the 2014 non-st-elevation mi guidelines—what’s new … · 2014 aha/acc guideline for the ......

The 2014 Non-ST-elevation MI Guidelines—What’s new and relevant to

clinical practice?

Jeffrey L. Anderson, MD, FACC, FAHA, MACP Professor of Internal Medicine, University of Utah

Associate Chief of Cardiology, Intermountain Medical Center Director of Cardiovascular Research, Intermountain Heart Institute

Vice-Chair of Research, Department of Internal Medicine, Intermountain Medical Center

Objectives:

• Describe the epidemiological and pathology of NSTEMI • Review pre-hospital measures and ED diagnosis in possible

NSTEMI • Describe decision making for invasive vs. noninvasive therapies

The 2014 Non-ST-Elevation-Acute Coronary Syndrome Guidelines—

What’s New and Relevant to Clinical Practice?

Jeffrey L Anderson, MD, FACC, FAHA, MACP

Intermountain Heart Institute Intermountain Medical Center Murray, Utah

Disclosures: Member of “Advances in ACS Expert Consensus Panel” (unrestricted CME grant from Sanofi-Aventis); Consultant, Medicines Company (minor)

Pathophysiology of Non-ST-elevation and ST-elevation Acute Coronary Syndromes

STEMI NSTEMI

HeartSite.com. http://www.heartsite.com/html/cad.html

Cross Section Longitudinal Section

Clot Totally Blocking Channel

Cross Section Longitudinal Section

Clot Partially Obstructing

Channel Ruptured Plaque

Hospitalizations in the U.S. Due to Acute Coronary Syndromes

Acute Coronary Syndromes

1.83 Million Hospital Admissions - ACS

UA/NSTEMI STEMI

1.42 million admissions per year

0.41 million admissions per year

National Hospital Discharge Survey. National Center for Health Statistics/Centers for Disease Control and Prevention 2007. 3

2014 AHA/ACC Guideline for the Management of Patients with Non-ST-Elevation Acute Coronary Syndromes

Sept 23, 2014

6

Key Management Questions

1. Dx/Pathway? STEMI? UA/NSTEMI? Prob/Poss UA? (history, exam, ECG)

2. Risk? (troponin, ECG; TIMI, GRACE risk scores) 3. General management: bedrest, aspirin, O2, NTG,

beta-blocker, morphine (?) 4. Initial strategy?

a. Invasive? B. Initial conservative/medical? 5. Antiplatelet: Clopidogrel? Prasugrel? Ticagrelor?

Glycoprotein IIb/IIIa inhibitor? 6. Anticoagulant: UFH? LMWH? Bival? Fonda?

Troponin Levels Predict Risk of Mortality in UA/NSTEMI

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

1 . 0 1 . 7

3 . 4 3 . 7

6 . 0

7 . 5

0

1

2

3

4

5

6

7

8

0 t o < 0 . 4 0 . 4 t o < 1 . 0 1 . 0 t o < 2 . 0 2 . 0 t o < 5 . 0 5 . 0 t o < 9 . 0 ≥ 9 . 0

Morta

lity at

42 da

ys; %

of pa

tients

831 174 148 134 50 67

% %

% %

%

%

C a r d i a c t r o p o n i n I ( n g / mL )

8

TIMI Risk Score 1. Age ≥65 y*

2. ≥3 CAD risk factors (high cholesterol, family history, hypertension, diabetes, smoking)*

3. Prior coronary stenosis ≥50%

4. Aspirin in last 7 days

5. ≥2 anginal events ≤24 h

6. ST-segment deviation*

7. Elevated cardiac markers* (Troponin or CK-MB)

Antman EM, et al. JAMA. 2000;284(7):835-842.

Number of Predictors

0

5

10

15

20

25

30

35

40

45

0/1 2 3 4 5 6/7

% D

eath

/ M

I / U

rgen

t Rev

asc

at 1

4 d

Non-ACS Causes of Elevated Troponin • Heart failure • Shock: septic, hypovolemic, cardiogenic • Injury: cardiac contusion, surgery, ablation, shocks • Inflammation: myocarditis, pericarditis • Cardiomyopathies: infiltrative, stress, hypertensive, hypertrophic • Aortic dissection, severe aortic stenosis • Tachycardias • Pulmonary: embolism/hypertension, respiratory failure • Neurologic: stroke, intracranial hemorrhage • Renal failure

AHA/ACC NSTE-ACS Guidelines: Early Risk Stratification

Perform rapid determination of likelihood of ACS, including a 12-lead ECG within 10 min of arrival at an ED. Perform serial ECGs at 15- to 30-min intervals during the first hour in symptomatic patients with initial non-diagnostic ECG. Measure cardiac troponin (cTnI or cTnT) in all patients with symptoms consistent with ACS. Measure serial cardiac troponin I or T at presentation and 3-6 h after symptom onset in all patients with symptoms consistent with ACS to identify a rising and/or falling pattern. Use risk scores to assess prognosis in patients with NSTE-ACS

I I I IIa IIa IIa IIb IIb IIb III III III I I I IIa IIa IIa IIb IIb IIb III III III I I I IIa IIa IIa IIb IIb IIb III III III IIa IIa IIa IIb IIb IIb III III III





2014 AHA/ACC NSTE-ACS Guideline. Circulation 2014 (Epub ahead of print, Sept 23, 2014)

Troponin-I Testing at Intermountain for Probable or Possible NSTE-ACS

AHA/ACC NSTE-ACS Guidelines: General Early Hospital Care

Administer supplemental oxygen only with oxygen saturation <90%, respiratory distress, or other high-risk features for hypoxemia. Administer sublingual NTG every 5 min x 3 for continuing ischemic pain, then assess need for IV NTG. Administer oral beta blockers within the first 24 h in the absence of HF, low-output state, risk for cardiogenic shock, or other contraindications to beta blockade. Calcium channel blockers are recommended for ischemic symptoms when beta blockers are not successful, are contraindicated, or cause unacceptable side effects. Initiate or continue high-intensity statin therapy in patients with no contraindications.







High-Intensity Statin and Peri-PCI MI Meta-analysis of 13 Randomized Studies

Test for heterogeneity: Chi2 = 9.02, df = 11 (P = 0.62), I2 = 0%. Test for overall effect: Z = 4.67 (P < 0.00001). OR = odds ratio. Patti G, et al. Circulation. 2011;123:1622-1632.

Study No. of Patients With

Event/Total No. of Patients OR (fixed) 95% CI

Weight %

OR (fixed) 95% CI High-dose statin Controls

ARMYDA 3/76 9/77 4.86 0.31 (0.08 – 1.20) ARMYDA-ACS 5/86 9/85 4.83 0.52 (0.17 – 1.63) ARMYDA-RECAPTURE 7/192 15/191 8.20 0.44 (0.18 – 1.11) Bozbas 1/59 0/34 0.35 1.77 (0.07 – 44.64) Briguori 27/226 37/225 18.48 0.69 (0.40 – 1.18) Cay 0/153 16/146 9.52 0.03 (0.00 – 0.43) Hara 6/15 7/22 1.13 1.43 (0.24 – 8.64) Jia 0/113 0/115 Not estimable Kinoshita 2/21 4/21 2.05 0.45 (0.07 – 2.76) NAPLES II 32/339 52/329 27.05 0.56 (0.35 – 0.89) STATIN-STEMI 13/86 17/85 8.21 0.71 (0.32 – 1.58) Veselka 10/100 12/100 6.11 0.81 (0.33 – 1.98) Yun 12/225 17/220 9.21 0.67 (0.31 – 1.44) Total (95% CI) 100.0 0.56 (0.44 – 0.71)

10 5 2 1 0.5 0.2 0.1 Favors

high-dose statin Favors controls

Considerations for Choice of Stategy Immediate invasive Refractory angina strategy Signs/symptoms of HF, new/worsening mitral regurgitation (within 2 h) Hemodynamic instability

Recurrent angina/ischemia at rest or low-level activity _____________________ Sustained VT or VF________________________________ Ischemia-guided Low-risk score (e.g., TIMI 0/1, GRACE <109) strategy Low-risk, troponin-negative females _____________________ Patient/clinician preference and no high-risk features_____ Early invasive strategy None of above, but GRACE risk score >140 (within 24 h) Temporal change in troponin _____________________ New or presumably new ST depression________________ Delayed invasive None of the above but diabetes mellitus strategy Renal insufficiency (GFR <60 ml/min/1.73 sq-m) (within 25-72 h) Reduced LV systolic function (EF<0.40)

Early post-infarction angina PCI within 6 months Prior CABG GRACE score 109-140; TIMI score >=2.

2014 AHA/ACC NSTE-ACS Guideline. Circulation 2014 ; Sept 23, 2014

Time (months) 0 1 2 3 4 5 6

0

4

8

12

16

20

% P

atie

nts

Conservative: Invasive:

O.R 0.78 95% CI (0.62, 0.97) P=0.025

19.4% 15.9%

TACTICS: Invasive vs Conservative Rx for Definite UA/NSTEMI Primary Endpoint: Death, MI, Rehospitalized for ACS at 6 Mo

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

*Low/intermediate risk=GRACE score <140 High risk=GRACE score ≥140 Early: Within 24 h (mean, 15 h); Delayed: After 36 h (mean, 50 h)

TIMACS: Timing of PCI in NSTE-ACS Rates of death, MI, or stroke within 6 mo by GRACE score:

HR (95% CI), early vs delayed invasive strategy

Mehta SR et al. N Engl J Med. 2009;310:2165-2175.

EARLY (%)

DELAYED (%)

Hazard Ratio (95% CI) P

Low/Intermediate (n=2070) 7.6 6.7 1.12 (0.88–

1.56) 0.48

High (n=961) 13.9 21.0 0.65 (0.48–

0.89) 0.006

Mechanisms of Platelet Aggregation and Antiplatelet Therapies in ACS

ADP = adenosine diphosphate, TXA2 = thromboxane A2, COX = cyclooxygenase. Adapted from Schafer AI. Am J Med. 1996;101:199-209.

Collagen Thrombin

TXA2

TXA2

ADP phosphodiesterase

ADP

(Aggregation) Gp IIb/IIIa

Activation

COX

clopidogrel

prasugrel

ticagrelor

aspirin

dipyridamole

cAMP

Heparins IIb/IIIa inhibitors

Aspirin Evidence: Secondary Prevention

Antithrombotic Trialist Collaboration. BMJ 2002;324:71–86

Category % Odds Reduction Acute MI Acute CVA Prior MI Prior CVA/TIA Other high risk CVD

(e.g. unstable angina, heart failure) PAD

(e.g. intermittent claudication) High risk of embolism (e.g. Afib) Other (e.g. DM) All trials

1.0 0.5 0.0 1.5 2.0 Control better Antiplatelet better

Effect of antiplatelet treatment* on vascular events**

*Aspirin was the predominant antiplatelet agent studied **Include MI, stroke, or death

Aspirin Evidence: Dose and Efficacy

0.5 1.0 1.5 2.0

500-1500 mg 34 19

160-325 mg 19 26

75-150 mg 12 32

<75 mg 3 13

Any aspirin 65 23

Antiplatelet Better

Antiplatelet Worse

Aspirin Dose No. of Trials (%) Odds Ratio for

Vascular Events

0 P<.0001

Indirect comparisons of aspirin doses on vascular events in high-risk patients

Antithrombotic Trialist Collaboration. BMJ 2002;324:71-86

Non-enteric-coated aspirin (162-325 mg/d) should be given to all NSTE-ACS patients promptly after presentation, and a maintenance dose (81-325 mg/d) should be continued indefinitely.

In NSTE-ACS patients unable to take aspirin because of hypersensitivity or GI intolerance, a loading dose of clopidogrel followed by a daily maintenance dose should be administered.

It is reasonable to use an aspirin maintenance dose of 81 mg per day in preference to higher maintenance doses in patients with NSTE-ACS treated either invasively or with coronary stent implantation


Aspirin Therapy for NSTE-ACS I I I IIa IIa IIa IIb IIb IIb III III III I I I IIa IIa IIa IIb IIb IIb III III III I I I IIa IIa IIa IIb IIb IIb III III III IIa IIa IIa IIb IIb IIb III III III



P2Y12 Inhibitor Basic Pharmacology

Clopidogrel Prasugrel Ticagrelor

Class Thienopyridine Thienopyridine Triazolopyrimidine

Reversibility Irreversible Irreversible Reversible

Activation Prodrug, limited by metabolism

Prodrug, not limited by metabolism

Active drug

Onset of Effect^ 2-4 hours 30 minutes 30 minutes

Duration of Effect 3-10 days 5-10 days 3-4 days

Withdrawal before major surgery

5 days 7 days 5 days

Hamm CW, et al. Eur Heart J. 2011. ^ 50% inhibition of platelet aggregation 22

0.00

0.02

0.04

0.06

0.08

0.10

0.12

0.14

Cu

mu

lati

ve H

azar

d R

Clopidogrel + ASA*

3 6 9

Placebo + ASA*

Months of Follow-Up

P = 0.00009† N = 12,562

0 12

* In addition to other standard therapies.

The CURE Trial Investigators. N Engl J Med. 2001;345:494-502.

Clopidogrel in NSTE-ACS with Medical Therapy: MI/Stroke/CV Death

Overall Relative Risk

Reduction

20%

CURE

0.15

0.10

0.05

0.0 0 100 200 300 400

Days of follow-up

12.6%

8.8%

P = 0.002 N = 2658

Clopidogrel + ASA*

Placebo + ASA*

Cum

ulat

ive

Haz

ard

Rat

e

* In addition to other standard therapies. PCI=percutaneous coronary intervention

Mehta. et al for the CURE Investigators. Lancet. 2001;358:527-533.

Composite of MI or cardiovascular death from randomization to end follow-up

PCI-CURE

Overall Relative Risk

Reduction

31%

Clopidogrel in NSTE-ACS with PCI: MI/Stroke/CV Death

Placebo + ASA*

N = 6303

Clopidogrel + ASA*

N = 6259

Major bleeding 2.7% 3.7% †

Life-threatening bleeding 1.8% 2.2% ‡

Non–life-threatening bleeding 0.9% 1.5% §

• Minor bleeding 2.4% 5.1%

End Point

* In addition to other standard therapies. † P = 0.001; ‡ P = NS; § P = 0.002; P < 0.001.

The CURE Trial Investigators. N Engl J Med. 2001;345:494-502.

CURE: Bleeding Results

Days

Cum

ulat

ive

Haz

ard

0.0

0.01

0.

02

0.03

0.

04

0 3 6 9 12 15 18 21 24 27 30

Clopidogrel: Double vs Standard Dose Primary Outcome: PCI Patients

Clopidogrel Standard

Clopidogrel Double

HR 0.85 95% CI 0.74-0.99

P=0.036

15% RRR

CV Death, MI or Stroke

Mehta. ESC 9/09

Variability in Antiplatelet Effect : Clopidogrel versus Prasugrel

IPA = inhibition of platelet aggregation Adapted from Brandt JT et al. Am Heart J. 2007;153:66.e9-e66.e16. Storey RF. Eur Heart J Suppl. 2008;10(suppl D):D30-D37.

-20

0

20

40

60

80

100

IPA

at 24

Hou

rs, %

Response to Prasugrel 60 mg

Response to Clopidogrel 300 mg

Clopidogrel Responder Clopidogrel Non-responder

Inte

rpat

ient

Varia

bilit

y Interpatient Variability

n = 64

TRITON-TIMI 38: Study Design

Double-blind: at cath, PCI planned

ACS (STEMI or UA/NSTEMI) & Planned PCI ASA

PRASUGREL 60 mg LD/ 10 mg MD

CLOPIDOGREL 300 mg LD/ 75 mg MD

1o endpoint: CV death, MI, Stroke 2o endpoints: CV death, MI, Stroke, Rehosp-Rec Isch CV death, MI, UTVR Stent Thrombosis (ARC definite/prob.) Safety endpoints: TIMI major bleeds, Life-threatening bleeds Key Substudies: Pharmacokinetic, Genomic

Median duration of therapy - 12 months

N= 13,600

Wiviott SD et al. Am Heart J. 2006;152:627-35.

Prasugrel vs Clopidogrel for NSTE-ACS and STEMI: TRITON-TIMI 38 Primary Results:

CV Death, MI, Stroke

0

5

10

15

0 30 60 90 180 270 360 450

HR 0.81 P=.0004 Prasugrel

Clopidogrel

HR 0.80 P=.0003

HR 0.77 P=.0001

Days

Prim

ary

End

Poin

t, %

12.1 (781)

9.9 (643)

NNT=46

ITT=13,608

Adapted from Wiviott SD, et al. N Engl J Med. 2007;357(20):2001-2015.

Primary endpoint = first occurrence of CV death, MI, or stroke

n Hazard Ratio Prasugrel

(%) Clopidogrel

(%) Females 320 13.6 20.5 Males 883 9.7 13.6

Age <75 979 9.3 13.0 Age ≥75 224 17.2 28.0

No Hx of DM 856 10.6 11.0 Hx of DM 347 11.7 27.0

UA/NSTEMI 893 12.1 15.2 STEMI 390 9.0 17.1

BMS only 571 10.7 17.0 DES 560 11.3 13.7

CrCl ≥60 1013 8.4 12.3 CrCI <60 176 26.2 31.7

TRITON-TIMI 38 Study: Subgroups

Murphy. Eur Heart J. 2008;29:2473-2479.

Prasugrel better

Clopidogrel better

0.2 1 5

TRITON TIMI 38 Bleeding Events – Safety Cohort (n=13,457)

% E

vent

s

ARD 0.6% HR 1.32 P=0.03

NNH=167

ARD 0.5% HR 1.52 P=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)

Wiviott SD et al. N Engl J Med. 2007;357:2001-2015.

Life Threatening

TIMI Major Bleeds

Clopidogrel Prasugrel

0.9

2.4

1.4

0

2

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

0.9 1.1

0.1 0.4 0.3 0.3

Nonfatal Fatal ICH

1.8

32 32

TRITON-TIMI 38: Net Clinical Benefit Bleeding Risk Subgroups

Post hoc analysis

OVERALL

≥60 kg

<60 kg

<75

≥75

No

Yes

0.5 1 2

Prior Stroke / TIA

Age

Wgt

Risk (%) + 37

-16

-1

-16

+3

-14

-13

Prasugrel Better Clopidogrel Better HR

Pint = .006

Pint = .18

Pint = .36

Wiviott SD, et al. N Engl J Med. 2007;357(20):2001-2015.

PLATO study design

Primary endpoint: CV death + MI + Stroke Primary safety endpoint: Total major bleeding

6–12-month exposure

Clopidogrel If pre-treated, no additional loading dose; if naive, standard 300 mg loading dose, then 75 mg qd maintenance; (additional 300 mg allowed pre PCI)

Ticagrelor 180 mg loading dose, then 90 mg bid maintenance; (additional 90 mg pre-PCI)

NSTE-ACS (moderate-to-high risk), STEMI (if primary PCI) Clopidogrel-treated or -naive; randomized within 24 hours of index event (N=18,624)

PLATO study design

James S et al. Am Heart J. 2009;157:599-605.

All patients received aspirin

PLATO: Ticagrelor vs. Clopidogel in NSTEMI and STEMI ACS

No. at risk

Clopidogrel Ticagrelor

9,291 9,333

8,521 8,628

8,362 8,460

8,124

Days after randomisation

6,743 6,743

5,096 5,161

4,047 4,147

0 60 120 180 240 300 360

12 11 10 9 8 7 6 5 4 3 2 1 0

13 C

V de

ath,

MI,

or C

VA in

cide

nce

(%)

9.8

11.7

8,219

HR 0.84 (95% CI 0.77–0.92), p=0.0003

Clopidogrel

Ticagrelor

K-M = Kaplan-Meier; HR = hazard ratio; CI = confidence interval NEJM 09; 361:1045

No. at risk

Clopidogrel

Ticagrelor

9,291

9,333

8,560

8,678

8,405

8,520

8,177


6,703

6,796

5,136

5,210

4,109

4,191

0 60 120 180 240 300 360

6

5

4

3

2

1

0

7

Cum

ulat

ive

inci

denc

e (%

)

Clopidogrel

Ticagrelor

5.8

6.9

8,279

HR 0.84 (95% CI 0.75–0.95), p=0.005

0 60 120 180 240 300 360

6

4

3

2

1

0

Clopidogrel

Ticagrelor

4.0

5.1

HR 0.79 (95% CI 0.69–0.91), p=0.001

7

5

9,291

9,333

8,865

8,294

8,780

8,822

8,589


7079

7119

5,441

5,482

4,364

4,419 8,626

Myocardial infarction Cardiovascular death

Cum

ulat

ive

inci

denc

e (%

)

PLATO: Secondary efficacy endpoints

PLATO: Non-invasive and Invasive Therapy Subgroups

0

4

8

12

16

20

0 60 120 180 240 300 360 Days after Randomization

Card

iova

scul

ar d

eath

, MI,

or S

trok

e (%

)

14.3%

12.0% HR 0.85 P=.04

Non-invasive Invasive

James SK, et al. BMJ. 2011.

Ticagrelor Clopidogrel

10.7%

9.0% HR 0.84 P=.0025

PLATO Major Bleeding: Non-CABG vs CABG

Kapl

an-M

eier e

stim

ated

rate

(%

)

Wallentin L et al. N Engl J Med. 2009;361:1045-1057.

P=0.026

P=0.025

NS

NS

Non-CABG PLATO major

bleeding

8

7

6

5

4

3

2

1

0 Non-CABG TIMI major bleeding

CABG PLATO major

bleeding

CABG TIMI major bleeding

4.5

3.8

2.8

2.2

7.4 7.9

5.3 5.8

Ticagrelor Clopidogrel

Ticagrelor Interaction with Aspirin Dose: HR Compared with Clopidogrel

Aspirin Dose (mg/day)

Hazard Ratio 95% CI

>= 300 1.45 1.01 – 2.09 >100 – <300 0.99 0.70 – 1.40 <=100 0.77 0.69 – 0.86

Warning: Aspirin Dose and Ticagrelor Effectiveness: Maintenance doses of aspirin above 100mg reduce the effectiveness of ticagrelor and should be avoided. After any initial dose, use with aspirin 75-100 mg per day (FDA-approved prescribing information, July 2011)

Summary • ASA 81 mg is the preferred dose after the initial

dose in ED or cath lab • Medically managed ACS

– Ticagrelor and clopidogrel indicated • Ticagrelor with superior efficacy/mortality

reduction – Prasugrel not indicated

• Invasively managed ACS – Ticagrelor, prasugrel, clopidogrel indicated – Ticagrelor, prasugrel superior efficacy

(ticagrelor mortality reduction) to clopidogrel with increased bleeding

• Duration of DAPT: generally one year

A loading dose of a P2Y12 receptor inhibitor (clopidogrel, prasugrel, or ticagrelor) should be given before the procedure in patients undergoing PCI with stenting.

It is reasonable to use ticagrelor in preference to clopidogrel for maintenance P2Y12 treatment in patients with NSTE-ACS who undergo an early invasive strategy or ischemia-guided strategy.

It is reasonable to choose prasugrel over clopidogrel in NSTE-ACS patients who undergo PCI and are not at high risk of bleeding.


P2Y12 Inhibitors in NSTE-ACS with PCI/Stents




A P2Y12 inhibitor (either clopidogrel or ticagrelor) in addition to aspirin should be given for up to 12 months for patients treated with either an early invasive or initial ischemia-guided strategy. It is reasonable to use ticagrelor in preference to clopidogrel for P2Y12 treatment in patients with NSTE-ACS who undergo an early invasive or ischemia-guided strategy. P2Y12 inhibitor therapy (clopidogrel, prasugrel, or ticagrelor) should be continued for at least 12 mo in post-PCI patients treated with coronary stents.


P2Y12 Inhibitor Therapy in NSTE-ACS (continued)




Early Discontinuation of Antiplatelet Therapy is An Important Risk Factor for

Stent Thrombosis

ST = stent thrombosis

Iakovou I et al. JAMA. 2005;293:2126-2130.

UA Thrombus Diabetes Unprotected Left Main

Bifurcation Lesion

Renal Failure

Prior Brachytherapy

Overall ST=1.3% (P=0.09, n=2229)

1.4 2.0 2.5 3.3 3.6 6.2

8.7

29.0

0

10

20

30

Premature Antiplatelet

Discontinuation

Inci

denc

e of

ST

(%)

If the risk of morbidity from bleeding outweighs the anticipated benefit of a recommended duration of P2Y12 inhibitor therapy after stent implantation, earlier discontinuation (e.g., <12 months) of P2Y12 inhibitor therapy is reasonable In patients referred for elective CABG, clopidogrel and ticagrelor should be discontinued for at least 5 days before surgery (LOE: B) and prasugrel for at least 7 days before surgery (LOE:C)

I I IIa IIa IIa IIb IIb IIb III III III I I I IIa IIa IIa IIb IIb IIb III III III I I IIa IIa IIa IIb IIb IIb III III III IIa IIa Ia IIb IIb I III III I

P2Y12 Inhibitor Therapy in NSTE-ACS (continued)




In patients with NSTE-ACS, anticoagulation, in addition to antiplatelet therapy, is recommended for all patients irrespective of initial treatment strategy. Treatment options include: --Enoxaparin (LOE:A) --Bivalirudin (LOE:B) --Fondaparinux (LOE:B) --Unfractionated heparin (LOE:B) If PCI is performed while the patient is on fondaparinux, an additional anticoagulant with anti-IIa activity (either UFH or bivalirudin) should be administered because of the risk of catheter thrombosis (LOE:B)

I I IIa IIa IIa IIb IIb IIb III III III I I I IIa IIa IIa IIb IIb IIb III III III I I IIa IIa IIa IIb IIb IIb III III III IIa IIa Ia IIb IIb I III III I

Anticoagulant Therapy for NSTE-ACS




Post-hospital systems of care designed to prevent hospital readmissions should be used to facilitate the transition to effective, coordinated outpatient care for all patients with NSTE-ACS. An evidence-based plan of care that promotes medication adherence, timely follow-up, appropriate dietary and physical activities, and compliance with secondary prevention should be provided to patients with NSTE-ACS. Annual influenza vaccination for all patients.

2014 AHA/ACC NSTE-MI Guidelines


General Plan of Outpatient Care for Patients with NSTE-ACS



Secondary Prevention* Recommendations COR LOE

Lipid management with lifestyle modification and lipid-lowering therapy

Beta blocker therapy

RAAS blocker therapy

Lifestyle modification I B

Statin therapy—mod/high intensity

I A

For 3 y in pts with normal LVF All pts with EF<40, HF, prior MI

I B A

ACEI if HTN, DM, EF<40, CKD Use ARBs if intolerant of ACEIs

I A

Blood pressure control (with a blood pressure goal of <140/90 mm Hg)

Lifestyle modification I B

Pharmacotherapy I A

Diabetes management (e.g., lifestyle modification and pharmacotherapy) coordinated with the patient’s primary care physician and/or endocrinologist.

I C

Complete smoking cessation I A

In addition, referral to a cardiac rehabilitation program (IB). *Comprehensive secondary prevention recommendations in the ACC/AHA Secondary Prevention and Risk Reduction 2011 and 2013 Updates and 2012 SIHD Guidelines GNL 2011

Performance Matters! Association Between Hospital Guideline

Adherence and In-hospital Mortality in CRUSADE

Adapted with permission from Peterson ED, et al. JAMA. 2006;295(16):1912-1920.

NSTE ACS = non–ST-segment elevation ACS.

8

7

6

5

4

3

2

1

0 1 2 3 4

In-H

ospi

tal M

orta

lity,

%

Hospital Composite Guideline Adherence Quartiles

NSTE ACS

CRUSADE = Can Rapid Risk Stratification of Unstable Angina Patients Suppress Adverse Outcomes With Early Implementation of the ACC/AHA Guidelines.

Impact of Adherence to Evidence-based

Therapies: Effect on 6-month Survival in the GRACE Registry Cohort*

OR = odds ratio *Registry of patients with ACS

Chew DP et al. Heart. 2010;96:1201-1206.

0.80 (0.52-1.26)

0.74 (0.48-1.13)

0.59 (0.39-0.90)

0.51 (0.33-0.78)

0.40 (0.26-0.62)

0.27 (0.16-0.44)

0.31 (0.17-0.57)

NUMBER OF THERAPIES (vs 0 or 1 therapy)

2 therapies

3 therapies

4 therapies

5 therapies

6 therapies

7 therapies

8 therapies

OR (95% CI)

0 0.5 1 1.5 2 OR

CONCLUSION

Early Diagnosis, Risk Stratification,

Strategy Selection, and Appropriate

Antithrombotic and Other Guideline-

Directed Medical Therapy Make a

Difference in ACS Outcomes!

Equally Important is Aggressive

Secondary Prevention after Discharge!

the 2014 non-st-elevation mi guidelines—what’s new … · 2014 aha/acc guideline for the ......

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