acs update
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ACUTE CORONARY
SYNDROMESR MAHARAJ
EMERGENCY MEDICINE
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INTRODUCTION
Coronary Artery Disease leading cause of morbidity & mortality in
industrialised nations.
Although decrease in cardiovascular mortality still major cause of
morbidity & burden of disease.
South African perspective of cardiovascular disease:
A World in One Country - Yusuf et al
Epidemiological transitions of cardiovascular disease.
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HIGH RISK POPULATION FOR CAD/ACS:
INDIAN/WHITE/COLOURED
INCREASING rate in Black population lifestyle/socioeconomic
changes, urbanisation
GF Jooste stats: 23.8% of admissions to resus. unit for chest
pain/acs related (stats 1Jan 2009 28 Feb 2009) 150/628 entries.
In US 2004 1.56 million admissions for ACS 669 000 for
unstable angina, 896 000 for MI
Higher prevelance for NSTEMI.
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DEFINITIONS
CAD is a continuum of disease.
Angina -> unstable angina -> AMI -> sudden cardiac death
Acute coronary syndrome encompasses unstable angina, NSTEMI,STEMI
Stable angina transient episodic chest pain d/t myocardial
ischaemia, reproducible, frequency constant over time.usually
relieved with rest/NTG.
Classification of anginaCanadian Cardiovascular Societyclassification.
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Canadian Cardiovascular Association Classification of
Angina
CLASS 1 NO PAIN WITH ORDINARY PHYSICAL ACTIVITY
CLASS 2 SLIGHT LIMITATION OF PHYSICAL ACTIVITY
PAIN OCCURS WITH WALKING, CLIMBING
STAIRS,STRESS
CLASS 3 SEVERE LIMITATION OF DAILY ACTIVITY PAIN
OCCURS ON MINIMAL EXERTION
CLASS 4 UNABLE TO CONDUCT ANY ACTIVITY WITHOUT
PAIN, PAIN AT REST
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UNSTABLE ANGINA
Pain occurring at rest duration > 20min, within one week of first
visit
New onset angina ~ Class 2 severity, onset with last 2 months
Worsening of chest pain increase by at least 1 class, increases infrequency, duration
Angina becoming resistance to drugs that previously gave good
control.
NB! ECG normal, ST depression(>0.5mm), T wave changes
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ACUTE MYOCARDIAL INFARCTION
ECC/ACC DEFNrise and fall in cardiac enzymes with one or more
of the following:
Ischaemic type chest pain/symptoms
ECG changes ST changes, pathological Q waves Coronary artery intervention data
Pathological findings of an acute MI
NSTEMI = UNSTABLE ANGINA SYMPTOMS/FINDINGS +
POSITIVE CARDIAC ENZYMES
STEMI = ST ELEVATION ON ECG + SYMPTOMS
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WHY IS IT IMPORTANT TO RECOGNISE PATIENTS WITH
UNSTABLE ANGINA??
5 -17% suffer an MI within a week after admission.
3 -15% die within a year.
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ACS PATHOPHYSIOLOGY
Distruption of coronary artery
plaque -> platelet
activation/aggregation
/activation of coagulation
cascade -> endothelial
vasoconstriction ->intraluminal
thrombus/embolisation ->
obstruction -> ACS
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APPROACH
Identifying those with chest pain suggestive of IHD/ACS.
Thorough history required:
Character of pain
Onset and duration
Location and radiation
Aggravating and relieving factors
Autonomic symptoms
TYPICAL VS ATYPICAL HISTORY Failure to recognise symptoms other than chest pain -> approx 2 hr
delay in seeking medical attention
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CHARACTERISTICS OF TYPICAL ANGINAL CHEST PAIN
(ADAPTED FROM ROSENS, EMERGENCY MEDICINE)
CHARACTERISTIC SUGGESTIVE OF ANGINA LESS SUGGESTIVE OF
ANGINA
TYPE OF PAIN DULL
PRESSURE/CRUSHING
PAIN
SHARP/STABBING
DURATION 2-5 MIN,
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ATYPICAL PAIN
RISK FACTORS FOR DEVELOPING ATYPICAL PAIN:
Diabetes, females, non white patients, elderly, dementia, no prior history ofMI
ATYPICAL SYMPTOMS:
GIT symptoms
Syncope SOB
Pleuritic/positional pain
Chest wall tenderness
No chest pain/symptoms
NRMI 2 STUDY MI without chest pain -> increased risk of death (23% vs9%)
More complications hypotension,heart failure, stroke
Delayed ED presentation, delayed intervention
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RISK STRATIFICATION IN ACS
Reasons :
Provides prognostic information
Determines treatment and level of intervention -> low risk patientsearly discharge, high risk -> admission to high care
Helps decongest the ED and make available medical resources tomore needy patients
Risk stratification should be ongoing at admission, 6-8 hrs, 24hrs,discharge
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TOOLS USED IN RISK STRATIFICATION
HISTORY
ECG
BIOCHEMICAL MARKERS
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ECG
First point of entry into ACS algorithm
Abnormal or normal
Neither 100% sensitive or 100% specific for AMI
Single ECG for AMI sensitivity of 60%, specificity 90%
Represents single point in timeneeds to be read in context
Normal ECG does not exclude ACS 1-6% proven to have AMI, 4%unstable angina
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GUIDELINES:
Initial 12 lead ECG goal door to ECG time 10min, read by
experienced doctor (Class 1 B)
If ECG not diagnostic/high suspicion of ACS serial ECGs initially
15 -30 min intervals (Class 1 B)
ECG adjuncts leads V7V9, RV 4 (Class 2a B)
Continuous 12 lead ECG monitoring reasonable alternative to serial
ECGs (Class 2a B)
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BIOCHEMICAL MARKERS
IDEAL MARKER:
High concentration in myocardium
Myocardium specific
Released early in injury
Proportionate to injury Non expensive testing
Troponins
CKMB Myoglobin
Other markers
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TROPONINS T/I
Troponin T vs I
both equivalent in diagnostic and prognostic abilities ( except in
renal failure Trop T less sensitive)
Elevation ~ 2hrs to 12hrs
~30 40% of ACS patients without ST elevation had normal
CKMB but elevated troponins on presentation
Meta-analysis (Heindereich et al) odds of death increased 3 to 8
fold with positive troponin
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Mortality at 42 days in troponin positive patients
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MYOGLOBIN
Rapid release within 2 hours
Not cardiac specific
Rule out for NSTEMI rather than rule in.
CKMB
Used in conjunction with troponinsUseful in diagnosing re-infarction
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MARKER CHANGE SCORES
2 hour delta CKMB mass
Aim to exclude MI within 6hrs of symptom onset
Determine changes in serum marker levels over certain timeintervalsdelta values
Increasing values while still within normal range suggestive of
ischaemia more rapid anti- ischaemic mxn.
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OTHER MARKERS
INDICATORS OF INFLAMMATION OR ACTIVATION OF
COAGULATION CASCADE:
Myeloperoxidase, soluble CD40 ligand, IL6, hsCRP, d dimer,
prothrombin fragment 1 & 2
Elevated before onset of irreversible injury
Lack specificity
Complex lab assays
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ISCHAEMIA MODIFIED ALBUMIN
Measured with albumin cobalt binding assay
In ischaemia -> decreased binding of albumin to cobalt
Increased with minutes of ischaemia elevated for 6-12hrs gone
by 24hrs
~90% negative predictive value Combined with myoglobin/CKMB/troponin increases diagnostic
sensitivity of ischaemia by 40%
Possible role for rule criteria in low risk patients
Positive IMA high risk patients more aggressive mxn
Positive in hypoxic disorders poor specificity in this setting
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Btype Natriuretic Peptide:
released from heart muscle in response to increased ventricular wall
stress.
Studies BNP not a specific marker but a strong predictor of ACS
especially in patients with chest pain, no ECG changes, nondiagnostic troponins.
Also positive in heart failure, PE, atrial arrythmias, renal failure
Pregnancy Associated Plasma Protein A (PAPP-A):
Released when plaque ruptures
Predictor of ischaemia
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HEART FATTY ACID BINDING PROTEIN (HF ABP)
Identifies AMI
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2007 ACC/AHA guidelines: Cardiac biomarkers measured in all patients with suspicion of ACS
(Class 1 B)
Troponin preferred marker( Class 1 B)
If troponin negative within 6 hours of onset, repeat 8-12hours
later(Class 1 B) Remeasuring of positive biomarkers to determine infarctsize/necrosis (Class 2a B)
Patients presenting within 6 hours of symptom onset myoglobin inconjunction with troponin measured (Class 2b B)
2hr delta CKMB/Delta troponin considered in
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RISK STRATIFICATION MODELS
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TIMI RISK SCOREincrease in mortality with increasing score ~40%
all cause mortality at 14 days for patients requiring urgent
revascularisation
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WHICH MODEL IS MOST APPROPRIATE??
2007 ACS/AHA GUIDELINES:
Risk stratification models useful in decision making with regard to
treatment options ( Class 2a B)
TIMI vs GRACE vs PURSUIT
PURSUIT & GRACE risk scores allow better discrimination of in
hospital and 1 year mortality in patients compared to TIMI. (Andrew
et al, Risk scores for risk stratification in ACS )
Whats appropriate in our setting???
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MANAGEMENT ALGORITHM
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MANAGEMENT UPDATE
2007ACS/AHA GUIDELINES:
Rapid catergorisation of patient (Class 1 C)
Possible ACS, non diagnostic ECG/biomarkers observed in facility
with cardiac monitoring (Class 1 C)
Alternative to in patient treatment: for those with 12hr ECG/markers
negative stress ECG in 72hrs (Class 1 C)
Giving precautionary treatment for those for OPD stress (Class 1 B)
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INITIAL INVASIVE
VS
INITIAL CONSERVATIVE STRATEGY
CLASS 1 RECOMMENDATIONS:
Early invasive strategy for refractory angina, hemodynamicinstability (LOE B)
Early invasive strategy for stabilised patients with elevated risk forclinical events.
High risk factors include: Recurrent angina, ischaemia at rest or minimal activity
Elevated troponins
New ST depression
Signs of heart failure/worsening mitral regurg.
Ventricular tachycardia
Prior CABG
PCI in last 6 months
High TIMI/GRACE scores
LVEF < 40%
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CLASS 2b
May opt for initial conservative strategy in stabilised high risk
patients dependent on patient/physician preference (LOE B)
CLASS 3 Invasive strategy -not recommended in patients with multiple co
morbidities, low risk patients, patients not consenting.(LOE C)
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UA/NSTEMIPHARMACOTHERAPY UPDATE
GENERAL:
IV B Blockers downgraded from Class 1 to 2a recommendation.
(COMMIT Trial)
Oral B Blockers in first 24hrs still Class 1 but not used in signs of
heart failure, cardiogenic shock and reactive airway disease.(LOE B)
MORPHINE downgraded from Class 1 to 2a findings from
CRUSADE Registry
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NSTEMI- PHARMACOTHERAPY UPDATE
ANTIPLATELET THERAPY:
CLASS 1 RECOMMENDATION
Aspirin to all patients as soon as possible and continued (if no C/I) (LOE A)
Initial dose 162 -325mg
Maintenance 75 -162mg
No added benefit from higher doses except post stenting
Clopidogrel for those allergic to aspirin or major GI bleeding (LOE A)
For initial invasive strategy aspirin + clopidogrel or IV glycoprotein 2b/3atherapy (LOE A)
Abciximab if no delay in angiography/PCI, eptifibatide/tirofiban if delayedangiography(LOE B)
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CLASS 2a
In patients managed conservatively who develop recurrent
ischaemia on clopidogrel/ASA/Anticoagulant can add
glycoprotein inhibitor. (LOE C)
Invasive strategy can use clopidogrel + glycoprotein
inhibitors(LOE C)
CLASS 2b
In patients managed conservatively can add glycoprotein inhibitortherapy, in addition to aspirin & anticoagulant (LOE B)
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CLASS 3
ABCIXIMAB should not be given if PCI not planned (LOE A)
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For initial conservative strategy:
Aspirin + Clopidogrel + anticoagulant administered for 1
month(LOE A), continued ideally up to 1 year(LOE B)
If initial conservative strategy selected but patient has recurrentischaemic symptoms/heart failure/arrythmias diagnostic
angiography recommended. Clopidogrel or Glycoprotein 2b/3a
inhibitors should be added before angiography.
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ANTICOAGULANT THERAPY
CLASS 1
Anticoagulant therapy should be added as soon as possible
For patients undergoing angiography/PCI enoxaparin/UFH (LOE
A) of Bivalirudin/ fondaparinux (LOE B)
For conservative strategy: enaxaparin, UFH (LOE A), fondaparinux
For patients with increased risk of bleeding with conservative
strategy fondaparinux
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CLASS 2a
Enoxaparin /fondaparinux vs UFH
Enoxaparin/fondaparinux preferred except in those undergoing
CABG within 24hrs (LOE B)
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ADDITIONAL MANAGEMENT
STRESS TEST should be performed for those managed
conservatively.
If stress test positive/ high risk needs diagnostic
angiography(Class 1 LOE A)
If classed as low risk
need to continue aspirin indefinitely ( LOE A)
Clopidogrel for at least 1 month(LOE A), ideally up to 1 year(LOE B)
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UA/NSTEMI ALGORITHM- INVASIVE STRATEGY
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UA/NSTEMI ALGORITHMCONSERVATIVE STRATEGY
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STEMI
PHARMACOLOGICAL UPDATE:
ANALGESIA changes from 2004 guidelines
MORPHINE: still remains Class 1 C for STEMI, titrated doses
NSAIDS/COX 2 INHIBITORS: those on it should have it
discontinued ( increased risk of mortality, re infarction, heart failure,
myocardial rupture) Class 1 C
NSAIDS should not be administered in hospital for MI (Class 3)
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BETA BLOCKERS
Modified recommendation
Oral Beta Blockers should be initiated in first24rs, if no contra-
indications (heart failure, risk of cardiogenic shock) Class 1 B
Patients with early contraindications -> re- evaluated later forpossible use
Role of IV B blockers used in hypertensive patients with STEMI
Class 2a B
Class 3 LOE A IV B blockers should not be administrated to
patients with heart failure, risk of cardiogenic shock
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No major changes to reperfusion strategies.
Emphasis on decreasing ischaemic time.
Increase use of prehospital 12 lead ECG emphasised.
In PCI capable hospital door to PCI time 90 min (Class 1 A)
In non PCI capable hospital door to needle time 30 min or timeous
transfer to PCI capable hospital. (Class 1 B)
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REPERFUSION STRATEGY
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FIBRINOLYTICS
AVAILABLE FIBRINOLYTICS: STREPTOKINASE 1.5mu infusion over 30min (1hourACLS)
rtPA accelerated infusion over 1.5hrs
- 15mg IV bolus, 0.75mg/kg over 30 min, 0.5mg/kg over 1hr
ANISTREPLASE 30 U IV over 5 min
TENECTEPLASE 30 TO 50 MG
RETEPLASE 10 U IV bolus, ffd. 10U IV after 30 min
WHICH FIBRINOLYTIC TO USE???
GISSI 2 trial tPA vs Streptokinase , no difference in mortality, marginallyhigher stroke rate with tPA (1.3% vs 1%)
GUSTO 1 trial early vessel patency post infract assoc. with better survival.
Accl. tPA/heparin cf comb. Streptokinase/tPA/heprain cf strep with IV vsS/C heparin
Outcome better flow rates with accl. tPA -> lower mortality rates
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ASSENT 2 TRIAL tenecteplase vs aTPA
- tenecteplase was equally or minimally more
effective, especially in those presenting > 4hrs after symptom onset.
Fibrinolysis combined with glycoprotein 2b/3a inhibitors no overalladvantage (ASSENT 3, GUSTO 5 trials)
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RESCUE PCI: CLASS 1 LOE B angiography with +/- PCI in patients (
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ANTICOAGULANT ADJUNCTS
NEW RECOMMENDATIONS:
CLASS 1
Patients undergoing fibrinolysis should be kept on anticoagulants for
atleast 48 hrs and preferably the duration of hospital stay. LOE A
Anti coagulants with proven efficacy:
Unfractionated Heparin - keeping aPTT 1.5 2 sec above control
(LOE C)
Enoxaparin (Clexane) initial dosage of 30mg IV bolus ffd by
1mg/kg 12hrly, caution in renal impairment (LOE A) Fondaparinux 2.5mg IV, ffd by 2.5mg dly S/C maintenance for
duration of hospitalisation (LOE B)
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ANTICOAGULANTS
CLASS 2a recommendation to use anticoagulants in STEMI without
reperfusion.
UFH (LOE B)
LMWH (LOE C)
Fondaparinux (LOE B)
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THIENOPYRIDINES
CLASS I
CLOPIDOGREL now recommended in all STEMI patients in
addition to aspirin, whether undergoing reperfusion or not. Dosage
75mg daily(LOE A)
Duration -14 days (LOE B)
CLASS 2 A
In patients < 75yrs Clopidogrel 300mg loading dose
recommended(LOE C)
Long term maintenance therapy should be considered, 75mg dly for 1year (LOE C)
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SECONDARY PREVENTION
INCREASED FOCUS ON SECONDARY PREVENTION:
SMOKING CESSATION
DIET MODIFICATION/WT CONTROL
BP CONTROL
LIPID MANAGEMENT
EXERCISE
DIABETES MANAGEMENT
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Despite good reperfusion strategies approx. 1/3 of patientsworldwide miss out.
Attributed to delayed presentation, atypical presentation,
complicated disease presentation, older age
SYMPTOMS OF INFARCT BUT NO ESTABILISHED ECG
CHANGES - keep in mind aortic dissection, GIT disease, other
chest pathology
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CONCLUSION
With increase burden of CVD, and lack of health resources riskstratification becomes important.
Emphasis should also be placed on primary &secondary prevention
of ACS.
Early intervention helps prevent complications, decreases morbidity
& mortality
The way forward fully equipped CHEST PAIN OBSERVATIONUNIT
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REFERENCES
EDITORS MARX ET AL, ROSENS EMERGENCY MEDICINE: CONCEPTS AND CLINICALPRACTICE, 6TH EDITION
PAUL PD ET AL, KEY ARTICLES IN MANAGEMENT OF ACS & PCI -2007 UPDATE,PHARMACOTHERAPY 2007:27(12), 1722 -1750
WHITE HD, DEFINING THE LIMITS OF ACS, CARDIOLOGY AT THE LIMITS IV, EDITORS:
OPIE LH, YELLON DM
YUSUF S, THE GLOBAL EPIDEMIC OF ATHEROSCLEROTIC CARDIOVASCULAR DISEASE,CARDIOLOGY AT THE LIMITS IV, EDITORS: OPIE LH, YELLON DM
FOX KA, MANAGEMENT OF ACS: AN UPDATE, HEART.2004 JUNE, 90(6):698 -706
ANDERSON ET AL, ACC/AHA 2007 GUIDELINES FOR MXN OF U/A,NSTEMI EXECUTIVESUMMARY DOWNLOADED content.onlinejacc.org
SIX AJ ET AL, CHEST PAIN IN THE ER: VALUE OF THE HEART SCORE, NETH. HEART J.2008 JUNE,16(6):191 -196
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ANTMAN EM ET AL, 2007 FOCUSSED UPDATE OF ACC/AHA 2004 GUIDELINES FOR MAXNOF PATIENTS WITH STEMI, DOWNLOADED http://circ.ahajournals.org
McCANN CJ ET AL, NOVEL BIOMARKERS IN EARLY DIAGNOSIS OF AMI COMPARED WITH
CARDIAC TROPONIN T, EUROPEAN HEART JOURNAL 2008,29(23): 2843 -2850
KING III SB ET AL, 2007 FOCUSSED UPDATE OF ACC..FOR PCI, JOURNAL OF
AMERICAN COLLEGE OF CARDIOLOGY, VOL 51, NO 2, 2008
http://circ.ahajournals.org/http://circ.ahajournals.org/