Guidelines AMI 1996.PDF Biblio 1

European Heart J ournal (1996) 17, 4363
Guidelines
Acute myocardial infarction: pre-hospital and in-hospital
management
The Task Force on the Management of Acute Myocardial Infarction of the
European Society of Cardiology
Introduction
The management of acute myocardial infarction has
undergonemajor changesinrecent years. Goodpractice
can now be based on sound evidence derived from
well-conducted clinical trials. Because of this, the
European Society of Cardiology decided that it was
opportune to provide guidelines and appointed a Task
Force to formulate these. I t must be recognised, how-
ever, that many aspects of treatment, such as theman-
agement of cardiac arrest and shock, depend upon
experience rather than upon randomized controlled
experiments. Furthermore, even when excellent clinical
trials have been undertaken, their results are open to
interpretation. Finally, treatment optionsmaybelimited
by resources; cost-eectiveness is an important issue
when deciding upon therapeutic strategies.
I n setting out these guidelines, the Task Force
has attempted to dene which treatment strategies are
based on unequivocal evidence and which are open to
genuine dierences of opinion. As always with guide-
lines, they are not prescriptive. Patients vary so much
fromoneanother that individual careisparamount and
there is still an important place for clinical judgment,
experienceand common sense.
Thenatural history of acutemyocardial
infarction
Thetruenatural historyof myocardial infarctionishard
to establish for a number of reasons: the common
occurrence of silent infarction, the frequency of acute
coronary death outside hospital and the varying
methodsusedinthediagnosisof thecondition. Commu-
nity studies
[1,2]
haveconsistently shown that theoverall
fatality of acuteheart attacksin therst month isabout
50%, andof thesedeathsabout one-half occur withinthe
rst 2h. This high mortality seems to havealtered little
over the last 30 years. By contrast with community
mortality, therehas been a profound fall in thefatality
of thosetreated in hospital. Prior to theintroduction of
coronary careunits in the1960s, thein-hospital mortal-
ityseemsto haveaveragedsome2530%
[3]
. A systematic
reviewof mortalitystudiesinthepre-thrombolyticeraof
themid-1980s showed an averagefatality of 18%
[4]
. The
overall one-monthmortalityhassincebeenreduced, but
remains high in spiteof thewidespread useof thrombo-
lytic drugs and aspirin. Thus, in the recent MONI CA
(monitoring trends and determinants in cardiovascular
disease) review of ve cities, the 28 day mortality was
1327%
[5]
. Other studies have reported one month
mortality gures of 1020%
[610]
.
I t wasfound many yearsago that certain factors
werepredictiveof death in patientsadmitted to hospital
with myocardial infarction
[3]
. Chief among these were
age, previous medical history (diabetes, previous infarc-
tion) indicators of large infarct size, including site of
infarction (anterior vs inferior), low initial blood pres-
sure, the presence of pulmonary congestion and the
extent of ischaemia as expressed by ST elevation and/or
depression on the electrocardiogram. These factors
remain operativetoday.
Aims of management
While the primary concern of physicians is to prevent
death, thosecaring for victims of myocardial infarction
aim to minimize the patients discomfort and distress
and to limit theextent of myocardial damage. Thecare
can bedivided conveniently into threephases:
(1) Emergencycarewhenthemainconsiderationsareto
relievepain and to prevent or treat cardiac arrest.
(2) Early care in which the chief considerations are to
initiate reperfusion therapy to limit infarct size
and to prevent infarct extension and expansion
and to treat immediatecomplications such as pump
failure, shock and life-threateningarrhythmias.
(3) Subsequent care in which the complications that
usually ensuelater areaddressed, and consideration
is given to preventingfurther infarction and death.
Key Words: Myocardial infarction, drug therapy, ischae-
mic heart disease.
Requests for reprints to: European Heart J ournal W. B. Saunders
2428 Oval Road, London NW1 7DX.
Correspondence: Professor D. J ulian, Flat 1, 7Netherhall Gardens,
London NW3 5RN.
0195-668X/96/010043+21 $12.00/0 1996 TheEuropean Society of Cardiology
These phases may correspond to pre-hospital care, the
coronary careunit (CCU), and thepost CCU ward, but
thereismuchoverlapandanycategorizationof thiskind
is articial.
Emergency care
I nitial diagnosis
A workingdiagnosis of myocardial infarction must rst
bemade. This is usually based on thehistory of severe
chest pain lastingfor 15min or more, not respondingto
nitroglycerine. But the pain may not be severe and, in
the elderly particularly, other presentations such as
dyspnoea, faintness or syncopearecommon. I mportant
clues are a previous history of coronary disease, and
radiation of thepain to theneck, lower jaw, or left arm.
There are no individual physical signs diagnostic of
myocardial infarction, but most patients have evidence
of autonomic nervous systemactivation (pallor, sweat-
ing) and either hypotension or a narrowpulsepressure.
Features may also include irregularities of the pulse,
bradycardia or tachycardia, a third heart sound and
basal rales. An electrocardiogramshould beobtained as
soon as possible. Even at an early stage, the ECG is
seldomnormal
[11,12]
. However, theECG isoftenequivo-
cal in the early hours and even in proven infarction it
may never show the classical features of ST elevation
and newQ waves. Repeated ECG recordings should be
obtained and, when possible, the current ECG should
be compared with previous records. ECG monitoring
should beinitiated as soon as possiblein all patients to
detect life-threatening arrhythmias. When thediagnosis
is in doubt, rapid testing of serummarkers is valuable.
I n dicult cases, echocardiography and coronary
angiography may behelpful.
Relief of pain, breathlessness and anxiety
Relief of pain is of paramount importance, not only for
humanereasons but becausethepain is associated with
sympathetic activation which causes vasoconstriction
and increases the work of the heart. I ntravenous
opioidsmorphine or, where available, diamorphine
are the analgesics most commonly used in this con-
text; intramuscular injections should be avoided. Re-
peated doses may be necessary. Side-eects include
nausea and vomiting, hypotension with bradycardia,
and respiratory depression. Antiemetics may beadmin-
istered concurrently with opioids. Thehypotension and
bradycardiawill usuallyrespondto atropine, andrespir-
atory depression to naloxone, which should always be
availableI f opioidsfail to relievethepain after repeated
administration, intravenousbeta-blockersor nitratesare
often eective. Paramedics have a limited choice of
non-addictiveopioidsthat they may use, theavailability
of whichvariesfromcountryto country. Oxygenshould
beadministeredespeciallyto thosewho arebreathlessor
who haveany features of heart failureor shock.
Anxiety is a natural responseto thepain and to
thecircumstances surrounding a heart attack. Reassur-
anceof patients and thoseclosely associated with them
is of great importance. I f the patient becomes exces-
sively disturbed, it may be appropriate to administer a
tranquilliser, but opioids are frequently all that is
required.
Cardiac arrest
n:sic iirr siiio1
Those not trained or equipped to undertake advanced
life support should start basic life support as recom-
mended by TheEuropean Resuscitation Council
[13]
.
:nv:Ncrn iirr siiio1
Trained paramedics and other health professionals
should undertakeadvanced lifesupport, as described in
theguidelinesof theEuropeanResuscitationCouncil
[14]
.
Early care
Restoring and maintaining patency of the
infarct related artery
For patientswiththeclinical presentationof myocardial
infarction and with ST elevation or bundle branch
block, early reperfusion should beattempted.
1noxnoix1ic 1r:1xrN1
1nr rvinrNcr ro nrNrri1. More than 100000 patients
havebeen randomized in trials of thrombolysis vs con-
trol, or one thrombolytic strategy compared with
another
[1520]
. For patients within 12h of the onset of
symptoms of infarction, the overall evidence for the
benet of treatment with thrombolysis is overwhelming.
For thosepresenting within 6h of symptomon-
set, and ST elevation or bundlebranch block, approxi-
mately30deathsarepreventedper 1000patientstreated,
with 20 deaths prevented per 1000 patients treated for
those between 7 and 12h. Beyond 12h there is no
convincingevidenceof benet for thegroup as a whole.
TheI SI S-2
[16]
study demonstrated theimportant
additional benet of aspirin so that there was a com-
bined reduction of approximately 50 lives per 1000
patients treated. There is consistency of benet across
pre-stratied subgroups and across the range of data
derived subgroup analyses. Overall, thelargest absolute
benet isseenamongpatientswiththehighest risk, even
though the proportional benet may be similar. Thus,
more lives are saved per 1000 higher risk patients
treated; for example, amongthoseover 65years of age,
thosewith presenting systolic pressure <100mmHg, or
thosewithanterior infarctionor moreextensiveevidence
of ischaemia.
44 Guidelines on acutemyocardial infarction
Eur Heart J , Vol. 17, J anuary 1996
Timeto treatment. Most benet is seen in thosetreated
soonest after the onset of symptoms. An analysis of
studies in which patients were randomized to pre-
hospital or in-hospital thrombolysissuggeststhat saving
an hour reduces mortality signicantly
[21]
, but the rela-
tively small sizeof thesestudies precludes precisequan-
tication of the benet. The brinolytic overview
[15]
reported a progressivedecreaseof about 16 deaths per
hour of delayper 1000patientstreated. Thiscalculation,
based on studies in which thetimeto treatment was not
randomized, must be interpreted with caution because
thetimeto presentation is not random.
Hazards of thrombolysis. Thrombolytic therapy is
associatedwithasmall but signicant excessof approxi-
mately39extrastrokesper 1000patientstreated
[15]
with
all of theexcess hazard appearing on therst day after
treatment. The early strokes are largely attributable to
cerebral haemorrhage; later strokes aremorefrequently
thrombotic or embolic. Thereis a non-signicant trend
for fewer thrombo-embolic strokesin thelater period in
those treated with thrombolysis. Part of the overall
excess of strokeis amongpatients who subsequently die
and is accounted for in the overall mortality reduction
(19excessper 1000). Thus, thereisanexcessof approxi-
mately two non-fatal strokes per 1000 patients treated.
Of these, half aremoderately or severely disabling. The
risk of stroke varies with age. There is a substantially
increased risk for thoseabove75 years of ageand also
for those with systolic hypertension. Other major non-
cerebral bleeds, requiring blood transfusion or that are
life-threatening, occur in about 7 per 1000 patients
treated. No specic subgroup is associated with an
excessof bleeds, but smaller studieshavedemonstrateda
clear association between arterial and venous punctures
and the development of major haematomas. The risks
are increased if arterial punctures are performed in the
presenceof a thrombolytic agent.
Administration of streptokinase and anistreplase
may be associated with hypotension, but severe allergic
reactions arerare. Routineadministration of hydrocorti-
soneisnot indicated. Wherehypotensionoccurs, it should
bemanagedbytemporarilyhaltingtheinfusion, lyingthe
patient at or elevatingthefeet. Occasionally atropineor
intravascular volumeexpansion may berequired.
Comparisonof thrombolytic agents. Neither theI nterna-
tional Trial
[19]
nor the Third I nternational Study of
I nfarct Survival (I SI S3)
[17]
found adierencein mortal-
itybetweentheuseof streptokinaseandtissueplasmino-
gen activator or anistreplase. Furthermore, theaddition
of subcutaneous heparin did not reducemortality com-
paredwiththeuseof no heparin. However, theGUSTO
Trial (Global Utilisation of Streptokinase and Tissue
Plasminogen Activator for occluded coronary ar-
teries)
[20]
employed an accelerated t-PA (tissue type
plasminogenactivator) regimengivenover 90minrather
than thepreviously conventional period of 3h. Acceler-
ated t-PA with concomitant aPTT (activated partial
thromboplastin time) adjusted intravenous heparin was
reported to result in 10 fewer deaths per 1000 patients
treated. The risk of stroke is higher with t-PA or
anistreplase than with streptokinase
[16,20]
. I n the
GUSTO trial, there were three per 1000 additional
strokeswithacceleratedt-PA andheparinincomparison
with streptokinase and subcutaneous heparin
[20]
, but
only one of these survived with a residual decit. I n
assessingthenet clinical benet, this must betaken into
account with thereduced death ratein thet-PA group.
The choice of reperfusion strategy will depend on an
individual assessment of risk, andalsoonfactorssuchas
availability and cost benet
[22]
.
Clinical implications. Based upon the substantial evi-
dencenowaccumulated, thereis unequivocal benet, in
terms of morbidity and mortality for prompt treatment
of acute myocardial infarction with thrombolysis and
aspirin, the two agents being additive in their eect.
Where appropriate facilities exist, with trained medical
or paramedical sta, pre-hospital thrombolysis may be
instituted provided that thepatient exhibits theclinical
features of myocardial infarction and the ECG shows
ST elevation or bundlebranch block.
Unless clearly contraindicated, patients with infarc-
tion, as diagnosed by clinical symptoms and ST
segment elevation or bundle branch block, should
receive aspirin and thrombolytic therapy with the
minimum of delay. I f the rst ECG does not show
diagnostic changes, frequent or continuous ECG
recordings should beobtained. Rapid enzymeanaly-
sis, echocardiography and, occasionally, coronary
angiography may be helpful. A realistic aim is to
initiate thrombolysis within 90min of the patient
calling for medical treatment (call to needle time).
I n patients with slowly evolving, or stuttering myo-
cardial infarction, a series of ECGs and clinical
assessments should be performed to detect evolving
infarction (with rapid cardiac enzyme analysis, if
available).
Thrombolytictherapyshouldnot begivento patients
in whom:
The potential for benet is low, e.g. if the ECG
remains normal, or demonstrates only T wave
changes as these patients are at low risk but exper-
ience all of the hazards of therapy. Trials have not
demonstrated benet in those with ST depression,
even though the risk in these patients is relatively
high; theyhavenot, however, excludedthepossibility
of somebenet;
infarction has been established for more than 12h,
unless there is evidence of ongoing ischaemia, with
theECG criteria for thrombolysis.
Contra-indications to thrombolytic therapy
Stroke
Recent major trauma/surgery/head injury (within
preceding 3 weeks)
Gastro-intestinal bleeding within thelast month
Known bleeding disorder
Dissecting aneurysm
Guidelines on acutemyocardial infarction 45
Relativecontra-indications
Transient ischaemic attack in preceding 6 months
Coumadin/warfarin therapy
Pregnancy
Non-compressiblepunctures
Traumatic resuscitation
Refractory hypertension (systolic blood pressure
>180mmHg)
Recent retinal laser treatment
Re-administration of thrombolytic agent. I f there is evi-
denceof re-occlusion or reinfarction with recurrenceof
ST elevation or bundlebranch block, further thrombo-
lytictherapyshouldbegiven, or angioplastyconsidered.
Streptokinase and anistreplase should not be re-
administered in the period between 5 days and a mini-
mumof 2yearsfollowinginitial treatment witheither of
these drugs. Antibodies to streptokinase persist for at
least 2 years, at levels which can impair its activity.
Alteplase(t-PA) andurokinasedo not result inantibody
formation.
Adjunctive antithrombotic and antiplatelet therapy. The
independent and additive benets of aspirin have been
describedabove. I t isnot clear whether aspirinworksby
enhancing thrombolysis, preventing reocclusion or by
limiting the microvascular eects of platelet activation.
I n studieson latereocclusion, aspirin wasmoreeective
in preventing recurrent clinical events than in main-
tainingpatency
[23]
. Therst doseof 150160mgshould
be chewed, and the same dosage given orally daily
thereafter.
Heparin has been extensively tested after throm-
bolysis, especially with tissue plasminogen activator.
Heparin does not improve immediate clot lysis
[24]
but coronary patency evaluated in the hours or days
followingthrombolytic therapy with tissueplasminogen
activator appears to be better with intravenous
heparin
[25,26]
. No dierence in patency was apparent in
patientstreatedwitheither subcutaneousor intravenous
heparin and streptokinase
[27]
. Prolonged intravenous
heparin administration has not been shown to prevent
reocclusion after angiographically proven successful
coronary thrombolysis, nor has intravenous heparin
followed by coumadin
[28]
. Heparin infusion after tissue
plasminogen activator therapy may be discontinued
after 2448h
[29]
. Closemonitoringof heparin therapy is
mandatory; aPTT valuesover 90sarecorrelatedwithan
unacceptable risk of cerebral bleeding. I n the I SI S-3
trial
[17]
, subcutaneous heparin (12500b.d.) did not
aect mortality when combined with aspirin and
streptokinase, duteplase, or anistreplase.
irci1:Nrois 1:NsiixiN:i cooN:x :Ncioii:s1x
(i1c:)
The role of coronary angioplasty (PTCA) during the
early hoursof myocardial infarction can bedivided into
primary angioplasty, angioplasty combined with throm-
bolytic therapy, and rescue angioplasty after failed
thrombolysis.
Methods of administration
Table1 Thrombolytic regimens for acutemyocardial infarction
I nitial treatment Heparin therapy
Specic
contra-indications
Streptokinase(SK) 15 million units Noneor Prior (>5 days)
100ml of 5%dextrose subcutaneous SK/anistreplase
or 09%salineover 3060min 12500u b.d.
Anistreplase 30 units in 35min i.v. Prior SK or
anistreplase >5 days
Known allergy to
SK/anistreplase
Alteplase(t PA) 15mg i.v. bolus i.v. for 48h*
075mg. kg
1
over 30min
then 05mg. kg
1
over 60min i.v.
Total dosagenot to
exceed 100mg.
Urokinase** 2 million units as an i.v. i.v. for 48h*
bolus or 15 million units
bolus +15 million units
over 1h
Thistabledescribesfrequentlyusedthrombolyticregimens. Alternativestrategiesandnewer agents
may confer advantages over theseregimens but thepotential advantages havenot been validated
in largescalestudies.
*Dosagedetermined by aPTT.
**Not licensed in somecountries for usein myocardial infarction.
N.B. Aspirin should begiven to all patients without contraindications.
Primary angioplasty. This is dened as PTCA without
prior or concomitant thrombolytic therapy, and is a
therapeutic option only when rapid access (<1h) to a
catheterization laboratory is possible. I t requires an
experienced team, which includes not only interven-
tional cardiologists, but also skilled supporting sta.
This means that only hospitals with an established
interventional cardiology programmecan usePTCA as
a routine treatment option for patients presenting with
thesymptoms and signs of acutemyocardial infarction.
For patients admitted to a hospital without thesefacili-
ties on site, a careful individual assessment should be
madeof thepotential benetsof PTCA inrelationto the
risks and treatment delay of transportation to thenear-
est interventional catheterization laboratory. I t should
bereservedfor thoseinwhomthebenetsof reperfusion
would be great but the risks of thrombolytic therapy
high.
Primary PTCA is eectivein securingand main-
tainingcoronary patency and avoids someof thebleed-
ing risks of thrombolysis. Randomized clinical trials
comparing primary PTCA with thrombolytic therapy
haveshown moreeectiverestoration of patency, better
ventricular function and a trend towards better clinical
outcome
[3032]
. PTCA may have a special role in the
treatment of shock.
Patients with contra-indications to thrombolytic
therapy have a higher morbidity and mortality than
thoseeligiblefor this therapy
[33]
. Primary PTCA can be
performed with success in a large majority of these
patients
[34]
, but experience is still limited and eective-
ness and safety outsidemajor centres may beless good
than they have been in trials. Large multicentre
randomized trials areneeded.
Angioplasty combined with thrombolysis. PTCA per-
formed as a matter of policy immediately after throm-
bolytic therapy, in order to enhance reperfusion or
reduce the risk of reocclusion, has proved disappoint-
ing in a number of trials
[3537]
, which have shown a
tendency to an increased risk of complications and
death. Routine PTCA after thrombolysis cannot,
therefore, berecommended.
Rescue angioplasty. Currentlytheonlyexceptiontothis
general ruleis rescuePTCA which is dened as PTCA
performedonacoronaryarterywhichremainsoccluded
despite thrombolytic therapy. Limited experience from
two randomized trials
[38,39]
suggests a trend towards
clinical benet if the infarct-related vessel can be re-
canalized at angioplasty. Although angioplasty success
rates are high, an unsolved problemis the unreliability
of non-invasivemethods in assessing patency.
cooN:x :1rx nxi:ss sicrx (c:nc)
Coronary artery bypass surgery has a very limited place
in the management of the acute phase of myocardial
infarction. I t may, however, be indicated when PTCA
has failed, when therehas been a sudden occlusion of a
coronary artery during catheterization, if PTCA is not
feasible, or in association with surgery for a ventricular
septal defect or mitral regurgitation due to papillary
muscledysfunction and rupture.
Pump failureand shock
The various haemodynamic states that can arise in
myocardial infarction aretabulated in Table2.
nr:1 r:iiir
Left ventricular failure during the acute phase of myo-
cardial infarction is associated with a poor short and
long-termprognosis
[40]
. Theclinical featuresarethoseof
breathlessness, athird heart sound and pulmonary rales
which areat rst basal but may extend throughout both
lung elds. However, pronounced pulmonary conges-
tioncanbepresent without auscultatorysigns. Repeated
auscultation of the heart and lung elds should be
practised in all patients during the early period of
myocardial infarction, together with theobservation of
other vital signs.
General measures include monitoring for ar-
rhythmias, checking for electrolyte abnormalities, and
for the diagnosis of concomitant conditions such as
valvular dysfunction or pulmonary disease. Pulmonary
congestion can be assessed by portable chest X-rays.
Echocardiography is valuable in assessing ventricular
function, and determining the mechanisms, such as
mitral regurgitation and ventricular septal defect, which
may be responsible for poor cardiac performance. I n a
fewcases, coronaryangiographymayprovideadditional
information of therapeutic value.
Table2 Spectrumof haemodynamic states in myocardial infarction
Normal Normal blood pressure, heart and respiration rates, good peripheral circulation
Hyperdynamic state Tachycardia, loud heart sounds, good peripheral circulation. ?beta-blocker therapy
Bradycardia-hypotension Warm hypotension, bradycardia, venodilatation, normal jugular venous pressure, decreased tissue
perfusion. Usuallyininferior infarction, but maybeprovokedbyopiates. Respondsto atropineor pacing
Hypovolaemia Venoconstriction, lowjugular venous pressure, poor tissueperfusion. Responds to uid infusion
Right ventricular infarction High jugular venous pressure, poor tissueperfusion or shock, bradycardia, hypotension. Seetext.
Pump failure Tachycardia, tachypnoea, small pulsepressure, poor tissueperfusion, hypoxaemia, pulmonary oedema.
Seetext.
Cardiogenic shock Very poor tissue perfusion, oliguria, severe hypotension, small pulse pressure, tachycardia, pulmonary
oedema. Seetext.
Thedegreeof failuremay becategorized accord-
ing to the Killip classication
[41]
: class 1: no rales or
thirdheart sound; class2: ralesover lessthan50%of the
lung elds or third heart sound; class 3: rales over 50%
of thelung elds; class 4: shock.
xiin :Nn xonr:1rix srvrr nr:1 r:iiir
Oxygen should beadministered early by mask or intra-
nasally, but caution is necessary in the presence of
chronic pulmonary disease.
Minor degreesof failureoftenrespondquicklyto
diuretics, such as frusemide 1040mg given slowly in-
travenously, repeated at 14 hourly intervals, if neces-
sary. I f there is no satisfactory response, intravenous
nitroglycerine or oral nitrates are indicated. The dose
should be titrated while monitoring blood pressure to
avoid hypotension. The initiation of ACE therapy
should be considered within the next 2448h in the
absenceof hypotension or renal failure.
srvrr nr:1 r:iiir
Oxygen should be administered and a loop diuretic
given as above. Unless thepatient is hypotensive, intra-
venous nitroglycerine should be given, starting with
025g. kg
1
per minute, and increasing every 5min
until afall inbloodpressureby15mmHgisobservedor
thesystolic blood pressurefalls to 90mmHg. Consider-
ation should be given to measuring the pulmonary
artery and wedgepressures, and thecardiac output with
a balloon otation catheter with a view to obtaining a
wedge pressure of less than 20mmHg and a cardiac
index in excess of 2l . min
1
.
I notropic agents may be of value if there is
hypotension. I f signs of renal hypoperfusion are
present, dopamine is recommended intravenously in a
dosageof 2550g. kg
1
. min
1
. I f pulmonary con-
gestion is dominant, dobutamine is preferred with a
initial dosage of 25g. kg
1
. min
1
. This may be
increased gradually at 510min intervals up to
10g. kg
1
. min
1
or until haemodynamic improve-
ment is achieved. ACE therapy and phosphodiesterase
inhibitors may also be considered.
Theblood gases should bechecked. Continuous
positive pressure airways pressure may be indicated if
an oxygen tension of more than 60mmHg cannot be
maintained inspite of 100% oxygen delivered at
810l . min
1
by mask and the adequate use of
bronchodilators.
Cardiogenic shock. Cardiogenic shock is dened as a
systolic blood pressure <90mmHg in association with
signsof circulatorydeteriorationexpressedasperipheral
vasoconstriction, low urinary output (<20ml . h
1
),
and mental confusion and dulling.
The diagnosis of cardiogenic shock should be
madewhenother possibilitiesfor hypotensionhavebeen
excluded such as hypovolaemia, vasovagal reactions,
electrolyte disturbance, pharmacological side-eects, or
arrhythmias. I t is usually associated with extensive left
ventricular damage, but may occur in right ventricular
infarction (vide infra). Ventricular function should be
evaluated by echocardiography, and haemodynamics
measured with a balloon otation catheter. A lling
pressure(pulmonarywedge) of at least 15mmHgshould
beaimed for with a cardiac index of >2l . min
1
. Low
dose dopamine 255g. kg
1
. min
1
may be given
to improve renal function and the additional admin-
istration of dobutamine 510g. kg
1
. min
1
should
beconsidered.
Patients in cardiogenic shock can be assumed
to be acidotic. Correction of acidosis is important as
catecholamines havelittleeect in an acid medium.
Emergency PTCA or surgery may belife-saving
and should be considered at an early stage. Supportive
treatment with a balloon pump is a valuable bridge to
such intervention.
Cardiac ruptureand mitral regurgitation
rrr v:ii ii1ir
This clinical entity is encountered in 1%3% of all
hospitalized patients with acute myocardial infarc-
tion
[42]
. I n 30%to 50%of thecases it occurs in therst
24h and in 80%and 90%in therst 2 weeks.
Acutefreewall rupture. This is characterized by cardio-
vascular collapsewithelectromechanical dissociationi.e.
continuing electrical activity with a loss of cardiac
output andpulse. I t isusuallyfatal withinafewminutes,
and does not respond to standard cardiopulmonary
resuscitation measures. Only very rarely is theretimeto
bring thepatient to surgery.
Subacutefreewall rupture. I n about 25%of cases, small
quantities of blood reach the pericardial cavity and
producea progressivehaemodynamic burden
[43,44]
. The
clinical picturemay simulatereinfarction becauseof the
recurrenceof pain and re-elevation of ST segments, but
morefrequently thereis sudden haemodynamic deterio-
ration with transient or sustained hypotension. The
classical signs of cardiac tamponade occur and can be
conrmed by echocardiography. I mmediate surgery
shouldbeconsideredirrespectiveof theclinical statusof
the patient, as an acute episode follows in most cases.
Surgical repair is performed by thesutureless technique
described by Padro et al.
[45]
, which does not require
cardiopulmonary bypass.
vrN1icii: sri1:i nrrrc1
Ventricular septal defect (VSD) appearsearlyafter myo-
cardial infarction, withanincidenceof about 12%of all
infarctions
[42]
. Without surgery, the mortality is 54%
within the rst week, and 92% within the rst year
[46]
.
Thediagnosis, rst suspected becauseof theoccurrence
of a loud systolic murmur accompanied by severeclini-
cal deterioration, isbest conrmedbyechocardiography
and/or by detecting a oxygen step-up in the right
ventricle. Themurmur may, however, besoft or absent.
Pharmacological treatment with vasodilators, such as
intravenous nitroglycerine, may producesomeimprove-
ment if there is no cardiogenic shock, but intra-aortic
balloon counterpulsation is the most eective method
of providing circulatory support while preparing for
surgery. Operation oers theonly chanceof survival in
largepost-infarction VSDs with cardiogenic shock
[47,48]
.
Theprimary goal of early surgery is thereliableclosure
of the defect using the technique of patch augmenta-
tion
[49]
. Pre-operative coronary angiography should be
performed provided it doesnot compromisethehaemo-
dynamic status or causeunduedelay to surgery. Bypass
grafts are inserted as necessary. Predictors of poor
postoperativeoutcomearecardiogenic shock, posterior
location, right ventricular dysfunction, age, and long
delay between septal ruptureand surgery
[47,48]
. Hospital
mortalityafter surgeryisestimatedto bebetween25and
60%
[50,51]
, and 95%of survivors areNYHA I or I I
[50]
.
xi1:i rcici1:1ioN
Most cases of mitral regurgitation after myocardial
infarction are mild and the reux is transitory. I n a
minorityof patients, however, major acuteregurgitation
is a catastrophic complication that is amendable to
aggressive therapy if promptly diagnosed and treated
surgically. Theincidenceof moderately severeor severe
mitral regurgitation is about 4% and the mortality
without surgery high at about 24%
[52]
. I t is usually
associated with signicant narrowing of both the right
and left circumex coronary arterieswith posteromedial
papillary muscleinvolvement.
Cardiogenic shock and pulmonary oedema with
severe mitral regurgitation require emergency surgery.
I ntra-aortic balloon pump placement may be helpful
during preparation
[50]
. Coronary angiography is per-
formed if thepatients condition permits. I n congestive
heart failure, primary catheterization and reperfusion of
theinfarct-related artery by thrombolysis or PTCA can
beattempted.
Valve replacement is the procedure of choice in
papillary muscle dysfunction and rupture, although re-
pair canbeattemptedinselectedcases
[53]
., Revasculariz-
ation is indicated for major vessel obstruction.
Arrhythmias and conduction disturbances
Arrhythmiasandconduction disturbancesareextremely
common duringtheearly hoursafter myocardial infarc-
tion. I n somecases, such as ventricular tachycardia and
ventricular brillation, they are life threatening and
require immediate correction. Often, however, arrhyth-
mias are not in themselves hazardous, but are a mani-
festation of a serious underlying disorder, such as
continuing ischaemia, vagal overactivity, or electrolyte
disturbance, that requires attention. The necessity for
treatment and its urgency depend mainly upon the
haemodynamic consequences of therhythmdisorder.
vrN1icii: :nx1nxi:s
Ventricular ectopic rhythms. Ventricular ectopic beats
are almost universal on the rst day, and complex
arrhythmias (multiform complexes, short runs, or the
R-on-T phenomenon) arecommon. Their valueas pre-
dictors of ventricular brillation is questionable; either
ventricular brillation follows so quickly that no pro-
phylactic measures can betaken or no serious arrhyth-
mia ensues.
Ventricular tachycardia. Short runsof ventricular tachy-
cardia may bewell tolerated and not requiretreatment,
but more prolonged episodes may cause hypotension
and heart failure. Lignocaineis thedrug of rst choice,
but several other agents are also eective. An initial
loadingdosageof 1mg. kg
1
of intravenouslignocaine
isusually given, with half thisdosebeingrepeated every
810min to a maximum of 4mg. kg
1
. This may be
followed by an intravenous infusion to prevent recur-
rences. Countershock is indicated if haemodynamically
signicant ventricular tachycardia persists.
I t is important to dierentiate true ventricular
tachycardia from accelerated idioventricular rhythm,
usually aharmlessconsequenceof reperfusion, in which
theventricular rateis less than 120 beats. min
1
.
Ventricular brillation. When a debrillator is available,
immediate debrillation should be performed. I f it is
not, aprecordial thump isworth trying. Therecommen-
dations of the European Resuscitation Council should
befollowed (Fig. 1)
[14]
.
sii:vrN1icii: :nx1nxi:s
Atrial brillation complicates some1520%of myocar-
dial infarctions, and is frequently associated with severe
left ventricular damage and heart failure. I t is usually
self-limited. Episodes may last from minutes to hours,
and are often repetitive. I n many cases, the ventricular
rateis not fast, thearrhythmia is well tolerated, and no
treatment is required. I n other instances, the fast rate
contributes to heart failure and prompt treatment is
needed. Digoxin is eectivein slowingtheratein many
cases, but amiodaronemay bemoreecaciousin termi-
nating the arrhythmia
[54]
. Countershock may also be
used, but should only be employed if mandatory as
recurrences areso common.
Other supraventricular tachycardiasarerare, but
usually self-limited. They may respond to carotid sinus
pressure. Beta-blockers may be eective, if not contra-
indicated, but verapamil is not recommended. Counter-
shock should be employed if the arrhythmia is poorly
tolerated.
siNis n:nxc:ni: :Nn nr:1 niocx
Sinusbradycardiaiscommonintherst hour, especially
in inferior infarction. I n somecases, opioidsarerespon-
sible. I t may be accompanied by quite severe hypoten-
sion, in which case it should be treated by intravenous
atropine, startingwith a dosageof 0305mg, repeated
up to a total of 1520mg. Later in the course of
myocardial infarction, it isusuallyafavourablesignand
requires no treatment. Occasionally it may, however, be
associatedwithhypotension. I f it thenfailstorespondto
atropine, temporary pacing may beadvisable.
First degreeheart block needs no treatment.
Type I second degree (Wenckebach) AV (atrio-
ventricular) block is usually associated with inferior
infarction and seldom causes adverse haemodynamic
eects. Should it do so, however, atropine should be
given rst; if this fails, pacing should beinstituted.
Type I I second degree (Mobitz) and complete
AV block are indications for the insertion of a pacing
electrode. Pacing should be undertaken if a slow heart
rate appears to be a cause of hypotension or heart
failure. I f the haemodynamic disturbance is severe,
consideration should begiven to AV sequential pacing.
Asystolemay followAV block, bi- or trifascicu-
lar block, or electrical countershock. I f a pacing elec-
trodeisinplace, pacingshouldbeattempted. Otherwise,
chest compression and ventilation should be initiated,
and external pacing started.
A transvenous pacing electrode should be in-
serted, as discussed above, in thepresenceof advanced
atrio-ventricular block, and considered if bifascicular or
trifascicular block develop. Many cardiologists prefer
the subclavian route but this should be avoided in the
presenceof thrombolysisor anticoagulation. Alternative
sites should bechosen in this situation.
Prophylactic therapies in theacutephase
Aspirin. Convincing evidence of the eectiveness of
aspirinwasdemonstratedbytheI SI S-2trial
[16]
, inwhich
it was shown that the benets of aspirin and strepto-
kinase were additive. I n this trial of more than 17000
patients, the rst 160mg tablet of aspirin was chewed;
subsequently one 160mg tablet was swallowed daily.
The mortality in those receiving aspirin in I SI S-2 was
94% compared with that of 118% in those receiving
placebo. I t waseectivebothinthosewho didandthose
who did not receivethrombolysis. I n an overviewof all
theaspirin trials
[55]
, a 29%odds reduction in death was
observed, with a vascular mortality of 117% in the
control population and 93% in those receiving
aspirinrepresenting 24 lives saved per 1000 patients
treated. There were also fewer non-fatal strokes and
non-fatal myocardial reinfarctions in thetreated group.
There are few contra-indications to the use of
aspirin, but it shouldnot begivento thosewithaknown
hypersensitivity, bleeding peptic ulcer, blood dyscrasia,
or severe hepatic disease. Aspirin may occasionally
trigger bronchospasm in asthmatics. Unlike the situ-
ation with thrombolysis, thereis no clear evidenceof a
relationship between eectivenessand thetimefromthe
onset of symptoms. Nonetheless, aspirinshouldbegiven
to all patients with an acute coronary syndrome as
soon as possibleafter thediagnosis is deemed probable.
This represents about 8595% of those sustaining a
myocardial infarction.
Anti-arrhythmic drugs. Although it has been demon-
strated that lignocaine can reduce the incidence of
ventricular brillation in theacutephaseof myocardial
infarction
[56,57]
, this drug signicantly increases therisk
of asystole
[57]
. A meta-analysis of 14 trials showed a
non-signiciantly higher mortality in lignocaine treated
patientsthan in controls
[58]
. Theprophylacticuseof this
drug does not appear justied.
Beta-blockers. Many trialsof intravenousbeta-blockade
havebeen undertaken in theacutephaseof myocardial
infarction, becauseof their potential to limit infarct size,
reducetheincidenceof fatal arrhythmias, and to relieve
pain. The16000 patient I SI S-1
[59]
study of intravenous
atenolol revealed a signicant (2P<005) 15%reduction
in mortality at 7days. The7day mortality of only 46%
in theplacebo armindicates that only a lowrisk group
were recruited. Pooling of 28 trials
[60]
of intravenous
beta-blockaderevealsanabsolutereductionof mortality
at 7days from43%to 37%or six lives saved per 1000
treated in this low risk group. I t is unknown whether
thesebenets can beextended to thoseat higher risk.
These studies were conducted prior to the
thrombolytic era. The only large trial of intravenous
Precordi al thump
DC shock 200 J 1
DC shock 200 J 2
DC shock 360 J 3
I f not al ready:
i ntubate
i .v. access
Adrenal i ne 1 mg i .v.
10 CPR sequences
of 5:1 compressi on/venti l ati on
DC shock 360 J 4
DC shock 360 J 5
DC shock 360 J 6
VF
or PULSELESS VT
The i nterval between shocks 3 and 4 shoul d not be >2 mi n.
Adrenal i ne gi ven duri ng l oop approx every 23 mi n.
Conti nue l oops for as l ong as defi bri l l ati on i s i ndi cated.
After 3 l oops consi der:
an al kal i si ng agent
an anti arrhythmi c agent.
Figure 1 European Resuscitation Council guidelines on
thetreatment of ventricular brillation
beta-blockade undertaken since the widespread use of
thrombolysiswasasubstudy of theTI MI -I I B
[61]
but the
number of events was too small to allowconclusions to
bedrawn. As discussed below, theuseof beta-blockade
in the acute phase of infarction in many countries is
extremelylow. Thereisagoodcasefor thegreater useof
an intravenous beta-blocker when there is tachycardia
(intheabsenceof heart failure), relativehypertension, or
pain unresponsiveto opioids. I t may beprudent to test
the patients response to this form of therapy by rst
using a short-acting preparation.
Nitrates. A meta-analysis of 10 trials of early intra-
venous nitrate therapy conducted in 2041 patients
showed a mortality reduction of about one-third
[62]
.
Each of thetrialswassmall and with only 329deathsin
all, the results although highly signicant had wide
condencelimits. TheGI SSI -3
[63]
trial also tested intra-
venousnitratetherapy(followedbytransdermal nitrate)
in 19394 patients; no signicant reduction in mortality
was observed, but this nding must be viewed with
caution as 44% of the patients assigned to the control
group received intravenous nitrate. The I SI S-4 trial
[64]
,
in which oral mononitratewasadministeredacutely and
continued for onemonth, also failed to showa benet.
Furthermore, abenet wasnot seenintheESPRI M trial
of molsidomine
[65]
, a nitric oxide donor. Again, how-
ever, bothinI SI S-4andESPRI M, thefrequent earlyuse
of intravenous nitrates in the control group makes
deductions dicult. The routine use of nitrates in the
initial phaseof myocardial infarction has, therefore, not
convincingly been shown to beof value.
Calciumantagonists. A meta-analysis of trials involving
calciumantagonistsearly in thecourseof acutemyocar-
dial infarction showed a non-signicant adverse
trend
[66]
. Thereis no casefor using calciumantagonists
for prophylactic purposes in the acute phase of myo-
cardial infarction.
Angiotensin converting enzyme (ACE) inhibitors. I t is
now well established that ACE inhibitors should be
started in thelater hospital period in patients who have
an impaired ejection fraction or who have experienced
heart failurein theearly phase(seelater). Recently, the
GI SSI -3
[63]
, I SI S-4
[64]
and ChineseStudy
[67]
haveshown
that ACE inhibitors started on the rst day reduce
mortality in the succeeding 46 weeks by a small but
signicant amount. TheCONSENSUSI I trial
[68]
, how-
ever, failedto showabenet. Thismayhavebeendueto
the play of chance, or the fact that treatment was
initiated with an intravenous formulation. A systematic
overview of trials of ACE inhibitions early in acute
myocardial infarction indicated that this therapy would
result in 46 fewer deaths per 1000 patients treated
[64]
.
Although it is recognised that subgroup analysis is
hazardous, it wouldseemprobablethat thistherapywas
especially valuable in certain high risk groups, such as
those presenting with heart failure or with previous
infarction. Thebenetsof ACE inhibitioninmyocardial
infarction patients appear to be a class eect. The
regimens used in thetrials of ACE inhibitors areshown
in Table3.
As discussed later, opinions dier as to whether
to administer ACE inhibitor therapy to all patients (for
whomit is not contraindicated) on therst day or start
it in a more selected group of patients shortly there-
after
[69,70,71]
. I n the view of the Task Force, there are
valid arguments on both sides. Certainly, there should
bealowthresholdfor usingtheseagentsearlyif features
Table3 Dosages in ACE inhibitor trials
I nitial dosage Target dosage
CONSENSUS I I
[68]
1mg i.v. enalaprilat over 2h up to 20mg daily
enalapril followed by 25mg b.d.
increasing to 20mg, if tolerated
GI SSI -3
[63]
5mg initially up to 10mg daily
lisinopril
I SI S-4
[64]
625mg initially, 125mg in 2h, up to 50mg b.d.
captopril 25mg at 1012h
CHI NESE
[67]
625mg initially, up to 125mg t.d.
captopril 125mg 2h later if tolerated
SMI LE
[117]
75mg initially, up to 30mg b.d.
zofenopril repeated after 12h and
repeatedly doubled if tolerated
AI RE
[116]
25mg b.d. increased up to 5mg b.d.
ramipril to 5mg b.d. if tolerated
SAVE
[115]
test of 625mg, increased if up to 50mg t.d.
captopril tolerated to 25mg t.d.
TRACE
[118]
test of 05mg up to 4mg daily
trandolapril
of heart failuredo not respond quickly to conventional
measures.
Magnesium. A meta-analysis of trials of magnesium
therapy in acute myocardial infarction suggested a sig-
nicant benet
[72,73]
, but the later large I SI S-4 trial
[64]
did not support this. Although it has been argued that
the magnesium regimen in I SI S-4 was not optimal
[74]
,
there does not at present seem enough evidence to
recommend its routineuse.
Management of specic types of infarction
sisirc1rn xxoc:ni:i iNr:c1ioN vi1noi1 s1
rirv:1ioN o niNnir n:Ncn niocx
Many patients present with symptoms suggestive of
recent myocardial infarction, but without the ECG
features of ST elevation or bundle branch block which
would qualify themfor thrombolytic therapy. Somewill
progresstoQwaveinfarction, andotherstonon-Qwave
infarction; many will eventually beclassied asunstable
angina. A sizeableproportionwill beregardedashaving
stable angina and yet others will have a non-cardiac
diagnosis. Themanagement will dependonthedegreeof
suspicion of infarction. Thus, if there has been a pre-
vious infarction, or there are denite ST and T wave
changes short of ST elevation or new Q waves, or if
the symptoms or physical signs suggest that this is an
acutecoronary syndrome, thepatient should beclosely
observed with repeated ECG recordings and enzyme
tests. I n the absence of contra-indications, all such
patients should be given aspirin and considered for
heparin therapy and beta-blockade. Continuing chest
pain should be treated with nitrates and, if severe,
opioids. I f pain persists or recurs in spite of this treat-
ment, cor-onary angiography should beconsidered with
a viewto early intervention by angioplasty or surgery.
NoN-q v:vr xxoc:ni:i iNr:c1ioN
A non-Q wave myocardial infarction is one with the
characteristic clinical features and enzyme abnormali-
ties, but without new Q waves in the ECG. The
incidence is reported as being from 20 to 40% of all
infarctions but may beincreasing in relation to Q wave
infarction
[75]
. Thisvariability could berelated to theuse
of reperfusion therapy and/or moresensitivetechniques
for enzymedetection
[75,76]
.
Hospital mortality is signicantly less than in Q
wave infarction. Conversely in the long term, higher
mortality and event rates arereported in non-Q infarcts
after hospital discharge, so that themortality is similar
at 35years
[75,76]
. A higher incidenceof residual ischae-
mia is a constant nding (50%90% more than in Q
waveinfarction)
[76,77]
.
Risk markers. I nitial and persistent ST depression, com-
plications present in the acute phase, post-infarction
angina with ECG changes, early reinfarction, and the
inability to performa stress test, areall associated with
a higher mortality
[78,79]
. A symptom-limited exercise
stress test should be performed as in Q wave infarc-
tion, but thalliumscintigraphy and stress echocardiog-
raphy may be more sensitive and specic in detecting,
quantifying, and localizing ischaemic myocardium in
asymptomatic non-Q wavepostinfarction patients
[75]
.
Management. Whether evolving infarction results in Q
waves or ends as a non-Q waveinfarction is established
only after a few days follow-up. Thus, at the time of
admission to CCU no distinction can bemadebetween
these two groups of patients. Thrombolytic therapy is
particularly indicatedin patientswith ST segment eleva-
tion dueto extensiveischaemiaresultingfromocclusion
of a coronary artery
[16]
. The I SI S-2
[16]
and GI SSI
[18]
trialsdemonstratednodecreaseinmortalitywiththrom-
bolysis in patients with myocardial infarction and ST
depression on admission; these patients have probably
not had a complete coronary occlusion. Recent data
from TI MI I I I B, conrmed no signicant benet in
mortality, or reinfarction ratewith t-PA in non-Q wave
infarction
[80]
.
Antithrombotic therapy with oral aspirin and
intravenousheparin reducestheincidenceof subsequent
reinfarction or death
[81,82]
. Thrombolysis may prevent
thedevelopment of Q waves in thosewho present with
ST elevation.
Two small trials have suggested that diltiazem
reduces early but not the total incidence of reinfarc-
tion;
[83,84]
further evidence is needed before this agent
can be recommended for this purpose. There are no
specic studies designed to demonstrate the eect of
betablockers in non-Q AMI . Retrospective analysis
of the non-Q subgroup in general trials has been
inconclusive
[85]
.
An early invasive strategysystematic cor-
onary angiography and revascularization <48hwas
explored in TI MI I I I B
[80]
. No dierence in death, re-
infarction or positiveexercisetest at 6weeks was found
comparing this with an early conservativestrategy.
Revascularization should beconsidered if spon-
taneous or readily provoked ischaemia can bedetected,
provided thecoronary anatomy is appropriatefor this.
At present, there are no data from controlled clinical
trialsthat comparethelong-termeectsof medical treat-
ment, PTCA or surgery in patients with non-Q wave
infarction and residual ischaemia. PTCA of the culprit
lesionissafeandeectivefor relievinganginaandrecur-
rent ischaemia
[86]
but many patients after non-Q wave
infarction arefound to havemultipleor severestenoses
for which surgical treatment is moresuitable
[87]
.
icn1 vrN1icii: iNr:c1ioN
Therecognitionof right ventricular infarctionisimport-
ant becauseit may manifest itself as cardiogenic shock,
but theappropriatetreatment strategy is quitedierent
from that for shock due to severe left ventricular
dysfunction.
Right ventricular infarction may besuspected by
thespecic, but insensitive, clinical triadof hypotension,
clear lungelds, and raised jugular venous pressurein a
patient with inferior myocardial infarction
[88]
. ST elev-
ation in V
4
R is very suggestiveof thediagnosis
[89]
; this
leadshouldcertainly berecordedinall casesof shock, if
not doneasaroutine. Q wavesand ST elevation in V
13
also suggest thediagnosis.
When right ventricular infarction can be impli-
cated in hypotension or shock, it is important to
maintain right ventricular preload. I t is desirable to
avoid (if possible) vasodilator drugssuch astheopioids,
nitrates, diuretics and ACE inhibitors. I ntravenous
loading is eectivein many cases; initially, it should be
administered rapidly, for exampleat a rateof 200ml in
10min. I t mayrequire121normal salineintherst few
hours, and 200ml . h
1
thereafter. Careful haemo-
dynamic monitoring should be instituted during intra-
venousuidloading. I f cardiacoutput doesnot improve
on this regimen, dobutamineshould begiven.
Right ventricular infarction is often complicated
by atrial brillation. This should becorrected promptly
as the atrial contribution to right ventricular lling is
important in thiscontext. Likewise, if heart block devel-
ops, dual chamber pacing should beundertaken. There
has been somequestion of theeectiveness of thrombo-
lytic therapy in right ventricular infarction, but it
certainly seems appropriate in the hypotensive patient.
Alternatively, direct angioplasty may result in rapid
haemodynamic improvement
[90]
.
xxoc:ni:i iNr:c1ioN iN ni:nr1ic i:1irN1s
Diabetic patients who sustain a myocardial infarction
havea high mortality. Strict attention to thecontrol of
hyperglycaemia with insulin has been claimed to reduce
long-term mortality
[91]
. Diabetes is not a contra-
indication to thrombolysis, even in the presence of
retinopathy.
Management of the later in-hospital
course
crNr:i x:N:crxrN1
Most patientsshould rest in bed for therst 1224h, by
which timeit will beapparent whether theinfarction is
going to be complicated. I n uncomplicated cases, the
patient cansit out of bedlateontherst day, beallowed
to use a commode and undertake self-care and self-
feeding. Ambulation can start the next day and such
patients can be walking up to 200m on the at, and
walking up stairs within a few days. Those who have
experienced heart failure, shock or serious arrhythmias
should bekept in bed longer, and their physical activity
increased slowly, dependent upon their symptoms and
theextent of myocardial damage.
nrri vriN 1noxnosis :Nn iiixoN:x rxnoiisx
Thesecomplicationsarenowrelatively uncommon after
infarction, except in patients kept in bed because of
heart failure. I n such patients, they can beprevented by
heparin. When they occur they should be treated with
heparin, followed by oral anticoagulation for 36
months.
iN1:vrN1icii: 1noxnis :Nn sxs1rxic rxnoii
Echocardiography will reveal intraventricular thrombi
inmanycases, especiallylargeanterior infarctions. I f the
thrombi are mobile or protuberant, they should be
treated initially with heparin and subsequently with oral
anticoagulants for 36 months.
iric:ni1is
Acute pericarditis may complicate myocardial infarc-
tion, givingriseto chest painthat maybemisinterpreted
as recurrent infarction or angina. Thepain is, however,
distinguished by its sharp nature, and its relationship to
posture and respiration. The diagnosis may be con-
rmedbyapericardial rub. I f thepainistroublesome, it
may betreated by high doseoral or intravenousaspirin,
non-steroidal anti-inammatory agents, or steroids. A
haemorrhagic eusion with tamponade is uncommon
and is particularly associated with anticoagulant
treatment. I t can usually be recognised echocardio-
graphically. Treatment is by pericardiocentesis if
haemodynamic embarrassment occurs.
i:1r vrN1icii: :nx1nxi:s
Ventricular tachycardia and ventricular brillation oc-
curring on the rst day carry only a small adverse
prognosis, but when thesearrhythmias develop later in
the course they are liable to recur and are associated
withahighrisk of death. Thisispartlyduetotheir usual
association with severe myocardial damage; a careful
assessment of coronary anatomy and ventricular func-
tion should always beundertaken. I f it is probablethat
the arrhythmia is induced by ischaemia, revasculariz-
ation by angioplasty or surgery should beconsidered. I f
this is unlikely, a variety of therapeutic approaches are
available which are, as yet, inadequately researched.
Theseincludetheuseof beta-blockers, amiodarone, and
electrophysiologically guided anti-arrhythmic therapy.
I n some cases, an implantable converter debrillator is
indicated.
ios1-iNr:c1ioN :NciN: :Nn iscn:rxi:
Mild angina occurring in those with a previous history
of the condition may respond satisfactorily to the
usual medical treatment, but new, especiallyrest, angina
in the early post-infarction phase requires further
investigation.
The routine use of elective PTCA following
thrombolytic therapy has been compared with a con-
servativeapproach in several randomized trials
[9294]
. I t
can be concluded that routine PTCA in the absence of
spontaneous or provocableischaemia does not improve
left ventricular function or survival. I n treating angina
or recurrent ischaemia, however, whether due to re-
occlusion or to a residual stenosis, PTCA has a denite
role. I t may also be of value in managing arrhythmias
associated with persistent ischaemia. Although analyses
fromseveral trialshaveidentiedapatent infarct-related
vessel as a marker for good long-termoutcome, it has
not been shown that late PTCA with the sole aim of
restoring patency inuences lateevents.
Coronaryarterybypasssurgerymaybeindicated
if symptoms are not controlled by other means or if
coronary angiography demonstrates lesions, such as
left main stenosis or three vessel disease with poor
left ventricular function, for which surgery improves
prognosis
[95]
.
Risk assessment, rehabilitation, and
secondary prevention
isx :ssrssxrN1
Risk assessment prior to dischargehas theobjectives of
estimating prognosis, deciding which further investiga-
tions are required, and assisting in devising the best
individual therapeutic strategy for patients who survive
the acute event. This assessment depends partly on
clinical data, including age, pre-existing risk factors,
previous infarction, diabetes, haemodynamic status and
arrhythmias during the acute phase, and partly on
functional investigations and imaging.
ciiNic:i isx s1:1iric:1ioN
Clinical risk stratication can beused to dividepatients
into high, intermediate and low risk categories. This
clinical stratication is important because the yield of
investigationsdependscriticallyonthepre-test probabil-
ity of a positiveresult.
Evaluationof highrisk cases. Patients at thehighest risk
arethosewith persistent heart failure, severely impaired
left ventricular function, persistent or early appearance
of angina at rest or on minimal exertion, or recurrent
arrhythmias, and those unable to perform a pre-
discharge exercise test
[9699]
. Such patients tend to be
older, to have multiple risk factors, and to have had
previous infarcts. Left ventricular function should be
evaluated by echocardiography and/or scintigraphy.
Coronary angiography providesindependent prognostic
information and acts as a guide to further treatment
such as revascularization
[100]
.
Evaluationof mediumrisk cases. Casesthat areclinically
at medium risk are likely to be older than 55 years,
have had transient heart failure, have had a previous
infarction or have risk factors such as hypertension or
diabetes. These patients should be assessed for left
ventricular dysfunction and for residual ischaemia. The
latter may be assessed by exercise electrocardiography,
myocardial perfusion scanning or stress echocardiogra-
phy, depending on local availability. Patients with
impaired left ventricular function and/or inducible is-
chaemia should be considered for angiography. This
approach to stratication is shown as a ow chart in
Figure2.
Evaluation of low risk patients. Low risk patients are
younger (age<55years), havehad no previous infarcts,
and have had an event-free clinical course. Exercise
electrocardiography isthemost useful rst investigation
in this group. This may taketheformof a submaximal
test before discharge or a symptom-limited test on
treadmill or cycle ergometer at 38 weeks post-
infarction, or both. Variablesreectingresidual exercise-
induced myocardial ischaemiado not seemto beclosely
related to mortality.
Patients who fail to achievea satisfactory work-
load on exercise testing, or who develop angina or
electrocardiographic signs of ischaemia, or severedysp-
noeashould beconsidered for further tests. By contrast,
MI
CLI NI CAL RI SK ASSESSMENT
Hi gh ri sk: persi sti ng or
reccurrent i schaemi a at
rest or on mi ni mal
exerti on; or persi sti ng
heart fai l ure + poor LV
I s i nterventi on a real i sti c
opti on?
Yes
Coronary angi ogram
I ntermedi ate ri sk:
previ ous MI , heart fai l ure
mul ti pl e ri sk factors
Exerci se ECG and measure
LV functi on
Poor exerci se/
i mpai red LV
Low ri sk: young age
smal l i nfarct
no heart fai l ure
Exerci se ECG
Poor or
i nadequate
exerci se
Good exerci se
tol erance:
Good exerci se
tol erance and
LV functi on
Reassure
ri sk factor
reducti on
Figure2 Strategiesfor assessment of risk.
the negative predictive accuracy for patients who can
completestageI I I of thestandard Bruceprotocol or its
equivalent without chest painor ischaemicECG changes
is high
[101]
. I n addition, the eect on patient morale is
positive, and the information is helpful in planning
rehabilitation. There is no necessity to discontinue
medication beforeexercisetesting.
:ssrssxrN1 ro iscn:rxi:
Patients who fail to achievea satisfactory workload on
exercisetesting, or who developanginaor electrocardio-
graphicsignsof ischaemiaat amediumworkloadshould
beconsidered for further evaluation in order to localize
thesiteandquantify theamount of myocardiumat risk,
as well as the extent of potentially viable myocardium.
Thechoicebetween stress echocardiography and radio-
isotopeperfusion scanningdependsupon theexperience
of the individual centre and the resources available.
I n competent hands, both these techniques are more
sensitiveand specic than exerciseelectrocardiography.
rv:ii:1ioN or iixi riNc1ioN
Evaluation of cardiac impairment by echocardiography
or radionuclide ventriculography is helpful in assessing
patients with no evidenceof cardiac failure, particularly
if performed under conditions of stress, though left
ventricular function is likely to bewell preserved in low
risk cases.
rv:ii:1ioN ro :nx1nxic isx
Holter monitoring and electrophysiological studies are
of value in the assessment of patients considered to be
at high risk of arrhythmias. Heart rate variability, QT
dispersion, baroreex sensitivity, and late potentials
have all been found to be of prognostic value after
myocardial infarction, but further clinical experience is
neededto establishwhether theyaddsubstantiallyto the
moreconventional prognostic tests.
rv:ii:1ioN or xr1:noiic isx x:xrs
I t is also important to measure metabolic risk markers
such as total, LDL and HDL cholesterol, fasting tri-
glycerideand plasma glucosein all patients.
iNnic:1ioNs ro cooN:x :Ncioc:inx
Coronary angiography should be undertaken in the
early post-infarction period when thereis:
Angina that does not respond to pharmacological
therapy
Angina or evidenceof myocardial ischaemia at rest
Exercise-inducedanginaor myocardial ischaemiaat a
low workload, or on Holter monitoring, when there
has been littleor no increasein heart rate.
Coronary angiography should be considered when
thereis:
Angina or objective evidence of provocable myo-
cardial ischaemia (in the absence of the features
described above)
Postinfarctionanginarespondingto pharmacological
therapy
Severeleft ventricular dysfunction
Complexventricular arrhythmiamorethan48hafter
theonset.
I n selected cases, especially in younger individuals, cor-
onary angiography can be considered for patients with
an uncomplicated course to evaluate the success of
reperfusion, to identify those with extensive coronary
artery disease, and to facilitateearly hospital discharge
and return to work.
Rehabilitation
Rehabilitation isaimed at restoringthepatient to asfull
a life as possible, and must take into account physical,
psychological and socio-economic factors. The process
shouldstart assoonaspossibleafter hospital admission,
and becontinued in thesucceeding weeks and months.
Thedetailsof rehabilitationwill not bediscussedhere, as
full considerationof itsprinciplesandmethodsaredealt
with in thereports of theWorking Group on Rehabili-
tation of theEuropean Society of Cardiology
[102]
.
Psychological and socio-economic aspects. Anxiety is
almost inevitable, both in patients and their associates,
so that reassuranceand explanation of thenatureof the
illness is of great importance and must be handled
sensitively. I t is also necessary to warn of the frequent
occurrence of depression and irritability that more
frequently occurs after return home. I t must also be
recognised that denial is common; while this may have
a protective eect in the acute stage, it may make
subsequent acceptanceof thediagnosis moredicult.
Thequestionof returnof work andother activit-
ies should bediscussed prior to hospital discharge.
Lifestyleadvice. Thepossiblecausesof coronary disease
should be discussed with patients and their partners
during hospitalization, and individualized advice on a
healthydiet, weight control, smokingandexercisegiven.
Physical activity. All patients should be given advice
with regard to physical activity based upon their recov-
ery fromtheheart attack, takinginto account their age,
their preinfarction level of activity, and their physical
limitations. Assessment is greatly aided by a pre-
discharge exercise test, which not only provides useful
clinical information but can be reassuring to the over-
anxious patient. A meta-analysis of rehabilitation pro-
grammes which included exercisesuggested asignicant
reduction in mortality
[103]
.
Secondary prevention
Smoking. Although no randomized trials have been
undertaken, compelling evidence from observational
studies shows that those who stop smoking have a
mortality in the succeeding years less than half that of
those who continue to do so
[104]
. This is, therefore,
potentiallythemost eectiveof all secondaryprevention
measures; much eort should be devoted to this end.
Most patients will not have smoked during the acute
phase and the convalescent period is ideal for health
professionals to help smokers quit the habit. Resump-
tion of smoking is common after return home and
continued support and adviceis needed duringrehabili-
tation. A randomized study has demonstrated theeec-
tiveness of a nurse-directed programme
[105]
: a smoking
cessation protocol should beadopted by each hospital.
Diet and dietary supplements. Thereis littleevidenceon
the eectiveness of dietary treatment of postinfarction
patients, but aweight reducingdiet shouldbeprescribed
for those who are overweight. All patients should be
advised to take a diet low in saturated fat and high in
fruit andvegetables. Onestudysuggeststhat takingfatty
sh at least twiceaweek reducestherisk of reinfarction
anddeath
[106]
. Theroleof antioxidantsintheprevention
of coronary diseasehas yet to beestablished.
Antiplatelet and anticoagulant treatment. The Anti-
platelet Trialists Collaboration
[55]
meta-analysis demon-
strated about a 25%reduction in reinfarction and death
in post-infarction patients. I n thetrialsanalysed, aspirin
dosages ranged from75 to 325mg daily. Thereis some
evidencethat thelower dosages areeectivewith fewer
side-eects.
Clinical trials undertaken beforethewidespread
useof aspirin showed that oral anticoagulants areeec-
tivein preventingreinfarction and death in survivors of
myocardial infarction
[107,108]
. Thepatients in thesetrials
were randomized at least two weeks after the index
infarction. Theroleof routineearlyoral anticoagulation
following acute myocardial infarction is less clear and
has only recently been evaluated after thrombolytic
therapy
[29,109]
. I n such patients there is no clear benet
over antiplatelet therapy. Possibly, subsets of patients,
e.g. those with left ventricular aneurysm, atrial brilla-
tionor echographicallyprovenleft ventricular thrombus
might benet fromearly oral anticoagulation, but large
randomized trialsin thiseld arelacking. Theambulant
useof subcutaneous heparin may behelpful
[110]
, but the
results should beconrmed in morestudies.
Combined anticoagulant and antiplatelet
therapy after myocardial infarction is currently being
investigated; therst results appear promising
[111]
.
Beta-blockers. Several trials and meta-analyses have
demonstrated that beta-adrenoceptor blocking drugs
reduce mortality and reinfarction by 2025% in those
who have recovered from acute myocardial infarc-
tion
[60,85]
. Positive trials have been conducted with
propranolol, metoprolol, timolol and acebutolol, but
studies with other beta-blockers, although not signi-
cant, are compatible with a comparable eect. About
25% of patients have contra-indications to beta-
blockadebecauseof uncontrolled heart failure, respira-
tory disease or other conditions. Of the remainder,
perhapshalf canbedenedasof lowrisk
[85,112]
, inwhom
beta-blockadeexerts only a marginal benet, bearingin
mind the minor though sometimes troublesome side-
eects. Opinion is divided as to whether beta-blockers
should beprescribed to all thosefor whomthey arenot
contra-indicated, or whether they should only be given
to thoseat moderaterisk who havethemost to gain.
Calcium antagonists. Trials with verapamil
[113]
and
diltiazem
[114]
have suggested that they may prevent
reinfarction and death,but caution must beexercised in
thepresenceof impaired ventricular function. They may
beappropriatewhen beta-blockers arecontra-indicated
(especially in obstructiveairways disease).
Trials with dihydropyridines
[66]
have failed to
show a benet in terms of improved prognosis after
myocardial infarction; they should, therefore, only be
prescribed for clear clinical indications, bearingin mind
the potentially adverse eects in those with poor left
ventricular function.
Nitrates. There is no evidence that oral or transdermal
nitrates improve prognosis after myocardial infarc-
tion, the I SI S-4
[64]
GI SSI -3
[63]
trials failing to show a
benet at 46weeks after theevent. Nitrates, of course,
continueto berst linetherapy for angina pectoris.
Angiotensinconvertingenzyme(ACE) inhibitors. Several
trials haveestablished that ACE inhibitors reducemor-
tality after acute myocardial infarction
[115118]
. I n the
SAVE trial
[115]
patients wereentered a mean of 11days
after theacuteevent if they had an ejection fraction less
40% on nuclear imaging, and if they were free of
manifest ischaemia on an exercise test. No mortality
benet was seen in the rst year, but there was a 19%
reductioninthesucceeding35yearsof follow-up(from
246 to 204%). Fewer re-infarctions and less heart
failurewere, however, seen even within therst year.
I n the AI RE trial
[116]
patients were randomized
to ramipril a mean of 5 days after the onset of a
myocardial infarction that wascomplicated by theclini-
cal or radiological features of heart failure. At an
average of 15 months later, the mortality was reduced
from226%to 169%(a27%reduction). I n theTRACE
study
[118]
, patients were randomized to trandolapril or
placebo a median of 4days after infarction, if they had
left ventricular dysfunction as demonstrated by a wall
motion index of 12 or less. At an averagefollow-up of
108weeks, themortality was347%in thetreated group
and423%intheplacebogroup. Takingthethreestudies
together, there is a strong case for administering ACE
inhibitorsto patientswho haveexperiencedheart failure
intheacuteevent, evenif no featuresof thispersist, who
have an ejection fraction of less than 40%, or a wall
motion index of 12 or less, provided there are not
contra-indications.
As discussed above, there is a case for admin-
istering ACE inhibitors to all patients with acute
infarction from admission, provided there are no
contra-indications. Against suchapolicyistheincreased
incidence of hypotension and renal failure in those
receiving ACE inhibitors in the acute stage, and the
small benet in those at relatively low risk, such as
patients with small inferior infarctions. With the very
early use of ACE inhibitors, consideration should be
given to discontinuing these agents at 46 weeks if the
clinical coursehas been uncomplicated and theejection
fraction greater than 40%.
Lipid-lowering agents. The Scandinavian Simvastatin
Survival Study(4S)
[119]
clearlydemonstratedthebenets
of lipid-loweringin apopulation of 4444anginal and/or
post-infarction patients with serum cholesterol levels
of 5580mmol . l
1
(212308mg. dl
1
) after dietary
measures had been tried. Patients werenot entered into
the trial until 6 months after an acute infarction, and
a relatively low risk group of patients was recruited.
Overall mortality at a median of 54 years was reduced
by 30%(from12to 8%). Thisrepresented 33livessaved
per 1000 patients treated over this period. There were
substantial reductions in coronary mortality, and in the
needfor coronarybypasssurgery. Patientsover 60years
of ageappeared to benet as much as younger patients.
Women beneted as far as major coronary events were
concerned, but a statistically signicant reduction in
death was not demonstrated; this may have been as a
result of therelativelysmall number of womenrecruited.
Lipid-lowering agents should, therefore, be pre-
scribed for patients who correspond to those recruited
into 4S, but controversy still exists as to how soon
treatment should bestarted after theevent, and whether
the criteria for treatment should be extended to those
with lower lipid levels.
Logistics of care
ir-nosii1:i c:r
Patient delay. The most critical time in an acute heart
attack istheveryearlyphase, duringwhichthepatient is
ofteninseverepainandliableto cardiacarrest. Further-
more, the earlier that some treatments, notably throm-
bolysis, are administered, the greater the benecial
eect. Yet, it is often an hour or more after the onset
before aid is requested. Sometimes this reects the fact
that thesymptoms arenot severe, or typical, or abrupt
in onset, but frequently immediate action is not taken
even when they are. I t should be a normal part of the
care of patients with known ischaemic heart disease to
inform them and their partners of the symptoms of a
heart attack and how to respond to it. I t is less certain
what should be the role of education of the general
public. Certainly, the public must be aware of how to
call the emergency services, but although they have
achieved somesuccess, it is questionablewhether public
education campaigns have had a signicant impact on
outcome
[120,121]
.
Public education in cardio-pulmonary resuscitation. The
techniques of basic life support should be part of the
school curriculum. Those most likely to encounter
cardiac arrest while at work, such as the police and
re service personnel, should be procient in cardio-
pulmonary resuscitation.
The ambulance service. The ambulance service has a
critical role in the management of acute myocardial
infarction and cardiac arrest. The quality of the care
given depends on thetrainingof thesta concerned. At
the most simple level, all ambulance personnel should
be trained to recognise the symptoms of myocardial
infarction, administer oxygen and pain relief, and pro-
vide basic life support. All emergency ambulances
should be equipped with debrillators and at least one
person on board trained in advanced life support.
Doctor-manned ambulances, available in only a few
countries, can provide more advanced diagnostic and
therapeutic skills, including the authorisation to give
opioids and thrombolytic drugs. I n some countries,
suitably trained nurses undertakethesefunctions.
I t is desirable for ambulance sta to record an
ECG for diagnostic purposes and either interpret it or
transmit it so that it canbereviewedbyexperiencedsta
in a coronary care unit or elsewhere. The recording of
an ECG prior to admission can greatly accelerate
in-hospital management
[122,123]
.
General practitioners. I n some countries, general prac-
titioners play a major rolein theearly careof myocar-
dial infarction. I nthesecountries, theyareoftentherst
to becalled by patients. I f they can respond quickly and
have been suitably trained, they can be very eective,
because they may know the individual patient, record
andinterpret anECG, beableto administer opioidsand
thrombolytic drugs, and undertakedebrillation
[123,124]
.
I n most areas, general practitioners are not so trained.
I n this circumstance, although it is desirable that
they attend the patient without delay, they should
immediately call for an ambulance.
Admission procedures. The processing of patients once
they arrivein hospital must bespeedy, particularly with
regard to diagnosis and the administration of throm-
bolysis, if indicated. I n somehospitals, direct admission
to a coronary care unit may be the best option, but
in most, patients are rst delivered to an Emergency
Department. Delays herecan besubstantial; it is essen-
tial that suitably qualied sta are available to assess
and treat patients with suspected myocardial infarction
in this environment. Patients with clear-cut features of
myocardial infarction, whose ECG demonstrate either
ST elevation or left bundlebranch block, should enter a
fast-track system, inwhichthrombolysisisinstitutedin
theEmergency Department so that thedoor-to-needle
time is no more than about 20min. Other cases may
require more detailed assessment which may be better
undertaken in thecoronary careunit.
1nr cooN:x (c:ni:c) c:r iNi1 (cci)
All patientswithsuspectedmyocardial infarctionshould
initially be assessed and cared for in a designated unit,
where appropriately trained sta are constantly avail-
ableand wherethenecessary equipment for monitoring
andtreatment areimmediatelyat hand. WheretheCCU
is used, as it usually is, for triage, it is important that
satisfactory arrangements exist for therapid transfer to
other wards of those not needing its highly specialised
facilities.
Non-invasivemonitoring. Electrocardiographic monitor-
ing for arrhythmias should be started immediately in
any patient suspected of having sustained an acute
myocardial infarction. This should be continued for at
least 24h or until an alternative diagnosis has been
made. Further ECG monitoring is dependent upon the
perceived risk to the patient and upon the equipment
available. When a patient leaves the CCU, monitoring
of rhythmmay becontinued, if necessary, by telemetry.
More prolonged monitoring is appropriate for those
who have sustained heart failure, shock or serious
arrhythmias in the acute phase as the risk of further
arrhythmias is high.
I nvasivemonitoring. All coronary careunitsshould have
theskillsand equipment to undertakeinvasivemonitor-
ing of the arterial and pulmonary artery pressures.
Arterial pressure monitoring should be undertaken in
patients with cardiogenic shock. Balloon otation cath-
eters, such as theSwan-Ganz catheter, areof valuefor
the assessment and care of patients with low cardiac
output. Theypermit measurement of right atrial, pulmo-
naryarteryandpulmonarywedgepressures, andcardiac
output. Balloon otation catheters are indicated in the
presenceof cardiogenic shock, progressiveheart failure,
and suspected ventricular septal defect or papillary
muscledysfunction.
Thecurrent useof therapies tested by
clinical trials
The results of clinical trials have often not been imple-
mented in practice and treatments which have been
shown to be of little or no value continue to be used
widely. I t hasbeendicult to obtainreliabledataonthe
utilization of therapies in myocardial infarction, except
fromclinical trials, which may not be truly representa-
tive of current practice. The European Secondary Pre-
vention Study Group have recently reported
[125,126]
on
the utilization of drugs in samples of 200520 repre-
sentative acute myocardial infarction patients from 11
countries. Thrombolytic therapy was given to an aver-
age of 35% of patients (range 13 to 52%). The use of
intravenous beta-blockade varied from 0554% (aver-
age 13%). Oral beta-blockade at discharge varied from
3381%(average 52%). These data emphasize the need
both for continuing medical education and for ongoing
audit to ensure the implementation of therapeutic ad-
vances. Centres which participatein multicentreclinical
trials are more likely to implement evidence-based
changes in clinical practice
[127]
.
Recommendations
Patients. Patients with a suspected heart attack have a
right to expect prompt diagnosis, pain relief, resusci-
tation and, if indicated, reperfusion treatment.
Patients with suspected or conrmed myocardial
infarction should be cared for by sta trained and
experienced in modern coronary care. They should have
access to advanced methods of diagnosis and treatment
either at the initial place of management or following
transfer to a specialist unit.
They should haveappropriatefacilities for post-
discharge follow-up, rehabilitation and secondary
prevention.
They and their associates should beinformed of
howto recogniseand respond to a further heart attack.
Cardiologists. Cardiologists, in association with emer-
gency care physicians and health authorities, should
ensure that an optimal system for the care of heart
attack patients is operative in their area. This should
includetheappropriatetrainingof ambulancepersonnel
and rst-line doctors, ecient arrangements for the
diagnosisand treatment of suspected myocardial infarc-
tions in the Emergency Department, and protocols for
theprompt administration of thrombolytic treatment.
Cardiologists, in association, with anaesthetists
and other relevant specialists, should ensurethat medi-
cal and paramedical hospital sta are competent in
resuscitation techniques.
Registersshouldbekept of thetimefromthecall
for care and the administration of thrombolysis (call-
to-needle time) and that from hospital admission to
thrombolysis(door-to-needletime). Theformer should
be no longer than 90min and for fast track patients
with clear indications for thrombolysis, the door-to-
needletime should not exceed 20min.
Registers should also be kept of the proportion
of patients with denitemyocardial infarction admitted
within 12h of theonset of symptoms with ST elevation
or bundlebranch block who receivethrombolysis. This
proportion should probably bein excess of 90%.
PTCA may be regarded as a viable and cost-
eective alternative to thrombolytic therapy when the
appropriateskillsand facilitiesareavailable. Theresults
of PTCA should berecorded in a national register.
A rehabilitation programme should be made
available for all patients, tailored to their individual
needs.
Thereshould bea policy for smoking cessation.
This must consist of a continuing programme run by
healthprofessionalsthat not onlyencouragespatientsto
stop, but endeavours to maintain cessation.
Records should bekept of secondary prevention
therapy prescribed to survivors of denite myocardial
infarction. Suggestedminimumtarget guresat thetime
of dischargearefor aspirin >85%, beta-blockers >35%
and ACE inhibitors >20%.
All patients should have their lipids measured,
preferably on the day of admission. Those with raised
lipids should rst receivedietary advice. Should this fail
to reduce raised lipid levels suciently, consideration
shouldbegivento lipid-loweringdrugs, accordingto the
criteriaof theScandinavian Simvastatin Survival Study.
General practitioners. Whengeneral practitionersarethe
rst point of contact for cases of suspected myocardial
infarction, they must either beableto respond immedi-
atelyor makeprovisionfor theemergencyservicesto do
so, or (preferably) both.
I f general practitioners can respond quickly
and are appropriately trained and equipped, they can
providedebrillation and thrombolysis eectively.
They should be involved in the co-ordinated
local programme for the management of cardiac
emergencies.
Theyshouldseepatientsassoonaspossibleafter
dischargefromhospital, ensurethat their rehabilitation
is properly organised, and oversee the appropriate
secondary prevention measures.
Health authorities. Health authorities should encourage
the training of the public in basic cardiopulmonary
resuscitationtechniquesandtheambulancepersonnel in
basic and advanced lifesupport.
They should ensure that an optimal system of
care is available for patients suspected of sustaining
cardiacarrest or myocardial infarction, byco-ordinating
the activities of the ambulance service, general practi-
tioners, and thehospital service.
They should ensure that Emergency Depart-
ments have appropriate protocols for the prompt
management of patients with suspected myocardial in-
farction, and that there are appropriately trained sta
availableat all times.
They should provide sucient beds for the
intensive care of patients with myocardial infarction.
Physicians with a formal trainingin cardiology must be
available.
They should make provision for the rehabili-
tation of patients discharged from hospital after
myocardial infarction.
They shouldensurethat facilitiesareavailablein
their own hospital or district for the advanced investi-
gation and treatment of patients with thecomplications
of myocardial infarction or, if not available locally,
arrangements have been made with tertiary centres
elsewhere.
Procedure of the Task Force. The Task Force on the
Management of Acute Myocardial I nfarction was cre-
ated by theCommitteefor Scientic and Clinical I nitia-
tivesof theEuropeanSocietyof CardiologyinFebruary
1995and asked to report to theCongress of theSociety
in August 1995. The members of the Task Force were
Prof. D. G. J ulian (Chairman) U.K., Prof. J .-P. Boissel
(France), Prof. D. P. De Bono (U.K.), Prof. K. A. A.
Fox (U.K.), Dr J Heikkila (Finland), Dr L. Lopez-
Bescos (Spain), Prof. K.-L. Neuhaus (Germany),
Prof. R. Schrder (Germany) Prof. P. Sleight (U.K.),
Prof. G. Specchia (I taly), Drs A. Sigurdsson and K.
Swedberg (Sweden), Prof. M. Turina, Dr M. Genoni
(Switzerland), Prof. F. W. A. Verheugt (The
Netherlands), Prof. F. van de Werf (Belgium), Dr F.
Zijlstra (TheNetherlands).
I ndividual members wereinvited to submit draft
papers in their area of expertise and these were rst
discussed at a meeting in London on 15 and 16 May.
After several revisions, and consultation with members
of theCommittee, themembers met again on 4 J uly in
Amsterdam. The document was redrafted and widely
circulated prior to submission of thenal document to
theCommitteefor its approval.
I nvaluableassistanceinprocessingthedocument
was provided by Mrs W. Thieme. The guidelines were
developed without any involvement of thepharmaceuti-
cal companies that provided nancial support of its
activities.
Financial support. TheTask Forcewishes to express its
appreciation of thenancial support provided by Astra
Hssle AB, Behringwerke AG, I nstitut de Recherches
I nternationales Servier, Knoll AG, Laboratoires Searle,
Merck, Sharp and Dohme, and Pzer Ltd.
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