acs-wrap

ACS-WRAPACS-WRAP

Charles V. Pollack, Jr., M.A., M.D., FACEP, FAHA

Professor and Chairman

Emergency Medicine, Pennsylvania Hospital

University of Pennsylvania Health System

Philadelphia

Charles V. Pollack, Jr., M.A., M.D., FACEP, FAHA

Professor and Chairman

Emergency Medicine, Pennsylvania Hospital

University of Pennsylvania Health System

Philadelphia

Non-ST-Segment-Elevation ACSNon-ST-Segment-Elevation ACS

Inclusive of unstable angina and NSTEMI

These are the same clinical syndrome, with the only distinction being the objective identification of myonecrosis with NSTEMI

Neither UA or NSTEMI are necessarily associated with ischemic ECG changes Result from partial or intermittent obstruction

of epicardial vessels, or complete obstruction of distal branches

In contradistinction, STEMI is complete obstruction of larger vessel, which is associated with ECG changes

Inclusive of unstable angina and NSTEMI

These are the same clinical syndrome, with the only distinction being the objective identification of myonecrosis with NSTEMI

Neither UA or NSTEMI are necessarily associated with ischemic ECG changes Result from partial or intermittent obstruction

of epicardial vessels, or complete obstruction of distal branches

In contradistinction, STEMI is complete obstruction of larger vessel, which is associated with ECG changes


UA/NSTEMI typically result from fissure or frank rupture of an atherosclerotic plaque Stimulates local activation of:

• platelets• coagulation cascade• complement

Platelet aggregate forms over site of plaque injury . . . but remains unstable and subject to shear forces from passing blood flow

No obstruction in situ, but downstream embolization can occur• perhaps resulting in ST↓ or troponin leak

UA/NSTEMI typically result from fissure or frank rupture of an atherosclerotic plaque Stimulates local activation of:

• platelets• coagulation cascade• complement

Platelet aggregate forms over site of plaque injury . . . but remains unstable and subject to shear forces from passing blood flow

No obstruction in situ, but downstream embolization can occur• perhaps resulting in ST↓ or troponin leak


Pharmacologic therapy in NSTE ACS is therefore directed at this triad of abnormal activity: Platelet activation—anti-activation and anti-

aggregation• ASA and clopidogrel• GPIs

Coagulation activation—anticoagulants Complement activation—anti-

inflammatories . . . ? statins

Pharmacologic therapy in NSTE ACS is therefore directed at this triad of abnormal activity: Platelet activation—anti-activation and anti-

aggregation• ASA and clopidogrel• GPIs

Coagulation activation—anticoagulants Complement activation—anti-

inflammatories . . . ? statins

Guidelines for NSTE-ACS diagnosis and management


Very complex disease state with broad ranges of risk and a multitude of therapeutic options

Many important and pertinent clinical studies

Information overload!

Need evidence-based guidelines to promote consistency of care and resulting better outcomes

Very complex disease state with broad ranges of risk and a multitude of therapeutic options

Many important and pertinent clinical studies

Information overload!

Need evidence-based guidelines to promote consistency of care and resulting better outcomes



AHCPR guidelines 1994: first attempt

ACC/AHA Joint Task Force: Sep 2000 Widely read, lots of interest Clear evidence scoring, sensible

recommendations, temporal sequencing• “soup to nuts”

Recapitulation, interpretation, and promulgation for upstream providers in Annals of Emergency Medicine

AHCPR guidelines 1994: first attempt

ACC/AHA Joint Task Force: Sep 2000 Widely read, lots of interest Clear evidence scoring, sensible

recommendations, temporal sequencing• “soup to nuts”

Recapitulation, interpretation, and promulgation for upstream providers in Annals of Emergency Medicine

Class I Benefit >>> Risk

Procedure/ Treatment SHOULD be performed/ administered

Class IIa Benefit >> RiskAdditional studies with focused objectives needed

IT IS REASONABLE to perform procedure/administer treatment

Class IIb Benefit ≥ RiskAdditional studies with broad objectives needed; Additional registry data would be helpful

Procedure/Treatment MAY BE CONSIDERED

Class III Risk ≥ BenefitNo additional studies needed

Procedure/Treatment should NOT be per-formed/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 considered

may/might be reasonable

usefulness/effectiveness is unknown /unclear/uncertain or not well established

is not recommendedis not indicatedshould notis not useful/effective/

beneficialmay be harmful

Applying Classification of Recommendations

“The Guidelines”Weighing the Evidence

“The Guidelines”Weighing the Evidence

Weight of evidence grades:= Data from many large, randomized trials= Data from fewer, smaller randomized trials,

careful analyses of nonrandomized studies, observational registries

= Expert consensus

Weight of evidence grades:= Data from many large, randomized trials= Data from fewer, smaller randomized trials,

careful analyses of nonrandomized studies, observational registries

= Expert consensus

• Braunwald E, Antman EM, Beasley JW, et al: ACC/AHA guidelines for the management of patients with unstable angina and non-ST-segment elevation myocardial infarction: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee on the Management of Patients with Unstable Angina). J Am Coll Cardiol 2000;36:970-1062 (2002 update at www.acc.org; summary in Circulation 2002;106:1893-1900)

• Pollack CV, Roe MT, Peterson ED: 2002 Update to the Pollack CV, Roe MT, Peterson ED: 2002 Update to the ACC/AHA guidelines for the management of patients with ACC/AHA guidelines for the management of patients with unstable angina and non-ST-segment elevation myocardial unstable angina and non-ST-segment elevation myocardial infarction: Implications for emergency department practice. infarction: Implications for emergency department practice. Ann Ann Emerg MedEmerg Med 2003;41:355-69. 2003;41:355-69.

NSTE ACS: Optimal Therapy, 2002-07NSTE ACS: Optimal Therapy, 2002-07

http://www.acc.org/

• Anderson JL, Adams CD, Antman EM, et al. 2007 guidelines for the management of patients with unstable angina/non-ST-segment-elevation myocardial infarction: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. J Am Coll Cardiol 2007;50:e1-e157, and Circulation 2007;116:e148-e304, and at www.acc.org and at www.americanheart.org.

• Pollack CV, Braunwald E: 2007 Update to the ACC/AHA Pollack CV, Braunwald E: 2007 Update to the ACC/AHA guidelines for the management of patients with unstable guidelines for the management of patients with unstable angina and non-ST-segment elevation myocardial angina and non-ST-segment elevation myocardial infarction: Implications for emergency department practice. infarction: Implications for emergency department practice. Ann Emerg MedAnn Emerg Med 2008, in press. 2008, in press.

NSTE ACS: Optimal Therapy, 8/6/07NSTE ACS: Optimal Therapy, 8/6/07

http://www.acc.org/

http://www.americanheart.org/

CRUSADE: A National CRUSADE: A National

Quality Improvement InitiativeQuality Improvement Initiative

CRUSADE: A National CRUSADE: A National

Quality Improvement InitiativeQuality Improvement Initiative

CCan an RRapid Risk Stratification of apid Risk Stratification of UUnstable Angina Patients nstable Angina Patients

SSuppress uppress ADADverse Outcomes with verse Outcomes with EEarly Implementation arly Implementation

of the ACC/AHA Guidelinesof the ACC/AHA Guidelines

2002-20072002-2007

CCan an RRapid Risk Stratification of apid Risk Stratification of UUnstable Angina Patients nstable Angina Patients

SSuppress uppress ADADverse Outcomes with verse Outcomes with EEarly Implementation arly Implementation

of the ACC/AHA Guidelinesof the ACC/AHA Guidelines

2002-20072002-2007

January 2007

443 Participating Sites205,528 Patients

AK(0)

WA(5)

OR(5)

CA(34)

ID(0)

NV(2)

MT(0)

WY(0)

CO(9)

NM(1)

ND(1)

SD(3)

NE (3)

KS(3)

OK(7)

TX(13)

MN(3)

IA(6)

MO(8)

AR(2)

LA(6)

WI(5) MI

(20)

MI

UT(1)

AZ(8)

HI (0)

IL(17)

IN(7)

KY(8)

TN (9)

MS(6)

AL(9)

GA(14)

FL(31)

SC(7)

NC(14)

VA(17)

OH(35)

WV(2)

PA(36)

NY(34)

MD (13)

ME(0)

VT (1)

NH (1)

NJ (12)

MA (10)

CT (7)

DE (3)

RI (1)

DC (1)

The CRUSADE Experience

Data on file, Duke Clinical Research Institute.Data on file, Duke Clinical Research Institute.

Hospital Link Between Overall Guidelines Adherence and MortalityHospital Link Between Overall Guidelines Adherence and Mortality

Peterson et al, JAMA 2006;295:1863-1912Peterson et al, JAMA 2006;295:1863-1912

5.95

5.16 4.97

4.16

5.064.63

4.15

6.31

0

1

2

3

4

5

6

7

<=25% 25 - 50% 50 - 75% >=75%

Hospital Composite Quality Quartiles

% I

n-H

osp

Mo

rtal

ity

Adjusted Unadjusted

5.95

5.16 4.97

4.16

5.064.63

4.15

6.31

0

1

2

3

4

5

6

7

<=25% 25 - 50% 50 - 75% >=75%

Hospital Composite Quality Quartiles

% I

n-H

osp

Mo

rtal

ity

Adjusted Unadjusted

Every 10% Every 10% in guidelines adherence in guidelines adherence 10% 10% in mortality (OR=0.90, 95% CI: 0.84-0.97) in mortality (OR=0.90, 95% CI: 0.84-0.97)

Management Strategies: 2002 GuidelinesConservative vs. Invasive StrategiesConservative vs. Invasive Strategies

Management Strategies: 2002 GuidelinesConservative vs. Invasive StrategiesConservative vs. Invasive Strategies

Early (within 48h) invasive strategy in high-risk patients with any of the following:

- Recurrent ischemia, despite meds- Recurrent ischemia, despite meds

- Elevated Troponin I or T- Elevated Troponin I or T

- New ST-segment depression- New ST-segment depression

- New CHF symptoms- New CHF symptoms

- High-risk stress test findings- High-risk stress test findings

- LV dysfunction (EF < 40%)- LV dysfunction (EF < 40%)

- Hemodynamic instability, sustained VT- Hemodynamic instability, sustained VT

- PCI within 6 months, prior CABG- PCI within 6 months, prior CABG

Early (within 48h) invasive strategy in high-risk patients with any of the following:

- Recurrent ischemia, despite meds- Recurrent ischemia, despite meds

- Elevated Troponin I or T- Elevated Troponin I or T

- New ST-segment depression- New ST-segment depression

- New CHF symptoms- New CHF symptoms

- High-risk stress test findings- High-risk stress test findings

- LV dysfunction (EF < 40%)- LV dysfunction (EF < 40%)

- Hemodynamic instability, sustained VT- Hemodynamic instability, sustained VT

- PCI within 6 months, prior CABG- PCI within 6 months, prior CABG

II IIaIIa IIbIIb IIIIII

Invasive Procedures 4Q 2006(among patients without contraindications to cath)

Invasive Procedures 4Q 2006(among patients without contraindications to cath)

Median TimesMedian Times

• Cath - 22 hrsCath - 22 hrs

• PCI - 21 hrsPCI - 21 hrs

• CABG - 69 hrsCABG - 69 hrs

83%

67%

53%

38%

12%

0%

20%

40%

60%

80%

100%

Cath Cath < 48 hr PCI PCI < 48 hr CABG

Management Strategies: 2007Early Invasive vs Selectively InvasiveEarly Invasive vs Selectively Invasive


Early invasive: diagnostic angiography with intent to perform revascularization cath anticipated within 4-24 hours follows a foundation of risk-directed medical therapy

Selectively invasive (or early conservative): invasive evaluation only if optimal medical management fails

Note: from ED perspective, both strategies involve risk-directed, evidence-based medical therapy

Early invasive: diagnostic angiography with intent to perform revascularization cath anticipated within 4-24 hours follows a foundation of risk-directed medical therapy

Selectively invasive (or early conservative): invasive evaluation only if optimal medical management fails

Note: from ED perspective, both strategies involve risk-directed, evidence-based medical therapy



EIS is indicated in initially stabilized UA/NSTEMI patients (without contraindications) who have an elevated risk for clinical events

EIS is indicated in UA/NSTEMI patients (without contraindications) who have refractory angina or hemodynamic or electrical instability

SIS may be considered in initially stabilized patients who have an elevated risk for clinical events (including ↑Tn)

EIS is indicated in initially stabilized UA/NSTEMI patients (without contraindications) who have an elevated risk for clinical events

EIS is indicated in UA/NSTEMI patients (without contraindications) who have refractory angina or hemodynamic or electrical instability

SIS may be considered in initially stabilized patients who have an elevated risk for clinical events (including ↑Tn)


Benefits of Early Catheterizationby Risk Group

Benefits of Early Catheterizationby Risk Group

0

2

4

6

8

10

12

Low Risk Moderate Risk High Risk

Early Cath No Early Cath

0

2

4

6

8

10

12

Low Risk Moderate Risk High Risk

Early Cath No Early Cath

- Bhatt AHA 2002- Bhatt AHA 2002

% I

nhos

pita

l Mor

talit

y%

Inh

ospi

tal M

orta

lity

Medical Management: 2007 GuidelinesMedical Management: 2007 GuidelinesAnti-Ischemic Therapy: Independent of StrategyAnti-Ischemic Therapy: Independent of Strategy

Medical Management: 2007 GuidelinesMedical Management: 2007 GuidelinesAnti-Ischemic Therapy: Independent of StrategyAnti-Ischemic Therapy: Independent of Strategy

NTG

Morphine

Beta-Blockers: emphasis on oral dosing

NTG

Morphine

Beta-Blockers: emphasis on oral dosing

IIII IIaIIaIIaIIa IIbIIbIIbIIb IIIIIIIIIIII

Medical Management: 2002 GuidelinesMedical Management: 2002 GuidelinesAnti-Thrombotic TherapyAnti-Thrombotic Therapy


Immediate aspirin

Clopidogrel, if aspirin contraindicated

Heparin (IV unfractionated, LMW) with antiplatelet agents listed above

Enoxaparin preferred over UFH unless CABG is planned within 24 hours

Immediate aspirin

Clopidogrel, if aspirin contraindicated

Heparin (IV unfractionated, LMW) with antiplatelet agents listed above

Enoxaparin preferred over UFH unless CABG is planned within 24 hours




In EIS:

enoxaparin or UFH

bivalirudin* or fondaparinux

In SIS:

enoxaparin or UFH

fondaparinux

In EIS:

enoxaparin or UFH

bivalirudin* or fondaparinux

In SIS:

enoxaparin or UFH

fondaparinux


Immediate ASAImmediate ASA



Relevant new studies for antithrombotic therapy:

SYNERGY, JAMA 2004 10,027 patients with high-risk NSTE ACS, randomized

to enox vs UFH, open-label, superiority

OASIS-5, NEJM 2006 20,078 patients with high-risk NSTE ACS, randomized

to fonda vs enox, double-blind, noninferiority

ACUITY, NEJM 2006 13,819 patients with moderate or high-risk NSTE ACS,

randomized to hep/GPI vs bival/GPI vs bival, open-label, noninferiority

Relevant new studies for antithrombotic therapy:

SYNERGY, JAMA 2004 10,027 patients with high-risk NSTE ACS, randomized

to enox vs UFH, open-label, superiority

OASIS-5, NEJM 2006 20,078 patients with high-risk NSTE ACS, randomized

to fonda vs enox, double-blind, noninferiority

ACUITY, NEJM 2006 13,819 patients with moderate or high-risk NSTE ACS,

randomized to hep/GPI vs bival/GPI vs bival, open-label, noninferiority

Anti-Aggregation Antiplatelet Tx: 2002Anti-Aggregation Antiplatelet Tx: 2002Platelet GP IIb/IIIa InhibitorsPlatelet GP IIb/IIIa Inhibitors

Anti-Aggregation Antiplatelet Tx: 2002Anti-Aggregation Antiplatelet Tx: 2002Platelet GP IIb/IIIa InhibitorsPlatelet GP IIb/IIIa Inhibitors

Any GP IIb/IIIa inhibitor + ASA/Heparin for all patients, if cath/PCI planned

Eptifibatide or tirofiban + ASA/Heparin for high-risk* patients in whom early cath/PCI is not planned

Any GP IIb/IIIa inhibitor for patients already on ASA + Heparin + clopidogrel, if cath/PCI is planned

Any GP IIb/IIIa inhibitor + ASA/Heparin for all patients, if cath/PCI planned

Eptifibatide or tirofiban + ASA/Heparin for high-risk* patients in whom early cath/PCI is not planned

Any GP IIb/IIIa inhibitor for patients already on ASA + Heparin + clopidogrel, if cath/PCI is planned


* High-risk: Age > 75; prolonged, ongoing CP; hemodynamic instability; rest CP w/ ST ; VT; positive cardiac markers * High-risk: Age > 75; prolonged, ongoing CP; hemodynamic instability; rest CP w/ ST ; VT; positive cardiac markers

Eptifibatide or tirofiban + ASA/Heparin for patients without continuing ischemia in whom PCI is not planned

Abciximab for patients in whom PCI is not planned

Eptifibatide or tirofiban + ASA/Heparin for patients without continuing ischemia in whom PCI is not planned

Abciximab for patients in whom PCI is not planned


Ant-Aggregation Antiplatelet Tx: 2002Ant-Aggregation Antiplatelet Tx: 2002Platelet GP IIb/IIIa InhibitorsPlatelet GP IIb/IIIa Inhibitors

Ant-Aggregation Antiplatelet Tx: 2002Ant-Aggregation Antiplatelet Tx: 2002Platelet GP IIb/IIIa InhibitorsPlatelet GP IIb/IIIa Inhibitors

Anti-Activation Antiplatelet Therapy: 2002Anti-Activation Antiplatelet Therapy: 2002ClopidogrelClopidogrel

Anti-Activation Antiplatelet Therapy: 2002Anti-Activation Antiplatelet Therapy: 2002ClopidogrelClopidogrel

Aspirin + clopidogrel, for up to 1 month*

Aspirin + clopidogrel, for up to 9 months*

Withhold clopidogrel for 5-7 days for CABG

Aspirin + clopidogrel, for up to 1 month*

Aspirin + clopidogrel, for up to 9 months*

Withhold clopidogrel for 5-7 days for CABG


* For patients managed with an early conservative strategy, and * For patients managed with an early conservative strategy, and those who are planned to undergo early PCIthose who are planned to undergo early PCI* For patients managed with an early conservative strategy, and * For patients managed with an early conservative strategy, and those who are planned to undergo early PCIthose who are planned to undergo early PCI

Guidelines do not specify initial timing of using Guidelines do not specify initial timing of using clopidogrel when coronary anatomy is unknownclopidogrel when coronary anatomy is unknownGuidelines do not specify initial timing of using Guidelines do not specify initial timing of using clopidogrel when coronary anatomy is unknownclopidogrel when coronary anatomy is unknown

Advanced Antiplatelet Tx: 2007Advanced Antiplatelet Tx: 2007Advanced Antiplatelet Tx: 2007Advanced Antiplatelet Tx: 2007


All patients receive ASA

EIS: upstream clopidogrel or IIb/IIIa

EIS: upstream IIb/IIIa should be small-molecule

SIS: if medical management fails, add IIb/IIIa or clopidogrel . . .

. . . upstream

All patients receive ASA

EIS: upstream clopidogrel or IIb/IIIa

EIS: upstream IIb/IIIa should be small-molecule

SIS: if medical management fails, add IIb/IIIa or clopidogrel . . .

. . . upstream

Advanced Antiplatelet Tx: 2007Advanced Antiplatelet Tx: 2007Advanced Antiplatelet Tx: 2007Advanced Antiplatelet Tx: 2007


SIS with recurrent ischemia on ASA, clopidogrel, and anticoag: add IIb/IIIa upstream

EIS: it is reasonable to give both clopidogrel and IIb/IIIa upstream

EIS: can omit IIb/IIIa if bivalirudin is anticoagulant + at least 300mg clopidogrel given > 6h prior to cath

SIS with recurrent ischemia on ASA, clopidogrel, and anticoag: add IIb/IIIa upstream

EIS: it is reasonable to give both clopidogrel and IIb/IIIa upstream

EIS: can omit IIb/IIIa if bivalirudin is anticoagulant + at least 300mg clopidogrel given > 6h prior to cath

Anti-Activation Antiplatelet Tx: 2007Anti-Activation Antiplatelet Tx: 2007More onMore on ClopidogrelClopidogrel

Anti-Activation Antiplatelet Tx: 2007Anti-Activation Antiplatelet Tx: 2007More onMore on ClopidogrelClopidogrel


Clopidogrel with full loading dose in ASA-allergic patients

EIS: clopidogrel or IIb/IIIa administered upstream

SIS: clopidogrel initiated “as soon as possible” and continued for at least one month . . .

. . . and preferably for one year

Clopidogrel with full loading dose in ASA-allergic patients

EIS: clopidogrel or IIb/IIIa administered upstream

SIS: clopidogrel initiated “as soon as possible” and continued for at least one month . . .

. . . and preferably for one year

Antiplatelet Drug TargetsAntiplatelet Drug Targets

PlateletThrombin

ADP

Thromboxane A2

Epinephrine

Serotonin

Collagen

PAR-1

PAR-4

P2Y1

P2Y12

TXA2-R

5HT2A

Anionicphospholipidsurfaces

GP IIbGP IIbGP IIIaGP IIIa

GP VI

Platelet

GP IIIaGP IIIaGP IIbGP IIb

Fibrinogen

GP Ia

Clopidogrel Prasugrel

Aspirin

Gp IIb/IIIa inhibitors

P2Y12

00

22

44

66

88

1010

1212

1414

Dea

th, M

I, o

r S

tro

keD

eath

, MI,

or

Str

oke

Clopidogrel Clopidogrel + ASA+ ASA

33 66 99

Placebo Placebo + ASA+ ASA

Months of Follow-UpMonths of Follow-Up

11.4%11.4%

9.3%9.3%

20% RRR20% RRRPP < 0.001 < 0.001

N = 12,562N = 12,562

00 1212

N Engl J Med. 2001N Engl J Med. 2001

CURE Primary ResultsCURE Primary ResultsCURE Primary ResultsCURE Primary Results

%%%%

CURE: Ischemic Endpoints Were Reduced within 24h of Randomization

CURE: Ischemic Endpoints Were Reduced within 24h of Randomization

Adapted from Adapted from Yusuf S, et al. Yusuf S, et al. Circulation.Circulation. 2003;107:966-972. 2003;107:966-972.

Hours After RandomizationHours After Randomization

Cu

mu

lati

ve H

azar

d R

ates

Cu

mu

lati

ve H

azar

d R

ates

0.00.0

0.0050.005

0.0100.010

0.0150.015

0.0200.020

0.0250.025

00 22 44 66 88 1010 1212 1414 1616 1818 2020 2222 2424

RR = 0.67RR = 0.67P P = 0.003= 0.003

PlaceboPlacebo+ ASA+ ASA

ClopidogrelClopidogrel+ ASA+ ASA

33%33%RRRRRR

0 1 2

ACUITY Composite Ischemia at 1-YearACUITY Composite Ischemia at 1-Year

Hazard ratio±95% CI

Hazard ratio±95% CI

Bivalalone

UFH/Enox+ IIb/IIIa

HR (95% CI) Pint

0.67

Bivalirudin alone betterBivalirudin alone better UFH/Enox + IIb/IIIa betterUFH/Enox + IIb/IIIa better

19.8% 19.2% 1.09 (0.96-1.23)

21.1% 20.7% 1.04 (0.79-1.36)

9.0% 9.6% 0.97 (0.76-1.24)

Actual Treatment

PCI (n=5179)

CABG (n=1040)

Medical (n=2994)

17.7%

14.6%

16.4%

16.1%

1.14 (0.99-1.30)

0.95 (0.80-1.14)0.11

Biomarkers (CK/Trop)

Elevated (n=5072)

Normal (n=3402)

16.2%

16.4%

17.2%

14.3%

0.97 (0.86-1.11)

1.20 (1.01-1.44)0.07

Pre Thienopyridine

Yes (n=5751)

No (n=3305)

UFH/Enoxaparin + GPIIb/IIIa vs. Bivalirudin alone1 yr KM estimate

ACUITY 1-Year Data as presented at ACC 2007.

P value interaction

only between subgroups

Clopidogrel Dosing and Duration of TherapyClopidogrel Dosing and Duration of Therapy Clopidogrel Dosing and Duration of TherapyClopidogrel Dosing and Duration of Therapy

ordinarily given with ASA (established in CURE)

labeled loading dose 300mg Many cardiologists prefer 600mg for faster onset of

action, no apparent additional safety concerns

labeled maintenance dose 75mg Some cardiologists prefer 150mg for first month after

stenting

CURRENT (OASIS-7) trial currently studying 600 vs 300, 150 vs 75 (first month), and low- vs high-dose ASA

Results in 2009?

ordinarily given with ASA (established in CURE)

labeled loading dose 300mg Many cardiologists prefer 600mg for faster onset of

action, no apparent additional safety concerns

labeled maintenance dose 75mg Some cardiologists prefer 150mg for first month after

stenting

CURRENT (OASIS-7) trial currently studying 600 vs 300, 150 vs 75 (first month), and low- vs high-dose ASA

Results in 2009?

Clopidogrel Dosing and Duration of TherapyClopidogrel Dosing and Duration of Therapy Clopidogrel Dosing and Duration of TherapyClopidogrel Dosing and Duration of Therapy

duration of therapy after ACS, whether or nor PCI performed with BMS, with 75-162mg ASA

75mg daily for at least 1 month (I-A) preferably 12 months (I-B)

duration of therapy after ACS and PCI performed with DES, with 162-325mg ASA for at least 3 months after sirolimus-eluting stent and 6 months after paclitaxel-eluting stent . . . then indefinitely thereafter

75mg daily for at least 12 months (I-B)

CHARISMA showed no net benefit from long-term clopidogrel therapy to patients with cardiac risk factors but no objectively demonstrated CAD

duration of therapy after ACS, whether or nor PCI performed with BMS, with 75-162mg ASA

75mg daily for at least 1 month (I-A) preferably 12 months (I-B)

duration of therapy after ACS and PCI performed with DES, with 162-325mg ASA for at least 3 months after sirolimus-eluting stent and 6 months after paclitaxel-eluting stent . . . then indefinitely thereafter

75mg daily for at least 12 months (I-B)

CHARISMA showed no net benefit from long-term clopidogrel therapy to patients with cardiac risk factors but no objectively demonstrated CAD

Chest Pain or ACS Committee

Meets quarterly or PRN PRN means after . . .

• Pertinent, “practice-changing” new study published

• ACC / AHA / TCT meetings

• M & M or sentinel event

• New guidelines published

Chest Pain or ACS Committee

Meets quarterly or PRN PRN means after . . .

• Pertinent, “practice-changing” new study published

• ACC / AHA / TCT meetings

• M & M or sentinel event

• New guidelines published

Optimal Management of NSTE ACS: ED to Cardiology — A Functional Model

Chest Pain or ACS Committee comprised of: Emergency physicians Interventional cardiologists Medical cardiologists Hospitalists CT surgeons ED nursing Cath lab nursing CCU nursing Lab Imaging

Chest Pain or ACS Committee comprised of: Emergency physicians Interventional cardiologists Medical cardiologists Hospitalists CT surgeons ED nursing Cath lab nursing CCU nursing Lab Imaging

Optimal Management of NSTE ACS ED to Cardiology — A Functional Model

Chest Pain or ACS Committee discusses: Protocols and standing orders Practice variations versus evidence Time to catheterization predictability Reduction of medical errors in ACS care DTB times QI issues (CRUSADE / NRMI / ACTION) Transfers in, transfers out New data: How should it impact our protocols?

Chest Pain or ACS Committee discusses: Protocols and standing orders Practice variations versus evidence Time to catheterization predictability Reduction of medical errors in ACS care DTB times QI issues (CRUSADE / NRMI / ACTION) Transfers in, transfers out New data: How should it impact our protocols?

Optimal Management of NSTE ACS ED to Cardiology — A Functional Model

ED physicians should be using optimal, evidence-based, guideline-consistent medical therapy for NSTE ACS

ED physicians must work with their colleagues in cardiology to develop pathways and approaches (EDICT for ACS) for proper use of antithrombotic and antiplatelet therapy at all levels

ED physicians should facilitate early invasive management of ACS whenever feasible and appropriate

ED physicians should address issues related to bleeding risk as well as ischemic risk.

A seamless transition of care is most likely to result in good outcomes.

ED physicians should be using optimal, evidence-based, guideline-consistent medical therapy for NSTE ACS

ED physicians must work with their colleagues in cardiology to develop pathways and approaches (EDICT for ACS) for proper use of antithrombotic and antiplatelet therapy at all levels

ED physicians should facilitate early invasive management of ACS whenever feasible and appropriate

ED physicians should address issues related to bleeding risk as well as ischemic risk.

A seamless transition of care is most likely to result in good outcomes.

Optimal Management of NSTE ACS ED to Cardiology — Summary and Game Plan

We should be using optimal medical therapy for NSTE ACS in the ED, just as in the CCU or the cath lab.

There must be cross-disciplinary collaboration (EM, CD, IM, HM, CTS, nursing throughout all levels of care) to develop pathways for proper use of antithrombotic and antiplatelet therapy at all levels, to facilitate early invasive management whenever feasible, and to address issues related to bleeding risk as well as ischemic risk.

We should be using optimal medical therapy for NSTE ACS in the ED, just as in the CCU or the cath lab.

There must be cross-disciplinary collaboration (EM, CD, IM, HM, CTS, nursing throughout all levels of care) to develop pathways for proper use of antithrombotic and antiplatelet therapy at all levels, to facilitate early invasive management whenever feasible, and to address issues related to bleeding risk as well as ischemic risk.

Conclusion: NSTE ACSConclusion: NSTE ACS

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Documents

nste acs

nsteacs diagnosis

broad ranges of risk

additional registry

risk procedure treatment

segmentelevation acsuanstemi

evidencebased guidelines

ecg changesnonst