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Optimal Antithrombotic Care for Patients with Acute Coronary SyndromesAcross the Continuum of Unstable Angina,

NSTEMI, and STEMI

TITLE GOES HERESubtitle Goes Here

FIRST NAME AND LAST, SUFFIX, XX, XxXXPresenter’s Title

Institution Name HereCity, State

Faculty Disclosures

The faculty reported the following relevant financial relationships that they or their spouse/partner have with commercial interests:

• Presenting Physician, MDCategory – Disclosures

TO BE FILLED IN BY PRESENTING PHYSICIAN

Steering Committee Disclosures

The Steering Committee reported the following relevant financial relationships that they or their spouse/partner havewith commercial interests:

• Deepak L. Bhatt, MD, MPH, FACC, FAHA, FSCAI: Principal Investigator: AstraZeneca, Bristol-Myers Squibb, Eisai, Sanofi-Aventis, The Medicines Company

• Charles V. Pollack Jr., MA, MD, FACEP, FAAEM, FAHA: Consultant: Sanofi-Aventis, Bristol-Myers Squibb; Speaker: Bristol-Myers Squibb; Researcher: Sanofi-Aventis

Non-faculty Disclosures

Non-faculty content contributors and/or reviewers reported the following relevant financial relationships that they or their spouse/partner have with commercial interests:

• Barry Watkins, PhD; Bradley Pine; Blair St. Amand; Jay Katz; Laurie Frueh, MD: Nothing to Disclose

Educational Objectives

This program is designed to address the following IOM competencies: provide patient-centered care and employ evidence-based practice.

At the conclusion of this activity, participants should be able to:

• Adopt ischemic risk assessment stratification strategies to best evaluate patients with chest pain syndrome

• Assess and stratify bleeding risk after antithrombotic treatment is initiated

• Make treatment choices based on an understanding of the different mechanisms of action among antithrombotic agents, and on pertinent clinical trial results

• Analyze pharmacologic and clinical trial results of newer antithrombotic agents to anticipate how they may impact standards of care of ACS patients

Chest Pain Case

• 68-year-old male presents at 1400 on Tuesday• Epigastric pain radiating to left shoulder for two hours;

onset was with exertion but continued at rest• Suspected CAD with abnormal stress test, but declined

catheterization one year ago; treated with beta-blockers and long-acting nitrates

• PMH significant only for hypertension

Chest Pain CaseECG

Chest Pain CaseTreatment Stratification Issues

• Choice of therapy depends at least in part on selection of management strategy for next 24h:– Invasive or conservative?

– Patient’s creatinine clearance is 45 cc/min, his first troponin is negative, and he is not anemic

– Once decided, medical therapy that supports that approach should be initiated:

• Anticoagulant?

- Which one? What dose?

• Oral antiplatelet (beyond aspirin)?

- Which one? What dose?

• GP IIb/IIIa antagonist?

- Small or large molecule? What dose?

• Beta blocker?

- IV or PO?

Chest Pain CaseTreatment Stratification Issues

• Two hours later, repeat troponin assay is positive, and patient’s diagnosis is changed from UA to NSTEMI

• Plan is to take him to cath lab as first case tomorrow morning if he remains stable and pain free

• Do your previous choices of anticoagulation, antiplatelet, and beta-blocker therapy now change?

• What therapy might you add (or change) in the cath lab?

Acute Coronary Syndromes (ACS)

Scope of the Problem

ACS: Scope of the Problem

• NSTEMI • STEMI

• CHD is the leading cause of death in the US; 835,000 deaths in 2006

• 1,365,000 annual hospital discharges for ACS

• 34% of those with a coronary event die within a year of having it

• Hospital adherence to ACC/AHA ACS treatment guidelines is only 75%

Roe MT et al. Arch Int Med. 2005;165:1630-1636.Fox KAA et al. JAMA. 2007;297:1892-1900.Lloyd-Jones D et al. Circulation. 2010;121:e46-e215.

Acute Coronary Syndromes

• Common Features of ACS– Similar pathophysiology– Similar presentation and early management rules

• Differentiating Features– Unstable Angina

Non-occlusive thrombus No diagnostic ECG changes, but ischemic ST-T changes confer higher risk Normal cardiac enzymes

– NSTEMI Occluding thrombus sufficient to cause myocardial damage No diagnostic ECG changes, but ischemic ST-T changes: higher risk Elevated cardiac enzymes

– STEMI Complete thrombus occlusion ST elevations or new LBBB Elevated cardiac enzymes More severe symptoms

Mortality in Acute Coronary SyndromesDeath from hospital admission to 6 months

16

12

8

4

00 30 60 90 120 150 180

% M

orta

lity

DaysFox KA et al. BMJ. 2006;333:1091.

STEMI

NSTEMI

UA

GRACE n=43,810


Clinical Spectrum and Presentation

Early Assessment

STEMIClinical concernPositive cardiac markerST elevation on ECG

Unstable AnginaClinical concern alone

NSTEMIClinical concernPositive cardiac markerAbsence of ST elevation

Chest Pain Suggestive of Ischemia

• 12 lead ECG

• Obtain initial cardiac enzymes

• Electrolytes, CBC lipids, BUN/ creatinine, glucose, coags

• Chest x-ray

Immediate Assessment within 10 Minutes

• Establish diagnosis

• Read ECG

• Identify complications

• Assess for reperfusion

Initial Labsand Tests

Emergent Care

History & Physical

• IV access

• Cardiac monitoring

• Oxygen

• Aspirin

• Nitrates

The Role of the Emergency Physician in the Management of Chest Pain

• Stabilization – When required

• Recognition – “Atypical is the new typical”

• Prompt STEMI management– ~15% of our ACS population

• Risk stratification of the rest– >50% don’t have ACS– Of those who do, fewer than 30% are high

(ischemic) risk in the ED


Risk Stratification

“Dynamic Risk Stratification” Tools• History and physical• Standard EKG and non-standard EKG leads

15-lead ECGs should, perhaps, be “standard” in all but very-low-risk patients

• Biomarkers CPK-MB, troponins I and T, myoglobin High-sensitivity troponin

• Non-invasive imaging Echocardiogram Stress testing Technetium-99m-sestamibi

• Predictive indices/schemes Better as research tools than for real-time clinical decision-making

Serum Enzymes

Troponin Levels Predict Risk of Mortality in UA/NSTEMI

Antman EM et al. N Engl J Med. 1996;335:1342-1949.

1.01.7

3.4 3.7

6.0

7.5

0

1

2

3

4

5

6

7

8

0 to <0.4 0.4 to <1.0 1.0 to <2.0 2.0 to <5.0 5.0 to <9.0 ≥ 9.0

Mor

talit

y at

42

days

; % o

f pat

ient

s

831 174 148 134 50 67

%%

%%

%

%

Cardiac troponin I (ng/mL )

PRESENTATION

TIMI RISK SCORE for UA/NSTEMIRisk Algorithms: GRACE, PURSUIT, TIMI;The Preponderence of Evidence Favors the TIMI Score

HISTORICAL

Age ≥ 65 ≥ 3 CAD risk factors(FHx, HTN, ↑ chol, DM, active smoker)Known CAD (stenosis ≥ 50%)ASA use in past 7 days

Recent (≤ 24H) severe angina↑ cardiac markersST deviation ≥ 0.5 mm

RISK SCORE = Total Points (0-7)

RISKSCORE

DEATHOR MI

DEATH, MI, ORURGENT REVASC

0/1 3 5 2 3 8 3 5 13 4 7 20 5 12 26 6/7 19 41

*Entry criteria: UA or NSTEMII defined as ischemic pain at rest within past 24H, with evidence of CAD (ST segment deviation or elevated cardiac marker)

Antman EM et al. JAMA. 2000;284:835-842.

RISK OF CARDIAC EVENTS (%) BY 14 DAYS IN TIMI 11B

Acute CoronarySyndromesEarly Hospital Care

Early Invasive Initial Conservative

Braunwald E et al. Available at: www.acc.org.Bowen WE, McKay RG. N Engl J Med. 2001;344:1939-1942.

* Also known as Q-wave MI† Also known as non-Q-wave MI

Treatment of Acute Coronary Syndrome

http://www.acc.org/

Optimal Upstream Management ofIschemic Risk Assessment

• Basis for assessment:– “Pain story”

– Background CVD risk– ECG– Troponin elevation in pertinent time frame– Predictive risk score

• Options:– Antiplatelet therapy increasingly important as ischemic risk increases– UFH and enoxaparin established– Bivalirudin and fondaparinux: New options that are non-inferior

Acute Therapy

• Oxygen, Bed Rest, ECG Monitoring

• Nitroglycerin

• Beta Blockers

• ACE Inhibitors

• Antiplatelet Therapy

• Anticoagulant Therapy

Current Medical Management ofUnstable Angina and NSTEMI*

Maintenance Therapy

• Antiplatelet Therapy

• Beta Blockers

• Calcium Channel Blockers

• Lipid-lowering Agents

• ACE Inhibitors

Braunwald E et al. Available at: www.acc.org.

* Also known as Q-wave MI.

http://www.acc.org/

Acute Coronary Syndrome

Patient Management Strategies for UA/NSTEMI:

Conservative or Invasive – Based on Risk Assessment

“An early invasive strategy (i.e. diagnostic angiography with intent to perform revascularization) is indicated in initially stabilized UA/NSTEMI patients (without serious comorbidities or contraindications to such procedures) who have an elevated risk for clinical events.”

“In initially stabilized patients, an initially conservative (i.e. a selectively invasive) strategy may be considered as a treatment strategy for UA/NSTEMI patients (without serious comorbidities or contraindications to such procedures) who have an elevated risk for clinical events, including those who are troponin positive.”

“The decision to implement an initial conservative (vs initial invasive) strategy in these patients may be made by considering physician and patient preference.”

UA/NSTEMI Strategy OverviewThe Big Picture: Early Invasive vs Initial Conservative Therapy

UA/NSTEMI Strategy OverviewThe Big Picture: Early Invasive vs Initial Conservative Therapy

ACC/AHA 2007 Guidelines for the Management of UA/NSTEMI. August 6, 2007. Circulation.

Conservative Therapy Option for UA/NSTEMI

• Early revascularization or PCI not planned• MONA + BAH (LMW or UFH)

– Morphine, oxygen, nitraglycerin, aspirin + beta blocker, ACEI, heparin• Antiplatelet therapy

– Aspirin– Thienopyridine (clopidogrel or prasugrel)

• Glycoprotein IIb/IIIa inhibitors– Only in certain circumstances

Planning PCI, elevated troponin• Surveillance in hospital

– Serial ECGs– Serial cardiac markers

Invasive Therapy Option for UA/NSTEMI

• Coronary angiography and revascularization within 12 to 48 hours after presentation to ED

• For high-risk ACS • MONA + BAH (UFH)

– Morphine, oxygen, nitraglycerin, aspirin + beta blocker, ACEI, heparin

• Antiplatelet therapy– Aspirin; thienopyridine (clopidogrel or prasugrel)– 20% reduction in death/MI/Stroke– 1 month minimum duration and possibly up to 9 months

• Glycoprotein IIb/IIIa inhibitor

ACC/AHA Guidelines 2007Early Invasive Strategies

High-risk patients with:- Refractory ischemia (’07)- Recurrent angina/ischemia- Elevated cardiac biomarkers (T)- New ST-segment depression- New CHF or worsening MR- High-risk on non-invasive testing- LV dysfunction (EF <40%)- Hemodynamic instability- Sustained VT- PCI within 6 months, prior CABG high-

risk score (TIMI, GRACE, FRISC)- Not in low-risk women (’07)

II IIaIIa IIbIIb IIIIII

Circulation. 2007.

Invasive Therapy Option for 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)

– Morphine, oxygen, nitraglycerin, aspirin + beta blocker, ACEI, heparin

• Clopidogrel or prasugrel

– Clopidogrel: 20% reduction death/MI/Stroke – CURE trial

– Clopidogrel: 1-month minimum duration and possibly up to 9 months

• Glycoprotein IIb/IIIa inhibitors

Time (months)0 1 2 3 4 5 6

0

4

8

12

16

20

% P

atie

nts

Conservative:

Invasive:

O.R 0.7895% CI (0.62, 0.97)P=0.025

19.4%

15.9%

TACTICS: Primary EndpointDeath, MI, Rehospitalized for ACS at 6 Months

Cannon CP et al. N Engl J Med. 2001;344:1879-1887.

Updated Meta-analysis: MortalityUpdated Meta-analysis: Mortality

Bavry, AA et al. J Am Coll Cardiol. 2006;48:1319-1325.

Study

FRISC-II

TRUCS

TIMI-18

VINO

RITA-3

ISAR-COOL

ICTUS

Deaths, n Follow-upInvasive Conservative Months

45 67 24

3 9 12

37 39 6

2 9 6

102 132 60

0 3 1

15 15 12

Deaths, n Follow-upInvasive Conservative Months

45 67 24

3 9 12

37 39 6

2 9 6

102 132 60

0 3 1

15 15 12

0.1 1 100.1 1 10FavorsEarly InvasiveTherapy

FavorsEarly InvasiveTherapy

FavorsConservativeTherapy

FavorsConservativeTherapy

Overall RR (95% CI)0.75 (0.63-0.90)

Invasive StrategyRationale for Early Catheterization

End point HR (95% CI) P

Death, MI, stroke* 0.85 (0.68–1.06) 0.15

Death, MI, refractory ischemia 0.72 (0.58–0.89) 0.002

Death, MI, stroke, refractory ischemia, repeat intervention

0.84 (0.71–0.99) 0.039

Refractory ischemia 0.30 (0.17–0.53) <0.00001

Mehta SR et al. American Heart Association 2008 Scientific Sessions; November 10, 2008; New Orleans, LA.

TIMACS: Primary and secondary outcomes in TIMACS hazard ratio (95% CI), early vs delayed strategies

*Primary end point

*Low/intermediate risk=GRACE score <140 High risk=GRACE score ≥140

TIMACS: Rates of death, MI, or stroke within 6 months according to GRACE risk level and HR (95% CI), early vs delayed invasive strategy

Mehta SR et al. American Heart Association 2008 Scientific Sessions; November 10, 2008; New Orleans, LA.

Risk level by GRACE score* Early (%) Delayed (%) HR (95% CI) P

Low/Intermediate(n=2070)

7.7 6.7 1.14 (0.82–1.58) 0.43

High (n=961) 14.1 21.6 0.65 (0.48–0.88) 0.005

COURAGEBenefits of Early Catheterization by Risk GroupCOURAGEBenefits of Early Catheterization by Risk Group

Bhatt D. American Heart Association 2002 Scientific Sessions; Chicago, IL .

0

2

4

6

8

10

12

Low Risk M oderate Risk High Risk

Early Cath No Early Cath

% I

n-ho

spita

l Mor

tality

% I

n-ho

spita

l Mor

tality

Mortality Rates by Early Catheterization

Bhatt DL et al. JAMA. 2004;292:2096-2104..

10

6

4

2

0

8

0.7

2.3

1.1

2.5

3.9

8.6Early Catheterization

No Early Catheterization

% In

-hos

pita

l Mor

talit

y

Low(n=4326)

Moderate(n=4492)

High(n=9108)

Modified PURSUIT Risk Category

Acute CoronarySyndromes

Specific Drug Treatment Options

Months of Follow-up

Yusuf S et al. N Engl J Med. 2001;345:494-502.

CURE Study Primary End Point: MI/Stroke/CV Death

Clopidogrel + Aspirin(n=6259)

Placebo + Aspirin(n=6303)

P<0.001n=12,562

3 6 90 12

20%Relative RiskReduction

0.12

0.14

0.10

0.06

0.08

0.00

0.04

0.02Cum

ulat

ive

Haz

ard

Rat

e

CREDOLong-Term (1 Year) Benefits of Clopidogrel in PCI Patients

MI, stroke, or death – ITT population

* Plus ASA and other standard therapies Steinhubl S et al. JAMA. 2002;288:2411-2420.

Com

bine

d en

dpoi

nt o

ccur

renc

e (%

)

Months from randomization

27% RRRP=0.02

Placebo*Clopidogrel*

0

5

10

15

8.5%

11.5%

0 3 6 9 12

Primary Endpoint (MI/Stroke/CV Death) in Patients with Previous MI, IS, or PAD*“CAPRIE-like Cohort”

RRR: 17.1 % (95% CI: 4.4%, 28.1%)P=0.01

Prim

ary

Out

com

e Ev

ent R

ate

(%)

0

2

4

6

8

10

Months Since Randomization 0 6 12 18 24 30

Clopidogrel + ASAPlacebo + ASA

n=9,478

* Post hoc analysis

Bhatt DL et al. J Am Coll Cardiol. 2007;49:1982-1988.

8.8%

7.3%

Days

TRITON – TIMI 38 CV Death, MI, Stroke

0

5

10

15

0 30 60 90 180 270 360 450

HR 0.81(0.73-0.90)P=0.0004

Prasugrel

Clopidogrel

Prim

ary

Endp

oint

(%)

12.1(781)

9.9 (643)

NNT= 46

ITT= 13,608 LTFU = 14 (0.1%)

Wiviott SD et al. N Engl J Med. 2007;357:2001-2005.

HR 0.80P=0.0003

HR 0.77P=0.0001

• A loading dose of thienopyridine is recommended for STEMI patients for whom PCI is planned.

• Regimens should be one of the following:

–Clopidogrel (at least 300 mg to 600 mg) should be given as early as possible before or at the time of primary or nonprimary PCI

–Prasugrel (60 mg) should be given as soon as possible for primary PCI

2009 ACC/AHA STEMI/PCI Guidelines Focused UdatesLoading Doses for Thienopyridines

C

Kushner FG et al. J Am Coll Cardiol. 2009;54:2205-2241.

Modified Recommendation

B


2007 ACC/AHA STEMI Focused UpdateAnticoagulants as Ancillary Therapy to Reperfusion Therapy in PCI

For patients undergoing PCI after having received an anticoagulant regimen, the following dosing recommendations should be followed:

• For prior treatment with UFH, administer additional boluses of UFH as needed to support the procedure, taking into account whether GP IIb/IIIa receptor antagonists have been administered. Bivalirudin may also be used in patients treated previously with UFH.

• For prior treatment with enoxaparin, if the last SC dose was administered within the prior 8 hours, no additional enoxaparin should be given; if the last SC dose was administered at least 8 to 12 hours earlier, an IV dose of 0.3 mg per kg of enoxaparin should be given.

• For prior treatment with fondaparinux, administer additional IV treatment with an anticoagulant possessing anti-IIa activity, taking into account whether GP IIb/IIIa receptor antagonists have been administered.

New Class I Recommendation

Antman EM et al. J Am Coll Cardiol. 2008;51:210-247.

Glycoprotein IIb/IIIa Inhibitors

• Only indicated in highest risk UA/NSTEMI patients (dynamic changes on ECG, elevated biomarkers, electrical instability) and/or in whom early PCI is planned

• Abciximab is the choice if early angiography and PCI are planned

• Eptifibatide or tirofiban indicated when no PCI planned

• Initiate in conjunction with your cardiologist

Anderson JL et al. J Am Coll Cardiol. 2007;50:e1-e157.

Acute CoronarySyndromesTreatment of STEMI

EMS Transport

Onset of symptoms of

STEMI

9-1-1EMS

dispatch

EMS on-scene• Encourage 12-lead ECGs• Consider prehospital fibrinolytic if

capable and EMS-to-needle within 30 min

GOALSPCI

capable

Not PCIcapable

Hospital fibrinolysis: door-to-needle within 30 min

EMS triage plan

Golden hr = 1st 60 min Total ischemic time: within 120 min

Patient EMS Prehospital fibrinolysisEMS-to-needlewithin 30 min

EMS transportEMS-to-balloon within 90 min

Patient self-transport Hospital door-to-balloon within 90 min

Dispatch1 min

5 min

8 min

Time to Treatment Is Critical in STEMI

Figure adapted with permission from Antman EM et al. J Am Coll Cardiol. 2008;51:210-247.

• Time to reperfusion is a critical determinant of the extent of myocardial damage and clinical outcomes in patients with STEMI

• Key factors in STEMI care are rapid, accurate diagnosis and keeping the encounter time to reperfusion as short as possible

0.4 million discharges per year for STEMI in US

Inter-hospitaltransfer

Effect of Door-to-Balloon Time on Mortality in Patients with STEMI

Reproduced with permission from McNamara RL et al. J Am Coll Cardiol. 2006;47:2180-2186.

In-hospital mortality and door-to-balloon time; P for trend <0.001

8

7

6

5

4

3

2

1

0≤90 >90-120 >120-150 >150

Door-to-Balloon Time (min)

In-h

ospi

tal M

orta

lity,

%

*P<0.05 for all

Bradley EH et al. N Engl J Med. 2006;355:2308-2320.

Door to Balloon (DTB) An Alliance for Quality Campaign

StrategyMean reduction in door-to-

balloon time, min*

Having emergency medicine physicians activate the cath lab 8.2

Having a single call to a central page operator activate the cath lab 13.8

Having the ED activate the cath lab while patient is still en route 15.4

Expecting staff to arrive at the cath lab within 20 minutes after page 19.3

Having an attending cardiologist always on site 14.6

Having staff in the ED and cath lab use and receive real-time feedback 8.6

Strategies Associated With a Significant Reduction in DTB Time

Class I Modified Recommendations

2007 ACC/AHA STEMI Focused UpdateReperfusion Therapy for STEMI

• STEMI patients presenting to a hospital with PCI capability should be treated with primary PCI within 90 minutes of first medical contact as a systems goal (Level of Evidence: A)

• STEMI patients presenting to a hospital without PCI capability and who cannot be transferred to a PCI center and undergo PCI within 90 minutes of first medical contact should be treated with fibrinolytic therapy within 30 minutes of hospital presentation as a systems goal unless fibrinolytic therapy is contraindicated (Level of Evidence: B)



STEMI patient who is a candidate for reperfusion

Initially seen at a PCI- capable facility

Initially seen at a non–PCI-capable facility

Diagnostic angio

Send to cath lab for primary PCI

(Class I, LOE: A)

At PCI facility,

evaluate for timing of diagnostic

angio

Prep antithrombotic (anticoagulant plus antiplatelet) regimen

Medical therapy only PCI CABG

NOT HIGH RISKTransfer to a PCI facility may be

considered (Class IIb, LOE: C), especially if

ischemic symptoms persist and failure to

reperfuse is suspected

HIGH RISKTransfer to a PCI

facility is reasonable for early diagnostic angio and possible PCI or CABG (Class

IIa, LOE: B),

High-risk patients as defined by 2007 STEMI Focused Update should

undergo cath (Class I, LOE: B)

Initial treatment with fibrinolytic therapy

(Class I, LOE: A)Transfer for primary PCI (Class I, LOE: A)

Selection of reperfusion strategy

2009 ACC/AHA STEMI/PCI Guidelines Focused UpdatePathway: Triage and Transfer for PCI in STEMI

PCI vs Fibrinolysis Systematic Overview

Short term (4-6 weeks)

Keeley EC et al. Lancet. 2003;361:13-20.

P=0.0002P=0.0003 P<0.0001

P<0.0001

P=0.0004

(23 RCTs, n=7,739)(23 RCTs, n=7,739)

8.5 7.3 7.2

22.0

2.0

7.24.9

2.8

6.8

1.00.0

5.0

10.0

15.0

20.0

25.0

Death DeathSHOCK

excl.

Reinfarction Recurrentischemia

Stroke

Perc

ent (

%)

LysisPCI

Medical Therapy for STEMI Managed by Primary PCI

ASA

Anticoagulant UFH (Bival)

Thienopyridine

Clopidogrel 600Prasugrel 60

Beta Blocker IV prn Oral within 24h

GP IIb/IIIa

EptifibatideAbciximab

Statin

Presentation Access—Wire—Balloon

EDCCL

2009 ACC/AHA STEMI/PCI Guidelines Focused UpdateUse of Thienopyridines

• In STEMI patients with a prior history of stroke and transient ischemic attack for whom primary PCI is planned, prasugrel is not recommended as part of a dual antiplatelet therapy regimen


New RecommendationC


CLARITY TIMI 28CV Death, MI, Recurrent Ischemia, Urgent Revascularization

Days

Perc

enta

ge w

ith e

ndpo

int (

%)

05

1015

0 5 10 15 20 25 30

Placebo

Clopidogrel

Odds Ratio 0.80(95% CI 0.65-0.97)

P=0.026

20%

Sabatine MS et al. N Engl J Med. 2005;352:1179-1189.


2009 ACC/AHA STEMI/PCI Guidelines Focused UpdateUse of GP IIb/IIIa Inhibitors in STEMI

• It is reasonable to start treatment with glycoprotein IIb/IIIa receptor antagonists at the time of primary PCI (with or without stenting) in selected patients with STEMI

• Abciximab

• Tirofiban and eptifibatide

A


Modified Recommendation

B

2009 ACC/AHA STEMI Focused UpdateAnticoagulants as Ancillary Therapy to Reperfusion Therapy in PCI

For patients undergoing PCI after having received an anticoagulant regimen, the following dosing recommendations should be followed:

• For prior treatment with UFH, administer additional boluses of UFH as needed to support the procedure, taking into account whether GP IIb/IIIa receptor antagonists have been administered; bivalirudin may also be used in patients treated previously with UFH

• For prior treatment with enoxaparin, if the last SC dose was administered within the prior 8 hours, no additional enoxaparin should be given; if the last SC dose was administered at least 8 to 12 hours earlier, an IV dose of 0.3 mg per kg of enoxaparin should be given

• For prior treatment with fondaparinux, administer additional IV treatment with an anticoagulant possessing anti-IIa activity, taking into account whether GP IIb/IIIa receptor antagonists have been administered

New Class I Recommendation


2009 ACC/AHA STEM Focused UpdateAnticoagulants as Ancillary Therapy to Reperfusion Therapy

• Patients undergoing reperfusion with fibrinolytics should receive anticoagulant therapy for a minimum of 48 hours (LOE: C) and preferably for the duration of the index hospitalization, up to 8 days (regimens other than unfractionated heparin [UFH] are recommended if anticoagulant therapy is given for more than 48 hours because of the risk of heparin-induced thrombocytopenia with prolonged UFH treatment) (LOE: A)

• Anticoagulant regimens with established efficacy include:

– UFH (LOE: C)

– Enoxaparin (LOE: A)

– Fondaparinux (LOE: B)

New Class I Recommendations


Anti-ischemic Effects vsBleeding Risk

Acute CoronarySyndromes

Recent ACS TrialsForging a New Paradigm for Upstream Management

ISC

HEM

IA: T

he tr

aditi

onal

, prim

ary

conc

ern

of th

e em

erge

ncy

phys

icia

n

BLEEDING: Newer, important concern for the cardiologist: A novel issue for the emergency physician

Mortality

Major Bleeding

TransfusionHypotension Cessation of ASA/Clopidogrel

Ischemia Stent Thrombosis Inflammation

Bhatt DL et al. In Braunwald: Harrison’s Online 2005.

Possible Relationship BetweenBleeding and Mortality

Bleeding Events – Safety Cohort(n=13,457)

% E

vent

s

ARD 0.6%HR 1.32P=0.03

NNH=167

ARD 0.5%HR 1.52P=0.01

ARD 0.2%P=0.23

ARD 0%P=0.74

ARD 0.3%P=0.002

Clop 0 (0) % Pras 6 (2.3)% (P=0.02)

Slide courtesy of Dr. Elliott Antman.

LifeThreatening

TIMI MajorBleeds

ClopidogrelPrasugrel

0.9

2.4

1.4

0

2

4ICH in patients with prior stroke/TIA (n=518)

0.91.1

0.10.4 0.3 0.3

Nonfatal Fatal ICH

1.8

Question and Answer Session

Optimal Antithrombotic Care for Patients with Acute Coronary SyndromesAcross the Continuum of Unstable Angina,

NSTEMI, and STEMI

Thank you for joining us today.

Please remember to turn in your evaluation form.

Your participation will help shape future CME activities.

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materials on ACS.

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