Acute Coronary Syndrome (ACS) encompasses a spectrum of conditions caused by reduced blood flow in the coronary arteries, including unstable angina and myocardial infarction (MI). It is typically diagnosed through a patient's symptoms, electrocardiogram (ECG) findings, and cardiac biomarker levels. For ACS patients presenting within 12 hours of symptoms, guidelines recommend obtaining an ECG within 10 minutes and starting reperfusion therapies like thrombolysis within 30 minutes to minimize heart muscle damage. Diagnosis is based on criteria including typical chest pain, ECG changes, and elevated troponin levels. Outcomes are generally worse in elderly patients and those with atypical presentations and longer treatment delays.

1. Acute Coronary
Syndrome (ACS)
Dr. B. K. Iyer

2. Goals of lecture
• Definition of ACS
• Diagnosis of ACS
• Treatment of ACS: Antiplatelet agents;
Antithrombin agents; Reperfusion therapies
• Role of the emergency physician in the
diagnosis and management of ACS

3. ACS: definition
• ACC/AHA definition: ”a group of clinical syndromes
compatible with acute myocardial ischemia”
• Physiologic definition: Plaque rupture leading to thrombus
formation, leading to partial or complete blockage of a
coronary artery with or without myocyte death.
• Spectrum includes unstable angina (No ST elevation, normal
biomarkers), NSTEMI (no ST elevation, abnormal
biomarkers), STEMI (ST elevation, abnormal biomarkers)
• Unstable angina includes: angina at rest, new angina,
increasing angina
• Anderson JL et al. ACC/AHA 2007 guidelines for the Management of Patients With
Unstable Angina/Non-ST-Elevation Myocardial Infarction. J AM Coll Cardiology 2007.
50(7); e8

4. Definition & spectrum
• Any constellation of
clinical symptoms that
are compatible with
acute myocardial
ischemia. It
encompasses
1.AMI (ST-segment
elevation and
depression, Q wave
and non-Q wave) as
well as
2.Unstable angina.
Acute Coronary Syndromes
No ST elevation ST elevation
Enzymes not ↑ Enzymes ↑
USA NSTEMI
STEMI
ECG

5. Pathopysiology
• Plaques: atheromatous plaques are formed in the
coronary arteries and when they rupture, exposing
endothelium, they trigger a cascade of events
• Thrombus: thrombin is deposited as well as fibrin, as
the fibrin aggregates, platelets are activated
• White: platelet-rich thrombi, more often partially
occlusive and associated with UA/NSTEMI
• Red: fibrin-rich thrombi, more often totally occlusive
and associated with STEMI
• Treatment of ACS is targeted at the root causes

6. Golden Hour
• Maximum damage to
heart muscle
• Maximum efficacy of
treatment seen
• Survival is best if
thrombolysis is given
within this period
“Time is muscle
and muscle is
time”
““Each minute of delay inEach minute of delay in
the first 3 hours confers 10the first 3 hours confers 10
lost days of survival”lost days of survival”

7. Process of care in emergency : 4 D’s
• Timed 0: onset of symptoms
• ED time 1: Door [arrival at ED]
• ED time 2: Data
[initial ECG]
• ED time 3: Decision
[to administer thrombolytics]
• ED time 4: Drug
[infusion of thrombolytic started
Time interval 1
Time interval 2
Time interval 3
Door
To
Drug
time

8. Door to Needle time
• < 30 min in 33% patients only
• Adjusted odds ratio of death if Door to Needle
time as observed:
– 61 - 90 min = 11%
– > 90 min = 23 %
• 11-23 % increased the odds of developing
EF<40%, if Door to Needle time was > 30 min.
• Door to Ballon time > 2 hrs associated with
41-62 % increase in adjusted odds ratio of
death.

9. Reducing treatment delays
• Heart attack awareness campaign
• Excellent Emergency Management System
• Ambulance transport with pre-hospital ECGs
• Pre-hospital thrombolysis : only when a
physician is present or if pre-hospital transport
time is > 6o min

10. Diagnosis of ACS
• No single factor from the history is a
powerful enough predictor to exclude
ACS.
• Increased likelihood of ACS in patients
with:
–Radiation of pain to the right arm (LR
4.7)
–Radiation of pain to both arms (LR 4.1)
– Value and limitations of chest pain history in the evaluation of patients
with suspected acute coronary syndromes. JAMA 2005; 294:2623-2629.

11. Diagnosis of ACS
• Presentation: Classic story most often seen in
younger (50-65) patients, males
• Those who present atypically tend to present
further on in their disease and have worse
outcomes (REACT)
• Typical versus Atypical
• Elderly: tend to present with shortness of breath
• Diabetics: vague symptoms
• Women: complain of feeling fatigued
• Missed Diagnosis of Acute Cardiac Ischemia in the Emergency Department. N Engl J
Med. 2000. April 20; 342 (16): 1163-70.

12. Symptoms
• Chest pain (variously described, but
classically it is pressure-like)
• Shortness of breath
• Nausea/Vomiting (especially in inferior MI)
• Diaphoresis
• Weakness
• Syncope

13. Signs
• Not terribly helpful to rule in or out ACS, but:
– JVD, S3, pulmonary edema, new heart murmur are
concerning for significant myocardial damage and
indicate a patient at high risk for death/MI
– Diaphoresis is never a good sign and should always
concern the wary clinician
– Can help discern alternate causes of chest pain
– Anderson JL et al. J Am Coll Card 2007. 50(7): e1-157

14. Emergency Room Triage in ACS
• Initial presentation
• 12 Lead ECG
• Cardiac Enzymes

15. Ischemic Chest Discomfort
ST Elevation
or New LBBB
ECG s/o Ischemia
ST dep, T inversion
Non-diagnostic
or Normal ECG
Assess initial ECG
Aspirin
Baseline CK, CK-MB
Assess C/I to thrombolysis
Anti-ischemic therapy
Reperfusion therapy
thrombolyse or Primary PTCA ]
Admit
Anti-ischemic therapy
Serial cardiac markers
2D Echo
E/o ischemia / MI
NoYes
DischargeAdmit
Goal 10 minutes
Goal
< 30 min for STK or
< 60 min for arrival in Cath Lab for PTCA
Triage of ACS

16. ↑ Biomarkers +
≥ of the following
Pathological
findings of AMI
Typical symptoms
of AMI + one of
the following
Procedural
myocardial damage
Typical symptoms of
myocardial ischemia
No other findings
required
ST segment
elevation in the
ECG
↑ cardiac biomarkers to
prespecified levels;
symptoms may be
absent; ECG changes
absent/nonspecific
Q waves in the ECG Increased levels of
cardiac biomarkers
ST segment elevation
or depression in the
ECG
Modified from Alpert J, Thygesen K, et al: Towards a new definition of myocardial infarction for
the 21st century. J Am Coll Cardiol 2000
Criteria For The Diagnosis Of
Acute Myocardial Infarction (AMI)

17. Initial Presentation

18. Common symptom history in acute MI
– Location
• Usually substernal
– Quality
• Crushing or squeezing
– Radiation
• Either Arm, Neck,
Jaw, Epigastrium, or
between Scapulae
– Duration
• Generally 30 minutes
to several hours
• Anginal Pain
Equivalents
• Dyspnoea
• Marked weakness
• Syncope
• Accompanied
diaphoresis, nausea,
vomiting
• Chest Pain

19. No pain ; No gain
• In a lot of cases with proven acute MI, chest
pain was absent at initial presentation [33%]
• These pts
– were at least 70 years older;
– Higher proportion were women[49% vs 38%];
diabetics; had h/o prior heart failure
– Had longer delay before hospital admission;
– Were less likely to receive thrombolysis or
primary PTCA; b-blockers, aspirin or heparin
– Had higher in-hospital mortality [23.3% vs 9.3%]

20. Recognition of high risk cases
• Demographic and historical factors associated
with poor prognosis
– Age > 70 years
– Female gender
– History of Diabetes mellitus
– Prior angina pectoris
– Previous MI
Peterson ED et al. Ann Intern Med 126:561-582,1997

21. Electrocardiogram
“standard of care”

22. ECG
• Very specific and a good test, particularly helpful if
positive:
– Should be done within 10 minutes of arrival on
anyone with suspected ACS
– Serial ECGs in the ED are a must when looking for
changes, especially if the patient is initially pain-free
or has atypical symptoms
– Can have a normal ECG with significant disease,
particularly if the patient is pain free
– Tells us the most likely artery affected and area of
myocardium affected
– Kumar, Amit, et al. Acute Coronary Syndromes: Diagnosis and Management, Part 1. Mayo
Clin Proc. October 2009;84(10):917-938

23. ECG: watch for
• Inferior: II, III, AVf
• Anterior: V1-V6
• Lateral: I, AVL, V5, V6
• Posterior: depression V1-V3 with tall R waves
• Right ventricular infarct: right sided leads
• Wellens (indicates significant LAD disease): T
wave inversions V2-V4 without pain
• NSTEMI: ST depressions; T wave inversions

24. ECG Patterns
In Acute Chest Pain In unstable angina
TIMI IIIb Investigators, Circulation 1994;89Hamm et al. NEJM 1997;337
23%
18%
11%
10%
30%
0%
5%
10%
15%
20%
25%
30%
T-wave inversion ST- depression ST- elevation
LBBB Normal
13%
57%
17%
12%
0%
10%
20%
30%
40%
50%
60%
T-wave inversion ST- depression
ST- elevation Normal

25. Prognostication through ECG
• ST elevation
• decisive role regarding thrombolytic therapy
• Worse prognosis / Increase mortality in
• Anterior MI > Inferior MI
• RVMI complicating IWMI
• Multiple leads with ST elevation & high sum of ST
elevation
• Persistent advanced heart block
• New IVCD (Bifascicular / trifascicular)
• Persistent ST depression / Q waves in many leads
• ST depression in anterior leads in IWMI
NEJM 330:1211-1217, 1994 , Ann Intern Med 126:556;1997

26. Risk of MI/ death during 1 year follow up
based on admission-ECG
0
5
10
15
20
25
30
60 120 180 240 300 360
Follow Up ( Days)
MIorDeath(%)
ST Elev + Dep
ST Dep
ST Elev
T Inv
NO ST/T
Changes
The RISC Study Group . J.Intern.Med.1993;234

27. Time of ECG and outcomes

28. Limitations of ECG
• It provides a snapshot view of a highly dynamic process.
• Lack of perfect detection in areas of myocardium it supplies.
• Small areas of ischemia or infarction may not be detected.
• Conventional leads do not directly examine right ventricle,
posterior basal or lateral walls very well.
• Baseline changes like BBBs, early repolarization, LVH, &
arrhythmias make interpretation difficult.
• AMI in LCx territory are likely to have non-diagnostic ECG.
• ECG is not very sensitive test & should always be considered
a supplement to, rather than a substitute for, physician
judgment.

29. Pseudo-infarction on ECG
• LVH
• Conduction disturbance
• Pre-excitation
• Primary myocardial
disease
• Traumatic heart disease
• Pericarditis
• Early repolarization
• Pneumothorax
• Pulmonary embolism
• I/C hemorrhage
• Hyperkalemia
• Amyloidosis
• Sarcoid cardiac
involvement

30. Inferior MI

31. Right Ventricular MI

32. Lateral MI

33. Wellen’s Syndrome

34. NSTEMI

35. Cardiac Markers

36. hFABP=heart fatty acid binding proteins; MLC=myosin light chain; cTnI=cardiac troponin I; cTnT=cardiac troponin T;
MB-CK=MB isoenzyme of creatinine kinase (CK); MM-CK=MM isoenzyme of CK; LD=lactate dehydrogenase;
MHC=myosin heavy chain; CP=chest pain
Markers, MW, Time to initial elevation, Mean time to peak,
Time to return to normal, Common sampling schedule

37. Appearance of cardiac markers in blood
versus time after onset of symptoms
• Peak A:
Myoglobin or
CK-MB isoforms
post AMI
• Peak B: cardiac
troponin post
AMI
• Peak C: CK-MB
post AMI
• Peak D: cardiac
troponin after
unstable angina.

38. Predictive value of troponin rapid testing
Predischarge TMT
+ Troponin
• If Both Normal
– 1 % risk of Death /MI
at 5 Months
• If both Abnormal
– 50 % risk of death/MI
at 5 Months

39. Troponins
• 30% patients with rest pain without ST-
elevation and were diagnosed as unstable
angina based on CPK_MB results are found
to have elevated troponins, converting these
to NSTEMI.

40. Clinical Status
GISSI-1 (%)
Killip Definition Incidence Control
Lytic
Class Mortality
Mortality
I No CHF 71 7.3 5.9
II S3 gallop or 23 19.9 16.1
basilar rales
III Pulmonary edema 4 39.0 33.0
(rales >1/2 up)
IV Cardiogenic shock 2 70.1 69.9
Killip T et al. Am J Cardiol 20:457;1967
GISSI. Lancet 1”397-401, 1986

41. Hospital Phase

42. Hospital Phase : Tools
• Risk stratification in ICU is done by:
– Clinical findings
– ECG monitoring
– Invasive hemodynamic monitoring
– LV Function
• Most important determinant of hospital mortality
– Echocardiography
• LVEF, diastolic function, hemodynamics,
degree of MR, mechanical complications

43. Hemodynamic Classification
Subset Definition PCWP CI Mortality
I Normal hemodynamics <18 >2.2 3%
II Pulmonary Congestion >18 >2.2 9%
III Peripheral hypoperfusion <18 <2.2 23%
IV Pulmonary congestion &
Peripheral hypoperfusion
>18 <2.2 51%
Forrester J et al. NEJM 295:1356:1976
PCWP = pulmonary capillary wedge pressure

44. Inpatient stratification

45. Risk Stratification
• GRACE (Global Registry of Acute Coronary Events) risk score and
PURSUIT (Platelet G IIb/IIIa in Unstable Angina: Receptor Suppression
Using Integrilin Therapy) risk score: too time consuming and complex for
regular use in the emergency department. Better for in-patient risk
stratification.
• TIMI (Thrombolysis in Myocardial Infarction) score (1 point for each):
– Age > 65
– Aspirin use in the last 7 days
– 3 or more conventional cardiac risk factors
– Severe angina (> 2 episodes in 24 hours)
– Positive cardiac markers
– ST changes > 0.5 mm
– > 3 TIMI score is high risk for ACS
• Hoekstra J, et al. Management of patients with unstable angina/non-ST-
elevation myocardial infarction: a critical review of the 2007 ACC/AHA
guidelines. Int J Clin Pract, April 2009, 63, 4, 642-655

46. Echocardiography
• Identification of location of infarction
• Estimation of infarct size
• Assessment of diastolic function
• Degree of MR
• Recognition of mechanical complications
• Determination of LVEF
– LVEF < 40% within 72 hrs of onset of AMI is
associated with increase risk of death
Berning et al. Am J Cardiol 69:1538-44;1992

47. Echocardiography
• Greater number of WMA
[wall motion
abnormalities] correlated
with
– Higher Killip class,
– Lower pO2,
– Higher CPK levels and
– Larger number of Q
waves on ECG
• Romano et al
• 30 day mortality
– WMA < 3 segments=
3.5%
– WMA 4-6 segments=
12.9%
– WMA 7-9 segments=
18.3%
– WMA > 9 segments=
37.8%
Am J Cardiol 81(12A):13G-16G;1998

48. Mitral inflow patterns
• Worse is the flow pattern, worse is the
prognosis
• A deceleration time < 130 msec indicates
future development of CHF
Normal
Relaxation
Defect
Pseudo-
Normalization
Restrictive
pattern
A
E
Poulsen et al , Eur Heart J 1997;18:1882

49. Complications
• LV systolic dysfunction
• Rupture
Free Wall
VSD
Papillary muscle rupture
Subepicardial aneurysm
MRCARDIAC RUPTURE VSD LV ANEURYSMLV ANEURYSM

50. Complications
• Mitral regurgitation LV dilatation
Papillary muscle dysfunction
Papillary muscle rupture
LV thrombus
Pericardial effusion/ tamponade
RV infarct
LV outflow tract obstruction

51. Echo: value in ACS
• Echo provides new and useful information in
29% of the patients admitted to ICU
• Decision about reperfusion strategy
• ACE-I therapy (SAVE trial)
• Unrecognized prior MI
• Titrating beta-blockers
• Need for invasive monitoring
• Standby IABP support

52. Management
• Goals
• Immediate relief of ischemia
• Prevention of serious
adverse outcomes
• Approach
• Anti-ischemic therapy
• Anti-platelet therapy
• Anti-coagulant therapy &
Reperfusion therapies
• Ongoing risk stratification
• Invasive procedures
• Adjunctive anti-ischemic
therapies: Beta-blockers,
Nitrates, Morphine, Calcium
channel blockers, O2, ACE
inhibitors
Match treatment to risk: More aggressive treatment in higher risk & unstable patients

53. Management – initial medical therapy
• Unstable Angina guidelines: Class 1
recommendations for antithrombotic therapy
Braunwald E et al , J. Am coll Cardiol 2000; 36:970-1002

54. Anti-Ischemic therapy for continuing
ischemia
• Bed rest with ECG
monitoring
• O2 to maintain SaO2
>90%
• NTG IV
• Beta-blockers
• Morphine
• IABP if ischemia or
hemodynamic instability
persists
• ACE I for control of
hypertension or LV
dysfunction, after MI
Class-I Recommendations, ACC/AHA practice guidelines

55. Anti Ischemic Therapy
• Nitrates
• Beta Blockers
• Calcium Channel Blockers

56. Nitrates in ACS
No.
Of Pts.
Mortality (%)Study Year
Tt Control
GISSI 3 94 18895 6.5 6.9
ISIS-4 95 58050 7.3 7.5

57. Beta blockers in ACS
Mortality
Study Year n
Tt C
MIAMI *
1985 5578 4.3 4.9
ISIS-1#
1986 16027 3.9 4.6
* Eur H Journal 1985;6
# Lancet 1986;ii

58. Calcium Channel Blockers in ACS
MortalityStudy Yr N
Tt C
Meta
analysis
1989 7351 5.9 5.2
Salim Yusuf, BMJ 1989; 299

59. Antiplatelet and Anticoagulation
Therapy
• Oral Antiplatelet therapy
• Aspirin
– Thienopyridines
Ticlopidine Clopidogrel
• Heparins
– UFH
– LMWH
• IV Antiplatelet therapy
• Abciximab
• Eptifibatide
• Tirofiban

60. Role of Anticoagulants in ACS
Mortality %Study Yr N
Tt c
UFH
[Meta-analysis]
1994 1353 6.5 6.9
LMWH
[FRISC 1]
1996 1506 1.8 3.8

61. New Anti-coagulants in ACS

62. Anticoagulants - Unfractionated
Heparin (UFH)
• Most widely used antithrombotic agent
• Recommendation is based on documented
efficacy in many trials of moderate size
• Meta-analyses of 6 trials showed a 33% risk
reduction in MI and death, but with a 2-fold
increase in major bleeding

63. Anticoagulants - Unfractionated
Heparin (UFH)
• Disadvantages include:
– Poor bioavailability
– No inhibition of clot-bound thrombin
– Dependent on antithrombin III (ATIII) cofactor
– Frequent monitoring (aPTT) to ensure
therapeutic levels
– Rebound ischemia after discontinuation
– Risk of heparin-induced thrombocytopenia
(HIT)

64. Anticoagulants - Low-Molecular-Weight
Heparin (LMWH)
• Fraction of standard (UFH) heparin
• Enoxaparin, dalteparin, reviparin, nadroparin,
fraxiparin
• Advantages over UFH:
– Greater bioavailability
– No need to closely monitor
– Resistant to inhibition by activated platelets
– Lower incidence of HIT Enhanced anti-factor
Xa activity
– Effective subcutaneous administration

65. ESSENCE Trial: (Efficacy and Safety of Subcutaneous
Enoxaparin in non-Q-Wave Coronary Events Study)
• LMWH (enoxaparin)+ASA vs UFH+ASA
• Patients:
– angina at rest or non-Q-wave MI;
• n = 3,171
• Composite triple endpoint:
– death/nonfatal MI/RA

66. 0
5
10
15
20
25
0
5
10
15
20
25
heparin enoxaparin Heparin enoxaparin
n=1564 n=1607 n=1564 n=1607
19.8%
16.6%
P=0.019
23.3%
19.8%
P=0.016
Day 14 Day 30
N Eng J Med 1997;337:447-452
ESSENCE Trial - Incidence of death, MI,
or recurrent angina

67. AntiThrombotic Therapy for ACS
• Anticoagulants
– Heparin
• UFH
• LMW
– Hirudin
– Coumarins
• Antiplatelets
– Aspirin
– Ticlopidine
– Gp IIb/IIIA Inhibitors
• Thrombolytics

68. Anti Platelet Therapy in ACS
• Aspirin
– Inhibits cyclo-oxygenase in platelets
• Ticlopidine
– Inhibits the ADP receptor on the platelet surface
• Gp iib/iiia receptor antagonist

69. Aspirin
Advantages
• In AMI, ASA reduced
the risk of death by 20-
25%
• In UA, ASA reduced the
risk of fatal or nonfatal
MI by
– 71% during the acute
phase,
– 60% at 3 months, and
– 52% at 2 years
Disadvantages
• Not Perfect
• Patients on ASA may
present with ACS
• ASA non-responders
20-30%
• Not adequate alone for
stent implantation
• Side effects

70. Incidence of Ischemic Events
0
2
4
6
8
10
12
14
16
No aspirin
(early 1980s)
Aspirin Aspirin + Heparin
16%
12%
9%
Incidence of death and MI

71. Thienopyridines
• Ticlopidine
• Clopidogrel
– Block ADP receptor resulting in inhibition of
transformation of GP IIb/IIIa into its high
affinity state

72. Aspirin & Ticlopidine in ACS

73. IV Anti-platelet Therapy
• GP IIb/IIIa inhibitors
• abciximab (monoclonal antibody)
• eptifibatide (peptide inhibitor)
• lamifiban and tirofiban (non-peptides)

74. Recommendations for Antiplatelet &
Anticoagulation Therapy
• Class 1:
– Antiplatelet therapy should be initiated promptly.
Aspirin is the first choice and is administered as soon
as possible after presentation and is continued
indefinitely. (Level of Evidence: A)
– Clopidogrel should be administered to patients who
are unable to take ASA because of hypersensitivity or
major gastrointestinal intolerance. (Evidence Level: A)
– In hospitalized patients in whom an early
noninterventional approach is planned, clopidogrel
should be added to ASA as soon as possible on
admission and administered for at least 1 month (Level
of Evidence : A) and for upto 9 months (Evidence
Level: B)

75. Recommendations for Antiplatelet &
Anticoagulation Therapy
• Class 1:
– In hospitalized patients for whom a PCI is planned, clopidogrel
should be started and continued for at least 1 month (Level of
Evidence : A) and for up to 9 months in patients who are not at
high risk for bleeding (Level of Evidence : B)
– In patients taking clopidogrel in whom CABG is planned, if
possible the drug should be withheld for at least 5 days, and
preferably for 7 days. (Level of Evidence :B)
– Anticoagulation with subcutaneous LMWH or intravenous UFH
should be added to antiplatelet therapy with ASA and/or
clopidogrel. (Level of Evidence : A)
– A platelet GP IIb/IIIa receptor antagonist should be administered,
in addition to ASA and heparin, to patients in whom
catheterization and PCI are planned. The GP IIb/IIIa antagonist
may also be administered just prior to PCI (Level of Evidence: A)

76. Early Conservative vs Invasive
Strategies - Recommendations Class I
• An early invasive strategy in patients with UA/NSTE-
MI and any of the following high risk indicators.
(Level A)
– Recurrent angina/ischemia at rest or with low-level
activities despite intensive anti-ischemic therapy
– Elevated TnT or TnI
– New or presumably new ST-segment depression
– Recurrent angina/ischemia with CHF symptoms, an S3
gallop, pulmonary edema, worsening rales, or new or
worsening MR
– High-risk findings on noninvasive stress testing
– Depressed LV systolic function (EF < 0.40)
– Hemodynamic instability
– PCI within 6 months
– Prior CABG

77. Early Conservative vs Invasive
Strategies - Recommendations Class I
• In the absence of these findings, either an
early conservative or an early invasive
strategy in hospitalized patients without
contraindications for revascularization (Level
of Evidence: B)

78. Indications of primary PTCA
• Cardiogenic Shock
• Large area of myocardium at risk
• Thrombolysis contraindicated
• Alternative to thrombolysis

79. Interventions in ACS
Rationale
• Prognosis of ACS is worse than Stable angina
• Inhospital death / Reinf. = 5 - 10 %
• Ist Mo Death / Reinf. = 5 - 10 %

80. Casualty protocol for acute chest pain

81. AMI: Parameters influencing prognosis
Acute
MI
At
Presentation
In
Hospital
At
Discharge
Size of
infarct
Recurrent
ischemia
LV systolic
dysfunction
Diastolic
dysfunction
Mechanical
complications
Residual
ischemia
LV
dysfunction
Risk of
arrhythmia
Age
Gender
ECG
features
Concomitant
Risk factors
Clinical
status

82. TIMI myocardial perfusion grade and
mortality

83. TIMI myocardial perfusion grade and
mortality

84. TIMI Risk Score for STEMI for
predicting 30-day mortality

85. The GUSTO Pyramid: 30 Day Mortality Model
Age (31%)Age (31%)
Systolic Blood Pressure (24%)Systolic Blood Pressure (24%)
Killip Class (15%)Killip Class (15%)
Heart Rate (12%)Heart Rate (12%)
MI Location (6%)MI Location (6%) Prior MI (3%)Prior MI (3%)
Age x Killip (1.3%)Age x Killip (1.3%) Height (1.1%)Height (1.1%)
Diabetes (1%)Diabetes (1%) Time-to-Rx (1%)Time-to-Rx (1%)
Smoker (0.8%)Smoker (0.8%) Weight (0.8%)Weight (0.8%)
Accel t-PA (0.8%)Accel t-PA (0.8%)
Prior CABG (0.8%)Prior CABG (0.8%)
HTN (0.6%)HTN (0.6%)
H/oH/o
CV DCV D
(0.4%)(0.4%)
Lee et al.
Circulation
1995;91:1659-
1668
Influence of Clinical characteristics on 30 day
mortality in thrombolyzed
Initial Presentation : Clinical

86. Summary

87. Treatment of ACS
• All patients receive aspirin
• Clopidogrel is also favored as an adenosine-mediated platelet blocker,
particularly in patients with aspirin allergy.
• ESSENCE trial (Efficacy and Safety of Subcutaneous Enoxaparin in Non–
Q Wave Coronary Events) has suggested a preference for LMWH
specifically, enoxaparin (Lovenox) over unfractionated heparin in ACS
• Finally, a platelet glycoprotein IIb/IIIa inhibitor is needed.
• Glycoprotein IIb/IIIa receptor blockers have been studied with
simultaneous use of unfractionated heparin and aspirin. Most of the trials
with these agents have involved coronary interventions and have shown
significant benefit.
• If no intervention is planned, abciximab is not indicated.
• Currently, tirofiban and eptifibatide are useful in patients with continuing
ischemia when no percutaneous intervention is planned. These latter two
medications are also indicated in patients with continuing ischemia or
other high-risk features in whom a percutaneous intervention is planned.

88. Rx of ACS
• TACTICS trial and TIMI-18 compared an early invasive and a conservative
strategy in patients treated with the tirofiban & showed that an early
invasive strategy reduces the incidence of major cardiac events.
• The data for high-risk AMI and non–Q wave MI suggest that angiography
should be part of the early plan.
• The data for unstable angina with no elevation in biochemical markers are
less clear.
• Because of cost considerations, abciximab with coronary intervention is
recommended in high-risk patients.
• In intermediate-risk patients, regardless of whether they are candidates for
coronary intervention, tirofiban or eptifibatide is recommended.
• Low-risk patients may not require either of these agents, but they should
receive heparin, probably low molecular-weight heparin, aspirin, and
clopidogrel at a dose of 300 mg to start and then 75 mg/d for at least 30
days.
• In addition, a “statin” should be started in that hospitalization (MIRACL) if
LDL cholesterol is greater than 130 mg/dL.

89. Antithrombotic Drug Therapy
Abciximab (ReoPro)
with unfractionated heparin & aspirin
0.25-mg/kg intravenous bolus followed by an infusion
of 0.125 μg/kg/min for 12–24 h up to 10 mg/min
Eptifibatide (Integrilin)
with unfractionated heparin & aspirin
180-μg/kg bolus followed by an infusion of
2 μg/kg/min up to 72 h for intervention. Max 15 mg/h
Tirofiban (Aggrastat)
with unfractionated heparin & aspirin
0.4 μg/kg/min × 30 min 0.1-μg/kg/min infusion × 48 h
up to 108 h (PRISM-Plus)
Enoxparin (clexane) 1 mg/kg q12 h
Clopidogrel (Plavix) 300 mg initially, followed by 75 mg/d

90. Findings in High-Risk Patients
• Recurrent ischemia at rest or low levels of
activity with medical management
• High-risk noninvasive stress testing with
depressed ejection fractions,
• Extensive wall motion abnormalities
• Hemodynamic instability
• Sustained ventricular tachycardia
• Recent revascularization with coronary
intervention or coronary bypass graft surgery

91. Post discharge Care
“ABCDE”
• A – Antiplatelets & Antianginals
• B – Beta blocker, Blood pressure control
• C – Cholesterol lowering, Cigarettes cessation
• D – Diabetes control, Diet
• E – Education & Exercise

92. Invasive therapy
• Percutaneous Coronary Intervention (PCI)
– Confers benefit in highest risk UA/NSTEMI
patients
– Multiple trials done over the last 20 years with
pendulum swinging from invasive to
conservative and back

93. Treatment of STEMI
• Many of the same anti-platelet and anti-
thrombin therapies used
• Fibrinolytics are indicated in STEMI but not in
UA/NSTEMI
• Emergency physicians in the United States
are held to multiple benchmarks for STEMI
(door to ECG, door to medications, door to
balloon time)

94. Fibrinolytics
• Indications:
– ST segment elevation of at least 1mm in two or more
contiguous leads
– Pain for < 12 hours
– Symptoms consistent with acute myocardial infarction
– No contraindications
• Fibrinolytics are particularly effective within the first six
hours after pain onset and in those with new left bundle
branch block and anterior wall myocardial infarctions
• Kumar, Amit and Christopher Cannon. Acute Coronary Syndrome: Diagnosis and Management, Part II. Mayo Clin Proc.
November 2009;84(11):1021-36

95. Fibrinolytics
• Absolute Contraindications:
– Any previous ICH
– Known structural cerebrovascular lesions
– Known malignant intracranial neoplasm
– Ischemic stroke within 3 months, except for acute
ischemic stroke within 3 hours
– Suspected aortic dissection
– Active bleeding or bleeding diathesis (excluding
menses)
– Severe closed head or facial trauma within 3 months

96. Fibrinolytics
• Streptokinase: reduces mortality significantly
(ISIS-1), lowest cost
• Retevase: no difference between Retevase
and tPA (GUSTO III) but easy dosing for ER
(10 mg bolus 30 minutes apart)
• Alteplase (tPA):GISSI-2, ISIS-3, GUSTO
showed likely more favorable outcome than
streptokinase; tPA slightly more likely to cause
intracranial hemorrhage
• Tenecteplase (TNK): equivalent to tPA, weight
based dosing may make it more difficult for

97. PCI in STEMI
• Coronary angioplasty with or without stenting
• Preferred at centers where available as some
studies point to better outcomes than
fibrinolytics (GUSTOIIb).
• Depends on whether it is available at your
facility and how quickly the patient can get to
the cath lab

98. Newer Modalities
• Coronary CT angiogram to diagnose CAD
and/or ACS
• Bivalirudin: ACUITY trial showed similar 30
day rates of death, MI or unplanned
revascularisation with lower bleeding rates in
the bivalirudin alone arm.
• Stone, GW et al. Bivalirudin for patients with acute coronary syndromes. N Engl J Med 2006; 355:
2203-16

99. Role of emergency physician
• No single historical or physical exam factor
can rule out ACS
• Diabetics, elderly and women present
atypically
– Less common risk factors such as lupus or
Kawasaki’s disease
• Serial ECGs are extremely important in
detecting on-going ACS

100. Role of emergency physician
• First line for diagnosis and treatment
• Earlier treatment = better outcomes
• Aspirin for everyone unless contraindicated
• We will miss some people with ACS, but we
can minimize it by being aware of the incorrect
assumptions

101. Thank you!