Acute coronary.ppt.Acute Coronary Syndrome

M

1. Acute Coronary Syndrome

2. Scope of Problem

4. DEATHS FROM CARDIOVASCULAR CAUSES
WORLDWIDE

5. AMI/ACS Epidemiology
1.57 million hospital admissions for ACS annually
1.24 million UA/NSTEMI cases
50% NSTEMI
50% STEMI

9. Acute Coronary Syndrome Definitions

10. Main Presentations of Unstable Angina
Braunwald E. Circulation1989;80:410-4

12. What do we mean by an MI?
0
10
20
30
40
50
60
70
80
02468121824324872
Hours After Onset of AMI
Multiple of
Upper
Reference
Range
TCK
CKMB
Myoglobin
TnI
TnT

13. Changing times, changing definition
“The World Health Organization definition, which has been
widely used, requires the presence of two of the following three
features: symptoms of myocardial ischaemia, elevation of
cardiac marker (enzyme) concentrations in the blood, and a
typical electrocardiographic pattern involving the development of
Q waves or persistent T wave changes.”
1959
2000
2007

14. MI incidence with TnTor CK-MB0%
20%
40%
60%
80%
100%
TnT CK-MB
Biomarker used
% of cases with raised TnT
Circulation 2006;114:790

15. TnT vs CK-MB defined MIs
0
20
40
60
80
100
Age (yrs)% female% NSTEMI% Multivessel% angio
TnT
CK-MB
Circulation 2006;114:790

16. E/O myocardial necrosis in a clinical setting consistent with
myocardial ischemia
Rise and/or fall of biomarkers (preferably troponin),
at least one value > 99th percentile of population
together with evidence of ischemia:
Symptoms
New ST-T wave changes/LBBB
Development of pathological Q waves
Imaging evidence of new loss of viable myocardium, or
new regional wall motion abnormality
Definition of myocardial infarction

17. Classification of MI
Type 1-due to primary coronary event
Type 2 -secondary to spasm, embolism,
anaemia, arrhythmia, blood pressure changes
Type 3 -sudden death before markers can be
measured
Type 4a -associated with PCI
Type 4b -stent thrombosis (angioor autopsy)
Type 5 -associated with CABG

18. Chronology of the
interface between the
patient and the
clinician through the
progression of plaque
formation and the
onset of complications
of STEMI.
Management
Before STEMI
4
1234 5 6
Onset of STEMI
-Prehospital issues
-Initial recognition and management
in the Emergency Department (ED)
-Reperfusion
Hospital Management
-Medications
-Arrhythmias
-Complications
-Preparation for discharge
Secondary Prevention/
Long-Term Management
Presentation
Working Dx
ECG
Cardiac
Biomarker
Final Dx
UA
NQMI QwMI
No ST Elevation
NSTEMI
Ischemic Discomfort
Acute Coronary Syndrome
Unstable
Angina
ST Elevation

19. Expanding Risk Factors
•Smoking
•Hypertension
•Diabetes Mellitus
•Dyslipidemia
–Low HDL < 40
–Elevated LDL / TG
•Family History—event
in first degree relative
>55 male/65 female
Age-->45 for
male/55 for female
Chronic Kidney
Disease
Lack of regular
physical activity
Obesity
Lack of diet rich in
fruit, veggies, fiber

20. Unstable
Angina
STEMINSTEMI
Non occlusive
thrombus
Non specific
ECG
Normal cardiac
enzymes
Occluding thrombus
sufficient to cause
tissue damage & mild
myocardial necrosis
ST depression +/-
T wave inversion on
ECG
Elevated cardiac
enzymes
Complete thrombus
occlusion
ST elevations on
ECG or new LBBB
Elevated cardiac
enzymes
More severe
symptoms

21. Acute Management
•Initial evaluation &
stabilization
•Efficient risk
stratification
•Focused cardiac
care

22. Evaluation
•Efficient & direct history
•Initiate stabilization interventions
Plan for moving rapidly to
indicated cardiac care
Directed Therapies
are
Time Sensitive!
Occurs
simultaneously

23. Chest pain suggestive of ischemia
–12 lead ECG
–Obtain initial cardiac
enzymes
–electrolytes, cbc lipids,
bun/cr, glucose, coags
–CXR
Immediate assessment within 10 Minutes
Establish diagnosis
Read ECG
Identify
complications
Assess for
reperfusion
Initial labs
and tests
Emergent care
History &
Physical
IV access
Cardiac
monitoring
Oxygen
Aspirin
Nitrates

24. Focused History
•Aid in diagnosis and
rule out other causes
–Palliative/Provocative
factors
–Quality of discomfort
–Radiation
–Symptoms associated
with discomfort
–Cardiac risk factors
–Past medical history -
especially cardiac
•Reperfusion
questions
–Timing of
presentation
–ECG c/w STEMI
–Contraindication to
fibrinolysis
–Degree of STEMI risk

26. Clinical Characteristics of Angina
Characteristic More likely to be anginaLess likely to be angina
Type of pain Dull, pressure Sharp, stabbing
Duration 2 to 5 min, always <15–20
min
Seconds or hours
Onset Gradual Rapid
Location Substernal Lateral chest wall, back
Reproducible With exertion With inspiration
Associated symptomsPresent Absent
Palpation of chest
wall
Not painful Painful, exactly reproduces
pain complaint

27. Targeted Physical
•Recognize factors that
increase risk
•Hypotension
•Tachycardia
•Pulmonary rales, JVD,
pulmonary edema,
•New murmurs/heart
sounds
•Diminished peripheral
pulses
•Signs of stroke
•Examination
–Vitals
–Cardiovascular
system
–Respiratory system
–Abdomen
–Neurological status

28. Presentation -ACS
Atypical Presentation
•10 –30% of patients with AMI
•Mortality rate is higher
•50% vs. 18% for classic presentation
•Patients: Elderly or Young, Diabetic
•Abdominal pain
•Vague complaints
•Confusion

29. ECG assessment
ST Elevation or new LBBB
STEMI
Non-specific ECG
Unstable Angina
ST Depression or dynamic
T wave inversions
NSTEMI

30. ED Evaluation of
Patients With STEMI
Aortic dissection
Pulmonary embolus
Perforating ulcer
Tension pneumothorax
Boerhaave syndrome
(esophageal rupture with
mediastinitis)
Differential Diagnosis of STEMI: Life-Threatening

31. ED Evaluation of
Patients With STEMI
Pericarditis
Atypical angina
Early repolarization
Wolff-Parkinson-White
syndrome
Deeply inverted T-waves
suggestive of a central
nervous system lesion or
apical hypertrophic
cardiomyopathy
LV hypertrophy with strain
Brugadasyndrome
Myocarditis
Hyperkalemia
Bundle-branch blocks
Hypertrophic
cardiomyopathy
Differential Diagnosis of STEMI: Other Cardiovascular and
Nonischemic

32. Gastroesophageal reflux
(GERD) and spasm
Chest-wall pain
Pleurisy
Peptic ulcer disease
Panic attack
Cervical disc or neuropathic
pain
Biliary or pancreatic pain
Somatization and
psychogenic pain disorder
Differential Diagnosis of STEMI: Other Noncardiac
ED Evaluation of
Patients With STEMI

33. Diagnosis -ACS
Electrocardiogram
•Diagnostic –50% of the cases of AMI
•ST Elevations
•Nondiagnostic50% of the time
•20% completely normal
•ST changes –depression
•T wave inversion or flattening
•Repolarizationchanges
•AV block or Bundle Branch Block

35. Normal ST-Segment Elevation and Normal Variants

36. Differentiation between viable and necrotic myocardium at the ischemic area at risk
Q waves that appear within 6 hours from onset of
symptoms do not signify irreversible damage
Early inversion of the T waves, along with
resolution of ST elevation, is a sign of reperfusion
the significance of negative T waves in leads with
ST elevation
ST elevation with negative T waves, especially if it occurs
in patients presenting more than 2 hours of onset of
symptoms, may be used as an ECG sign of a more
advanced stage of infarction or presence of irreversible
damage

37. Electrocardiographic Predictors of LAD Occlusion Site

38. Electrocardiographic Diagnosis of Myocardial Infarction during Left Bundle Branch Block

39. The admission ECG pattern is the most informative
noninvasive tool for the diagnosis, triage, and risk
stratification in patients who have STEMI
Three ECG patterns especially relevant:
(1) right ventricular infarction accompanying acute inferior
STEMI
(2) a very proximal LAD occlusion in anterior STEMI
(3) patients at higher risk (ie, those who have grade 3 ischemia,
ST depression in V4–V6 concomitant with inferior STEMI,
and ST elevation in lead aVR)

40. VPBs K
+
, Mg
++
, beta blocker
VT Antiarrhythmics, DC shock
AIVR Observe unless hemodynamic
compromise
NPJT Search for cause (e.g., dig toxicity)
Arrhythmia Treatment
Arrhythmias During Acute Phase of STEMI:
Electrical Instability

41. Arrhythmias During Acute Phase of STEMI:
Pump Failure / Excess Sympathetic Tone
Sinus TachTreat cause; beta blocker
Afib / FlutterTreat cause; slow ventricular rate; DC shock
PSVT Vagal maneuvers; beta blocker,
verapamil / diltiazem; DC shock
Arrhythmia Treatment

42. Arrhythmias During Acute Phase of STEMI:
Bradyarrhythmias
Sinus BradyTreat if hemodynamic compromise;
atropine / pacing
JunctionalTreat if hemodynamic compromise;
atropine / pacing

43. Arrhythmias During Acute Phase of STEMI:
AV Conduction Disturbances
Escape Rhythm His Bundle Distal
< 120 ms > 120 ms
45 -60 Often < 30
Duration of AVB2 -3 days Transient
Mortality Low High (CHF, VT)
Rx Observe PM (ICD)
Proximal Distal

44. 0 1 2 3 4 5 6 78
Cardiac troponin-no reperfusion
Days After Onset of STEMI
Multiples of the URL
Upper reference limit
1
2
5
10
20
50
URL = 99th %tile of
Reference Control Group
100
Cardiac troponin-reperfusion
CKMB-no reperfusion
CKMB-reperfusion
Alpert et al. J Am Coll Cardiol 2000;36:959.
Wu et al. Clin Chem 1999;45:1104.
Cardiac Biomarkers in STEMI

45. Cardiac markers
•Troponin ( T, I)
–Very specific and more
sensitive than CK
–Rises 4-8 hours after
injury
–May remain elevated for
up to two weeks
–Can provide prognostic
information
–Troponin T may be
elevated with renal dz,
poly/dermatomyositis
•CK-MB isoenzyme
–Rises 4-6 hours after injury
and peaks at 24 hours
–Remains elevated 36-48
hours
–Positive if CK/MB > 5%
of total CK and 2 times
normal
–Elevation can be predictive
of mortality
–False positives with
exercise, trauma, muscle
dz, DM, PE

46. Other causes of raised troponin
Cardiac trauma
Heart failure
Aortic dissection
HCM
Arrhythmias
Tako-tsuboCM
Rhabdomyolysiswith
cardiac injury
PE, severe PHT
Renal failure
Acute neurological
insult
Cardiac infiltration
Cardiac inflammation
Drug toxicity
Critical illness
Extreme exertion

47. Causes of raised TnT in 514 cases
with other condition
Heart failure
27%
Hypotension
27%
Critical illness (including sepsis)
17%
Cardiac & muscle trauma
13%
Severe hypertension
7%
Acute neurological disease
5%
Pulmonary embolism3%
Various metabolic
1%
Circulation 2006;114:790

48. TnT in the general population:
Dallas Heart Study
≥0.03µg/L
(DM, CKD, CHF factor or LVH)
No TnT 99.3%
TnT 0.7%
Circulation 2006;113:1958-1965

49. Risk Stratification
UA or NSTEMI
-Evaluate for Invasive vs.
conservative treatment
-Directed medical
therapy
Based on initial
Evaluation, ECG, and
Cardiac markers
-Assess for reperfusion
-Select & implement reperfusion
therapy
-Directed medical therapy
STEMI
Patient?
YES NO

50. Cardiac Care Goals
•Decrease amount of myocardial necrosis
•Preserve LV function
•Prevent major adverse cardiac events
•Treat life threatening complications

53. Reperfusion
Greater use of
9-1-1
Prehospital Rx
MI protocol
Critical pathway
Quality
improvement
program
Bolus lytics
Dedicated PCI
team
5min<30 min
D-B ≤ 90 min
D-N ≤ 30 min
Goals
Prehospital
ECG
Patient Transport Inhospital Reperfusion
Methods of
Speeding Time
to Reperfusion

54. STEMI cardiac care
•STEP 1: Assessment
–Time since onset of symptoms
–Is this high risk STEMI?
–KILLIP classification
–If higher risk may manage with more invasive rx
–Determine if fibrinolysis candidate
–Meets criteria with no contraindications
–Determine if PCI candidate
–Based on availability and time to balloon rx

55. STEMI cardiac care
•STEP 2: Determine preferred reperfusion
strategy
Fibrinolysispreferred if:
<3 hours from onset
PCI not available/delayed
door to balloon > 90min
door to balloon minus
door to needle > 1hr
Door to needle goal <30min
No contraindications
PCIpreferred if:
PCI available
Door to balloon < 90min
Door to balloon minus
door to needle < 1hr
Fibrinolysis
contraindications
Late Presentation > 3 hr
High risk STEMI
Killup3 or higher
STEMI dxin doubt

58. Fibrinolysis indications
•ST segment elevation >1mm in two
contiguous leads
•New LBBB
•Symptoms consistent with ischemia
•Symptom onset less than 12 hrs prior to
presentation

59. Absolute contraindications for fibrinolysis therapy in
patients with acute STEMI
Absolute
Contraindications
•Any prior intracranial hemorrhage
•Known structural cerebral vascular lesion
(e.g., arteriovenous malformation)
•Known malignant intracranial neoplasm
(primary or metastatic)
•Ischemic stroke within 3 months EXCEPT
acute ischemic stroke within 3 hours
NOTE: Age restriction for fibrinolysis has been removed
compared with prior guidelines.

60. •Suspected aortic dissection
•Active bleeding or bleeding diathesis
(excluding menses)
•Significant closed-head or facial trauma
within 3 months
Absolute contraindications for fibrinolysis
therapy in patients with acute STEMI

61. •Recent (< 2 to 4 weeks) internal bleeding
•Noncompressiblevascular punctures
•For streptokinase/anistreplase: prior exposure (> 5
days ago) or prior allergic reaction to these agents
•Pregnancy
•Active peptic ulcer
•Current use of anticoagulants: the higher the INR,
the higher the risk of bleeding
Relative
Contraindications
Relative contraindications for fibrinolysis
therapy in patients with acute STEMI

62.  Initial treatment Co-therapy Contraindications
Streptokinase (SK) 1.5 million U in 100 mL None or iv Prior SK or
5% dextrose or 0.9% salineheparin x 2448 hours anistreplase
over 3060 min
Alteplase(tPA)15 mg iv bolus, then iv heparin x 2448 hours
0.75 mg/kg over 30 min,
then 0.5 mg/kg iv over 60 min
Total dose not over 100 mg
Reteplase(rPA)10 U + 10 U iv bolus given iv heparin x 2448 hours
30 min apart
TenecteplaseSingle iv bolus iv heparin x 2448 hours
(TNK-tPA) 30 mg if <60 kg
35 mg if 60 kg to <70 kg
40 mg if 70 kg to <80 kg
45 mg if 80 kg to <90 kg
50 mg if ≥90 kg
Common Thrombolytic Regimens for STEMI
Van de WerfF et al. EurHeart J2003; 24: 2866

63. Relative contraindications for fibrinolysis therapy in
patients with acute STEMI
•History of chronic, severe, poorly controlled
hypertension
•Severe uncontrolled hypertension on
presentation (SBP > 180 mm Hg or DBP >
110 mm Hg)
•History of prior ischemic stroke greater than
3 months, dementia, or known intracranial
pathology not covered in contraindications
•Traumatic or prolonged (> 10 minutes) CPR
or major surgery (< 3 weeks)
Relative
Contraindications

66. Comparing outcomes

68. Why not PPCI for all?
Is it the last remaining (Big) question

78. Should we interfere following
thrombolysis?

79. PCI After FibrinolysisIIIIIaIIaIIaIIbIIbIIbIIIIIIIIIIIIIIaIIaIIaIIbIIbIIbIIIIIIIIIIIIIIaIIaIIaIIbIIbIIbIIIIIIIIIIIaIIaIIaIIbIIbIIbIIIIIIIII IIIIIaIIaIIaIIbIIbIIbIIIIIIIIIIIIIIaIIaIIaIIbIIbIIbIIIIIIIIIIIIIIaIIaIIaIIbIIbIIbIIIIIIIIIIIaIIaIIaIIbIIbIIbIIIIIIIII IIIIIaIIaIIaIIbIIbIIbIIIIIIIIIIIIIIaIIaIIaIIbIIbIIbIIIIIIIIIIIIIIaIIaIIaIIbIIbIIbIIIIIIIIIIIaIIaIIaIIbIIbIIbIIIIIIIII
In patients whose anatomy is suitable, PCI should be
performed for the following:
Objective evidence of recurrent MI
Moderate or severe spontaneous/provocable
myocardial ischemia during recovery from STEMI
Cardiogenic shock or hemodynamic instability.

80. PCI After Fibrinolysis
It is reasonable to perform routine PCI in patients
with left ventricular ejection fraction (LVEF) ≤ 0.40,
CHF, or serious ventricular arrhythmias.
It is reasonable to perform PCI when there is
documented clinical heart failure during the acute
episode, even though subsequent evaluation
shows preserved LV function (LVEF > 0.40).IIIIIaIIaIIaIIbIIbIIbIIIIIIIIIIIIIIaIIaIIaIIbIIbIIbIIIIIIIIIIIIIIaIIaIIaIIbIIbIIbIIIIIIIIIIIaIIaIIaIIbIIbIIbIIIIIIIII IIIIIaIIaIIaIIbIIbIIbIIIIIIIIIIIIIIaIIaIIaIIbIIbIIbIIIIIIIIIIIIIIaIIaIIaIIbIIbIIbIIIIIIIIIIIaIIaIIaIIbIIbIIbIIIIIIIII IIIIIaIIaIIaIIbIIbIIbIIIIIIIIIIIIIIaIIaIIaIIbIIbIIbIIIIIIIIIIIIIIaIIaIIaIIbIIbIIbIIIIIIIIIIIaIIaIIaIIbIIbIIbIIIIIIIII
Routine PCI might be considered as part of
an invasive strategy after fibrinolytic therapy.

81. REPERFUSION THERAPY 2008
prehospital ECG: STEMI
experienced PCI within 90 min
yes no
primary PCI
w/o facilitation
fibrinolysis
no yes
rescue PCI delayed PC
Risk assessment

82. Rescue PCI

83. Rescue PCI

84. Rescue PCI
Rescue PCI should be performed in patients less
than 75 years old with ST elevation or LBBB who
develop shock within 36 hours of MI and are
suitable for revascularization that can be
performed within 18 hours of shock.
Rescue PCI should be performed in patients with
severe CHF and/or pulmonary edema (Killip class
3) and onset of symptoms within 12 hours.IIIIIaIIaIIaIIbIIbIIbIIIIIIIIIIIIIIaIIaIIaIIbIIbIIbIIIIIIIIIIIIIIaIIaIIaIIbIIbIIbIIIIIIIIIIIaIIaIIaIIbIIbIIbIIIIIIIII IIIIIaIIaIIaIIbIIbIIbIIIIIIIIIIIIIIaIIaIIaIIbIIbIIbIIIIIIIIIIIIIIaIIaIIaIIbIIbIIbIIIIIIIIIIIaIIaIIaIIbIIbIIbIIIIIIIII

85. Rescue PCI
IIIIIaIIaIIaIIbIIbIIbIIIIIIIIIIIIIIaIIaIIaIIbIIbIIbIIIIIIIIIIIIIIaIIaIIaIIbIIbIIbIIIIIIIIIIIaIIaIIaIIbIIbIIbIIIIIIIII
Rescue PCI is reasonable for selected patients 75
years or older with ST elevation or LBBB or who
develop shock within 36 hours of MI and are
suitable for revascularization that can be performed
within 18 hours of shock.
It is reasonable to perform rescue PCI for patients
with one or more of the following:
a. Hemodynamic or electrical instability
b. Persistent ischemic symptoms. IIIIIaIIaIIaIIbIIbIIbIIIIIIIIIIIIIIaIIaIIaIIbIIbIIbIIIIIIIIIIIIIIaIIaIIaIIbIIbIIbIIIIIIIIIIIaIIaIIaIIbIIbIIbIIIIIIIII

86. PCI for CardiogenicShock

87. PCI for CardiogenicShock
Primary PCI is reasonable for selected patients
75 years or older with ST elevation or LBBB or
who develop shock within 36 hours of MI and
are suitable for revascularization that can be
performed within 18 hours of shock. IIIIIaIIaIIaIIbIIbIIbIIIIIIIIIIIIIIaIIaIIaIIbIIbIIbIIIIIIIIIIIIIIaIIaIIaIIbIIbIIbIIIIIIIIIIIaIIaIIaIIbIIbIIbIIIIIIIII IIIIIaIIaIIaIIbIIbIIbIIIIIIIIIIIIIIaIIaIIaIIbIIbIIbIIIIIIIIIIIIIIaIIaIIaIIbIIbIIbIIIIIIIIIIIaIIaIIaIIbIIbIIbIIIIIIIII
Primary PCI is recommended for patients less than
75 years with ST elevation or LBBB or who develop
shock within 36 hours of MI and are suitable for
revascularization that can be performed within 18
hours of shock.

88. Right Ventricular Infarction
Clinical findings:
Shock with clear lungs, elevated JVP
Kussmaul sign
Hemodynamics:
Increased RA pressure (y descent)
Square root sign in RV tracing
ECG:
ST elevation in R sided leads
Echo:
Depressed RV function
Rx:
Maintain RV preload
Lower RV afterload (PA---PCW)
Inotropic support
Reperfusion
V
4R
Modified from Wellens. N Engl J Med
1999;340:381.

89. Ventricular Septal
Rupture
Incidence 1-2% 1-6% 1-2%
Timing 3-5 d p MI 3-6 d p MI 3-5 d p MI
Phy Exam murmur 90% JVD, EMD murmur 50%
Thrill Common No Rare
Echo Shunt Peric. Effusion Regurg. Jet
PA cath O
2step up Diast Press Equal.c-v wave in PCW
Free Wall
Rupture
Mitral Regurgitation
(Pap. M. dysfunction)
Images:Courtesy of W D Edwards (Mayo Foundation)
Data: Lavocitz. CV Rev Rpt 1984;5:948; Birnbaum. NEJM 2002;347:1426.

90. Cardiogenic Shock
Early Shock, Diagnosed on
Hospital Presentation
Fibrinolytic therapy if all of the
following are present:
1.Greater than 90 minutes to PCI
2.Less than 3 hours post STEMI
onset
3. No contraindications
Arrange prompt transfer to invasive
procedure-capable center
IABP
Delayed Onset Shock Echocardiogram
to Rule Out Mechanical Defects
IABP
Arrange rapid transfer to invasive
procedure-capable center
1-2 vessel CAD Moderate 3-vessel CAD Severe 3-vessel CAD Left main CAD
PCI IRA PCI IRA
Immediate CABG
Staged Multivessel
PCI
Staged CABG
Cannot be
performed
Cardiac Catheterization and Coronary
Angiography
PCI for Cardiogenic Shock

91. Medical Therapy
MONA + BAH
•Morphine(class I, level C)
•Analgesia
•Reduce pain/anxiety—decrease sympathetic tone,
systemic vascular resistance and oxygen demand
•Careful with hypotension, hypovolemia, respiratory
depression
•Oxygen(2-4 liters/minute) (class I, level C)
•Up to 70% of ACS patient demonstrate hypoxemia
•May limit ischemic myocardial damage by increasing
oxygen delivery/reduce ST elevation

92. •Nitroglycerin(class I, level B)
•Analgesia—titrate infusion to keep patient pain free
•Dilates coronary vessels—increase blood flow
•Reduces systemic vascular resistance and preload
•Careful with recent ED meds, hypotension, bradycardia,
tachycardia, RV infarction

94. Aspirin(160-325mg chewed & swallowed) (class I, level A)
Irreversible inhibition of platelet aggregation
Stabilize plaque and arrest thrombus
Reduce mortality in patients with STEMI
Careful with active PUD, hypersensitivity, bleeding
disorders

97. Clopidogrel in ACS
STEMI NSTEMI Elective PCI
CLARITY: 28
days Rx (loading
dose given)
CURE (up to 12
months mean 9
months)
CREDO (all got
clopidogrel for
28 days then
randomised up to
1 year)
COMMIT 28
days Rx (no
loading dose)

98. Early and Long-Term Benefits of Clopidogrel
in UA/NSTEMI

102. Odds ratio & 95% CI
Clopidogrel betterPlacebo better
Outcome Clopidogrel Placebo
after re-MI (n=22,958) (n=22,891)
Fatal MI 209 (0.9%) 223 (1.0%)
Non-fatal MI 273 (1.2%)330 (1.4%)
ALL 482 (2.1%)553 (2.4%)
13%
reduction
p=0.02
0.40.60.81.01.21.41.6
Clopidogrel Decreased Re-Infarction
1.Chen ZM et al. Oral presentation, ACC 2005

103. Summary of Trials of Beta-Blocker Therapy
Phase of
Treatment
Acute
treatment
Secondary
prevention
Overall
Total No.
Patients
28,970
24,298
53,268
0.5 1 2
Relative risk (RR) of death
Beta blocker
better
RR (95% CI)
Placebo
better
0.87 (0.77-0.98)
0.77 (0.70-0.84)
0.81 (0.75-0.87)
Antman E, Braunwald E. Acute Myocardial Infarction. In:
Braunwald E, Zipes DP, Libby P, eds. Heart Disease: A
textbook of Cardiovascular Medicine, 6th ed.,
Philadelphia, PA: W.B. Sanders, 2001, 1168.

104. •Beta-Blockers(class I, level A)
•14% reduction in mortality risk at 7 days at 23% long
term mortality reduction in STEMI
•Approximate 13% reduction in risk of progression to
MI in patients with threatening or evolving MI
symptoms
•Be aware of contraindications (CHF, Heart block,
Hypotension)
•Reassess for therapy as contraindications resolve

105. ACC/AHA STEMI Guidelines 07
2007 STEMI Focused
Update Recommendation
Comments
2004 STEMI Guideline
Recommendation
*Risk factors for cardiogenic shock (the greater the number of risk factors, the higher the risk of developing cardiogenic shock) are age gender greater than
70 years, systolic blood pressure less than 1.20 mm Hg, sinus tachycardia greater than 100 hpm or heart rate less than 60 bpm, and increased time since
onset of symptoms of STEMI.
i.v. indicates intravenous; LOE: level of evidence; LV: left ventricular; PCI = percutaneous coronary intervention; and STEMI, ST elevation myocardial
infarction
IV beta blockers promptly to
STEMI patients without
contraindications, especially if
a tachyarrhythmia or
hypertension is present. It is
reasonable to administer
(Level of Evidence: B)
Class IIa
1. It is reasonable to administer IV beta blocker to STEMI pts
at presentation who are hypertensive & do not have: 1) signs
of HF; 2) evidence of low output; 3) increased risk* for
cardiogenic shock; 4) other relative beta blocker
contraindications (PR > 0.24 secs, 2
nd
or 3
rd
degree HB,
active asthma, or reactive airway disease) (LOE: B)
Beta Blockers
Modified
recommendation
(changed text)
New
Class III
1. IV beta blockers should not be administered to STEMI pts
who have: 1) signs HF; 2) evidence of a low output ; 3)
increased risk* for cardiogenic shock, or 4) other relative
contraindications to beta blockers (PR > 0.24 secs, 2
nd
or 3
rd
degree HB, active asthma, or reactive airway disease) (LOE:
A)
New
Class III
1. IV beta blockers should not be administered to STEMI pts
who have: 1) signs HF; 2) evidence of a low output ; 3)
increased risk* for cardiogenic shock, or 4) other relative
contraindications to beta blockers (PR > 0.24 secs, 2
nd
or 3
rd
degree HB, active asthma, or reactive airway disease) (LOE:
A)
New

106. All-Cause Mortality
Years
Probability of Event
0
0.05
0.
1
0.15
0.2
0.25
0.3
0 1 2 3
0.35
0.4
4
ACE-I
Placebo
OR: 0.74 (0.66–0.83)
ACE-I: 702/2995 (23.4%)
Placebo: 866/2971 (29.1%)
TRACE
Echocardiographic
EF 35%
AIRE
Clinical and/or
radiographic
signs of HF
SAVE
Radionuclide
EF 40%
ACE-I2995 2250 1617 892 223
Placebo2971 2184 1521 853 138
Flather MD, et al. Lancet. 2000;355:1575–1581

107. Captopril
0
0.05
0.1
0.15
0.2
0.25
0.3
0 6 12 18 24 30 36
Probability
Mortality by Treatment
Months
Valsartan vs. Captopril: HR = 1.00; P = 0.982
Valsartan + Captopril vs. Captopril: HR = 0.98; P = 0.726
Valsartan
Valsartan + Captopril
Captopril4909 4428 4241 4018 2635 1432 364
Valsartan4909 4464 4272 4007 2648 1437 357
Valsartan + Cap4885 4414 4265 3994 2648 1435 382
Pfeffer, McMurray, Velazquez, et al. N Engl J Med2003;349

108. P = 0.008
RR = 0.85 (95% CI, 0.75–0.96)
EPHESUS: All-Cause Mortality
Eplerenone3319 3044 2463 1260 336 0 0
Placebo3313 2983 2418 1213 323 2 0
Month 6 12 18 24 30 36
0
5
10
15
20
25
Cumulative Incidence (%)
0
Eplerenone
Placebo
Pitt et al. N Engl J Med2003;348:1309-1321

109. ACE/ARB: Within 24 Hours
An ACE inhibitor should be administered orally
within the first 24 hours of STEMI to the following
patients without hypotension or known class of
contraindications:
•Anterior infarction
Pulmonary congestion
LVEF < 0.40
An ARB should be given to ACE-intolerant patients
with either clinical or radiological signs of HF or LVEF
< 0.40.IIIIIaIIaIIaIIbIIbIIbIIIIIIIIIIIIIIaIIaIIaIIbIIbIIbIIIIIIIIIIIIIIaIIaIIaIIbIIbIIbIIIIIIIIIIIaIIaIIaIIbIIbIIbIIIIIIIII IIIIIaIIaIIaIIbIIbIIbIIIIIIIIIIIIIIaIIaIIaIIbIIbIIbIIIIIIIIIIIIIIaIIaIIaIIbIIbIIbIIIIIIIIIIIaIIaIIaIIbIIbIIbIIIIIIIII

110. ACE/ARB: Within 24 Hours
An intravenous ACE inhibitor should not be given to
patients within the first 24 hours of STEMI because
of the risk of hypotension (possible exception:
refractory hypotension).IIIIIaIIaIIaIIbIIbIIbIIIIIIIIIIIIIIaIIaIIaIIbIIbIIbIIIIIIIIIIIIIIaIIaIIaIIbIIbIIbIIIIIIIIIIIaIIaIIaIIbIIbIIbIIIIIIIII IIIIIaIIaIIaIIbIIbIIbIIIIIIIIIIIIIIaIIaIIaIIbIIbIIbIIIIIIIIIIIIIIaIIaIIaIIbIIbIIbIIIIIIIIIIIaIIaIIaIIbIIbIIbIIIIIIIII
An ACE inhibitor administered orally can be useful
within the first 24 hours of STEMI to the following
patients without hypotension or known class
contraindications:
Anterior infarction
Pulmonary congestion
LVEF < 0.40.

111. Aldosteroneblockers(class I, level A)
Post-STEMI patients
no significant renal failure (cr< 2.5 men or 2.0 for
women)
No hyperkalemis> 5.0
LVEF < 40%
Symptomatic CHF or DM

112. •Heparin(class I, level C to class IIa, level C)
–LMWH or UFH(max 4000u bolus, 1000u/hr)
•Indirect inhibitor of thrombin
•less supporting evidence of benefit in era of reperfusion
•Adjunct to surgical revascularization and thrombolytic /
PCI reperfusion
•24-48 hours of treatment
•Coordinate with PCI team (UFH preferred)
•Used in combo with aspirin and/or other platelet
inhibitors
•Changing from one to the other not recommended

119. Compared with UFH, enoxaparin was a/w with superior efficacy as adjunctive
antithrombin therapy among 49 000 patients across the ACS spectrum
Although bleeding was increased with enoxparin this increase was offset by a
reduction in death or MI. The net clinical benefit in favour of enoxaparin was
evident among the STEMI population and was neutral among the NSTEACS
population

130. ACC/AHA STEMI Guidelines 07
Anticoagulants Ancillary Reperfusion
New
Class IIa
1. Patients undergoing reperfusion with fibrinolytics:
2007 STEMI Focused
Update Recommendation
Comments
Should receive anticoagulant therapy for minimum of 48 hours
(LOE:C) & preferably for duration index hospitalization up to 8 days
(regimens otherthan UFH recommended if anticoagulant therapy is
given for > 48 hrs because of risk of HIT with prolonged Rx (LOE: A)
Anticoagulant regimens with established efficacy include:
a) UFH (initial IV bolus 60 U/ kg {max 4000 U} followed by IV infusion
12 U/ kg/hr per hour (max 1000 U/ hour) initially, adjusted to maintain
APTT at 1.5 to 2.0 x control (approximately 50 to 70 secs) (LOE: C).
(Note: available data do not suggest benefit of prolonging duration
UFH infusion > 48 hrs in absence of ongoing indications; more
prolonged infusions increase risk of HIT)
2004 STEMI
Guideline
Recommendation

131. ACC/AHA STEMI Guidelines 07
Anticoagulants Ancillary Reperfusion (ii)
Class IIa
New1. Patients undergoing reperfusion with fibrinolytics:
Anticoagulant regimens with established efficacy include:
b) Enoxaparin (provided creatinine < 2.5 mg in men & 2.0 mg/dL in
women); for pts < 75 yrs, an initial 30 mg IV bolus, followed 15 minutes
later by SC 1.0 mg/kg q12 hrs; for pts >75 yrs, omit initial IV bolus &
reduce SC dose to 0.75 mg/kg q 12 hrs. Regardless of age, if CrCl
(Crockroft-Gault ) during Rx is < 30 mL /min, the SC regimen is 1.0 mg/kg
q 24 hrs. Maintenance dosing with enoxaparin should be continued for the
duration of the index hospitalization, up to 8 days. (LOE: A)
c) Fondaparinux (provided serum creatinine < 3.0 mg/dL): initial dose 2.5
mg IV; subsequently SC 2.5 mg once daily. Maintenance dosing with
fondaparinux should be continued for the duration of the index
hospitalization, up to 8 days. (LOE: A)
2007 STEMI Focused
Update Recommendation
Comments
2004 STEMI
Guideline
Recommendation

132. ACC/AHA STEMI Guidelines 2007
Anticoagulants Ancillary Reperfusion (iii)
2007 STEMI Focused
Update Recommendation Comments
a. For prior Rx with UFH, administer additional boluses of UFH as needed to support
the procedure, taking into account whether GP IIb/IIIa antagonists have been
administered. (LOE:C). Bivalirudin may also be used in pts treated previously
with UFH. (LOE:C).
b.For prior treatment with enoxaparin, if last SC dose < 8 hrs, no additional
enoxaparin should be given; if last SC dose > 8 to 12 hrs earlier, an IV dose of
0.3 mg/kg of enoxaparin should be given (LOE:B)
c. For prior treatment with fondaparinux, administer additional IV Rx with an
anticoagulant possessing anti-IIa activity taking into account whether GP IIb/IIIa
receptor have been administered. (LOE:C).
Class III
1. Because of risk of catheter thrombosis, fondaparinux should not be used as the
sole anticoagulant to support PCI. An additional anticoagulant with anti-IIa activity
should be administered. (LOE:C)
New
2004 STEMI
Guideline
Recommendation
Class I
New
2. For patients undergoing PCI
after receiving an anticoagulant, the following dosing recommendation should be
followed:

133. Additional medication therapy
•Clopidodrel(class I, level B)
•Irreversible inhibition of platelet aggregation
•Used in support of cath / PCI intervention or if
unable to take aspirin
•3 to 12 month duration depending on scenario
•Glycoprotein IIb/IIIa inhibitors
(class IIa, level B)
•Inhibition of platelet aggregation at final common
pathway
•In support of PCI intervention as early as possible
prior to PCI

135. ACC/AHA STEMI Guidelines 07
Thienopyridines
2007 STEMI Focused
Update Recommendation
Comments
2004 STEMI Guideline
Recommendation
1.In patients taking clopidogrel in whom CABG is planned, the drug
should be withheld for at least 5 days and preferably 7 days
unless the urgency for revascularization outweighs the risks of
excess bleeding. (LOE: B)
2.Clopidogrel 75mg per day orally should be added to aspirin in
patients with STEMI regardless of whether they undergo
reperfusion with fibrinolytic therapy or do not receive reperfusion
therapy. (LOE: A) Treatment with clopidogrel should continue for
at least 14 days.(LOE: B)
Class I
Class IIa
New
New
New
Class IIa
1.In patients <75 years who receive fibrinolytic therapy or who do
not receive reperfusion therapy, it is reasonable to administer an
oral loading dose of clopidogrel 300 mg. (LOE: C) (No data are
available to guide decision making regarding an oral loading dose
in patients >75 years.)
2.Long-term maintenance therapy (e.g. 1 year) with clopidogrel (75
mg/day orally) is reasonable in STEMI patients regardless of
whether they undergo reperfusion with finrinolytics therapy or do
not receive reperfusion therapy. (LOE: C)
2004 recommendation
remains current in
2007 update
In patients taking
clopidogrel for whom
CABG is planned, the drug
should be withheld for at
least 5 days and preferably
7 days unless urgency for
revascularizationoutweighs
the risk of excess bleeding
(LOE: B)

136. STEMI care CCU
•Monitor for complications:
•recurrent ischemia, cardiogenic shock, ICH, arrhythmias
•Review guidelines for specific management of
complications & other specific clinical
scenarios
•PCI after fibrinolysis, emergent CABG, etc…
•Decision making for risk stratification at
hospital discharge and/orneed for CABG

137. Unstable angina/NSTEMI cardiac care
•Evaluate for conservative vs. invasive therapy
based upon:
•Risk of actual ACS
•TIMI risk score
•ACS risk categories per AHA guidelines
Low
Intermediate
High

138. TIMI Risk Score
Predicts risk of death, new/recurrent MI, need for urgent
revascularization within 14 days

139. ACS risk criteria
Low Risk ACS
No intermediate or high
risk factors
<10 minutes rest pain
Non-diagnositic ECG
Non-elevated cardiac
markers
Age < 70 years
Intermediate Risk ACS
Moderate to high likelihood
of CAD
>10 minutes rest pain,
now resolved
T-wave inversion > 2mm
Slightly elevated cardiac
markers

140. High Risk ACS
Elevated cardiac markers
New or presumed new ST depression
Recurrent ischemia despite therapy
Recurrent ischemia with heart failure
High risk findings on non-invasive stress test
Depressed systolic left ventricular function
Hemodynamic instability
Sustained Ventricular tachycardia
PCI with 6 months
Prior Bypass surgery

141. Low
risk
High
risk
Conservativ
e therapy
Invasive
therapy
Chest Pain
center
Intermediate
risk

142. Early Invasive versus no early invasive

145. Invasive therapy option
UA/NSTEMI
•Coronary angiography and revascularization
within 12 to 48 hours after presentation to ED
•For high risk ACS (class I, level A)
•MONA + BAH(UFH)
•Clopidogrel
–20% reduction death/MI/Stroke –CURE trial
–1 month minimum duration and possibly up to 9 months
•Glycoprotein IIb/IIIa inhibitors

146. Conservative Therapy for UA/NSTEMI
•Early revascularization or PCI notplanned
•MONA + BAH(LMW or UFH)
•Clopidogrel
•Glycoprotein IIb/IIIa inhibitors
–Only in certain circumstances (planning PCI, elevated
TnI/T)
•Surveillence in hospital
–Serial ECGs
–Serial Markers

150. Clinical suspicion of ACS
Physical examination
Electrocardiogram (ECG) monitoring, blood samples
Undetermined
diagnosis
Persistent
ST-segment elevation
No persistent
ST-segment elevation
ASA, LMWH,
clopidogrel*, beta-blockers, nitrates
Thrombolysis
PCI
High risk Low risk
GPIIb/IIIa,
coronary angiography
Stress test,
coronary angiography
Second troponin measurement
Positive Twice negative
ASA
PCI, CABG or medical management
depending upon clinical and angiographic features
*Omit clopidogrel if
the patient is likely to
go to CABG within 5
days
ESC Recommended Strategy in ACS Patients
Eur Heart J2002; 23; 18091840

151. Adjunctive medical therapy for ACS

155. Secondary Prevention
•Disease
–HTN, DM, HLP
•Behavioral
–smoking, diet, physical activity, weight
•Cognitive
–Education, cardiac rehab program

157. Summary
•ACS includes UA, NSTEMI, and STEMI
•Management guideline focus
–Immediate assessment/intervention (MONA+BAH)
–Risk stratification (UA/NSTEMI vs. STEMI)
–RAPID reperfusion for STEMI (PCI vs.
Thrombolytics)
–Conservative vs Invasive therapy for UA/NSTEMI
•Aggressive attention to secondary prevention
initiatives for ACS patients
•Beta blocker, ASA, ACE-I, Statin

158. Thank you for your attention !