction, more frequent pump failure and higher mortality

138. Heart failure
• 15-20% of AMI patients have some degree of heart failure
• 1/3 of these have shock
• The greater the LV dysfunction, the greater the mortality
• Mortality for AMI
• No HF - 10%
• Mild HF 15-20%
• Frank pulmonary oedema 40%
• Cardiogenic shock 50-80%
• Raised BNP early on portends worse 30-day outcome

139. Mechanical complications
• Ventricular free wall rupture
• 10% of AMI fatalities
• Usually 1-5 days after infarction
• Rupture of LV free wall = >90% lead to tamponade and death
• Tearing or sudden severe pain
• Surgical therapy required
• Rupture of IV septum
• Size of defect determines degree of shunt and prognosis
• Presents with chest pain, dyspnoea, new holosystolic murmur with palpable thrill and heart best at lower left sternal border
• Most common in anterior MI and extensive three-vessel CAD
• Surgical therapy required

140. Mechanical complications
• Papillary muscle rupture
• 1% of AMI and mostly inferior MI
• Usually 3-5 days post-MI
• Often occurs with small to medium sized infarcts (as opposed to free wall or IV septal
rupture)
• Present with acute dyspnoea, worsening heart failure and new holosystolic murmur
consistent with MR
• Posteromedial papillary muscle is most commonly ruptured as it receives blood supply
from only one coronary artery, usually the RCA

141. Pericarditis
• Early post-AMI pericarditis seen in <5% (previously 20% prior to PCI)
• More common with transmural AMI or delayed presentations
• Usually 2-4 days post-MI
• Resorption rate of any pericardial effusion (if even present) is many months
• Treatment is symptomatic with aspirin or colchicine
• Dressler’s syndrome
• Late post-AMI syndrome seen 2-10 weeks after AMI with chest pain, fever and
pleuropericarditis

142. Right ventricular infarction
• Isolated RV infarction is rare but is seen as part of 1/3 of inferior MI
• Significant increase in mortality and cardiovascular complications
• RV infarction with concurrent LV dysfunction has a particularly devastating
effect on haemodynamic function
• Pulmonary congestion already exists with raised PAP
• Each contraction of the LV causes the IV septum to move into the RV and expel blood
into the pulmonary circulation
• Pre-morbid CO already reduced and further diminished by reduced LV filling pressures

143. RV infarction
• Factors that reduce preload, increase RV afterload (LV failure) or impair
atrial function (AF/flutter, atrial infarction) all lead to significant
haemodynamic derangements
• Treatment consists of increasing preload, avoiding nitrates, reducing RV
afterload and early inotropic support (dobutamine if 1-2L of crystalloid fails
to show improvement)
• High-degree AV block is common and restitution of AV synchrony is crucial
and may require AV sequential pacing

144. Other complications
• LV thrombus
• Arterial embolisation
• VTE
• Post-infarction angina
• Infarct extension

145. Recurrent or refractory ischaemia
• Options include continued medical management (e.g. GTN infusions), rescue
angioplasty, CABG
• Warrants cath and antithrombin/antiplatelet therapy
• If haemodynamically unstable or cath not immediately available, intra-aortic
balloon pump counterpulsation may be used to improve coronary flow and
cardiac output, thereby decreasing oxygen demand and myocardial ischaemia

146. Post-procedure chest pain
• Assume abrupt vessel closure until proven otherwise
• Seen in 4% of patients 2-14 days after stent placement
• Bare metal more likely to re-stenose in short term and drug-eluting more
likely to re-stenose at 9-12 months after clopidogrel ceased
• Can be confused with post-MI pericarditis

147. Amphetamine-induced ACS
• AMI occurs in 6% of patients with chest pain after cocaine use
• Beta-blockers are contraindicated in first 24 hours after cocaine use but
otherwise treatment is the same
• Cocaine-associated STEMI still warrants PCI
• Benzodiazepines are effective in addition to usual therapy

148. Acute medical disorders and ACS
• GI bleeding, stroke and severe infection carry risk of AMI
• GI bleeders admitted to ICU have 13% risk of MI and may have increased risk of death (33 vs 8% in one study of
all GI bleeders, not just ICU admits)
• 17% of acute stroke have raised troponin, associated with 3.2 relative risk of death
• Conversely, risk of stroke post-MI is 0.6-1.8% but carries 17-27% risk of in-hospital mortality
• SAH shows elevated troponins in 28% and transient ECG changes + LV dysfunction but simultaneous STEMI is
very uncommon
• AMI occurs in 5.3% of admitted CAP patients and 15% of those with severe pneumonia

149. OMI Manifesto
• Aims to change paradigm from STEMI vs. NSTEMI to
• Occlusion Myocardial Infarction (OMI) vs. Non-occlusion Myocardial Infarction
(NOMI)

150. OMI Manifesto
• History of reperfusion
• Fibrinolytic therapy trialists (FTT) in 1994 showed in 60 000 patients randomized to thrombolysis
vs. placebo a NNT of 56 for mortality benefit
• 4 out of 9 included trials had no ECG criteria
• 1/3 of patients had no ST elevation appreciable
• Subgroup analysis of ST elevation NNT improved to 43 for mortality
• ST depression and normal subgroup analysis found no benefit to thrombolysis and these terms were not defined
• Primary indicator for thrombolysis was concerning story and undefined ECG findings
• Did not have any angiographic confirmation of acute coronary occlusion or not

151. OMI Manifesto
• Schmitt et al. 2001
• 25-30% of ‘NSTEMI’ have acute coronary occlusion
• 50% of these misses were left circumflex territory
• Wang et al. 2009
• 27% of NSTEMI had acute coronary occlusion
• Coronary occlusion group had higher 6-month risk-adjusted mortality
• Pride et al. 2010
• 26% of anterior ST segment depressions had occluded culprit arteries despite not meeting STEMI criteria
• 50% of these were LCx lesions

152. OMI Manifesto
• Khan et al. 2007
• Meta-analysis showed ¼ of NSTEMI had acute occlusion with increased all-cause
mortality in short and long term

153. OMI manifesto
• Early vs. delayed angiography for NSTEMI
• Mehta et al. TIMACS 2009
• Early <=24 hrs vs. delayed >= 36 hrs
• Mean time 14 vs. 50 hours (not actually early)
• Early is considered <2 hours
• No difference in death, MI or stroke

154. OMI Manifesto
• Hoedemaker et al. ICTUS 2017
• Early within 24-48 hours vs. selective invasive
• No difference in 1-year mortality or spontaneous MI
• No difference at 10 year mortality or spontaneous MI
• Patients excluded if refractory ischaemia, haemodynamic instability or congestive heart
failure

155. OMI Manifesto
• Van’t Hof et al. ELISA 2003
• Early vs. late – Mean 6 vs. 50 hours
• No difference at 30 days
• Refractory ischaemia excluded
• Still not early (<2 hours)

156. OMI Manifesto
• Thiele et al. LIPSIA-NSTEMI 2012
• Immediate <2 hours vs. 10-48 hours (Mean 18 hours)
• No difference in MI or death at 6 months
• Excluded refractory ischaemia
• Most likely explanation is that those with refractory ischaemia also had acute occlusion
and so were excluded from study

157. OMI Manifesto
• Montelascot et al. JAMA 2009
• Refractory ischaemia excluded
• Immediate or next working day
• 70min vs. 21 hours
• No difference in TnT, death, MI or revascularization at 1 month
• Likely no difference due to refractory ischaemia exclusion (= OMI)

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