DEFINITION

Acute myocardial infarction can be defined from a

number of different perspectives related to clinical,
electrocardiographic (ECG), bio-chemical, and
pathological characteristics.
The present guidelines pertain to patients presenting
with ischaemic symptoms and persistent ST-segment
elevation on the ECG (STEMI).
The great majority of these patients will show a typical
rise of biomarkers of myocardial necrosis and progress
to Q-wave myocardial infarction.
Separate guidelines patients presenting with ischaemic
symptoms but withoutpersistent ST-segment elevation.
2012 by the European Society of Cardiology, American College
of Cardiology Foundation, American Heart Association, Inc., and
the World Heart Federation

Criteria for Acute, Evolving, or Recent MI Either of the

following criteria satisfies the diagnosis for acute, evolving, or
recent MI:

1. Typical rise and/or fall of biochemical markers of

myocardial
necrosis with at least one of the
following :
a. Ischemic symptoms
b. Development of pathologic Q waves in the ECG
c. Electrocardiographic changes indicative of ischemia (STsegment elevation or depression)
d.Imaging evidence of new loss of viable myocardium or new
regional wall motion abnormality

2. Pathologic findings of an acute myocardial infarction

2012 by the European Society of Cardiology, American
College of Cardiology Foundation, American Heart Association,
Inc., and the World Heart Federation

EPIDEMIOLOGI

PATHOGENESIS
The hallmark is the sudden imbalance between myocardial oxygen
consumption (MVO2) and demand,which is usually the result of
coronary artery obstruction.
The imbalance may also be caused by other conditions, including
excessive myocardial oxygen demand in the setting of a stable flowlimiting lesion; acute coronary insufficiency due to other causes (e.g.,
vasospastic, angina, coronary embolism, coronary arteritis);
Noncoronary causes of myocardial oxygen supply-demand mismatch
(e.g. hypotension, severe anemia, hypertension, tachycardia,
hypertrophic cardiomyopathy, severe aortic stenosis);
Nonischemic myocardial injury (e.g., myocarditis, cardiac contusion,
cardiotoxic drugs); and multifactorial
Causes that are not mutually exclusive (e.g., stress cardiomyopathy
,pulmonary embolism, severe heart failure [HF], sepsis).

Expanding Risk Factors

Smoking
Hypertension
Diabetes Mellitus
Dyslipidemia
Low HDL < 40
Elevated LDL / TG

Family Historyevent
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 Etoh intake
Lack of diet rich in
fruit, veggies, fiber

Type Miocardial Infarction

2012 by the European Society of Cardiology, American College of Cardiology Foundatio

American Heart Association, Inc., and the World Heart Federation

 2012 by the European Society of Cardiology, American College of Cardiology Foundatio

American Heart Association, Inc., and the World Heart Federation

 2012 by the European Society of Cardiology, American College of Cardiology Foundatio

American Heart Association, Inc., and the World Heart Federation

CLINICAL PRESENTATION
Chest pain is the usual symptom which brings these patients
to medical attention. Pain is severe, diffuse, retrosternal and
radiates to arms or from jaws to umbilicus. Pain does not get
relieved with sublingual nitrates or usual pain killers. It is often
associated with eructations and retrosternal burning.
Commonly patients mistake it for acid peptic symptoms and
waste precious time with antacids. It is accompanied with
vomiting, sweating
and breathlessness. About 15-20% of infarcts can be painless
specially in elderly and diabetics. Equal number may have less
characteristic pain than described above. The pain needs to be
distinguished from other causes of acute severe chest pain
which can bring patients to emergency room.
Pandey et al, 2011

 Thus, although pain of myocardial infarction is quite

distinctive it may be mimicked by other conditions. A
good short history of type of pain, duration,
accompanying symptoms, risk factors and preceding
activities before the pain can be useful.
Examination of pulse and blood pressure and
respiratory rate help greatly in risk stratification of
these patients.
Palpation and auscultation are also helpful in these
acutely distressed individuals.
In the hurry to do an early ECG these things should
not be missed.
Pandey et al, 2011

Electrocardiography
ECG is generally the first investigation available for
making a diagnosis in a patient presenting with acute
severe chest pain.
Tall T waves and ST elevation are the hallmarks of
early presentation within minutes of onset of pain.
The third change appearance of Q waves, is
delayed and seen after 6 hours of onset. Q waves
denote significant myocardial necrosis.
The initial changes of upright and tall T wave with
concave upward ST segment elevation subsequently,
gives way to T wave inversion and ST coving with
convexity upwards over one day to one week.
Pandey et al, 2011

 Shortly after occlusion of a coronary artery, serial

ECG changes are detected by leads facing the
ischemic zone
First, the T waves become tall, symmetrical, and
peaked (grade 1 ischemia).
Second, there is ST elevation (grade 2 ischemia)
without distortion of the terminal portion of the QRS.
Third, changes in the terminal portion of the QRS
complex may appear (grade 3 ischemia).
The changes in the terminal portion of the QRSare
explained by prolongation of the electrical conduction
in the Purkinje fibers in the ischemic region.
Pandey et al, 2011

Echocardiography
Echocardiography is helpful in the
evaluation of chest pain, especially
during active chest pain.
The absence of LV wall motion
abnormalities during chest pain usually
but not always excludes myocardial
ischemia or infarction, and the presence
of regional wall motion abnormalities
helps in confirming the diagnosis
Pandey et al, 2011

CARDIAC BIOMARKERS
Cardiac biomarkers have conventionally being
used for diagnosis of acute myocardial infarction.
These have also been used in patients with
NSTEMI and unstable angina for finding high risk
individuals.
Elevation of CPK, CPK-MB and Troponins I and T
occurs in all patients with myocardial necrosis
that is seen in myocardial infarction.
Serial CK-MB estimations were done earlier for
estimation
of
infarct
size
before
echocardiography.
Pandey et al, 2011

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

Initial Risk Stratification Scheme

Chest Pain
History, Physical
EKG

STEMI

UA/NSTEMI/
High Risk

Mod Risk

Low Risk

Definite
Non-Cardiac

Risk Stratification

YES

STEMI
Patient?

- Assess for
reperfusion
- Select &
implement
reperfusion
therapy
- Directed medical
therapy

Based on initial
Evaluation, ECG, and
Cardiac markers

NO

UA or NSTEMI
- Evaluate for
Invasive vs.
conservative
treatment
- Directed medical
therapy

STEMI cardiac care

STEP 1: Assessment
Time since onset of symptoms
90 min for PCI / 12 hours for fibrinolysis

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
2008 by the European Society of Cardiology,
rx

STEMI cardiac care

STEP 2: Determine preferred reperfusion strategy

Fibrinolysis preferred
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

PCI preferred if:

PCI available
Door to balloon <
90min
Door to balloon
minus door to needle
< 1hr
Fibrinolysis
contraindications
Late Presentation >
3 hr
High risk STEMI

2008 by the European Society of Cardiology,

Killup 3 or higher

Medical Therapy

Morphine
Analgesia
Reduce pain/anxietydecrease sympathetic
tone, systemic vascular resistance and
oxygen demand
Careful with hypotension, hypovolemia,
respiratory depression

Oxygen
Up to 70% of ACS patient demonstrate
hypoxemia
May limit ischemic myocardial damage by
increasing oxygen delivery/reduce ST
elevation
2008 by the European Society of Cardiology,

 Nitroglycerin
Analgesiatitrate infusion to keep patient
pain free
Dilates coronary vesselsincrease blood
flow
Reduces systemic vascular resistance and
preload
Careful with recent ED (erectile dysfunction)
meds, hypotension, bradycardia,
tachycardia, RV infarction

Aspirin

(160-325mg chewed & swallowed)

Irreversible inhibition of platelet aggregation
Stabilize plaque and arrest thrombus
Reduce mortality in patients with STEMI
2008 by the European Society of Cardiology,
Careful with active gastrointestinal bleeding,

 Beta-Blockers
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

ACE-Inhibitors / ARB
Start in patients with anterior MI, pulmonary
congestion, LVEF < 40% in absence of
contraindication/hypotension
Start in first 24 hours
2008 by the European Society of Cardiology,
ARB as substitute for patients
unable to use

 Heparin
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 Used in combo with
aspirin and/or other platelet inhibitors
Changing from one to the other not recommended

2008 by the European Society of Cardiology,

Additional medication therapy

Clopidodrel
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

Inhibition of platelet aggregation at final
common pathway
In support of PCI intervention as early as
possible prior to PCI
2008 by the European Society of Cardiology,

Unstable angina/NSTEMI
care

cardiac

Evaluate for conservative vs. invasive

therapy based upon:
Risk of actual ACS
TIMI risk score
ACS risk categories per AHA guidelines

Low

High
Intermediate

Risk Stratification to Determine the Likelihood of

Acute Coronary
Findings indicating
Findings indicating
Syndrome Findings indicating
Assessment
HIGH likelihood of ACS

INTERMEDIATE

LOW likelihood of ACS

likelihood of ACS in
absence of highlikelihood findings

in absence of high- or
intermediate-likelihood
findings

History

Chest or left arm pain or

discomfort as chief
symptom
Reproduction of previous
documented angina
Known history of coronary
artery disease, including
myocardial infarction

Chest or left arm pain or

discomfort as chief
symptom
Age > 50 years

Probable ischemic
symptoms
Recent cocaine use

Physical
examination

New transient mitral

regurgitation,
hypotension, diaphoresis,
pulmonary edema or rales

Extracardiac vascular
disease

Chest discomfort
reproduced by palpation

ECG

New or presumably new

transient ST-segment
deviation (> 0.05 mV) or Twave inversion (> 0.2 mV)
with symptoms

Fixed Q waves
Abnormal ST segments or
T waves not documented
to be new

T-wave flattening or
inversion of T waves in
leads with dominant R
waves
Normal ECG

Serum cardiac
markers

Elevated cardiac troponin

T or I, or elevated CK-MB

Normal

Normal

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

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

LOW
RISK

INTERMEDIAT
E RISK

HIGH RISK

Chest Pain
center

Conservati
ve therapy

Invasive
therapy

Conservative Therapy for

UA/NSTEMI
Early revascularization or PCI not
planned
MONA + Anticoagulant
Clopidogrel
Glycoprotein IIb/IIIa inhibitors
Only in certain circumstances (planning PCI,
elevated TnI/T)

Surveillence in hospital
Serial ECGs
Serial Markers

Invasive therapy option

UA/NSTEMI
Coronary angiography and
revascularization within 12 to 48 hours
after sign and symptom
For high risk ACS (class I, level A)
MONA + Anticoagulant
Clopidogrel
20% reduction death/MI/Stroke
1 month minimum duration and possibly up to 9
months

Glycoprotein IIb/IIIa inhibitors