ACS differentiation: With or without ST- elevation

STEMI NSTEMI UAP

Myocardial Nekrosis

• Starts 30-45min after occlusion• 90min: 40-50% nekrotized• 6 hrs: nekrosis often complete

• However collaterals can modify time-course• Occlusion can be subtotal/fluctuating• Protective agents ?

AHA Textbook of Advanced Cardiac Life Support, 1999Courtesy Dr. Lars Aaberge, Oslo

Primary PCIPrimary PCI

••preferred treatment if performed by preferred treatment if performed by experienced team <90min after first experienced team <90min after first medical contactmedical contact

••indicated for patients in shock and those indicated for patients in shock and those with contraindications to fibrinolytic with contraindications to fibrinolytic therapytherapy

• Treatment before PPCI– ASA 300 mg– Clopidogrel 300-600 mg– Unfractioned heparin 5000 - (70 IE/kg) < 70 år

• Treatment during PPCI– Heparin 100 IE/kg bolus or Enoxaparin 30 mg iv + 1 mg/kg sc– Ev. Abciximab bolus, reduce Hep 70 IE/kg

• Treatment after PPCI– Evt Abciximab infusion 12 hrs– ASA + Clopidogrel 75 mg x 1

P(rimary)PCI

Courtesy Dr. Lars Aaberge, Oslo

Reperfusion therapyReperfusion therapy

Reperfusion therapy is indicated in all Reperfusion therapy is indicated in all patients with history of chest patients with history of chest pain/discomfort of <12h and associated pain/discomfort of <12h and associated with ST-segment elevation or (presumed) with ST-segment elevation or (presumed) new bundle-branch block on the ECGnew bundle-branch block on the ECG

ThrombolysisThrombolysis

Within the first 3 hours after onset of Within the first 3 hours after onset of chest pain fibrinolysis is a viabale chest pain fibrinolysis is a viabale alternative.alternative.

Within the first 3 hours of chest pain Within the first 3 hours of chest pain primary PCI and fibrinolysis are equally primary PCI and fibrinolysis are equally effective in reducing infarct size and effective in reducing infarct size and mortality.mortality.

Kontraindikationer mot trombolys

·        Tidigare intracerebral blödning ·        Inom 2 månader efter övriga stroke eller cerebrovaskulära händelser ·        Känt intrakraniellt neoplasm ·        Pågående invärtes blödning (inkluderar icke menstruation)

– ASA 300 mg– Clopidogrel 300-600 mg– One-dose rTPA (tenecteplase) + Enoxaparin 30

mg iv + 1 mg/kg sc

– Morphin - Oxgen – Nitrates - Betablokker

Pre-hospital Thrombolysis

Resuce PCIResuce PCI

after failed thrombolysis in patients with after failed thrombolysis in patients with large infarcts large infarcts

ReperfusionReperfusion

50 % av ST höjningen går i regress 90 min 50 % av ST höjningen går i regress 90 min efter start av trombolys.efter start av trombolys.

Om ej reperfusion efter trombolys, Om ej reperfusion efter trombolys, ställningstagande till rescue PTCAställningstagande till rescue PTCA

STEMISTEMI

NSTEMINSTEMI

KITKIT

KoagulationKoagulationIschemiIschemiTrombocyterTrombocyter

BehandlingBehandling

Icke ST höjnings Icke ST höjnings infarktinfarkt

ST höjningsinfarktST höjningsinfarkt

KoagulationKoagulation EnoxaparinEnoxaparin PCI (Trombolys)PCI (Trombolys)

IschemiIschemi BetablockadBetablockad

Ev nitroglycerinEv nitroglycerinBetablockadBetablockad

Ev nitroglycerinEv nitroglycerin

TrombocyterTrombocyter ASAASA

ClopidogrelClopidogrelASAASA

ClopidogrelClopidogrel

Antithrombotic Trialists’ Collaboration: Evidence Supports Low Dose ASA (75–150mg)1

1. Antithrombotic Trialists’ Collaboration. BMJ 2002; 324: 71–86.

ASA dose % odds reduction

500–1500 mg daily

160–325 mg daily

75–150 mg daily

< 75 mg daily

Any ASA dose 23% ±2

(p < 0.0001)

1.00.50.0 1.5 2.0

Control betterASA better

1. The CURE Study Investigators. Eur Heart J 2000; 21:2033–41

CURE-trial

Double-blind treatment up to 12 months

ASA 75–325 mg od

Clopidogrel75mg od

(n = 6,259)

Placebo1 tab od

(n = 6,303)

ASA 75–325 mg od

Day

1

6 m

onth

vis

it9

mon

th v

isit

12 m

onth

or fi

nal v

isit

Clopid

ogrel

300m

g load

ing

dose

3 m

onth

vis

it

Dis

char

ge v

isit

1 m

onth

vis

it

Patients withACS

(unstable angina or non-Q-wave

MI)

Plac

ebo

load

ing

dose

R = randomisation

n = 12,562

28 countries

R

NON-STEMI

CURE: early and long-term benefits of clopidogrel1

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

0.00

0.02

0.04

0.06

0.08

0.10

0.12

0.14

0 3 6 9 12Months of follow-up

Cu

mu

lati

ve h

azar

d r

ate Placebo*

(n = 6,303)

Clopidogrel* (n = 6,259)

20% relativerisk reduction

p = 0.00009

Cumulative events(MI, stroke or cardiovascular death)

*On top of standard therapy (including ASA)

Revascularization in NSTEMI/UAP

• Risk stratification– High (GPIIb/IIIa and fast PCI)– Intermediate (neg trop, delayed invasive dx)– Low (elective invasive dx or search for ischemia)

• Basistreatment– ASA 300 mg, 75-160 mg– Clopidogrel 300 mg 75 mg for 9-12mths– LMWH (Enoxaparin/Dalteparin)

– (Betablokker, Nitrates, Statins)

UAP / NSTEMI - Treatment

Courtesy Dr. Lars Aaberge, Oslo

• Treatment prior to PCI– ASA 300 mg 75 x1– Clopidogrel 300-600 mg 75x1– Enoxaparin / Dalteparin sc

• Treatment during PCI– Heparin 100 IE/kg bolus or Enoxaparin 30 mg iv + 1

mg/kg sc (ACT 250-350)– Possible: GPIIb/IIIa (reduce Hep to 70 IE/kg, ACT<250)

• Treatment post PCI– ASA + Clopidogrel 75 mg x 1 – (GP IIb/IIIa)

UAP/NSTEMI

Cholesterol

0

50

40

30

20

10

0

0.5

LRCCARE

POSCH

WOS4S

LIPID

AFCAPS

1.0 1.5 2.0 2.5

HPS

Adapted from:

LRC, JAMA 1984;251:351-364 Downs JR et al., JAMA 1998;279:1615-1622

LIPID Study Group, N Engl J Med 1998;339:1349-57 Shepherd J et al., N Engl J Med 1995;333:1301-7

Sacks FM et al., N Engl J Med 1996;335:1001-9 Buchwald H et al., N Engl J Med 1990;323:946-955

4S Group, Lancet 1994;344:1383-89 HPS Collaborative Group, Lancet 2002;360:7-22

Reduction in cholesterol (mmol/l)

Reduct

ion in c

ard

iovasc

ula

r events

(%

)

Relationship between reduction of cholesterol and decrease of cardiovascular events in various trials

1 mmol LDL- 21% CHD-