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Principle Managementof

Acute Coronary Syndrome

Nahar Taufiq

Bagian Kardiologi dan Kedokteran Vaskuler FK UGM

Yogyakarta



Atherothrombosis* is theLeading Cause of Death Worldwide1

*Atherothrombosis defined as ischemic heart disease and cerebrovascular disease.1The World Health Report 2001. Geneva: WHO; 2001.Reprod.with permission from Cannon CP. Atherothrombosis slide compendium. Available at:

22.3

19.3

12.6

9.7

9

6.3

0 5 10 15 20 25 30

Atherothrombosis*

Infectious Disease

Cancer

Injuries

Pulmonary Disease

AIDS

Causes of Mortality (%)



Atherothrombosis: A Generalized andProgressive Disease

Unstableangina

MI

Ischemicstroke/TIA

Critical legischemia

Intermittent

claudicationCV death

ACS

Atherosclerosis

Stable angina/Intermittent claudication

Stable angina/Intermittent claudication

Atherothrombosis

Atherothrombosis

MI = Myocardial infarction

ACS = Acute coronary syndromes

CV = CardiovascularAdapted from Libby P. Circulation 2001; 104: 365–372



Thrombus Formation and ACS

UAP NQMI STE-MI

Plaque Disruption/Fissure/Erosion

Thrombus Formation

Non-ST-SegmentElevation

Acute Coronary

Syndrome (NSTE-ACS)

ST-SegmentElevation

Acute

Coronary

Syndrome

(STE-ACS)

OldTerminology:

NewTerminology:

UAP



Pathophysiology

Ruptured Plaque with Occlusive Thrombus Formation

UAP orNON STEMI-ACS

STEMI-ACS



Initial RecognitionInitial Recognition

in the Emergencyin the EmergencyDepartmentDepartment



ED Evaluation of PatientsED Evaluation of Patients

1. Airway, Breathing, Circulation (ABC)

2. Vital signs, general observation

3. Presence or absence of jugular venous distension

4. Pulmonary auscultation for rales

5. Cardiac auscultation for murmurs and gallops

6. Presence or absence of stroke

7. Presence or absence of pulses

8. Presence or absence of systemic hypoperfusion (cool,clammy, pale, ashen)

Brief Physical Examination in the ED

P ExP Ex




Aortic dissection

Pulmonary Emboli

Perforating ulcer

Differential Diagnosis of STEMI: Life-Threatening

Tension pneumothorax

Boerhaave syndrome

(esophageal rupture with

mediastinitis)

P ExP Ex




Pericarditis

Atypical anginaEarly repolarizationWolff-Parkinson-White

syndromeDeeply inverted T-

waves suggestive of a central nervoussystem lesion orapical hypertrophiccardiomyopathy

LV hypertrophy with

strainBrugada syndrome

Myocarditis

Hyperkalemia

Bundle-branch blocks

Vasospastic angina

Hypertrophiccardiomyopathy

Differential Diagnosis of STEMI:Other Cardiovascular and Nonischemic

P ExP Ex



Gastroesophagealreflux (GERD) and

spasmChest-wall pain

Pleurisy

Peptic ulcer disease

Panic attack

Cervical disc orneuropathic pain

Biliary or pancreatic pain

Somatization andpsychogenic paindisorder


Differential Diagnosis of STEMI: Other Noncardiac

P ExP Ex



ElectrocardiogramElectrocardiogram

If the initial ECG is not diagnostic of STEMI,

serial ECGs or continuous ST-segment

monitoring should be performed in the

patient who remains symptomatic or if there

is high clinical suspicion for STEMI.

III IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIIaIIaIIa IIbIIbIIb IIIIIIIII

DxDx



ElectrocardiogramElectrocardiogram

Show 12-lead ECG results to emergency

physician within 10 minutes of ED arrival in all

patients with chest discomfort (or anginal

equivalent) or other symptoms of STEMI.

In patients with inferior STEMI, ECG leads

should also be obtained to screen for right

ventricular infarction.



DxDx



Laboratory ExaminationsLaboratory Examinations

Laboratory examinations should be performed as partof the management of STEMI patients, but should not

delay the implementation of reperfusion therapy.

Serum biomarkers for cardiac damage

Complete blood count (CBC) with platelets International normalized ratio (INR)

Activated partial thromboplastin time (aPTT)

Electrolytes and magnesium

Blood urea nitrogen (BUN) Creatinine

Glucose

Complete lipid profile


DxDx



Cardiac-specific troponins should be used as

the optimum biomarkers for the evaluation

of patients with STEMI who have coexistent

skeletal muscle injury.

For patients with ST elevation on the 12-lead

ECG and symptoms of STEMI, reperfusion

therapy should be initiated as soon aspossible and is not contingent on a

biomarker assay.

Biomarkers of Cardiac DamageBiomarkers of Cardiac Damage

III IIaIIaIIa IIbIIbIIb IIIIIIII IIII IIaIIaIIa IIbIIbIIb IIIIIIII IIII IIaIIaIIa IIbIIbIIb IIIIIIII IIIaIIaIIa IIbIIbIIb IIIIIIII I

III IIaIIaIIa IIbIIbIIb IIIIIIII IIII IIaIIaIIa IIbIIbIIb IIIIIIII IIII IIaIIaIIa IIbIIbIIb IIIIIIII IIIaIIaIIa IIbIIbIIb IIIIIIII I

DxDx



InitialInitial ManagementManagement

in the Emergencyin the EmergencyDepartmentDepartment



Supplemental oxygen should be administered to

patients with arterial oxygen desaturation (SaO2

< 90%).

It is reasonable to administer supplemental

oxygen to all patients with uncomplicated STEMI

during the first 6 hours.

OxygenOxygen



TxTx



Patients with ongoing ischemic discomfortshould receive sublingual NTG (0.4 mg) every 5minutes for a total of 3 doses, after which anassessment should be made about the need forintravenous NTG.

Intravenous NTG is indicated for relief of

ongoing ischemic discomfort that responds to

nitrate therapy, control of hypertension, or

management of pulmonary congestion.

NitroglycerinNitroglycerin



TxTx



Nitrates should not be administered topatients with:

Nitrates should not be administered topatients who have received aphosphodiesterase inhibitor for erectiledysfunction within the last 24 hours (48 hoursfor tadalafil).

• systolic pressure < 90 mm Hg or ≥ to 30 mm Hg

below baseline

• severe bradycardia (< 50 bpm)• tachycardia (> 100 bpm) or • suspected RV infarction.

NitroglycerinNitroglycerin



TxTx



AnalgesiaAnalgesia

Morphine sulfate (2 to 4 mg intravenously

with increments of 2 to 8 mg intravenously

repeated at 5 to 15 minute intervals) is theanalgesic of choice for management of pain

associated with STEMI.


TxTx



AspirinAspirin


Aspirin should be chewed by patients who

have not taken aspirin before presentation

with STEMI. The initial dose should be 162

mg (Level of Evidence: A) to 325 mg (Level

of Evidence: C)

Although some trials have used enteric-coated aspirin for initial dosing, more rapid buccalabsorption occurs with non–enteric-coated formulations.


TxTx



0

5

10

15

0 5 10 20 25 30

Endp

oint*(%)

Days

Placebo

Clopidogrel

20%

P=0.03

* Cardiovascular death, recurrent MI, or recurrent ischemia

leading to the need for urgent revascularization

Sabatine MS et al for the CLARITY-TIMI 28 Investigators. N Engl J Med 2005;352:1179-89

CLARITY-TIMI 28

ClopidogrelClopidogrelTxTx



1.9

1.6

3.4

1.7

0.9

2.7

0

1

2

3

4

P=0.80P=0.12

P=0.24

%

of

pati

en

ts

Major bleeding Minor bleeding Major or minor

bleeding

CLARITY-TIMI 28: Tingkat keamanan dalam 30hari

ASA + CLO

ASA



1 Dabaghi SF et al. Am J Cardiol 1994;74:720-3. 2. Savcic M et al. Semin Thromb Hemost 1999;25:15-19

3 Quinn MJ, Fitzgerald DJ. Circulation 1999;100:1667-72 4. Hochholzer W et al. Circulation

2005;111:2560-4 5. Lubbe DF, Berger PB. J Interv Cardiol

Agent Dose Onset

Aspirin Dosis 80 - 320 mg1 15 - 30 minutes

Clopidogrel 75 mg maintenance dose2

300 mg loading dose3

600 mg loading dose4

900 mg loading

dose3

Max at 3-7 days Max

at 24 to 48 h Max at

2 h same with

600 mg loading dose

Ticlopidine 250 mg 2x perhari5 50% pada 5 hari dan maksimum

8-11 hari

Onset of antiplateletTxTx



Mona_Mona_

CoCo

InitialInitial ManagementManagement in the EDin the ED

1 2 3



Reperfusion Therapy and

RecommendationsSTEMI

11



ReperfusionReperfusion

The medical system goal is to facilitate rapid

recognition and treatment of patients with STEMI

such that door-to- needle (or medical contact–

to-needle) time for initiation of fibrinolytic

therapy can be achieved within 30 minutes or

that door-to-balloon (or medical contact–to-

balloon) time for PCI can be kept within 90

TxTx



Symptom

Recognition

Call to

Medical System

ED-Hospital Cath LabPreHospital

Delay in Initiation of Reperfusion Therapy

Increasing Loss of Myocytes

Treatment Delayed is Treatment DeniedTreatment Delayed is Treatment Denied



Fibrinolysis generally preferred Early presentation ( ≤ 3 hours from symptom

onset and delay to invasive strategy)

Invasive strategy not an option Cath lab occupied or not available

Vascular access difficulties

No access to skilled PCI lab

Delay to invasive strategy Prolonged transport

Door-to-balloon more than 90 minutes

> 1 hour vs fibrinolysis (fibrin-specific agent) now

Reperfusion Options for STEMI PatientsReperfusion Options for STEMI Patients Select Reperfusion Treatment.Select Reperfusion Treatment.

If presentation is < 3 hours and there is no delay to an invasive

strategy, there is no preference for either strategy.



Contraindications and CautionsContraindications and Cautions

for Fibrinolysis in STEMIfor Fibrinolysis in 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.





AbsoluteContraindications

• Suspected aortic dissection

• Active bleeding or bleeding diathesis

(excluding menses)

• Significant closed-head or facial traumawithin 3 months





• 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





RelativeContraindications

• Recent (< 2 to 4 weeks) internal bleeding• Noncompressible vascular 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

f i i f i



Invasive strategy generally preferred Skilled PCI lab available with surgical backup

Door-to-balloon < 90 minutes

• High Risk from STEMI

Cardiogenic shock, Killip class ≥ 3

Contraindications to fibrinolysis, including

increased risk of bleeding and ICH

Late presentation

> 3 hours from symptom onset

Diagnosis of STEMI is in doubt

Reperfusion Options for STEMI PatientsReperfusion Options for STEMI Patients Select Reperfusion Treatment.Select Reperfusion Treatment.

If presentation is < 3 hours and there is no delay to an invasive strategy,

there is no preference for either strategy.



Antithrombin Therapyand Recommendations

Non-STEMI & UAP

2-32-3

ACC/AHA R d ti f



ACC/AHA Recommendations forAntithrombin Therapy in Patients with

NSTE-ACS

• Class I

– Anticoagulation with subcutaneous LMWH or intravenousUFH should be added to antiplatelet therapy

– Dose of UFH 60-70 U/kg (max 5000) IV followed byinfusion of 12-15 U/kg/hr (initial max 1000 U/hr) titratedto aPTT 1.5-2.5 times control

– Dose of enoxaparin 1 mg/kg subcutaneously q12 hr; thefirst dose may be preceded by a 30-mg IV bolus

– Fundaparinoux SC

• Class IIa– Enoxaparin is preferable to UFH as an anticoagulant

unless CABG is planned within 24 hours

Available at: www.acc.org/clinical/guidelines/unstable/unstable.pdf.

1 2 3



1 2 3



Secondary Prevention

andLong Term Management

S



Secondary Prevention and Long Term Management

• Assess tobacco use.

• Strongly encourage patient and familyto stop smoking and to avoid secondhand

smoke.

• Provide counseling, pharmacologicaltherapy (including nicotine replacement

and bupropion), and formal smokingcessation programs as appropriate.

SmokingGoal: Complete Cessation

Goals Recommendations

S d P ti d L T M t




If blood pressure is 120/80 mm Hg or greater:

• Initiate lifestyle modification (weight control,physical activity, alcohol moderation, moderatesodium restriction, and emphasis on fruits,

vegetables, and low-fat dairy products) in allpatients.

If blood pressure is 140/90 mm Hg or greater or130/80 mm Hg or greater for individuals with

chronic kidney disease or diabetes:

• Add blood pressure-reducing medications,emphasizing the use of beta-blockers and inhibitorsof the renin-angiotensin-aldosterone system.

Blood pressurecontrol:Goal: < 140/90 mm Hg or <130/80 mm Hg if chronic kidney disease or diabetes


S d P ti d L T M t




• Assess risk, preferably with exercise test, to

guide prescription.

• Encourage minimum of 30 to 60 minutes ofactivity, preferably daily but at least 3 or 4 times

weekly (walking, jogging, cycling, or other aerobic

activity) supplemented by an increase in daily

lifestyle activities (e.g., walking breaks at work,gardening, household work).

• Cardiac rehabilitation programs are

recommended for patients with STEMI.

Physicalactivity:Minimum goal: 30 minutes 3 to

4 days per week; Optimal daily


S d P ti d L T M t




• Start dietary therapy in all patients (< 7% of totalcalories as saturated fat and < 200 mg/dcholesterol). Promote physical activity and weightmanagement. Encourage increased consumption ofomega-3 fatty acids.

• Assess fasting lipid profile in all patients,preferably within 24 hours of STEMI. Add drugtherapy according to the following guide:

Lipidmanagement:(TG less than200 mg/dL)Primary goal: LDL-C << than 100 mg/dL


LDL-C < 100 mg/dL (baseline or on

treatment):Statins should be used to lower LDL-C.

LDL-C ≥ 100 mg/dL (baseline or ontreatment):

Intensify LDL-C–lowering therapy with drugtreatment, giving preference to statins.

S d P ti d L T M t




If TGs are ≥ 150 mg/dL or HDL-C is < 40 mg/dL:Emphasize weight management and physical

activity. Advise smoking cessation.

If TG is 200 to 499 mg/dL:

After LDL-C–lowering therapy, consider addingfibrate or niacin.

If TG is ≥ 500 mg/dL:

Consider fibrate or niacin before LDL-C–lowering

therapy.

Consider omega-3 fatty acids as adjunct for high

TG.

Lipidmanagement:

(TG 200 mg/dL

or greater)

Primary goal:

Non–HDL-C <<130 mg/dL




NCEP ATP III Guidelines

Patients withPatients withDrug therapyDrug therapy

considered if LDLconsidered if LDL

* TLC: therapeutic lifestyle changes* TLC: therapeutic lifestyle changesNational Cholesterol Education Program, Adult Treatment Panel III.National Cholesterol Education Program, Adult Treatment Panel III. JAMA JAMA 2001;2001;285285:2486–2497:2486–2497

Initiate TLC*Initiate TLC*if LDLif LDL

LDLLDLtreatmenttreatment

goalgoal

00 1 risk factors1 risk factors ≥160 mg/dL160 mg/dL†† ≥ 190 mg/dL190 mg/dL

(160(160–189 mg/dL:189 mg/dL:drug optional)drug optional)

<160 mg/dL<160 mg/dL††

2 risk factors2 risk factors(10(10 year riskyear risk 20%)20%)

≥130 mg/dL130 mg/dL††

1010 year risk 10year risk 10–

20%:20%: ≥ 130 mg/dL130 mg/dL10-year risk <10%:10-year risk <10%:

≥ 160 mg/dL160 mg/dL

<130 mg/dL<130 mg/dL††

CHD and CHD riskCHD and CHD risk

equivalentsequivalents

(10(10 year risk >20%)year risk >20%)

≥100 mg/dL100 mg/dL†† <100 mg/dL<100 mg/dL††

†† 100 mg/dL = 2.6 mmol/L; 130 mg/dL = 3.4 mmol/L; 160 mg/dL = 4.1 mmol/L100 mg/dL = 2.6 mmol/L; 130 mg/dL = 3.4 mmol/L; 160 mg/dL = 4.1 mmol/L

≥ 130 mg/dL130 mg/dL

drug optional)drug optional)

(100–129 mg/dL:(100–129 mg/dL:






Calculate BMI and measure waistcircumference as part of evaluation. Monitorresponse of BMI and waist circumference totherapy.

Start weight management and physical activityas appropriate. Desirable BMI range is 18.5 to24.9 kg/m2.

If waist circumference is ≥ 35 inches in women

or ≥ 40 inches in men, initiate lifestyle changesand treatment strategies for metabolicsyndrome.

Weightmanagement:Goal: BMI 18.5 to 24.9 kg/m 2

Waist circumference: Women: < 35 in.Men: < 40 in.





Appropriate hypoglycemic therapy to

achieve near-normal fasting plasma

glucose, as indicated by HbA1c.

Treatment of other risk factors (e.g.,

physical activity, weight management,

blood pressure, and cholesterol

management).

Diabetes

management:

Goal:

HbA1c < 7%



Guidelines for the Use of Enoxaparin in Patientswith NSTE-ACS

• 1 mg/kg SQ q12 hours (actual body weight)

– An initial 30 mg IV dose can be considered

• Adjust dosing if CrCl <30 cc/min

– 1 mg/kg SQ q24 hours

•Do not follow PTT; do not adjust based on PTT

• Stop if platelets ↓ by 50% or below 100,000/mm3

• If patient to undergo PCI:

– 0-8 hours since last SQ dose: no additional antithrombin therapy

– 8-12 hours since last SQ dose: 0.3 mg/kg IV immediately prior to PCI

Applying Classification ofApplying Classification of



Class I Benefit >>> Risk

Procedure/ TreatmentSHOULD be performed/administered

Class IIa Benefit >> Risk

Additional studies withfocused objectives needed

IT IS REASONABLE toperformprocedure/administer treatment

Class IIb Benefit ≥ Risk

Additional studies withbroad objectives needed;

Additional registry datawould be helpful

Procedure/TreatmentMAY BE CONSIDERED

Class III Risk ≥ Benefit No additional studiesneeded

Procedure/Treatment should NOT beperformed/administered SINCE IT IS NOT HELPFUL

AND MAY BE HARMFUL

shouldis recommendedis indicatedis useful/effective/ beneficial

is reasonablecan be useful/effective/

beneficialis probably recommended or

indicated

may/might be consideredmay/might be reasonableusefulness/effectiveness is

unknown /unclear/uncertain or not well established

is not recommendedis not indicatedshould notis not useful/effective/beneficialmay be harmful

Applying Classification of Applying Classification of

Recommendations and Level of EvidenceRecommendations and Level of Evidence

Applying Classification of



Level A

Multiple (3-5) population risk strata evaluated

General consistency of

direction and magnitude of effect

Class I

• Recommen-dation thatprocedure or treatment isuseful/ effective

• Sufficient

evidence frommultiplerandomizedtrials or meta-analyses

Class IIa

• Recommen-dation in favor of treatment or procedure beinguseful/ effective

• Some conflicting

evidence frommultiplerandomized trialsor meta-analyses

Class IIb

• Recommen-dation’susefulness/efficacy less wellestablished

• Greater

conflictingevidence frommultiplerandomized trialsor meta-analyses

Class III

• Recommen-dation thatprocedure or treatment notuseful/effectiveand may be

harmful• Sufficient

evidence frommultiplerandomized trialsor meta-analyses

Applying Classification of

Recommendations and Level of Evidence




Level B

Limited (2-3) population risk strata evaluated

Class I

• Recommen-dation thatprocedure or treatment isuseful/effective

• Limited evidence

from singlerandomized trialor non-randomizedstudies

Class IIa

• Recommen-dation in favor of treatment or procedure beinguseful/ effective

• Some conflicting

evidence fromsinglerandomized trialor non-randomizedstudies

Class IIb


• Greater

conflictingevidence fromsinglerandomized trialor non-randomizedstudies

Class III

• Recommen-dation thatprocedure or treatment notuseful/effectiveand may be

harmful• Limited evidencefrom singlerandomized trialor non-randomizedstudies

pp y gpp y g


Applying Classification ofApplying Classification of





Level C

Very limited (1-2) population risk strata evaluated

Class I

• Recommen-dation thatprocedure or treatment isuseful/ effective

• Only expert

opinion, casestudies, or standard-of-care

Class IIa

• Recommen-dation in favor of treatment or procedure beinguseful/effective

• Only diverging

expert opinion,case studies, or standard-of-care

Class IIb


• Only diverging

expert opinion,case studies, or standard-of-care

Class III

• Recommend-ation thatprocedure or treatment notuseful/effectiveand may be

harmful• Only expertopinion, casestudies, or standard-of-care

P th t Th b i



Pathway to Thrombosis

B t Bl kB t Bl k



Oral beta-blocker therapy should beadministered promptly to those patients without

a contraindication, irrespective of concomitant

fibrinolytic therapy or performance of primary

PCI.

It is reasonable to administer intravenous beta-

blockers promptly to STEMI patients without

contraindications, especially if a

tachyarrhythmia or hypertension is present.

Beta-BlockersBeta-Blockers



TxTx

S f T i l f B t Bl k ThS mmar of Trials of Beta Blocker Therap



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)

Placebobetter

0.87 (0.77-0.98)

0.77 (0.70-0.84)

0.81 (0.75-0.87)

Summary of Trials of Beta-Blocker TherapySummary of Trials of Beta-Blocker Therapy

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.

C i f H i + ASA ASA Al



RR:Death/MI

ASA Alone68/655=10.4%

Heparin + ASA55/698=7.9%

0.1 1 10

Summary Relative Risk

0.67 (0.44-0.1.02)

Theroux

RISC

Cohen 1990

ATACS

Holdright

Gurfinkel

Comparison of Heparin + ASA vs ASA Alone

ASA indicates acetylsalicylic acid; RISC, Research on InStability in Coronary artery disease; ATACS, Antithrombotic Therapy in Acute

Company Syndromes; RR, relative risk; and MI, myocardial infarction.

Data from Oler A, Whooley MA, Oler J, et al. Adding heparin to aspirin reduces the incidence of myocardial infarction and death in

patients with unstable angina: a meta-analysis. JAMA. 1996;276:811-815. Slide reproduced with permission from Cannon CP.

Atherothrombosis slide compendium. Available at: www.theheart.org.

ESSENCE Results



ESSENCE Results

30%

25%

20%

15%

10%

09 13

Days After Randomization

17 215

5%

25 29

Unfractionated Heparin

Enoxaparin (Lovenox)

Death,MI

or

Recu

rren

tAngina

P = 0.02

Risk Reduction 16.2%

Adapted with permission from Cohen M, Demers C, Gurfinkel EP, et al. A comparison of low-molecular-weight

heparin with unfractionated heparin for unstable coronary artery disease. Efficacy and Safety of Subcutaneous

Enoxaparin in Non-Q-Wave Coronary Events Study Group. N Engl J Med. 1997;337:447-452. Copyright © 1997,Massachusetts Medical Society. All rights reserved.

TxTx

TIMI 11B Eno aparin sTIMI 11B Enoxaparin vs



D e a t h

, M I

o r

U r g

e n

t R

e v a

s c

u l

a r i z

a t i

o n

Unfractionated Heparin

Enoxaparin (Lovenox)

Days

20

16

12

8

4

2 4 6 8 10 12 140

16.7%

14.2 %

p = 0.03

Relative Risk Reduction = 15%

TIMI 11B: Enoxaparin vs.Heparin in NSTE-ACS

TIMI 11B: Enoxaparin vs.Heparin in NSTE-ACS

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