update acute coronary syndromes - np forum

UPDATE ACUTE CORONARY SYNDROMESDr. Wayne Tymchak

April 7, 2017

Spontaneous RuptureUnstable Angina

Myocardial Infarction

Ischemic Discomfort

Non-ST ST

Unstable Angina

Non-Q Wave MI*

Q Wave MI** positive cardiac enzymes/markers

Classification: Acute Coronary Syndromes

Declining AMI Mortality Over Declining AMI Mortality Over Four DecadesFour Decades

% sh

ort-t

erm

mor

talit

y 30

13

7

0

5

10

15

20

25

30

35

40Resuscitation recognition

& Rx of dysrhythmiaPrehospital care

Infarct size limitationHemodynamic monitoringvasodilators/mechanical

assistReperfusionthrombolysis

PTCA Evidence-based practiceProcess of care

Early testing/intervention/combination therapies

1970s

1980s

1990s2000s

1960s

Pre-CCU era CCU era Reperfusion eraAdapted from Armstrong P. Can J Cardiol 1996;12:909

OBJECTIVES

• ACS Risk Assessment• Invasive vs. Conservative Therapy for ACS• ACS Dual Antiplatelet NSTEACS• ACS Dual Antiplatelet STEMI• ACS Dual Antiplatelet Duration• Pharmaco‐Invasive Approach To STEMI• STEMI Systems Of Care

26‐4‐2017 Eduard van den Berg, cardio.nl 9

ACS Risk Scoring• TIMI

– Age ‐ Use of aspirin– Risk Factors ‐ Known CAD– > 1 episode rest pain ‐ ST segment deviation– Cardiac risk markers

• PURSUIT– Age, Sex ‐ CCS class in last 6/52– Signs of CCF ‐ ST depression on ECG

• GRACE– Age ‐ Heart rate and systolic BP– Creatinine ‐ CCF (Killip class)– Cardiac arrest at admission– Elevated cardiac markers ‐ ST segment deviation

TIMI Risk Score for Patients with Definite ACS

• Age > 65• Documented CAD• Cardiac risk factors• ASA usage previous7 days

• > 2 anginal events in past 24 hours

• ST deviation• Elevated cardiac markers

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

Risk Score

Cardiac Even

ts (%

)

50

40

30

20

10

00/1 2 3 4 5 6/7

Key point: People have can significant disease with low scores.Must continuously reassess risk stratification

4.78.3

13.2

19.926.2

40.9p<0.001 by x2 for trendN=1957

26‐4‐2017 Eduard van den Berg, cardio.nl 11

At Admission Risk Model

>140=high risk

OBJECTIVES

• Invasive vs. Conservative Therapy for ACS

Invasive Therapy for Non‐ST Segment Elevation ACS

• New trials support an invasive approach in high risk patients with Non‐ST Segment Elevation ACS

• High risk– Recurrent chest pain– Dynamic ST‐T changes– Positive markers for myocardial injury– Hemodynamic instability

• Invasive Therapy– Planned catherization in all suitable high risk patients

without contraindication– Subsequent revascularization where feasible

Primary Endpoint: Death or MI at 6 months

Invasive vs. Non-Invasive

FRISC II -

12.1

9.4

0.0

5.0

10.0

15.0

Death or MI

% o

f Pat

ient

s

Non-Invasive (n=1226) Invasive (n=1207)

22 % p=0.031

Lancet 1999; 354: 708-15

0 1 2 3 4 5 6Time (months)

0

4

8

12

16

20

% P

atie

nts

CONSINV

O.R 0.7895% CI (0.62, 0.97)

p=0.025

19.4%

15.9%

Primary EndpointTACTICS

Death, MI, Rehosp for ACS at 6 Months

TIMING OF INTERVENTION

TIMACSTIMACS

Preliminary Results as of Nov 7, 2008

Design, Eligibility Criteria and Protocol

UA or NSTEMI2 of 3 Criteria: Age > 60, ischemic ECG or biomarker

AND suitable for revascularization

RANDOMIZE*

Early InvasiveCoronary angio as soon as

possible (<24 hours)

Delayed InvasiveCoronary angio

>36 hrs

*Randomization ratio 1:1, 1:2 or 2:1

Follow-up up to 180 days

TIMACSTIMACS

Preliminary Results as of Nov 7, 2008

Primary OutcomeDeath, MI, or Stroke

Days

Cum

ulat

ive

Haz

ard

0.0

0.02

0.06

0.10

0 30 60 90 120 150 180

Death/MI/Stroke at 180 days

Early

No. at Risk

DelayedEarly

1438 1328 1269 1254 1234 1229 12111593 1484 1413 1398 1391 1382 1363

Delayed

HR 0.8595% CI 0.68-1.06

P= 0.15

Days

Cum

ulat

ive

Haz

ard

0.0

0.05

0.10

0.15

0.20

0.25

0 30 60 90 120 150 180

Delayed

Early

Delayed

Early

High RiskGRACE Score >140

Low/Intermediate RiskGRACE Score 0-140

TIMACS HIGH RISK > 141 VS. LOW RISKPrimary Outcome

Mehta SR et al. N Engl J Med 2009;360:2165-75

OBJECTIVES

• ACS Dual Antiplatelet NSTEACS

Timing of Randomization in Dual Antiplatelet Trials

< 24 hrs

NSTE ACS < 72 hrsSTEMI < 12 hrs

CUREClopidogrel

PLATOTicagrelor

Presentation

Selective Invasive

Early Invasive

CoronaryAngiography

CABG

PCI

Medical Management

TRITONPrasugrel

SymptomOnset

James SK, et al. BMJ. 2011;342:d3527. Wiviott SD, et al. N Engl J Med. 2007;357(20):2001–2015. Yusuf S, et al. N Engl J Med. 2001;345(7):494–502.

CURE

0.00

0.02

0.04

0.06

0.08

0.10

0.12

0.14

Cum

ulat

ive

Haz

ard

Rat

e

Clopidogrel + ASA*

3 6 9

Placebo + ASA*

Months of Follow-Up

11.4%

9.3%

20% RRRP < 0.001

N = 12,562

0 12

* In combination with standard therapy

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

Primary End Point - MI/Stroke/CV Death

0.15

0.10

0.05

0.00 100 200 300 400

Days of follow-up

12.6%

8.8%

31% RRRP = 0.002N = 2658

Clopidogrel+ ASA*

Placebo+ ASA*

Cum

ulat

ive

Haz

ard

Rat

e

* In combination with standard therapy

Mehta, SR. et al for the CURE Trial Investigators. Lancet. August 2001.

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

Overall Long-Term ResultsPCI-CURE

PLATO study design

6–12 months treatment

PCI = percutaneous coronary intervention; CV = cardiovascular; PI = principal investigator

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

At randomization, 13,408 (72%) of patients were specified by the Investigator: intent for invasive strategy

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

Clopidogrel (n=6,676)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 (n=6,732)180 mg loading dose, then

90 mg bid maintenance;(additional 90 mg pre-PCI)

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

Cardiovascular Death All‐Cause Mortality

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

PLATO: Secondary Efficacy OutcomesTicagrelor Reduced Mortality in ACS

Clopidogrel(n=9291)

Ticagrelor(n=9333)

5.94.5

Incidence at 1 year (%)

HR 0.7895% CI 0.69–0.89p<0.001(nominal)

Cum

ulat

ive

inci

denc

e (%

)

Months after randomization

Clopidogrel (n=9291)

Ticagrelor(n=9333)

HR 0.7995% CI 0.69–0.91p=0.001

0 2 4 6 8 1210

0

1

2

3

4

5

6

7

21%RRR

Inci

denc

e (%

)

0

1

2

3

4

5

6

PLATO: Noninvasive Management

James SK, et al. BMJ. 2011;342:d3527 doi: 10.1136/bmj.d3527. Cannon CP, et al. Lancet .2010;375:283–293.

Subgroup Analysis of 5216 Patients (28% of overall cohort)

9.0

10.7

12.0

14.3

CV Dea

th/M

I/Stroke (%)

Days after randomization

0

4

8

12

20

0 60 120 180 240 300 360

16

Invasive SubgroupNoninvasive Subgroup

Ticagrelor (n=2601)

Clopidogrel (n=2615)Ticagrelor (n=6732)

Clopidogrel (n=6676)

p for interaction = 0.89

HR 0.8595% CI 0.73‐1.00p=0.045

HR 0.8495% CI 0.75‐0.94p=0.0025

InvasiveFigure 9: Rates of bleeding according to different definitions

CABG=coronary artery bypass graft; PLATO=PLATelet inhibition and patient OutcomesTIMI=Thrombolysis In Myocardial InfarctionGUSTO=Global Use of Strategies To Open occluded coronary arteries.

Non-CABG-related bleeding onlyp=0.8803

0

Kap

lan-

Mei

er e

stim

ated

rate

(% p

er y

ear)

PLATO-defined major bleeding

1

2

3

4

5

6

7

8

9

10

12

11

13

TIMI-defined major bleeding GUSTO-defined severe bleeding

11.5611.45

p=1.000

7.937.91

p=0.3785

3.242.94

Ticagrelor Clopidogrel Ticagrelor Clopidogrel Ticagrelor Clopidogrel

CABG-related bleeding onlyBoth non-CABG-related and CABG-related bleeding

Cannon CP, et al. Lancet 2010;375:283–293

Fondaparinux vs Enoxaparin in NSTE ACS Similar Ischemic Outcomes but Less Major Bleeding

Death/MI/Refractory Ischemia Major Bleeding

0

Fondaparinux(n=10,057) Enoxaparin

(n=10,021)

1

2

3

4

5

6

10 2 3 4 5 6 7 8 9

Days Days10 2 3 4 5 6 7 8 9

0

1

2

3

4

30‐Day and 6‐Month Results

Event Fondaparinux(n=10,057)

Enoxaparin(n=10,021) HR (95% CI) p‐value

Mortality (30 day) 2.9% 3.5% 0.83 (0.71–0.97) 0.02

Mortality (6 mo) 5.8% 6.5% 0.89 (0.80–1.00) 0.05

HR 1.0195% CI 0.90–1.13p=0.007

HR 0.5295% CI 0.44–0.61p<0.001

OASIS-5 – Yusuf S, et al. N Eng J Med. 2006;354:1464–1476.

Cumulative Hazard (%

)

Cumulative Hazard (%

)

Enoxaparin(n=10,021) Fondaparinux

(n=10,057)

Algorithm for Management of Patients With Definite or Likely NSTE-ACS

†In patients who have been treated with fondaparinux (as upfront therapy) who are undergoing PCI, an additional anticoagulant with anti-IIa activity should be administered at the time of PCI because of the risk of catheter thrombosis.

OBJECTIVES

• ACS Dual Antiplatelet STEMI

Study Design

Fibrinolytic, ASA, Heparin

Clopidogrel300 mg + 75 mg qd

Coronary Angiogram(2-8 days)

Primary endpoint:Occludedartery (TIMI Flow Grade 0/1)or D/MI by timeof angio

randomize

Placebo

Double-blind, randomized, placebo-controlled trial in3491 patients, age 18-75 yrs with STEMI < 12 hours

StudyDrug

30-day clinical follow-up

Open-labelclopidogrelper MD in

both groups

Primary Endpoint:Occluded Artery, D, MI at ANGIOGRAPHY

15.0

21.7

0

5

10

15

20

25

Occ

lude

d A

rter

y or

Dea

th/M

I (%

)

PlaceboClopidogrel

P=0.00000036P=0.00000036

Odds Ratio 0.64(95% CI 0.53-0.76)

Odds Ratio 0.64(95% CI 0.53-0.76)

1.00.4 0.6 0.8 1.2 1.6

Clopidogrelbetter

Placebobetter

n=1752 n=1739

36%Odds Reduction

36%Odds Reduction

CV Death, MI, RI Urg Revasc30 Days

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%20%

Conclusion• Clopidogrel offers an effective, simple, inexpensive,

and safe means by which to improve infarct-related artery patency and reduce ischemic complications.

• Bleeding complications were not increased

M A R C H 9, 2 0 0 5

Sabatine MS, Cannon CP, Gibson CM, Lopez-Sendon JL, Montalescot G, Theroux P, Claeys MJ,Cools F, Hill KA, Skene AM, McCabe CH and Braunwald E

for the CLARITY-TIMI 28 Investigators.

Beijing (48)

Shanghai (16)

Tianjin (21)

Shanxi (58)

Hebei (115)

Liaoning (92)

Jilin (50)

Heilongjiang (53)

Jiangsu (63)

Anhui (28)

Shandong (148)

Zhejiang (12)Jiangxi (20)

Fujian (22)Hunan (37)

Hubei (54)

Henan (121)

Guangdong (49)

Guizhou (11)

Hainan (7)

Sichuan (49)

Yunnan (12)

Shaanxi (43)

Gansu (25)

Qinghai (4)

Nei Mongol (38)

Guangxi (30)

Ningxia (8)

Xinjiang (7)

Chongqing (11)

COMMIT/CCS-2(ClOpidogrel & Metoprolol in Myocardial Infarction Trial)

45,852 patients from 1250 centres in China

TREATMENT: Clopidogrel 75 mg daily vs placebo, (aspirin 162mg daily in both groups)

INCLUSION: Suspected acute MI (ST change orLBBB) within 24 h of symptom onset

EXCLUSION: Primary PCI or high-risk of bleeding

1 OUTCOMES: Death & death, re-MI or stroke up to 4 weeks in hospital (or prior discharge)

Mean treatment and follow-up: 16 days

COMMIT: Study design

COMMIT: Effects of CLOPIDOGREL onDeath, Re-MI or Stroke

Days since randomisation (up to 28 days)

Event (%)

9% (SE3) relative riskreduction (2P=0.002)

Placebo + ASA: 2311 events (10.1%)

Clopidogrel + ASA:2125 events (9.3%)

Type Clopidogrel Placebo(n=22,958) (n=22,891)

CerebralFatal 39 40Non-fatal 16 15

Non-cerebralFatal 36 37Non-fatal 46 36

Any major bleed 134 124(0.58%) (0.54%)

COMMIT: Major bleed in hospital

COMMIT: Conclusions

Adding 75 mg daily CLOPIDOGREL to aspirin in acute MI prevents major vascular events

No excess of cerebral, fatal or transfused bleeds (even with fibrinolytic therapy and in older people)

Each million MI patients treated for ~2 weeks would avoid 5000 deaths and 5000 non-fatal events

OBJECTIVES

• ACS Dual Antiplatelet Duration

These slides have been provided, on request by AstraZeneca Scientific Affairs. AstraZeneca does not, under any circumstances,

promote its products for off-label or unapproved uses.

PEGASUSStable patients with history of MI 1–3 years prior

+ 1 additional atherothrombosis risk factor

Follow-up visitsQ4 months for 1st year, then Q6 months

Planned treatment with ASA 75–150 mg/d &standard background care

Followed for median of 33 months

Primary endpoint: CV death, MI, stroke

P2Y12 inhibitor therapy may have been stopped at any time prior to randomization

Bonaca MP et al. N Engl J Med 2015;372:1791–1800

Ticagrelor90 mg bid

Ticagrelor60 mg bid Placebo

RANDOMIZEDDOUBLE-BLIND



10

Background

Months from randomization

CV

deat

h, M

I, or

str

oke

(%)

3 6 9 120 15 18 21 24 27 30 33 36

Placebo (9.0%)

Ticagrelor 90 mg (7.8%)Ticagrelor 60 mg (7.8%)

6

5

4

3

9

8

7

2

1

0

N=21,162Median follow-up 33 months from randomization

Ticagrelor 60 mg BDHR 0.84 (95% CI 0.74, 0.95)

P=0.004

Ticagrelor 90 mg BDHR 0.85 (95% CI 0.75, 0.96)

P=0.008

CVD / MI / Stroke

Bonaca MP et al. N Engl J Med 2015;372:1791–1800



Reduction in CV death, MI or stroke with ticagrelor by time from P2Y12 inhibitor

withdrawal

Ticagrelor 90 mgTicagrelor 60 mgPooledPlacebo betterTicagrelor better

0.70 (0.57, 0.87)

0.75 (0.61, 0.92)

0.73 (0.61, 0.87) <0.001

0.90 (0.72, 1.12)

0.82 (0.65, 1.02)

0.86 (0.71, 1.04) 0.11

0.96 (0.73, 1.26)

1.06 (0.81, 1.38)

1.01 (0.80, 1.27) 0.96

1.0

HR (95% CI) P value

≤30 daysn=7181

>30 daysto 1 yearn=6501

>1 yearn=5079

Time from P2Y12 inhibitor withdrawal to randomization

Bonaca MP. Presented at ESC Congress 2015 (Abstract 3918)

P-interaction 0.0097

27% RRR

14% RRR

RRR

0.7 0.9 1.1



TIMI major bleeding at 3 years with ticagrelor by dose

Placebo betterTicagrelor better 1.0

≤30 daysn=7093

>30 daysto 1 yearn=6446

>1 yearn=5031

Time from P2Y12 inhibitor withdrawal to randomization

P trend NS

3-year Kaplan-Meier rate (%)Ticagrelor Placebo HR (95% CI) P value

Ticagrelor 90 mgTicagrelor 60 mgPooled

2.36 3.44 (1.88, 6.28)

2.63 3.30 (1.80, 6.03)

2.50 0.74 3.36 (1.91, 5.92) <0.001

2.76 2.85 (1.59, 5.10)

2.75 2.94 (1.66, 5.22)

2.75 1.20 2.89 (1.69, 4.94) <0.001

2.98 3.28 (1.70, 6.33)

1.88 2.10 (1.05, 4.22)

2.42 0.90 2.67 (1.43, 4.98) 0.002


1.5 3.00.5



Conclusions

• Continuing P2Y12 inhibition beyond 1 year after MI offers robust ischaemic benefit

• Re-initiation of P2Y12 inhibition in patients who have been stable on aspirin alone for more than a year does not appear to offer benefit and increases bleeding

• Ongoing research using clinical, biochemical and genetic factors may enable us to further refine, in a prospective manner, the optimal patient populations for long-term therapy


Two Recent Meta‐Analysis With Second Generation DES

• Shorter term 3‐6 months– Did not disadvantage patients

• No Increase in Mortality• No Increase in In‐stent thrombosis

– Resulted in less bleeding

• Extended Term > 12 months – Improved Mortality– Reduced in‐stent thrombosis– More bleeding events– Risk stratify using tools such as DAPT SCORE

OBJECTIVES

• Pharmaco‐Invasive Approach To STEMI

Pharmaco-Invasive Approach to STEMI

• Pharmaco-invasive approach to STEMI care has now become widely accepted as standard therapy

• Primary PTCA still preferred mode of therapy, must be done in a timely fashion with first medical contact to balloon inflation of < 90 minutes

65

ACC/AHA 2009 Joint STEMI/PCI Guidelines Focused Update

64

CARESS-IN-AMI: Primary Outcomeprimary outcome (composite of all cause mortality, reinfarction, & refractory MI within 30 days)

10.7%

4.4%

HR=0.40 (0.21-0.76)

Di Mario et al. Lancet 2008;371.

www. Clinical trial results.org

Endpoints (30 days and 6 months):Composite of death, reinfarction, recurrent unstable ischemia, or

stroke

Endpoints (30 days and 6 months):Composite of death, reinfarction, recurrent unstable ischemia, or

stroke

CAPITAL AMI TrialCAPITAL AMI Trial

Presented at ACC Scientific Sessions 20Presented at ACC Scientific Sessions 20

170 patients presenting with ST elevation acute MI with chest pain ≥30 minutes and within six hours of

symptom onsetRandomized, open-label, multicenter

170 patients presenting with ST elevation acute MI with chest pain ≥30 minutes and within six hours of

symptom onsetRandomized, open-label, multicenter

Thrombolytic TherapyFull-dose Tenectaplase (TNK)

n=84

Thrombolytic TherapyFull-dose Tenectaplase (TNK)

n=84

Thrombolytic Therapy,Transfer, and PCI

Full-dose Tenectaplase (TNK) followed by transfer and subsequent percutaneous

coronary intervention (PCI)n=86

Thrombolytic Therapy,Transfer, and PCI

Full-dose Tenectaplase (TNK) followed by transfer and subsequent percutaneous

coronary intervention (PCI)n=86


21.4%

8.1%

0%

5%

10%

15%

20%

25%

TNK TNK+PCI

21.4%

8.1%

0%

5%

10%

15%

20%

25%

TNK TNK+PCI

In-Hospital Composite Event Rate

p=0.017


CAPITAL AMI TrialCAPITAL AMI Trial%

•The composite in-hospital event rate of death, reinfarction, recurrent unstable ischemia, or stroke was lower in the TNK+PCI arm compared with the TNK alone arm, driven by a reduction in reinfarction and recurrent unstable ischemia.

11.9%

17.9%

3.5%

5.8%

0%

5%

10%

15%

20%

11.9%

17.9%

3.5%

5.8%

0%

5%

10%

15%

20%

TNK TNK+PCI

TNK TNK+PCI

In-Hospital Reinfarction

p=0.046

In-Hospital Recurrent

Unstable Ischemiap=0.02


21.4%

9.3%

0%

5%

10%

15%

20%

25%

TNK TNK+PCI

21.4%

9.3%

0%

5%

10%

15%

20%

25%

TNK TNK+PCI

Primary Composite Endpoint at 30 days

p=0.034


CAPITAL AMI TrialCAPITAL AMI Trial%

• Composite event rate remained lower in the TNK+PCI arm at 30 days, again driven by reductions in reinfarction and recurrent unstable ischemia, with no difference in mortality (2.3% vs. 3.6%).

• Length of hospital stay shorter in the TNK+PCI arm (5 vs. 6 days, p=0.009).

11.9 %

17 .9 %

4 .7 %7 .0 %

0%

5%

10%

15%

20%

11.9 %

17 .9 %

4 .7 %7 .0 %

0%

5%

10%

15%

20%

TNK TNK+PCI

TNK TNK+PCI

30-Day Reinfarction

30-Day Recurrent Unstable Ischemia

9803mo01, 70

PCI CentreCath Lab

CommunityHospitalEmergencyDepartment

Cath / PCI within 6 hrs regardless of

reperfusion status

Cath and Rescue PCI

GP IIb/IIIa Inhibitor

TNK + ASA + Heparin / Enoxaparin + Clopidogrel

“PharmacoinvasiveStrategy”

Urgent Transfer to PCI Centre Assess chest pain, ST resolution

at 60-90 minutes after randomization

‘High Risk’ ST Elevation MI within 12 hours of symptom onset

Failed Reperfusion* Successful Reperfusion

Elective Cath PCI

> 24 hrs later

“Standard Treatment”

* ST segment resolution < 50% & persistent chest pain, or hemodynamic instability

Repatriation of stable patients within 24 hrs of PCI

Randomization stratified by age (≤75 vs. > 75) and by enrolling site

9803mo01, 71

02468

1012141618

0 5 10 15 20 25 30

10.6

16.6

Days from Randomization

% of Patients

Standard PCI > 24 hrs (n=496)Invasive < 6 hrs (n=508)

n=496n=508

422468

415466

415463

414461

414460

412457

Primary Endpoint: 30-Day Death, re-MI, CHF, Severe Recurrent Ischemia,

Shock

OR=0.537 (0.368, 0.783); p=0.0013

RR= 0.64, 95 CI% (0.47-0.87)

OBJECTIVES

• STEMI Systems Of Care

F. Van de Werf, ACC 2013


A strategy of early fibrinolysis followed by coronary angiography within 6-24 hours or rescue PCI if needed

was compared with standard primary PCI in

STEMI patients with at least 2 mm ST-elevation in 2 contiguous leads presenting within 3 hours of symptom onset and unable to undergo primary PCI within 1 hour.

“Pharmaco-Invasive vs. Primary PCI In STEMI”

STUDY AIM


62

Sx onset1st Medical

contact

611 Hour 2 Hoursn=1892

29

Randomize IVRS

9

Rx TNK

31 86

Sx onsetRx PPCI

100 min

178 min

MEDIAN TIMES TO TREATMENT (min)

1st Medicalcontact

78 min differenceRandomize IVRS


PRIMARY ENDPOINT

TNK 12.4%

PPCI 14.3%

TNK vs PPCIRelative Risk 0.86, 95%CI (0.68‐1.09)

p=0.24

Dth/Sho

ck/CHF/Re

MI (%)

The 95% CI of the observed incidence in the pharmaco-invasive arm would exclude a 9% relative excess compared with PPCI


CONCLUSIONS

A strategy of fibrinolysis with bolus tenecteplase and contemporary antithrombotic therapy given before transport to a PCI-capable hospital coupled with timely coronary angiography :

circumvents the need for an urgent procedure in about two thirds of fibrinolytic treated STEMI patients.

is associated with a small increased risk of intracranial bleeding.

is as effective as primary PCI in STEMI patients presenting within 3 hours of symptom onset who cannot undergo primary PCI within one hour of first medical contact.

79

VHR – Vital Heart Response

• Evidence Based Guidelines (ACCF/AHA and ESC)• Developing a “System of Care” approach to

STEMI• First Medical Contact (FMC) to fibrinolysis in < 30

minutes• FMC to PPCI in < 90 minutes • Early reperfusion provides best outcomes• 1 in 3 patients reperfused within 1 hr of onset

have negligable myocardial damage

80

Alberta, Canada• 661,848 km2 (255,500 mi2)• 4.1 million people

Edmonton, Alberta• 782,439 city• 1,155,383 metro• 1.8 – 2.0 million referral

population

Texas: 268,820 square miles (696,200 km2), and a pop of 25.1 million residents

81

“Avoid reperfusion decision paralysis”

82

VHR Protocol Overview

83

STEMI Acute Care Overview

• Adding GP‐2b‐3a Inhibitors to ASA, Anticoagulation and DAPT in ACS patients implies a very high risk patient which require invasive investigation in a timely fashion.patients implies ve‐2b‐3a Inhibitors to ASA,

• GP‐2b‐3a Inhibitors not to be used concomitantly with Thrombolytics– Major increase in serious bleeding

• Ticagrelor not to be used concomitantly with Thrombolytics– Not studied

• If using Fondaparinux for ACS– Must reload with unfractionated heparin in patients going for

invasive approach– Increase catheter thrombosis

update acute coronary syndromes - np forum

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