acs management

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Acute coronary syndromesA national clinical guideline

1 Introduction 1

2 Presentation, assessment and diagnosis 4

3 Initial management 6

4 Reperfusion therapy for ST elevationacute coronary syndromes 12

5 Risk stratifcation and non-invasive testing 17

6 Invasive investigation and revascularisation 19

7 Early pharmacological intervention 21

8 Treatment of hypoxia and cardiogenic shock 26

9 Patient support and information needs 29

10 Implementation, audit and research 33

11 Development of the guideline 35

Abbreviations 39

Glossary 41

Annexes 42

References 48

Updates 54

February 2007(Section 3.3 updated June 2010)

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COPIES OF ALL SIGN GUIDELINES ARE AVAILABLE ONLINE AT WWW.SIGN.AC.UK

Scottish Intercollegiate Guidelines Network

Part of NHS Quality Improvement Scotland

SIGN


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keytoevIdencestatementsandGradesoFrecommendatIons

levelsoFevIdence

1++ High quality meta-analyses, systematic reviews of randomised controlled trials(RCTs), or RCTs with a very low risk of bias

1+ Well conducted meta-analyses, systematic reviews of RCTs, or RCTs with a lowrisk of bias

1-

Meta-analyses, systematic reviews of RCTs, or RCTs with a high risk of bias2++ High quality systematic reviews of case control or cohort studies

High quality case control or cohort studies with a very low risk of confounding orbias and a high probability that the relationship is causal

2+ Well conducted case control or cohort studies with a low risk of confounding orbias and a moderate probability that the relationship is causal

2 - Case control or cohort studies with a high risk of confounding or bias andasignifcantriskthattherelationshipisnotcausal

3 Non-analytic studies, eg case reports, case series

4 Expert opinion

GRADES OF RECOMMENDATION

Note: The grade of recommendation relates to the strength of the evidence on which therecommendation is based. It does not reect the clinical importance of the recommendation.

a At least one meta-analysis, systematic review of RCTs, or RCT rated as 1++

and directly applicable to the target population; or

A body of evidence consisting principally of studies rated as 1+, directly applicableto the target population, and demonstrating overall consistency of results

b A body of evidence including studies rated as 2++, directly applicable to the target

population, and demonstrating overall consistency of results; orExtrapolated evidence from studies rated as 1++ or 1+

c A body of evidence including studies rated as 2+, directly applicable to the targetpopulation and demonstrating overall consistency of results; or

Extrapolated evidence from studies rated as 2++

d Evidence level 3 or 4; or

Extrapolated evidence from studies rated as 2+

GOOD PRACTICE POINTS

Recommended best practice based on the clinical experience of the guidelinedevelopment group

This document is produced from elemental chlorine-free material and is sourced from sustainable forests


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Scottish Intercoegiate Guideines Netor

Acute coronar sndroes

A natina cinica gidin

Fba 2007


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Scttish Intcgiat Gidins NtwkISBN 1899893 74 1Fist bishd 2007

SIGN cnsnts t th htcing f this gidin f ths f intatin in NHSSctand

Scottish Intercoegiate Guideines Netor28 Thiste Street, Edinburgh EH2 1EN

.sign.ac.u


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1 INTRODUCTION

1 Introduction

Th act cna snds ncass a sct f nstab cna at disasf nstab angina t tansa cadia infactin. A ha a cn atig in thformation of thrombus on an inamed and complicated atheromatous plaque. The principlesbhind th sntatin, instigatin and anagnt f ths snds a siia withitant distinctins dnding n th catg f act cna snd.

1.1 GUIDElINE REmIT

This gidin ids idnc basd cndatins n th in-hsita anagnt fatints with an act cna snd (ACS). An xctin t this is in th cas f cidgs fwing nn-ST atin ACS wh th SIGN Cna Hat Disas ct stinggroup requested that the guideline development group examine the evidence base aroundth datin f cidg s bnd hsita dischag. Th gidin ds nt addssth anagnt f ndiffntiatd chst ain act hat fai athgh th tatnt

f hxia and cadignic shck in atints with act cna snds is cnsiddin section 8. Annex 1 provides a ow chart broadly summarising the recommendations fromth gidin.

.. pATIeNT verSIoN

A atint sin f this gidin is aaiab f th SIGN wbsit, .sign.ac.u

..2 ADDITIoNAl ADvICe To NHSSCoTlAND From NHS quAlITy ImprovemeNTSCoTlAND AND THe SCoTTISH meDICINeS CoNSorTIum

NHS qIS csss ti tchng aaisas (mTAs) f NHSSctand that ha bndcd b th Natina Institt f Hath and Cinica excnc (NICe) in engand andWas. Th Scttish mdicins Cnsti (SmC) ids adic t NHS Bads and thiAa Dg and Thatics Citts abt th stats f a nw icnsd dicins andan a nw indicatins f stabishd dcts. SmC adic and NHS qIS aidatd NICemTAs ant t this gidin a saisd in th sctin n intatin.

1.2 DEfINITION Of ACUTE CORONARy SyNDROmES

The denition of acute coronary syndrome depends on the specic characteristics of eachnt f th tiad f cinica sntatin (incding a hist f cna at disas),ctcadigahic changs and bichica cadiac aks. An act cna snda ccasina cc in th absnc f ctcadigahic changs atins inbichica aks, whn th diagnsis is std b th snc f i dcntdcoronary artery disease or subsequent conrmatory investigations.

Th idiat anagnt f a atint with an act cna snd is dtindb th chaactistics f th snting ctcadiga and, in atica, th snc absnc f ST sgnt atin. In cbinatin with th cinica sntatin (see section 2),an ST segment elevation acute coronary syndrome is dened by the presence of 1 mm STelevation in at least two adjacent limb leads, 2 mm ST elevation in at least two contiguouscdia ads, nw nst bnd banch bck. In th absnc f ST sgnt atin(nn-ST sgnt atin act cna snd), atints a initia anagd withtgnc fsin tha.


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ACUTE CORONARy SyNDROmES

Th ain diagnstic catgis f act cna snd, nstab angina and cadiainfarction, are dened by the serum concentration of cardiac enzymes and markers.2 Thcadiac aks, tnin T and tnin I, a xt snsiti t cadia in anddamage. Minimal damage can be detected, allowing identication of micro-infarcts wherethere is an elevation in the troponin concentration without a signicant rise in creatine kinase

or other cardiac enzymes. One consequence of the use of troponin measurement has been abing f th distinctin btwn nstab angina and cadia infactin. Th eanScit f Cadig (eSC) and Aican Cg f Cadig (ACC) stat that an atin,however small, of a troponin or the creatine kinase MB (muscle, brain) isoenzyme is evidenceof myocardial necrosis and that the patient should be classied as having myocardial infarction,hw sa.3,4 Th gba gist f act cna nts (GrACe) ss ths diagnsticcitia f act cadia infactin and nstab angina as shwn in Annx 2. This hascatgisd an atints with sa iss in tnin cncntatins as haing sstainda cadia infactin dsit th absnc f a tiss daag. mdst iss in tnincncntatin a assciatd with a sbstantia incas in th isk f dath and atints withdst tnin iss ha a siia n and six nth tait t ths sstaining a acinica cadia infactin (see Table 1).

Sinc th intdctin f tnin asnt and th nw eSC and ACC gidins, anstudies have used this changed denition of acute myocardial infarction. In order to synthesiseth idnc n tatnt f act cadia infactin f bf and sinc this chang, thBritish Cardiac Society (BCS) working group denition of myocardial infarction has been usedthroughout the guideline. The BCS denition has three categories for acute coronary syndromes,with a thshd f s tnin cncntatin ab which a cinica cadia infactinis diagnsd.2 This approximates to the previous World Health Organisation (WHO) denitionf cadia infactin.5 patints with a tnin cncntatin bw this thshd bt abth fnc ang a dsignatd as haing an act cna snd with idnc fct ncsis (see Table 1).

Table 1 Current denitions and prognosis of acute coronary syndrome according to troponinT concentration.

2h s tnin T cncntatin (g/)

< 0.0 0.01 and


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1 INTRODUCTION

1.3 PROGNOSIS IN ACUTE CORONARy SyNDROmES

patints with ACS cntin t ha a tc dsit adancs in dn thais(see Table 1).6 In ths adittd with sd ACS, 36% wi tiat b diagnsd withcadia infactin ding thi indx adissin.8 Th 30-da and 6-nth tait f

atints with act cna snd is atica high in ths with atd tnincncntatins bt is as atd in ths atints with nstab angina (tnin ngati).Th snc f ST sgnt diatin is a stng dict f an ads tc thanatins in tnin cncntatins.9,0

1.4 STATEmENT Of INTENT

This gidin is nt intndd t b cnstd t s as a standad f ca. Standadsf ca a dtind n th basis f a cinica data aaiab f an indiida cas andare subject to change as scientic knowledge and technology advance and patterns of care. Adhnc t gidin cndatins wi nt ns a sccssf tc in cas, n shd th b cnstd as incding a thds f ca xcdingth acctab thds f ca aid at th sa sts. Th tiat dgnt st b

ad b th aiat hathca fssina(s) snsib f cinica dcisins gadinga atica cinica cd tatnt an. This dgnt shd n b aid atfwing discssin f th tins with th atint, cing th diagnstic and tatntchoices available. It is advised, however, that signicant departures from the national guidelineor any local guidelines derived from it should be fully documented in the patients case notesat th ti th ant dcisin is takn.

1.5 REvIEw AND UPDATING

This gidin was issd in 2007 and wi b cnsidd f iw in th as. An datst th gidin in th inti id wi b ntd n th SIGN wbsit: .sign.ac.u


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3

2 Presentation, assessent and diagnosis

2.1 ClINICAl PRESENTATION AND ImmEDIATE ASSESSmENT

A high quality systematic review of 21 studies examined the usefulness of 16 different clinicalsigns and sts in th diagnsis f act cna snds. Takn in isatin, nsing sign st was disciinat. A sstatic iw b th Agnc f Hath Cafnd that st chaactistics w as nhf as gnstic facts.2 Th cntAican Hat Assciatin/Aican Cg f Cadig (AHA/ACC) gidins cndthat ve factors should be considered together when assessing the likelihood of myocardialischaia ating t act cna snds. Ths a th nat f th sts, histf ischaic hat disas, sx, incasing ag, and th nb f taditina cadiasca iskfacts snt. High isk fats incd wsning angina, ngd ain (>20 ints),pulmonary oedema (Killip class 2, see glossary), htnsin and ahthias.4

The diagnosis and management of a patient with suspected acute coronary syndrome requires adtaid cinica assssnt and th cding f a 2 ad ctcadiga. man tatnts,

scia f ST atin act cna snd, a citica ti dndnt and thidiat cinica assssnt f a atints with a ssctd act cna snd isssntia.3,4,3

Th indicatins f fsin tha (see section 4) a basd iai n th ta-analysis of the Fibrinolytic Therapy Trialists Collaboration (FTTC) group.4 Th td thatelectrocardiographic predictors of mortality benet from brinolytic therapy were the presencef ST sgnt atin nw nst bnd banch bck (see section 1.2). Th FTTC gdid nt distingish btwn ft and ight bnd banch bck athgh sa gidins andtrials specically stipulate left bundle branch block only.4 rgist data f act cadiainfactin shw that ight bnd banch bck is as cn as, and has a high taitthan, ft bnd banch bck.5 Th ait f atints snting with act cadiainfactin and ight bnd banch bck ha assciatd ST sgnt atin. It is nknwn

whth atints with act cadia infactin snting with ight bnd banch bckin the absence of ST segment elevation will derive benet from reperfusion therapy.

No specic evidence was identied on when to record serial electrocardiograms or on whichatints th shd b caid t.

D Patients ith suspected acute coronar sndroe shoud be assessed iediate b anappropriate heathcare proessiona and a 12 ead eectrocardiogra shoud beperored.

rat 2 ad ctcadigas shd b fd if th is diagnstic nctaint a chang in th cinica stats f th atint, and at hsita dischag.

patints with sisting bnd banch bck ST sgnt chang shd b gin ac f thi ctcadiga t assist thi ft cinica anagnt shd thsnt with a ssctd act cna snd.

Cntins ST sgnt niting, additina ad niting and ct cadigah aat id aab ng t gnstic infatin, bt thi in th assssnt and diagnsisf act cna snd has t t b stabishd.6-25


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2 PRESENTATION, ASSESSmENT AND DIAGNOSIS

2.. SelF meDICATIoN IN pATIeNTS WITH CoroNAry ArTery DISeASe

In atints with knwn cna hat disas, sf dicatin with gc tinitat idsaid st if f angina ain, bt its ffct asts f ss than 60 ints. 26,27

patints with knwn cna hat disas shd b gin ca adic n hw t sf

dicat with gc tinitat t i th sts f thi angina:

an initia ds shd b takn at st nst

if necessary, a further two doses should be taken at ve minute intervals

if symptoms have not settled within ve minutes of taking the third dose (15 minutesin tta f nst f sts) gnc dica sics shd b cntactd.

2.2 BIOCHEmICAl DIAGNOSIS IN ACS

The measurements of troponin I and T are of equal clinical value.28Th is a ag and cnsistntbd f idnc that th ti ti t as tnin (I T) f diagnsis gnsticrisk stratication is 12 hours from the onset of symptoms.28-32 Wh th is nctaint andti f st nst, tnin shd b asd 2 hs f sntatin. 32

In atints with an act cna snd wh snt t th gnc datnt withinsix hs f ain nst, and haf wi ha an atd tnin I n adissin.33 Sstaticiw f tnin asnt


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ACUTE CORONARY SYNDROMES

2++

2+

4

1+

3 Initial management

This section provides recommendations regarding the management of patients within the rst12 hours of an acute coronary syndrome.

3.1 SERVICE DELIVERY

Retrospective studies suggest that patients are more likely to receive appropriate evidence basedtherapies when treated by cardiology specialists than by general internal physicians.37-39 It isunclear whether this benet is attributable to the specialist physician in isolation or reects theoverall care and treatment of patients within a specialist cardiology service. A systematic reviewsuggests that this increased provision of evidence based therapy is associated with improvedclinical outcomes including mortality.40

C Patients with an acute coronary syndrome should be managed within a specialistcardiology service.

3.2 CARDIAC MONITORING

Ventricular brillation (VF) and pulseless ventricular tachycardia are common in patients withacute coronary syndromes. Prompt debrillation and cardioversion are effective and life saving(see SIGN guideline 94 on management of cardiac arrhythmias in coronary heart disease).41Continuous cardiac rhythm monitoring facilitates prompt recognition and treatment of theseforms of cardiac arrest.3,4,13

D Patients with an acute coronary syndrome should have continuous cardiac rhythmmonitoring.

3.3 OXYGEN THERAPYA Cochrane review found no conclusive evidence from randomised controlled trials to supportthe routine use of inhaled oxygen in patients with acute AMI.231

There is no evidence that routine administration of oxygen to all patients with the broad spectrumof acute coronary syndromes improves clinical outcome or reduces infarction size.

3.4 ANTIPLATELET THERAPY

3.4.1 ASPIRIN

In comparison with placebo, aspirin halves (absolute risk reduction; RR 5.3%, relative RR 46%)the rate of vascular events (cardiovascular death, non-fatal myocardial infarction and non-fatalstroke) in patients with unstable angina and reduces it by nearly a third (absolute RR 3.8%,relative RR 30%) in those with acute myocardial infarction.44

A Patients with an acute coronary syndrome should be treated immediately withaspirin (300 mg).

Updated

June 2010


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3 INITIAl mANAGEmENT

3.4.2 ComBINATIoN ASpIrIN AND ClopIDoGrel THerApy

Non-ST elevation acute coronary syndrome

In th Cure tia, cbind asiin (300 g stat and 75-50 g dai) and cidg (300g stat and 75 g dai)tha was ffcti than asiin tha an. Cbinatin

tha idd a fth 2.% abst rr (20% ati rr) in th cbind nd int fcadiasca dath, stk cadia infactin in high isk atints (ctcadigahicidnc f ischaia atd cadiac aks) with nn-ST atin act cnasnds.45 This benet was seen within 24 hours and was principally due to a reduction incadia infactin fact ischaia.45,46

ST elevation acute coronary syndrome

Th ClArITy-TImI 28 (cidg 300 g stat and 75 g dai) and CommIT/CCS (cidg75 g dai) tias ha dnstatd an incasd atnc at f th infact-atd at anddcd tait whn caing cbinatin asiin and cidg tha with asiinan in atints with ST atin act cna snd.47,48 Th dctins in th atf dath, infactin stk (0.9% abst rr, 9% ati rr) and in at f dath (0.6%

abst rr, 7% ati rr) w achid witht an xcss a bding and wpredominantly seen when clopidogrel was administered within the rst 12 hours.

A In the presence o ischaeic eectrocardiographic changes or eeation o cardiacarers, patients ith an acute coronar sndroe shoud be treated iediateith both aspirin (300 mg) and copidogre (300 mg) therap.

3.4.3 GlyCoproTeIN IIB/IIIA reCepTor ANTAGoNISTS


In a ta-anasis f six tias (n=3,402) atints with nn-ST atin act cnasnds tatd with a gctin IIb/IIIa ct antagnist had % abst rr (9%ati rr) in th dds f dath cadia infactin at 30 das.49 Th abst tatnt

benet was largest in those at high risk, such as patients with an elevated troponin concentration.ma bding cicatins a w incasd b gctin IIb/IIIa ct antagnists(2.4% s .4%). Intacania bding did nt incas.

In a saat anasis f th sa data, th s f gctin IIb/IIIa ct antagnistsdcd 30-da tait in atints with diabts (n=6,458, 4.6% s. 6.2%) bt nt in thswithout diabetes (n=23,072). This benet was greatest in patients with diabetes who underwentctans cna intntin (pCI) ding thi indx adissin (n=,279, tait.2% s 4.0%).50 Th was as a w 30-da at f dath cadia infactin (0.7%s 2.7%) with gctin IIb/IIIa ct antagnists in atints ndging pCI (n=6,337),scia whn fd ding dg infsin (n=2,249, 0.5% s 3.6%).5 Th ISAr-reACT2 trial conrmed that glycoprotein IIb/IIIa receptor antagonism conferred a further additionalbenet (absolute RR 2%; relative RR 25%) in patients pre-treated with aspirin (500 mg) and

cidg (600 g).52 These benets were again seen in high-risk patients, such as those withan atd tnin cncntatin.

B High-ris patients ith non-ST eeation acute coronar sndroe shoud be treated ithan intraenous gcoprotein IIb/IIIa receptor antagonist, particuar i the areundergoing percutaneous coronar interention.


There is little benet in routine use of glycoprotein IIb/IIIa receptor antagonists in patients withST atin act cna snd ciing thbtic tha. Th is a sa dctinin -infactin ats, an incas in a bding and n ffct n tait. 53,54

Th s f gctin IIb/IIIa ct antagnists in atints ndging ia ctans

cna intntin f ST atin act cna snd is discssd in sctin 4...


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3.5 ANTICOAGUlANT THERAPy

3.5. uNFrACTIoNATeD HepArIN


In atints with a nn-ST atin act cna snd, nfactinatd hain (uFH)tatnt f at ast 48 hs dcs th cbind nd int f dath cadia infactin(abst rr 2.5%; ati rr 33%).55 This is dinant din b a dctin in nn-fatacadia infactin.


In atints with ST atin act cna snd fwing asiin and thbsis withbrin-specic agents, unfractionated heparin reduces the rate of re-infarction (0.3% absoluterr) and dath (0.5% abst rr).56

3.5.2 loW moleCulAr WeIGHT HepArIN


A Cchan iw f sn andisd cntd tias (rCTs) (n=,092) td that wca wight hain tatnt (incia nxaain) dcd cadia infactinand cna ascaisatin cd ats cad t nfactinatd hain. Thwas n diffnc in tait a bding isds. Th nb f atints ndd ttat (NNT) with w ca wight hain ath than nfactinatd hain t ntn cadia infactin was 25 and t nt n xta ascaisatin cd was50. Benets from low molecular weight heparin remain evident well beyond the duration oftatnt and in th TImI IIB tia w sti idnt at n a.57 extndd s f w cawight hain bnd th inatint sta f than ight das is f n a. 58

Whn sd in cbinatin with gctin IIb/IIIa ct antagnists, w ca wightheparin is no more efcacious than unfractionated heparin but is associated with similar59

fw

60

bding cicatins.ST elevation acute coronary syndrome

rCTs caing w ca wight hain with nfactinatd hain in ST atinact cna snds shw s adantags f w ca wight hain, incianxaain.60-62 Meta-analysis conrms that, in patients treated with thrombolytic therapy, lowca wight hain (nxaain) is assciatd with btt tcs (cadia infactin,abst rr 2.3%, ati rr 4%; cnt ischaia abst rr 2.0%, ati rr 30%;dath cadia infactin, abst rr 2.9%, ati rr 26%; and dath, cadiainfactin cnt ischaia abst rr 4.8%, ati rr 28%) bt n dcas intait whn cad with nfactinatd hain.63 Th is an incas in a bdingatica whn sing nxaain with atas tnctas (% abst isk incas,44% ati isk incas). This is sn dinant in atints 75 as f ag wh

th ds f nxaain a nd t b dcd.64

These ndings have been conrmed in a large RCT (ExTRACT; n=20,506) of enoxaparin giventhght hsita adissin ss nfactinatd hain f at ast 48 hs. Th iand int f dath cnt cadia infactin was dcd (abst rr 2.%, atirr 7%) athgh a tait was nchangd. ma bding was incasd at 30 das(absolute risk increase 0.7%, relative risk increase 53%). Although superior efcacy of enoxaparinwas aant b 48 hs, this tia bsd a is in nt ats aft nfactinatd hainwas discontinued suggesting that 48 hours of anticoagulation is insufcient.65


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3.5.3 DIreCT THromBIN INHIBITorS

A ta-analsis f andisd tials has dnstatd dst siit f dict thbininhibits, sch as hidin bialidin, uFH in atints with act cna snds.66Althgh th was n ffct n talit, th was a 20% lati rr (0.7% abslt dctin)in -infactin at sn das, aintaind at 30 and 80 das. In caisn with uFH, thwas n xcss blding isk, xct whn sd in atints with ST latin act cnasnd haing thblsis wh th 30% lati rr in -infactin at f das wasffst b a 32% lati isk incas in dat blding.67.

Althgh th ha bn n caati stdis btwn dict thbin inhibits and lwlcla wight hain in act cna snds, dict thbin inhibits aa thave a similar magnitude of benet over unfractionated heparin to that seen with low molecularwight hain.58,66

3.5.4 SyNTHeTIC peNTASACCHArIDeS


In th oASIS-5 rCT (n=20,078) th snthtic ntasacchaid, fndaainx (sbctansinjection 2.5 mg daily), had similar clinical efcacy to enoxaparin (subcutaneous injection g/kg twic dail) bt with dcd isk f aj blding (abslt rr .9%; lati rr 48%).Althgh th ia nd ints (dath, cadial infactin fact ischaia) wsiila, bth sht (30 da) and lng t (80 da) talitis w lw with fndaainx(abslt rr 0.6 % and 0.7%; lati rr 7% and % sctil).68


In th oASIS-6 rCT (n=2,092), intans bls fllwd b dail sbctans fndaainxinjctin (2.5 g) dcd th ia nd int f dath cnt cadial infactinat 30 das (abslt rr .5%; lati rr 4%) cad t tatnt with lacb nfactinatd hain. Dath ats at all ti ints (9, 30 and 80 das) w dcd (30das; abslt rr .%, lati rr 3%) and th incidnc f aj blding was naffctd.

These benets were only seen in those patients not treated with primary percutaneous coronaryintntin.69

D t ltil std gs and tatnt gins, th inttatin f th oASIS-6 tialis clx. In cntast t th oASIS-5 tial, th was n dict had-t-had caisn ffndaainx with lw lcla wight hain. m, nal 50% f atints citd didnt ha a cla indicatin f anticaglatin and w andisd t lacb fndaainx.Th oASIS-6 tial incldd atints snting t 24 hs f st nst. Alst aquarter of the patients had no reperfusion therapy, and in those that did, streptokinase was thedinant (73%) thbltic agnt.

Bcas f th diffncs in inclsin citia, std dsign and lngth f anticaglantthais, th oASIS-6 and exTrACT tials d nt lnd thsls t dict caisn. Th

ExTRACT trial was limited to those patients receiving predominantly (80%) brin-specicthbltic tha. In th sbg f oASIS-6 wh did ci thbltic tha andw andisd t ith fndaainx nfactinatd hain (n=2,666), th was adctin in dath (abslt rr 3.2%, lati rr 2%) and in dath cnt cadialinfactin (abslt rr 4.%, lati rr 23%) in ths atints tatd with fndaainx. Thiswas a modest sized subgroup analysis and should be interpreted with caution.

3.5.5 overvIeW AND reCommeNDATIoNS

us f anticaglant tha in atints with act cna snds fas gssillw lcla wight hains and lngd (>48 hs) datins f tha. Thpentasaccharides appear to have the best efcacy and safety prole with a reduction in adverseblding nts cld with a dctin in sht t di t talit. Fndaainx is th

nl ntasacchaid cntl aailabl f clinical s. Th is a cncn that lw lclaweight heparins and pentasaccharides do not provide adequate anticoagulation in patientsndging pCI.


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lag sca rCTs (oASIS-5 and oASIS-6) aa t fa th s f fndaainx w ca wight hains. Th aant siit f fndaainx in atints withnn-ST atin act cna snds is basd n a sing ag rCT (oASIS-5) anddinant ats t sht t dctins in bding isk and aant ng tmortality benets.68,69

In atints with ST sgnt atin act cna snds, th ack f a dict caisnbtwn fndaainx and w ca wight hains, and th akd diffing incsincriteria, make specic recommendations challenging. In the relevant clinical trials currentevidence suggesting superiority of fondaparinux is insufcient to recommend its use in preferencet w ca wight hain. Th oASIS-6 tia was distingishd b th incsin fatints with ST sgnt atin act cna snd wh did nt ci fsintherapy. Its use in this subpopulation did confer therapeutic benet and fondaparinux shouldb th agnt f chic in this g.69

Th ag and w cndctd rCTs (exTrACT, oASIS-5 and oASIS-6) ha dnstatdthat a therapeutic strategy of 48 hours of anticoagulation is insufcient, with an increased riskf cadia infactin aant fwing a cssatin f tha. 65,68,69

A In the presence o ischaeic eectrocardiographic changes or eeation o cardiacarers, patients ith an acute coronar sndroe shoud be treated iediateith o oecuar eight heparin or ondaparinu.

B Patients ith an ST eeation acute coronar sndroe ho do not receie reperusiontherap shoud be treated iediate ith ondaparinu.

Anticagant tha shd b cntind f ight das, nti hsita dischag cna ascaisatin.

3.6 BETA BlOCkERS

3.6. NoN-ST elevATIoN ACuTe CoroNAry SyNDrome

Th a n ag sca rCTs f bta bck tha in atints with nn-ST atin actcna snds. mta-anasis f sa rCTs in atints with nstab angina sggststhat bta bcks dc th at f gssin t cadia infactin b 3%. 70 Gintheir secondary preventative benets in patients with a recent myocardial infarction (see SIGNguideline 97 on risk estimation and the prevention of cardiovascular disease) 7bta bcksshould be the rst line anti-anginal agent of choice in patients with non-ST elevation ACS.

3.6.2 ST elevATIoN ACuTe CoroNAry SyNDrome

The ISIS-1 trial described an early (seven day) benet in cardiovascular mortality of intravenousbta bck tha in atints with cadia infactin with a 5% ati rr (0.68%

abst rr).72 This benet was of borderline signicance and appeared to be mediatedthgh a dctin in cadiac t.73 This tia was cndctd bf th widsad sof thrombolytic therapy and it is unclear how relevant these ndings are in the contemporarytatnt f cadia infactin.

Th CommIT/CCS rCT f 45,852 atints with ST atin act cna snddnstatd that idiat intans (t 5-5 g) fwd b a (t50 mg four times daily for the rst 24 hours followed by 200 mg controlled-release metoprololdai thaft) bta bckad had n ffct n tait th c-ia nd ints f dath,-infactin cadiac ast. Th was a 0.5% abst rr in -infactin (8% atirr) and ahthic dath (7% ati rr) bt at th xns f an abst isk incas f.% (ati incas f 30%) in cadignic shck. Th dctin in dath f nticabrillation was counterbalanced by an increase in death from cardiogenic shock. The risk of

cardiogenic shock was seen within the rst day of presentation and in patients presenting withhtnsin in Kii cass III.74


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pis rCTs 72,75 and a ta-anasis 76 have failed to demonstrate a mortality benet of earlybeta blockade. A subsequent meta-analysis (conducted by the COMMIT/CCS authors) of RCTsf a bta bckad in 52,645 atints with ST atin act cna snd in Kiicass I (n cinica idnc f hat fai) with sstic bd ss >05 Hg andhat at >65/in fnd that intans fwd b a bta bckad dcs tait

(abst rr 0.7%, ati rr 3%), -infactin (abst rr 0.5%, ati rr 22%) andcadiac ast (abst rr 0.7%, ati rr 5%).74

B In the absence o bradcardia or hpotension, patients ith an acute coronar sndroein kiip cass I shoud be considered or iediate intraenous and ora betabocade.

3.7 GlyCAEmIC CONTROl

eatd bd gcs at hsita adissin is a stng indndnt isk ak f atintswith cadia infactin.77 Th ha bn tw a rCTs instigating th ffcts f insinand gcs infsin in diabtic atints with act cadia infactin. In th DIGAmI

tia (n=620), intnsi tabic cnt sing insin and gcs infsin in atints withdiabetes mellitus or a blood glucose >11.0 mmol/l conferred a marked mortality benet atn a (8.6% s 26.%).78 The subsequent DIGAMI 2 trial (n=1,253) investigated whetherng t insin tha shd b cnsidd in atints with t 2 diabts itsand act cadia infactin. It dnstatd that ng t insin was f n additinabenet, although there was extensive use of insulin at discharge in all treatment groups makinginterpretation difcult. For patients with type 2 diabetes mellitus, insulin is not required beyondthe rst 24 hours unless clinically required for the management of their diabetes.79

B Patients ith cinica ocardia inarction and diabetes eitus or aredhpergcaeia (>11.0 mmol/l) shoud hae iediate intensie bood gucose contro.This shoud be continued or at east 24 hours.


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4 Reperusion therap or ST eeation acute

coronar sndroes

This section provides further recommendations regarding the immediate (within the rst 12hs) anagnt f atints with ST atin act cna snds, fcsing n bthia ctans cna intntin and thbsis.

4.1 PRImARy PERCUTANEOUS CORONARy INTERvENTION

A chnsi sstatic iw80 and ta-anasis8 f rCT data shwd that iactans cna intntin is si t thbsis f th tatnt f atintswith ST atin act cna snd. Whn cad with thbsis, ia pCIdcd sht and ng t tait, stk, -infactin, cnt ischaia and th ndf cna at bass gaft (CABG) sg as w as th cbind nd int f dath nn-fata -infactin (see Table 2). This benet was consistent across all patient subgroups

and was independent of the thrombolytic agent used. The greatest benet was seen in thoseatints tatd within 2 hs f st nst.80,8

Table 2 Advantages of primary percutaneous coronary intervention over thrombolysis.80

Cinica indices Eent Rate Absoute

RR

Reatie

RRNNT

Throbosis PCI

Sht t tait (4-6 wks) 8% 5% 3% 36% 33

lng t tait (6-8 nths) 8% 5% 3% 38% 33

Stk 2%


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4 REPERfUSION THERAPy fOR ST ElEvATION ACUTE CORONARy SyNDROmES

Intracoronary stenting

In a ta-anasis f nin tias (n=4,433) f ctans cna intntin, intacnastnting dcd -infactin (abst rr .2%; ati rr 33%) and tagt ssascaisatin (abst rr 4.4%; ati rr 52%) at 2 nths whn cad withisolated balloon angioplasty. These benets did not affect short or long term mortality.84

A Intracoronar stent ipantation shoud be used in patients undergoing priarpercutaneous coronar interention.

4.2 THROmBOlyTIC THERAPy

Whn cad with acb, thbtic tha dcs 35-da tait (.9% abstrr, 8% ati rr) in atints snting with an ST atin act cna snd.4,85

4.2. TImING oF TreATmeNT

Compared with primary PCI, the benet of thrombolysis on six month mortality is more time-dndnt86 and is assciatd with a ss dg f cadia saag at a ti ints. 87eidnc is acking gading th cis acctab da f ia pCI thbsis.Cnsidd xt inin sggsts that whn ia pCI cannt b fd within 90ints f diagnsis, thbtic tha shd b adinistd.3,4 This is basd nasstins that th is a 30 int da f th adinistatin f thbsis and that thsiit f ia pCI is st ca whn th ti diffnc btwn adinistatin fthrombolysis and balloon ination is 60 minutes.

D when priar percutaneous coronar interention cannot be proided ithin 90inutes o diagnosis, patients ith an ST eeation acute coronar sndroe shoudreceie iediate throbotic therap.

4.2.2 THe FIrST TWo HourS

The time-dependent benets of thrombolysis (versus placebo) may be non-linear. A meta-analysissuggests that there are major mortality benets in the very early phase (2 hours) of ST segmentatin act cna snds.88 This anasis has bn citicisd f th scti hasison certain small trials that may exaggerate this apparent early benet.89 Whth th 90-intti da ains aiat in this a has ains t b stabishd.

In n rCT that cad a statg f -hsita thbsis with di f a atints tan intntina cnt with faciitis f sc pCI (in 26% f cass) t a statg f iapCI, th was n diffnc in th csit nd int f dath, cadia infactin andstk at 30 das.90 In a subsequent post hoc subgroup analysis of this trial, patients presentingwithin tw hs f st nst had a tnd twads a w tait whn gin -hsita thbsis.9 This difference was not statistically signicant (p>0.05) and relied on

a sa nb f nts (8 daths in 460 atints). Th a b a f -hsitathbsis in ths atints snting a (


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4.2.3 ServICe DelIvery

Administration of immediate thrombolysis

Since the clinical benets of thrombolysis are time dependent with an increase of 1.6 deaths perh f da ,000 atints tatd,4 ais statgis ha bn d t iniis

th da btwn diagnsis and initiatin f thbsis.

p-hsita thbsis shtns th ti btwn th ca f h and th adinistatinf thbsis.4

A ta-anasis sggsts that -hsita thbsis as dcs a-cas hsita taitwhn cad t in-hsita thbsis (abst rr .3%, ati rr 7%).95 This ta-anasis ind htgns atint atins, dis hathca ssts, diffntthbtic agnts and aing s f st f th dcisin aks.

Signicant improvements in door-to-needle times are achieved by administration of thrombolysiswithin th gnc datnt. This can b faciitatd b an xincd cadig ns96and accishd witht cising th aiatnss f its adinistatin. 97-99

Transfer of patients to interventional centres

Two randomised trials have conrmed that emergency transfer of patients to interventionalcnts f pCI can b ndtakn saf.00,0 pt tansf f atints f ia pCI wasassciatd with a dctin in th csit nd int f dath, -infactin and stk at 30das (abst rr 6%, ati rr 40%; 00 abst rr 7%, ati rr 45%0) whn cadto thrombolysis. This benet was primarily driven by a reduction in re-infarction (absolute RR4.7%, ati rr 75%;00 abst rr .7%, ati rr 55%0). In bth tias, th was ndiffnc in tait cad t thbsis, xct wh ti f st nst wasgat than th hs, which fad pCI.

C loca protocos shoud be deeoped or the rapid treatent o patients presenting ithST eeation acute coronar sndroes. Consideration shoud be gien to pre-hospitaand adission throbosis, and to the eergenc transer o patients to interentiona

centres or priar percutaneous coronar interention.

4.2.4 CoNTrAINDICATIoNS To THromBolySIS

Abst cntaindicatins f thbsis incd cnt hahag, taa sg, ca, ischaic stk within th nths, atic dissctin, bding diathss,knwn stcta cbasca sins incding nass, and an i intacbahahag.3,4,80 A f ist f cntaindicatins can b fnd in th Bitish Natina Fa(BNF; www.bnf.g). Axiat 40-50% f atints a dd inigib f thbtictha. This is st ftn (in 35% f inigib atints) d t dad sntatin (>2hs f st nst).02 patints inigib bcas f cntaindicatins t thbtictha (0-40%) shd b cnsidd f ia pCI.02,03 pia pCI incs a sa bding

isk f th adinistatin f antiatt and anticagant thais, and s aticntaindicatins a b cn t bth fsin statgis.

patints with an ST atin act cna snd and cntaindicatins tthbtic tha shd b cnsidd f idiat ia ctans cnaintntin.


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4.2.5 CHoICe oF THromBolyTIC AGeNT

Early trials of thrombolytic therapy established the mortality benets of both brin-specic(tissue plasminogen activator; alteplase) and non-brin-specic agents (streptokinase) in acutemyocardial infarction. Subsequent trials directly comparing the efcacy of these two classes ofthrombolytic agents demonstrated similar mortality benets at 30-35 days post-infarction, asconrmed by systematic review and meta-analysis.85,89,04

Th GuSTo tia (n=40,539) was distinct f a is tias sinc it sd an accatdgin f atas: adinistatin 90 ath than 80 ints. Accatd adinistatinf atas std in a gat dctin in tait whn cad with sttkinas(abst rr .%, ati rr 4%).05 Inttatin f th GuSTo tia in th cntxt fprevious trials is controversial. Collins and colleagues have argued that the mortality benetsf th accatd gin a dst and cannt b attibtd t ai fsin. 89Incorporation of the GUSTO trial into a meta-analysis demonstrates no mortality benet ofatas sttkinas.89 Others have argued that the accelerated regimen is sufcientlydistinct t nt its incsin in a ta-anasis f th tias sing th sw adinistatinof alteplase. They highlight a plausible mechanism of benet through more rapid restoration of

cna at atnc. Th as sggst that n w cndctd ag andisd cntdtia ids stng idnc than a ta-anasis f sa sa tias. 85

Tw cbinant tant asingn actiats, tas and tnctas, ha a ngdasa haf-if faciitating bs aicatin.Ths agnts ha bn cad with sttkinasand accelerated alteplase in non-inferiority and equivalence trials. Tenecteplase has been shownt b as ffcti as accatd atas with a w at f intacania hahag, andtas is at ast as ffcti as sttkinas.06-08

The potential mortality benets favour the use of brin-specic thrombolysis. The imperative todc tatnt das and th cnstaints f adinistatin in th -hsita stting fabs agnts.

B Thrombolysis should be conducted with a brin-specic agent.

A bolus brin-specic agent is preferred on practical grounds, particularly in the pre-hsita stting.

4.3 COST EffECTIvENESS Of REPERfUSION THERAPIES IN ST ElEvATION ACUTE

CORONARy SyNDROmE

4.3. prImAry pCI CompAreD WITH IN-HoSpITAl THromBolySIS

A sstatic iw f 0 stdis with ng t fw fnd cnsistnt idnc f wtta csts with ia pCI cad t in-hsita thbsis.80 Ths dcd csts wassociated with reduced length of hospital stay through early identication and discharge of low

risk patients, and need for fewer subsequent procedures.09,0

Nn f th stdis cntaindsc cst infatin dict ant t th NHS.

To apply these ndings to the UK, an economic model was developed using NHS costs (for thea 2003) and th cinica ffctinss data did b ta-anasis f ffctinss stdis.In this d, ia pCI was cad t thbsis sing tas. pia pCI had ahigh cst cas (~550) bt a gain in hath stats f 0.08, giing an incnta cstffctinss ati f abt 6,500 f ach nit f hath stat gaind.80 using sttkinasath than tas incasd th incnta cst ffctinss ati t ast 29,00 nit f hath stat gaind.80 This cnic aatin is iitd t a six nths fw anddoes not consider the longer term consequences of treatment with either therapy.

The analysis did not use the conventional health outcome measure of a quality adjusted lifeyear (QALY) but rather expressed benet as a unit of health state gained. Thus the conventional

thshds f cst qAly cannt b aid. rath th sts sggst ia pCI cdb cst ffcti cad t thbsis sing tas bt a incncsi in sct fia pCI cad t thbsis sing sttkinas.

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4.3.2 prImAry pCI CompAreD WITH pre-HoSpITAl THromBolySIS

Wh th is accss t a pCI cnt within tw hs f st nst, n cnicaatin, sing Fnch csts and cinica data f a andisd cntd tia,82cncdd that it was cst ffcti t fs ST atin ACS atints b pCI thanb -hsita thbsis. Th n a ia nd ints f th cinica nt-ats fdath, nn-fata cadia infactin, and stk w nt diffnt aft ia pCI and -hsita thbsis with sc pCI, bt csts w w f ia pCI. Th ain asnsf th w csts in th ia pCI a w w initia ngth f sta and a w at fsubsequent revascularisations.

4.3.3 A CompArISoN oF DIFFereNT THromBolyTIC AGeNTS

on sstatic iw f th cinica and cst ffctinss f diffnt thbtic agntscncdd that th diffncs in cinica tc a s sa that s f th chast dctshd b adcatd.85 As at f this std an cnic d was dd f an NHSscti, sing th BNF ist ics f thbtic agnts and xcding an diffncsin th cst f adinistatin. Ths ics d nt tak int accnt th discnts aaiab t

diffnt akts and ggahica aas. Th dd sts w high snsiti t aiatinsin th dg csts and th std cncdd that th chic f agnts shd b gnd b thati ics f th dgs, assing n diffnc in adinistatin csts.

4.4 RESCUE PERCUTANEOUS CORONARy INTERvENTION

rsc pCI is ndtakn within 2 hs f thbsis whn th is an aant fait fs th infact-atd at. rfsin is takn t ha ccd whn th is a>50% fa in ST sgnt atin nw nst f idintica hth.2,3

pis gidins cnd sc pCI as th fd statg f atints wh fai tfs aft thbsis.3,4 Rescue PCI is of particular benet in those with large areas ofcadi at isk, hadnaic cis, idnc f hat fai ctica instabiit

and total occlusion or minimal ow in the infarct-related artery.4

A sstatic iw f tias f sc pCI against cnsati tha aft faid thbsisconrmed a reduction in early severe heart failure (absolute RR 8%, relative RR 68%) and onea tait in atints with cinica cadia infactin (abst rr 5%, ati rr 38%).4on sing-cnt andisd tia td n diffnc in 30-da a-cas tait withsc pCI aft faid thbsis with sttkinas, athgh a dctin in th csitnd int f dath, -infactin, stk and gnt ascaisatin was sn with sc pCI(abst rr 3%, ati rr 26%).5 Anth andisd tia f sc pCI ss dad(elective) PCI (at a mean of 12 days post-infarction) conrmed a reduction in the composite endint f dath, -infactin, ascaisatin and ischaic nts at six nths (abst rr25%, ati rr 49%) faing sc pCI.6

In th reACT tia f atints wh cid thbsis within six hs f st nst

(n=427), rescue PCI, performed at median of 414 minutes (interquartile range 350-505) fromst nst, was assciatd with a akd dctin in th csit ia nd intf dath, -infactin, stk s hat fai (abst rr 5%, ati rr 53%). Thiswas dinant din b a dctin in -infactin.7

B Patients presenting ith ST eeation acute coronar sndroe ithin si hours ospto onset, ho ai to reperuse ooing throbosis, shoud be consideredor rescue percutaneous coronar interention.


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5 RISk STRATIfICATION AND NON-INvASIvE TESTING

5 Risk stratication and non-invasive testing

5.1 RISk STRATIfICATION

Th is indict idnc that idntifing high isk indiidas fwing adissin awssctin f atints f a instigatin and intntin. Data f th TACTICS TImI-8and FrISC II tias8,9 in atints with nn-ST atin act cna snds sggstthat the short term (6-12 months) benets of invasive investigation were predominantly seenin those at medium to high risk. Analysis of long term (ve year) outcome in the RITA-3 trialhas also demonstrated that those patients at moderate to high risk benet most from coronaryangigah and ascaisatin.20 Inasi instigatin with cna angigah with aview to revascularisation appears to be appropriate for patients with one- and ve-year event(dath cadia infactin) ats f >0% and >20% scti. patints at w iskdo not appear to benet.20

C Risk stratication using clinical scores should be conducted to identify those patientswith an acute coronary syndrome who are most likely to benet from early therapeutic

interention.

5.. rISK STrATIFICATIoN SCoreS

There are several clinical risk stratication scoring systems that can predict death or myocardialinfactin in atints with act cna snds: th st cn sd scs incdGrACe (see Annex 4),9,0 TImI,2,22 purSuIT,23 and FrISC.8 A a did f rCTpopulations except the GRACE registry which is obtained from an international real lifeobservational registry. It provides a unied scoring system for both ST elevation and non-STatin ACS. In scti aatins, th GrACe gist was th st dicti ftc24 and has bn aidatd sing indndnt xtna datasts.25

Gat gnaisabiit and accac fas th s f th GrACe sc f isk

stratication in acute coronary syndromes.

5.2 ASSESSmENT Of CARDIAC fUNCTION

A sstatic iw f bsatina stdis in atints with cinica cadia infactinsggsts that aks f ft ntica dsfnctin and hat fai id btt gnsticinfatin than stss tsting.26 This is cnsistnt with cht stdis that sggst asa bainnatitic tid cncntatins and asnts f ctin factin id cntagnstic infatin.27,28

Th sctin f ctain thais, sch as adstn ct antagnists (see section 7.7)29may require the assessment of left ventricular function before initiation of therapy.

C In patients ith an acute coronar sndroe, assessent o cardiac unction shoud beconducted in order to identi those patients at high ris and to aid seection oappropriate therapeutic interentions.


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5.3 STRESS TESTING

A sstatic iw f 54 bsatina stdis incating 9,874 atints with cinicacadia infactin indicats that -dischag stss tsting ids iitd additinagnstic infatin t gid atint anagnt.26 A fs f nn-inasi stss tsting

demonstrate similar sensitivities and specicities for the prediction of future cardiac events.

26

Athgh th ngati dicti a is high (~94%), th siti dicti a is w(


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6 INvASIvE INvESTIGATION AND REvASCUlARISATION

6 Inasie inestigation and reascuarisation

6.1 NON-ST ElEvATION ACUTE CORONARy SyNDROmE

A ta-anasis f sn tias td that, in caisn with a cnsati aach, in thabsnc f indcib ischaia, tin cna angigah and ascaisatin dcdats f cadia infactin, s angina and hsitaisatin athgh a taitwas unchanged (5.5% vs 6.0%; 0.5% absolute RR; 8% relative RR, 95% condence interval;CI -9 t 23%) aft a an fw f 7 nths. Th ffcts n tait aid with ti;with an early (in-hospital) hazard (1.8% vs 1.1%; 0.7% absolute risk increase; 60% relativerisk increase, 95% CI, 14 to 125%) and a late (post-discharge) benet (3.8% vs 4.9%; 1.1%abst rr; 24% ati rr, 95% CI, 6 t 38%).30 The meta-analysis is limited by signicanthtgnit btwn th sn tias and th high at f css f a cnsati t aninvasive strategy in most of the trials. This makes it difcult to disentangle the potential benetsf an a inasi statg.

F ag rCTs (n>,000)3-35 and ve smaller RCTs (n=131-993)36-40 ha cad an

a inasi with a cnsati statg in atints with nstab angina and nn-ST atinacute coronary syndromes. There was signicant heterogeneity amongst these nine trials oftenwith high css ats t an inasi statg.

Th FrISC II tia3,32 (n=2,457) had stict adhnc t std andisatin (0 daascaisatin f 7% ss 9% in th cnsati a) and dnstatd a 26% atidctin (95% CI, 8 t 40%; 3.0% abst rr) in cadia infactin and a 43% atirr (95% CI, 0 t 64%; .7% abst rr) in tait at n a.

Similar benets in myocardial infarction but not mortality were seen in the TACTICS-TIMI 18tia (n=2,220).33 This tia had a high css at with 5% f atints in th cnsatistatg g ndging in-hsita cna angigah sting in dst diffncsin ascaisatin ats (in-hsita ascaisatin f 37% with a cnsati statg

ss 6% in th inasi statg a). This a ha d t ndstiatin f tatntbenets.

Bth th FrISC II and TACTICS TImI-8 tias sstatica biasd th diagnsis f cadiainfactin accding t tatnt g with ths ndging ascaisatin haing a highbichica thshd f cadia infactin than ths wh did nt. This a ha d tan overestimation of the benets on this end point.

Th rITA-3 tia (n=,80)34 citd dat isk atints with nn-ST atin actcna snds: n-a tait was 8.3% cad t 4.% in th FrISC II tia. Italso demonstrated a benet of early invasive investigation and revascularisation with a 34%ati dctin (95% CI, 5 t 59 %, abst rr 4.9%) in th isk f th cbind iand int f dath, cadia infactin fact angina at f nths. A haing ffact angina iai d this nd int. Th w n diffncs in tait. Whn

employing the new ESC/ACC denition of myocardial infarction an early invasive strategy alsodcd cadia infactin ats b 33% (95% CI, 4 t 49%) at n a. Fi-a fwup data have conrmed that the reductions in the combined end point of death or myocardialinfactin a sstaind.20

The ICTUS trial (n=1,200) failed to demonstrate a signicant benet of early invasive interventionin w isk atints with nn-ST atin ACS. Th was a high at (>50%) f cnaangiography in the conservative treatment group and the overall mortality in the trial wasxctina w at 2.5% (cf 4% in th FrISC tia). 35 Th idnc sggsts that a tininasi aach is indicatd n in atints at di t high isk.

B Patients ith non-ST eeation acute coronar sndroes at ediu or high riso ear recurrent cardioascuar eents shoud undergo ear coronar angiograph

and reascuarisation.


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6.2 ST ElEvATION ACUTE CORONARy SyNDROmE

Initia tias assssing an a inasi statg aft thbtic tha sggstd that, inthe absence of inducible ischaemia, there was no benet in the clinical outcomes of death,cadia infactin, ft ntica ctin factin cna at bass sg.4-44

An idiat statg f angigah and angiast aft thbtic tha incasdbidit, bding ats and th nd f gnt cna at bass sg. 4

Ths tias w cndctd bf th widsad s f stnts and gctin IIb/IIIa ctantagnists, and incdd atints witht ST atin act cna snds. Th saftof percutaneous coronary intervention has improved signicantly over the last 10 years andths a tias a ik t b nsntati f cnta actic.

There have been four small (n=164-500) contemporary RCTs that have assessed the benetf a (within 24 hs) cna angigah and ascaisatin in atints with STatin act cna snds tatd with thbtic tha.6,45-47 A tias sggsta faab tc with a ctans cna intntin. In th agst std, thGrACIA- tia, th ait f atints in th intntin g ndwnt pCI (84%) cna at bass sg (2%) in caisn t 20% in th cnsati (ischaia-din)

tatnt a.45 At n-a fw , th ia nd int f dath, cadia infactin ascaisatin was dcd (abst rr 2%, ati rr 56%, 95% CI, 30 t 72%) inth inasi tatnt a. Th incatin f cna ascaisatin int th iaend point biased the apparent benet in favour of the intervention group. Although there wasan aant tnd, th aiat scnda nd int f dath -infactin was ntdcd (abst rr 5%, ati rr 4%, 95% CI, -5 t 67%). This was a it std and thapparent clinical benets need to be established in larger denitive RCTs.

A statg f ia pCI a cna angigah is assciatd with a sht dianngth f hsita sta80 because, in conjunction with clinical risk stratication, it enables theidentication of low-risk patients who can be safely discharged home early.09,

Th Task Fc f pctans Cna Intntins f th ean Scit f Cadig

cnd tin -dischag cna angigah in atints wh ha cidsccssf thbsis.92

C Patients ith ST eeation acute coronar sndroes treated ith throbotic therapshoud be considered or ear coronar angiograph and reascuarisation.

Hsitas adting a inasi intntin f atints with act cna sndsshould consider the early discharge of patients at low risk of subsequent events.


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7 EARly PHARmACOlOGICAl INTERvENTION

7 Ear pharacoogica interention

This sctin ids cndatins f th haacgica anagnt f ACS bndthe rst 12 hours and up to hospital discharge. With the exception of clopidogrel (see section

1.1), th datin f ng t tha bnd hsita dischag was nt within th it fthis gidin dnt g. See SIGN guideline 97 on risk estimation and the prevention

of cardiovascular disease.71

7.1 ANTIPlATElET THERAPy

7.. ASpIrIN

In additin t th act ffcts f asiin (see section 3.4), th ng t scnda ntatibenets of aspirin are well established in patients with coronary heart disease (absolute RR2.7%, ati rr 37%).44,48

A fooing an acute coronar sndroe a patients shoud be aintained on ong teraspirin therap.

A ds f 75-50 g asiin da is cndd in atints with act cnasnd.

7..2 ClopIDoGrel


In th Cure tia (see section 3.4.2), cidg (75 g dai) was adinistd f btwnth and 2 nths (dian nin nths) aft th act cna snd.45 Athgh thstudy was not powered to assess temporal effects, the clinical benets were predominantlyseen in the rst three months of therapy (see Table 3).46 Th w n diffncs in cinicatc bnd th nths46 athgh bding isks with cidg w cnsistnthigh.49 Cidg tha dcd th ia csit nd int f cadiasca dath,cadia infactin stk bt this was incia din b a dctin in cnt nn-fata cadia infactin. Th was n dnstab ffct n tait.

The CURE trial specically targeted recruiting centres with no routine policy for the earlys f inasi cds. Sinc this tia, tin cinica actic has d t th widsad inasi instigatin f a di-t-high isk atints (see section 5) t dcthe incidence of recurrent myocardial infarction. The benets of clopidogrel therapy are likelyt b stiatd in th dn a f intntina actic.

In th CHArISmA tia ng t cbinatin asiin and cidg tha (dian fwup 28 months) demonstrated no additional benet in comparison to aspirin alone.50 Th

appeared to be a modest benet in the subgroup of patients with clinically evident atheroscleroticdisas that incdd axiat 30% f atints with a hist f cadia infactinwithin the previous ve years. The magnitude of this apparent benet was similar to that seenin th Cure tia bnd th nths f th indx nt (see Table 3).

B In addition to ong ter aspirin, copidogre therap shoud be continued or threeonths in patients ith non-ST eeation acute coronar sndroes.


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Table 3 Clinical benets of clopidogrel therapy with time

Tiinta

(nths)

pia nd int ntats

Cidg

(%)

pacb

(%)

Abst

rr(%)

rati

rr(%)

95% CIs NNT

(inta)

NNT

(nth)

CURE tria 45,149

0- 4.3 5.5 .2 22 9 t 33% 84 84

>-3 .8 2.7 0.8 32 3 t 46% 20 240

>3-6 .7 .8 0.0 3* -27 t 27% ,725 5,74

>6-9 .3 .4 0. 7* -34 t 34% ,057 3,7

>9-2 . .3 0.2 5* -32 t 44% 533 ,600

0-2 0.3 2.6 2.4 9 42 507

NNT nth (0-2 nths) t cas a a bd was ,89

CHARISmA tria 150

0-28 6.8 7.3 0.5 7* -5 t 7% 200 5,59

0-28 6.9 7.9 .0 2 0 t 23% 00 2,800* p= not signicant Sbg f atints with cinica idnt athsctic disas

A cst ffctinss d f cidg s f a uK scti dgd that it was cstffcti t scib cidg f a 2 nth id f th initia nt.49 Th d,assd a cnstant ati isk dctin acss a ti ids which is nik t b a aidasstin.46 In additin, basin cinica nt at data a ain f 998 and ik tstat basin isk cad t cnt actic. Bnd th nths, th NNT t aida fth nt is ag (see Table 3) and nds t b iwd in th cntxt f incasd abding th 2 nths (abst isk incas %, ati isk incas 38%).

Patients treated with drug-eluting stent(s)

Three months of clopidogrel therapy may be inadequate for patients treated with drug-elutingstnts, wh th ngth f tha a nd t b xtndd t six nths aft stnt iantatin(see SIGN guideline 96 management of stable angina).151


In th CommIT/CCS tia, cidg was adinistd f t f wks (dian 6 das)aft ST atin act cna snd (see section 3.4).48

A In addition to ong ter aspirin, copidogre therap shoud be continued or up toour ees in patients ith ST eeation acute coronar sndroes.


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7.2 ANTICOAGUlANT THERAPy

A ta-anasis f rCTs in atints with cna hat disas fnd that, cad withno aspirin control, warfarin reduces subsequent mortality and myocardial infarction but isassciatd with an incas in a bding. Cad with asiin, wafain tha did

nt dc th cbind tc f dath, cadia infactin stk bt it incasda bding 2.4-fd (95% CI, .6 t 3.6; 0.0). Ths data sggst thatf ,000 atints tatd with wafain s asiin (instad f asiin an) 54 ascants wd b ntd and 6 a bds casd.

A ta-anasis f 0 tias incating 5,938 atints with act cna sndsindicates that, compared to aspirin alone, warfarin (INR target 2.0) plus aspirin reduces theanna at f cadia infactin (abst rr, .9%; ati rr, 44%), ischaic stk(abst rr, 0.4%; ati rr, 54%) and cna ascaisatin (abst rr, 2.0%;

ati rr, 20%).53 This is assciatd with an incasd isk f a bding (abst iskincas, 0.9%; ati isk incas, 50%) and n int in a tait. Th tiasxcdd atints wh had intacna stnt iantatin and th data cannt b xtaatdt atints ciing this intntin.

Th ti cbinatin f asiin, cidg and wafain has nt bn tstd. Th ha bnn tias t ca cbinatin asiin and cidg tha with cbinatin asiin andwafain tha athgh th abst dctins a siia f bth cbinatins.45,53 Thpotential additional benets of warfarin and aspirin are unlikely to outweigh the similar benetsf da antiatt tha with asiin and cidg. Whn assssing th aiatnssf wafain tha, sa facts shd b cnsidd incding bding isk, atint andphysician preference, deliverability of therapy, the absence of a mortality benet, and the higherats f cna ascaisatin in cnta actic.

7.3 STATIN THERAPy

Th ia54,55 and scnda56-59 preventative benets of statin therapy such as simvastatin40 g dai, a stabishd (see SIGN Guideline 97 on risk estimation and the preventionof cardiovascular disease).71 Th initia a rCTs xcdd atints in th a st-infarction period (rst 4-6 months) and it was unclear whether early statin therapy was safe orbenecial.

obsatina stdis ha sggstd that a statin tha (within 24 hs) is assciatdwith major benets although these studies are open to patient selection bias and are likely tooverestimate the benets of therapy.60-62 Two large RCTs have reported modest benets afterfour months of statin therapy when commenced early (within one to ve days of admission or

sts) aft an act cna snd (abst rr 2.6%, ati rr 6%) in ia ndint f dath, -infactin, sscitatd cadiac ast hsitaisatin f ischaia.63,64Meta-analysis conrms that early statin therapy is safe but apparent short term (four months)benets are limited to the prevention of recurrent ischaemia rather than mortality.65

B Patients ith an acute coronar sndroe shoud be coenced on ong ter statintherap prior to hospita discharge.

7 EARly PHARmACOlOGICAl INTERvENTION


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7.4 BETA BlOCkER AND ANTIANGINAl THERAPy

7.4. BeTA BloCKer THerApy

Acute coronary syndrome without clinical myocardial infarction

Th a n a sa nb f andisd cntd tias t assss bta bck thain atints with nstab angina (see section 3.6). mta-anasis f ths tias sggsts adctin in gssin t cadia infactin.70 The benets of short and long term betabck tha f atints with nstab angina a basd n xtaatd idnc fthe proven secondary preventative benets in patients with clinical myocardial infarction orft ntica fai (see SIGN guideline 95 on management of chronic heart failure),66 andth dctin f static angina in atints with stab angina. 67,68

C Patients ith unstabe angina or eidence o octe necrosis shoud be aintainedon ong ter beta bocer therap.

Acute coronary syndrome with clinical myocardial infarction

A ta-anasis f 25 rCTs ining 20,000 atints n ng t bta bck thaaft cadia infactin shwd a 23% ati isk dctin in tta tait and a 32%ati isk dctin in sddn dath.76

Clinical myocardial infarction with left ventricular failure

Th CAprICorN tia (n=,959) in atints with w ctin factin (


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These ndings have been conrmed in the EUROPA trial of 13,655 patients with stablecna hat disas.75 pindi 8 g dai d t a 20% ati rr in th ikihd fcadiasca dath, cadia infactin cadiac ast: 50 atints ndd t b tatdf f as t aid n nt.Th peACe tiacntasts with th Hope and europA tiasin that it did not demonstrate a benet of trandolipril in 8,290 patients with stable coronary heart

disas.76 Th nt at in this tia was ch w than th at in th tatnt as fbth th Hope and europA tias.74,75 Gin that atints with an act cna sndhave a higher event rate than patients in the EUROPA and HOPE trials, it seems justiable toextrapolate the evidence to recommend that angiotensin converting enzyme (ACE) inhibitortha shd b gin t a atints with an act cna snd iscti f thsnc f hat fai ft ntica dsfnctin.

B Patients ith unstabe angina or octe necrosis shoud be coenced on ong terangiotensin conerting enze inhibitor therap.

Acute coronary syndrome with clinical myocardial infarction or left ventricular failure

The major morbidity and mortality benets of ACE inhibitor therapy have been widely

stabishd in atints with hat fai with ft ntica dsfnctin fwing cadiainfactin.77,78

Meta-analysis of almost 100,000 patients receiving therapy with a converting enzyme inhibitorwithin 36 hours of acute myocardial infarction and continued for at least four weeks, conrmedthat ACE inhibitors reduce mortality and that most of the benets appeared to occur during therst few days, when mortality was highest. Patients at higher risk appeared to obtain a greaterabsolute benet.77

A Patients ith cinica ocardia inarction shoud be coenced on ong terangiotensin converting enzyme inhibitor therapy within the rst 36 hours.

7.6 ANGIOTENSIN RECEPTOR BlOCkERS

ACE inhibitor drugs have signicant side effects and are not well tolerated by up to a third ofatints.74,75 Angitnsin ct bcks (ArBs) a btt tatd and id a sitabatnati.79 Th vAlIANT tia80 has dnstatd nn-infiit f asatan(60 g twicdai) t cati in atints wh ha sstaind a cnt cadia infactin cicatdb hat fai ft ntica sstic dsfnctin. Nt a had-t-had caisns hacnsistnt dnstatd nn-infiit (see glossary) t ACe inhibitin (opTImAAl tia).79Tias in atints with chnic hat fai8-83 as dnstat that ArBs a a sitabatnati in atints intant f ACe inhibits (see SIGN guideline 95 on management ofchronic heart failure).66

A Patients ith cinica ocardia inarction copicated b et entricuar dsunctionor heart aiure shoud be coenced on ong ter angiotensin receptor bocer

therap i the are intoerant o angiotensin conerting enze inhibitor therap.

No trials have been identied that assess the use of a combination of an ACE inhibitor with anangitnsin ct bck in atints with act cna snd.

7.7 AlDOSTERONE RECEPTOR ANTAGONISTS

In an rCT, nn (25-50g) was cncd within 3-4 das f infactin and cntindf at ast 6 nths.84,85 Patients were required to have an ejection fraction of


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8 Treatent o hpoia and cardiogenic shoc

Th anagnt and tatnt f act ahthias and chnic hat fai a cnsiddin SIGN gidin 94 n cadiac ahthias in cna hat disas and SIGN gidin 95n anagnt f chnic hat fai.4,66

8.1 NON-INvASIvE vENTIlATION

Nn-inasi ntiatin a i sht t tcs in atints with act cadignicna da. Th ait f stdis ca cntins siti aiwa ss(CpAp) against standad xgn tha and cnsistnt t that nn-inasi ntiatin aid is sts and sht t hsigica aats, and as dcsth nd f intbatin and inasi ntiatin.86-92 There is no denitive evidence thatCpAp dcs tait athgh a sstatic iw and sa f th d data hafnd id tait in atints tatd with CpAp.93,94 A ta-anasis f 5 sa-scatias has sggstd that nn-inasi ntiatin dcs tait (abst rr 9%, ati

rr 45%) and th nd f intbatin (abst rr 8%, ati rr 57%).95 This idnc isnot denitive because of study heterogeneity and the small patient numbers recruited to eachindiida tia.

The symptomatic and physiological benets of non-invasive ventilation are predominantlysn a (n h) and a siia t standad xgn tha b six hs fwingtatnt.94

B Patients ith an acute coronar sndroe copicated b acute cardiogenic puonaroedea and hpoia shoud be considered or non-inasie positie aira pressureentiation.

8.2 INTRAvASCUlAR vOlUmE lOADING AND INOTROPIC THERAPy

Th a n ag rCTs f intic tha intaasca ading in atints withcadignic shck scnda t an act cna snd.

Th ait f atints with ntica dsfnctin and hadnaic cis fwingan acute coronary syndrome demonstrate evidence of elevated cardiac lling pressures andad, and intaasca ading is nt indicatd. In cass f ight ntica infactin cx cinica scnais ining ti athgis, sch as cncitant ssis,intravascular volume loading should be considered to ensure adequate cardiac lling pressuresand ad, atica bf institting intic tha.4

Th a sa stdis xaining th ffcts f diffnt intic agnts n sgat ass,such as lling pressures and cardiac output, but not on clinical outcomes. One meta-regressionanasis f 2 stdis ining 632 atints with s hat fai fnd that th wasn cnincing idnc f static int, and that th a b an incas intait (dds ati .50, 95% CI, 0.5 t 3.92) assciatd with intic tha.96 In thisanasis, st stdis xcdd atints with an act cna snd and andatdadequate cardiac lling pressures.

In th absnc f cinica tia idnc, cnsidd xt inin is that th s f intaascavolume loading and inotropic therapy is of benet in patients with hypotension and cardiogenicshock. This is based on clinical experience of efcacy and on surrogate haemodynamic measures.4

D In the absence o cinica eidence o oue oeroad, patients ith an acute coronarsndroe copicated b hpotension and cardiogenic shoc shoud be consideredor intraascuar oue oading.

D In the presence o cinica eidence o oue oeroad, patients ith an acute coronarsndroe copicated b hpotension and cardiogenic shoc shoud be consideredor inotropic therap.


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8 TREATmENT Of HyPOxIA AND CARDIOGENIC SHOCk

8.3 INTRA-AORTIC BAllOON COUNTERPUlSATION

Inta-atic ban cntsatin is cna fsin and dcs ft nticaaftad in hadnaica cisd atints with act cna snds.

obsatina stdis indicat that, in atints with cadignic shck, tatnt with

inta-atic ban cntsatin is assciatd with id in-hsita sia (70%ss 50%).97 Th is a high ikihd f bias as atints tatd with inta-atic bancntsatin a ik t ndg gnc cna ascaisatin (70%ss 20%), a ng and ha ss cbidit. A std f 22,663 atints sggsts thatinta-atic ban cntsatin is sccssf in atints with act cadia infactinrequiring haemodynamic support.98,99

The evidence regarding the use of intra-aortic balloon counterpulsation in high-risk patients withact cadia infactin ndging ia sc ctans cna intntinis incnsistnt.200-202 The original ndings of modest benet in the rst trial (n=182)200 wnot replicated in subsequent larger trials (n=238 and 437)20,202 which fnd n diffnc ininfact-atd at ccsin, -infactin, cadia c cinica tc. Inths tias, atints with cadignic shck w ith xcdd th tc andatd

css t inta-atic ban cntsatin.

In patients revascularised by cardiac surgery, one small RCT (n=60) of high-risk patients,incding ths with nstab angina, td that ati inta-atic bancntsatin dcd ngth f intnsi ca nit and hsita sta bt th w ndiffncs in a cinica tcs.203 obsatina stdis sggst that ati inta-atic ban cntsatin a i cinica tcs, bt th ains cncn bias in atint sctin.204,205

As cinica tia idnc is acking, th cndatins n th s f inta-atic bancountepulsation in patients with ACS are based on clinical experience of efcacy, potentiallybiasd bsatina data and cnsidd xt inin.

D Patients ith an acute coronar sndroe copicated b cardiogenic shoc,ocardia rupture (ventricular septal defect and papillary muscle rupture) or reractorischaeia shoud be considered or intra-aortic baoon counterpusation especiahen contepating eergenc coronar reascuarisation or correctie surger.

8.4 CORONARy REvASCUlARISATION

Two small RCTs suggest an early revascularisation strategy may be of benet in patients withact cadia infactin cicatd b cadignic shck d t ft ntica fai.206, 207Both trials were unable to recruit the pre-specied study population: the SMASH trial (n=55)207did not reach a denitive conclusion but reported ndings consistent with the SHOCK trial.Th SHoCK tia (n=302)208 showed a benet of early revascularisation on long term (6-12nth; 20% ati rr) bt nt a (30 da) tait atica in ng (


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8.5 CARDIAC SURGERy

Cohort studies suggest that early (within the rst 24-48 hours) corrective surgery is benecial inatints with chanica cicatins f act cadia infactin.208,20,2 Th is cncn sctin bias in that atints with ss cbidit and btt a gnsis wd b

ik t ndg ccti sg.In th absnc f andisd cinica tia idnc, th cndatin is basd n cnsiddxt inin that t sgica ai f chanica dfcts is indicatd.

D Patients ith echanica copications o acute ocardia inarction (ventricularseptal, free wall or papillary muscle rupture) shoud be considered or correctie surgerithin 24-48 hours.


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9 PATIENT SUPPORT AND INfORmATION NEEDS

9 Patient support and inoration needs

This sctin ids cndatins f schscia intntins cncd withinthe rst 72 hours/phase 1 of cardiac rehabilitation. See also SIGN guideline 57 on cardiac

habiitiatin.22

9.1 EARly PSyCHOSOCIAl INTERvENTIONS

Stdis f th ffctinss f schscia intntins st-cadia infactin (mI) shwca idnc f bias: wn, init thnic gs, d and ths with acbiditis a nd-sntd. In th fw stdis wh -bid ass f anxitand dssin w takn, ths w sd t xcd atints with cbiditis. It is ssibthat those patients who would have beneted most from psychosocial input were excluded ornd-sntd.23-26

pschgica and dcatina intntins a dis and this htgnit cats bswhen attempting to evaluate their efcacy. There is evidence that early identication of, andintntin in, ths st at isk can dc schgica distss, hsita adissinats and anxit and dssin scs at n a.27 Physicians and nurses subjectivedgnts f atint anxit a nt as accat as asnts f anxit n aidatdscas.4 Standadisd scning ts, sch as th Hsita Anxit and Dssin Sca, asf in schgica assssnt. It is atica itant t scn f dssin in tha st nt has.22

Fas bifs abt cadiac inss can cas atd ngati tins (dnia, fa, ang)affcting tatnt cianc and habiitatin.22 Intntins ccting cadiaciscnctins i atint knwdg and dc stss (bth idiat and at na fw ) f bth atint and atn fai.28-220 pschscia intntin asis fnctina tc b dcing angina sts, and hing c and tnt wk.29 Psychosocial interventions have no denitive effect on other physical outcomes ortait. Isatd intntins sch as sic and axatin,22 n sssin sking cssatinadic,222 -dischag aditas,223 st-dischag id tas224 st-dischag thncnsing,225 do not confer sustained emotional or physical benet but are thought to helpboth patients and family members knowledge and involvement as part of wider cardiachabiitatin.

B Patients ith acute coronar sndroes shoud be oered ear pschosocia assessentand indiiduaised pschosocia interention ith an ephasis on identiing andaddressing heath beies and cardiac isconceptions.

pschscia intntin fs at f th fa cadiac habiitatin ga andshd b iwd as a cntins css thght th atint ca athwa.

9.2 INfORmATION NEEDS Of PATIENTS

Ding adissin with an act cna snd atints wi want and nd infatinn a ang f tics, incding infatin abt thi inss, its cass, cs and gnsis,tatnt, ncssa ifst chang, actiit s and hw t anag th cnditin.23,226,227patints ha ankd infatin abt isk facts as bing st itant fwd b anatand hsig, dicatins and hsica actiit.226 Indiida atint nds a bth disand specic, depending on issues such as gender, ethnicity, educational reading age and socialdeprivation group. Patients receptivity to new information may be limited by physical ill health,and schgica and cgniti ( and attntin) actins. Hathca wks d ntawas cct ci th infatin nds and iitis f th indiida atint and

ths can chang thght th atint athwa f ca.23


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effcti infatin giing ins a cbinatin f gd cnicatin skis, assssntof a patients prior knowledge, readiness and ability to know more and use of effective teachingstatgis.

patints ci th hsician t b th hath ca fssina wh can bst tach thabt st ascts f thi inss st-mI whn cad with nss, dititians, haacistsand ths, athgh th hsician is nt awas th fd infatin id. extinin cnsids that th hsician ids a high cdib sc f infatin and thatintsna cntact with and ncagnt f hsicians is a ita cnnt f thpatients overall health education. Partner/family inclusion in receiving information has alsobn shwn t b itant.4,224,226 eidnc basd inatint dcatin can t ifstchangs scia in th aas f sking cssatin and xcis. 4,228

C Proision o patient inoration shoud be deterined b indiidua patient needs.Partner/ai incusion in receiing inoration shoud be considered and appropriateaudioisua aterias epoed.

D Phsicians shoud be inoed in proiding inoration to patients.

9.3 SOURCES Of fURTHER INfORmATION AND SUPPORT fOR PATIENTS AND

CARERS

Action on Soing and Heath (ASH)8 Fdick Stt, edinbgh eH2 2HBT: 03 225 4725 Fax: 03 225 4759www.ash.g.k eai: [email protected]

ASH Sctand is a nta ganisatin iding xt infatin and adic n a asctsf tbacc. pids a ang f wittn infatin incding adic n assi sking, skingand ng , sking cssatin and sking icis in th wkac.

Bood Pressure Association60 Can Tac, lndn SW7 0qST: 020 8772 4994 (Bst ti t thn: 9.30a - 5.30, mnda t Fida)Fax: 020 8772 4999www.bassc.g.k eai Infatin Sic: www.bassc.g.k/aif.ht

Th Bd pss Assciatin (BpA) hs with high bd ss t bc ind in cnting thi cnditin. pids a ang f infatin incding anagntf htnsin, dicatins, ifst changs and th isk facts.

British Cardiac Patients Association2 Statin rad, Swas, Cabidg CB4 5qjT: 0800 479 2800 Fax: 0954 202 022

www.bcpa.co.uk Email: [email protected] Bitish Cadiac patints Assciatin is a chaitab ganisatin n b nts idingst, adic and infatin t cadiac atints and thi cas.

British Heart foundation (Scotand)4 Sh pac, edinbgh eH6 6WWT: 03 555 589Hat Infatin in: 08450 70 80 70 (Aaiab: 9a-5, mnda t Fida) www.bhf.g.k eai:[email protected]

pids a thn infatin sic f ths sking infatin n hat hath isss.As ids a ang f wittn atias ffing adic and infatin t CHD atints andcas. Tics incd hsica actiit, sking and diabts.


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Chest Heart and Stroe Scotand65 Nth Cast Stt, edinbgh eH2 3lTT: 03 225 6963 Hin: 0845 0776000www.chss.g.k eai: [email protected]

Provides a 24 hour advice line offering condential, independent advice on all aspects of chest,hat and stk inss. A sis f infatin bkts, factshts and ids a aaiab ff chag t atints and cas. Th a 30 cadiac st gs in Sctand which aafliated to CHSS, patients can contact CHSS for details of their nearest local support group.

Depression Aiance Scotand3 Gsn Gadns, edinbgh eH2 5juT: 03 467 3050www.dssinaianc.g eai: [email protected]

pids infatin and st f in Sctand wh ha dssin.

Diabetes Uk0 pakwa, lndn NW 7AA

T: 020 7424 000Cain: 0845 20 2960 (Bst ti t thn: 9.30a - 5.30, mnda t Fida)www.diabts.g.k eai: [email protected]

Diabts uK is a natina ganisatin iding infatin and adic n a ascts f diabtssuch as diabetic care and diet. Provides a series of information leaets including Diabetes UKsown magazine Balance.

Heart Surger in Great Britainhtt://hatsg.hathcacissin.g.k/

This wbsit has bn dd b th Hathca Cissin and th Scit fCadithacic Sg in Gat Bitain and Iand t h hat sg atints ak infdchics abt thi tatnt. It ids atints and cas with infatin n th diffnt

operations available and the benets of having heart surgery.

Heart Uk7 Nth rad, maidnhad, Bkshi Sl6 peT: 0628 628 638 (Bst ti t thn: 9.30a - 4, mnda t Fida)Fax: 0628 628 698www.hatk.g.k eai: [email protected]

Hat uK is a natina chait aiing t ff infatin and st t ann at high iskf CHD, atica faiis with inhitd high chst. pids a ang f infatinincding anagnt f CHD b ifst, dgs and dit.

High Bood Pressure foundation

Datnt f mdica Scincs, Wstn Gna Hsitaedinbgh eH4 2XuT: 03 332 92 (Bst ti t thn: 9.30a - 5, mnda t Fida)Fax: 03 332 92www.hbf.g.k eai: [email protected]

Th High Bd pss Fndatin is a gistd chait which ais t i th assssnt,treatment and public awareness of high blood pressure. Provides a range of information leaetsincding ndstanding high bd ss and chst and cadiasca isk.

9 PATIENT SUPPORT AND INfORmATION NEEDS


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menta Heath foundation (Scotand)Merchants House30 George Square, Glasgow G2 1EGT: 04 572 025www.ntahath.g.k eai: [email protected]

Th mnta Hath Fndatin hs nt, c with and c f ntahath bs. pids a ang f factshts n nta hath isss incding anxit anddssin.

NHS Heath ScotandWdbn Hs, Canaan lan, edinbgh, eH0 4SGT: 03 536 5500 Txthn: 03 535 5503 Fax: 03 535 550www.hbs.c

eai: [email protected] (infatin n btaining Hath Sctand bicatins);[email protected] (help with general health information enquiries)

NHS Hath Sctand is a scia hath bad within NHSSctand. Th ganisatin ids

information on projects, publications, support groups and information leaets relating toCHD.

NHS 24T: 08454 24 24 24www.nhs24.c

NHS 24 is a ns-d sic f bs f th bic. It is a hin ffing hathinfatin, adic and h th thn.

Scotands Heath on the webwww.shw.sct.nhs.k

This wbsit ids bic accss t bicatins ating t CHD sch as th statg f

CHD and stk in Sctand.

Scottish Association or menta Heath (SAmH)Cba Hs, 5 Catn Ct, Gasgw, G5 9jpT: 04 568 7000 (Bst ti t thn: 2 - 4.30, mnda t Fida)www.samh.org.uk Email: [email protected]

pids atints and cas with infatin n a ascts f nta hath.


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10 ImPlEmENTATION, AUDIT AND RESEARCH

10 Ipeentation, audit and research

10.1 lOCAl ImPlEmENTATION

Intatin f natina cinica gidins is th snsibiit f ach NHS Bad and isan ssntia at f cinica gnanc. It is acknwdgd that Bad cannt int gidin idiat n bicatin, bt chaniss shd b in ac t nsthat th ca idd is iwd against th gidin cndatins and th asns fan diffncs assssd and, wh aiat, addssd. Ths discssins shd inbth cinica staff and anagnt. lca aangnts a thn b ad t int thnatina gidin in indiida hsitas, nits and actics, and t nit cianc. Thismay be done by a variety of means including patient-specic reminders, continuing educationand taining, and cinica adit.

10.2 kEy POINTS fOR AUDIT

ISD Scotlands coronary heart disease (CHD) and stroke national clinical datasets developmentgas a wking t d natina standad datasts f intatin in IT sstssting atint ca. Th fwing cinica datasts ha bn dd and a aaiabat www.datadictina.sct.nhs.k

CHD c

Act cna snds

Cadiac habiitatin

Hat fai

ecthsig.

There is a need for high quality Scottish audit of outcomes in acute coronary syndromes.

10.3 RECOmmENDATIONS fOR RESEARCH

instigatin int th cinica ffcts f cssatin f cidg tha in atints withcna hat disas f snthtic ntasacchaids in atints with ST sgnt atin ACS

comparison of effectiveness of pre-hospital thrombolysis versus primary PCI in the rst twohs fwing st nst in ST atin ACS

f a angigah in atints with ST sgnt atin ACS nt tatd bia pCI

f -dischag stss tsting in atints with ACS

f intic tha in atints with ACS

f inta-atic ban cntsatin in atints with ACS

nn-inasi siti ss ntiatin in act cadignic na daa dischag f atints fwing ACS

assssnt f atint infatin nds, incding angag f isk whn giing infatinabout the hazards and side effects of medications and interventions.


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10.4 ADDITIONAl ADvICE TO NHSSCOTlAND fROm NHS qIS AND THE SCOTTISH

mEDICINES CONSORTIUm

0.4. NHS qIS ApproveD NICe mTAS

As SIGN has iwd th cinica ffctinss and cst ffctinss idnc, th cntSIGN gidin ssds NHS qIS aa f NICe tchng aaisa gidanc N. 80Cidg in th tatnt f nn-ST-sgnt-atin.229

0.4.2 SmC ADvICe

Th Scttish mdicins Cnsti has issd adic n th s f cidg f tatntf atints with act cna snd (witht ST sgnt atin) in cbinatin withasiin.

SmC adic has as bn issd n th s f nn aft cadia infactin.

Adic n a nb f indiida dcts within th fwing dg casss; statins, angitnsinct bcks, bta bcks and dict thbin inhibits is as aaiab.

Fth dtais a aaiab f www.scttishdicins.g.k


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11 DEvElOPmENT Of THE GUIDElINE

11 Deeopent o the guideine

11.1 INTRODUCTION

SIGN is a cabati ntwk f cinicians, th hathca fssinas and atintganisatins and is at f NHS qait Int Sctand. SIGN gidins a ddb tidisciina gs f actising cinicians sing a standad thdg basd n asstatic iw f th idnc. Fth dtais abt SIGN and th gidin dntmethodology are contained in SIGN 50: A Guideline Developers Handbook, available at.sign.ac.u

11.2 THE GUIDElINE DEvElOPmENT GROUP

D Iain Finda Consultant Cardiologist, Royal Alexandra Hospital, Paisley

(Chai)

pfss Daid Nwb Professor of Cardiology and Consultant Cardiologist,(vic Chai) Royal Inrmary of Edinburgh

D Daid pd Consultant in Emergency Medicine, The James Cook(Scta) University Hospital, Middlesbroughm Gff Bg Clinical Director of Cardiac Surgery,

Western Inrmary, Glasgow

D Daid Casa Specialist Registrar, Emergency Medicine,Royal Inrmary of Edinburgh

ms mhaii Cab Physiotherapist/Cardiac Rehabilitation Coordinator,Royal Alexandra Hospital, Paisley

ms jc Caig Senior Health Economist,NHS Quality Improvement Scotland, Glasgow

ms Shi Dgas-Kgh Senior Nurse/Ward Manager, Royal Inrmary of Edinburghms Dian edga Cardiac Nurse Specialist/Lead Clinician CHD MCN,Borders General Hospital, Melrose

D rbt Finni General Practitioner, Dedridge Health Centre, Livingston

Dr Nicholas Goodeld Consultant Cardiologist, Stobhill Hospital, Glasgow

D Gaha Hiis Consultant Cardiologist, Aberdeen Royal Inrmary

D mik langan General Practitioner, Aviemore Health Centre, InvernesshireD Andw masdn Medical Director, Scottish Ambulance Service, Edinburgh

Dr Crawford McGufe Consultant in Emergency Medicine,Crosshouse Hospital, Kilmarnock

Dr Denis St J OReilly Consultant Clinical Biochemist, Glasgow Royal Inrmary

D mag osbn Consultant Clinical Psychologist,

Southern General Hospital, Glasgowm Gg Skik Lay Representative, Edinburgh

e. Ing. Gani Swa Lay Representative, Orkney

D Cab Tait Consultant Haematologist, Glasgow Royal Inrmary

D lna Thsn Programme Manager, SIGN

m Gdn Thsn Principal Pharmacist, Ninewells Hospital, Dundee

D Na un Consultant Cardiologist, Royal Inrmary of Edinburgh

ms janna Wsh Information Ofcer, SIGN

The membership of the guideline development group was conrmed following consultationwith th b ganisatins f SIGN. A bs f th gidin dnt gmade declarations of interest and further details of these are available on request from the SIGN

excti. Gidin dnt and itat iw xtis, st and faciitatin widd b th SIGN excti.


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11.3 THE STEERING GROUP

A steering group comprising the chairs of the ve SIGN CHD guidelines and other invitedxts was stabishd t s th gss f th gidin dnt. This g tga thght th dnt f th gidins.

D Kin jnnings Co-chair and Consultant Cardiologist,Aberdeen Royal Inrmary

pfss lwis ritchi Co-chair and Mackenzie Professor of General Practice,University of Aberdeen

D Aan Bgg Chair of SIGN stable angina guideline

D Nick Bn Consultant Cardiologist, Royal Inrmary of Edinburgh

ms ma Bns Director for Scotland, British Heart Foundation

m Daid Cak Chief Executive, Chest, Heart and Stroke Scotland

pfss Stat Cbb Chair of SIGN arrhythmias guideline

ms jc Caig Senior Health Economist,NHS Quality Improvement Scotland

D Iain Finda Chair of SIGN acute coronary syndromes guideline

pfss Kith Fx Professor of Cardiology, University of Edinburgh

D jas Gant Chair of SIGN prevention guideline

m jas Gant Lay representative, Balerno

D Gac lindsa Reader in Clinical Nursing Research,Glasgow Caledonian University

D ma Nain Programme Manager, SIGN

pfss Aan Stths Chair of SIGN chronic heart failure guideline

D lna Thsn Programme Manager, SIGN

11.4 SySTEmATIC lITERATURE REvIEw

Th idnc bas f this gidin was snthsisd in accdanc with SIGN thdg.A sstatic iw f th itat was caid t sing a sach statg disd b a SIGNInformation Ofcer. Databases searched include Medline, Embase, Cinahl, PsychINFO, and theCchan liba. F st sachs, th a ang cd was 999-2005. Intnt sachsw caid t n ais wbsits incding th Nw Zaand Gidins pga, NelHGidins Find, and th uS Natina Gidins Cainghs. Th mdin sin f thain sach statgis can b fnd n th SIGN wbsit, in th sctin cing sntaguideline material. The main searches were supplemented by material identied by individualbs f th dnt g.

11.5 CONSUlTATION AND PEER REvIEw

.5. NATIoNAl opeN meeTING

A natina n ting is th ain cnstati has f SIGN gidin dnt, atwhich the guideline development group presents its draft recommendations for the rst time.The national open meeting for the ve SIGN guidelines on coronary heart disease was heldn 6 Stb 2005 and was attndd b 600 sntatis f a th k sciatisant t th gidin. Th daft gidin was as aaiab n th SIGN wbsit f aiitd id at this stag t aw ths nab t attnd th ting t cntibt t thdnt f th gidin.


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.5.2 SpeCIAlIST revIeW

This gidin was as iwd in daft f b th fwing indndnt xt fs,wh w askd t cnt iai n th chnsinss and accac f inttatinf th idnc bas sting th cndatins in th gidin. SIGN is gatft a f ths xts f thi cntibtin t th gidin.

m B Gaha B Lay Representative, Edinburgh

D jhn Bikhad Medical Consultant, Northampton General Hospital

pfss Chistin Bnd Professor of Primary Care (Pharmacy),University of Aberdeen

D Nichas Bks President, British Cardiovascular Society, London

miss Gwn Cad Charge Nurse, Intensive Care, Raigmore Hospital, Inverness

pfss Sin Caw Professor of Clinical Epidemiology, University of Liverpool

D pa Cinsn Diabetologist, St Georges Medical School,University of London

D Sthn Css Consultant Physician/Cardiologist,

Raigmore Hospital, Invernessm ewn Cins Health Economist, McMaster Consultants Ltd, Glasgow

D Daid C Daidsn General Practitioner and Chair of National AdvisoryCommittee for CHD MCN Subgroup, Paisley

D mak d Bd Consultant Cardiologist, The James Cook UniversityHospital, Middlesbrough

pfss micha Gas Head of School of Medicine, Aberdeen University

ms jnn Ha Clinical Research Fellow, Dundee Health ServiceResearch Unit

pfss Si Bc Kgh Professor of Cardiac Surgery, The Heart Hospital, London

D Ci laid British Association for Immediate Care, Scotland

m Sctt mclan Cardiology Nurse Specialist, Royal Inrmary of EdinburghD jas mclnachan Consultant Cardiologist, Leeds General Inrmary

D Dth mi Director of Public Health, NHS Lanarkshire

D Sthn Nash Chair, Clinical Effectiveness Committee,British Association of Emergency Medicine

D rd Stabs Consultant Cardiologist, Cardiothoracic Centre, Liverpool

D Kan Sith Clinical Research Fellow (Cardiac Nursing),Ninewells Hospital, Dundee

ms Nica Stck Head of Clinical Psychology,Astley Ainsley Hospital, Edinburgh

D mag Thw Lecturer, Division of Physiotherapy,Glasgow Caledonian University

D Iain C Tdd Consultant in Cardiovascular Rehabilitation,Astley Ainslie Hospital, Edinburgh

pfss T Wa Director of HTA Programme, University of Liverpool

pfss Daid j What British Heart Foundation Professor of Cardiac Surgery,University of Glasgow

11 DEvElOPmENT Of THE GUIDElINE


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.5.3 SIGN eDITorIAl Group

As a nal quality control check, the guideline was reviewed by an editorial group comprisingmembers of SIGN Council to ensure that the specialist reviewers comments have been addressedadequately and that any risk of bias in the guideline development process as a whole has beeniniisd. Th ditia g f this gidin was as fws.

D Kith Bwn Member of SIGN Council

pfss Ian Cab Member of SIGN Council

pfss Hia Ca Member of SIGN Council

D Kin jnnings Co-chair SIGN CHD Steering Group and ConsultantCardiologist, Aberdeen Royal Inrmary

pfss Gdn lw Chair of SIGN; Co-Editor

ms Ann matthw Member of SIGN Council

ms Fina mcmian Member of SIGN Council

Dr Saa Qureshi SIGN Programme Director; Co-Editor

pfss lwis ritc

acs management

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