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| Journal of the New Zealand Medical Association,
07-October-2005, Vol 118 No 1223
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ST-elevation myocardial infarction: New Zealand
management guidelines
ST-Elevation Myocardial Infarction Guidelines Group and the
New Zealand Branch of the Cardiac Society of Australia and New Zealand
Glossary
PurposeThese guidelines apply to the management of patients with
ST-elevation myocardial infarction (STEMI). The purpose of these guidelines are
to provide a summary of the most up-to-date New Zealand and overseas evidence
and to make recommendations based on the evidence that will lead to the best
practice for patients with STEMI in New Zealand. The guidelines are aimed at all
health providers who care for patients with STEMI.
For a detailed description of the levels of evidence cited
in these guidelines, please see Appendix 2. These guidelines are intended for
best clinical practice. Where physicians or hospitals are not able to meet the
guidelines it is important that there is documentation that there have been
communications between clinicians and managers clearly defining the clinical
implications of any resource shortages.
ManagementSustained ST segment elevation on the electrocardiogram
(ECG) in the context of an acute coronary syndrome (ACS) is usually indicative
of an occluded epicardial artery. Included within this subset are those patients
presenting with presumed new left bundle branch block pattern on the initial
ECG.
When patients first present with ischaemic symptoms (chest
pain or a surrogate) lasting for more than 20 minutes, their management (Figure 1) depends on whether ST elevation is present
on the ECG or not. If the symptoms are within 12 hours, urgent reperfusion;
fibrinolytic, or catheter-based reperfusion is mandatory.1++A
(See Appendix 2 for explanation)
Good nursing care is a very important component of the care
of patients with STEMI.
DiagnosisThe diagnosis of STEMI is defined as ST elevation of
≥2 mm in chest leads V1–3 or ≥1
mm in 2 contiguous leads or presumed new left bundle branch block (LBBB).
InvestigationsECGsAn ECG should be performed and reviewed immediately on first
assessment. All patients with inferior infarctions must have
V3R and V4R leads
recorded to detect right ventricular infarction. Posterior recordings
(V7-V9) should be
performed if a posterior infarction is suspected.
If the initial ECG is normal, and there is a high clinical
suspicion of ongoing MI, serial ECGs should be performed at 5 to 10 minute
intervals and optimally continuous ST segment monitoring should be performed.
ECGs should be obtained every 6 to 8 hours in all other patients until an
established diagnosis has been made.D4
The criteria required are:
Patients who present with a
history consistent with acute myocardial ischaemia and have an ECG with new or
presumed new LBBB should be classified and managed as a STEMI. In this context,
the presence of one of three of the following ECG criteria adds independent
diagnostic value:
The ECG leads in which ST segment changes
occur are helpful in localising the regions of ischaemia of the left ventricular
myocardium and this in turn can help predict the culprit coronary artery
involved:
Q
waves:
The absence of
ST elevation or a new LBBB pattern does not exclude the presence of complete
epicardial coronary artery occlusion, but the benefit of reperfusion has not
been demonstrated among these patients. With a posterior MI due to circumflex
artery occlusion there may be marked ST segment depression in leads
V1 to V4
associated with tall R waves and upright T waves in the right precordial leads
(V1 to V3).
In patients with STEMI, initiation of reperfusion therapy
based on the initial ECG should take priority over cardiac marker analysis.
Subsequent confirmation of MI can be determined by initial and subsequent
biomarker levels.
Cardiac biomarkersBlood samples for measurement of troponin levels, which are
the preferred cardiac markers for ACS,1 should
be obtained within 10 minutes of presentation.D4
Measurement should be repeated 6 to 8 hours later
particularly if the baseline level was normal. Troponin levels assessed 8 hours
after admission will detect most MIs but requires 12 hours after the onset of
symptoms to detect all MIs.
Many patients who present within 3 to 6 hours of the onset
of symptoms will have normal troponin and CKMB levels. Myoglobin levels will
usually be elevated in these patients and maybe of clinical value to guide
management when there is uncertainty about the diagnosis of STEMI particularly
in patients with LBBB.
Due to its rapid rise and fall CKMB is preferred over
troponin T or I (which may remain elevated for 2 weeks) for the diagnosis of
re-infarction.
Troponins (which are the most specific cardiac markers),
however, may be elevated in conditions other than an ACS.
Other blood testsBlood should also be obtained for FBC, electrolytes,
glucose, liver function, renal function and lipids. A CXR should be performed
(but in the absence of clinical features suggesting aortic dissection or other
differential diagnoses), not before initiation of
treatment.D4
EchocardiographyOn occasions acute echocardiography demonstrating a regional
wall motion abnormality may be a useful adjunct for diagnosis and assessment of
complications such as ventricular septal defect, sub acute rupture and LV
thrombus. In situations where left bundle-branch block is present on the initial
electrocardiogram an early rising cardiac marker such as myoglobin may aid
diagnosis.D4
ManagementEarly risk stratificationThere are a number of risk scores. The TIMI STEMI risk score
for early risk stratification in patients with STEMI is used most commonly for
predicting mortality 30 days after the MI (Table
1).2 Risk assessment plays an important role in
predicting patient prognosis and initiating appropriate evidence-based therapies
in patients who are most likely to benefit from them.D4
Reperfusion therapy in patients with ST elevationUrgent reperfusion of the ischaemic myocardium by
restoration of flow in the occluded epicardial coronary artery is the primary
therapeutic goal in patients with STEMI who present within 12 hours of symptom
onset. If reperfusion therapies are initiated early after symptom onset, the
infarctions are smaller, complications are reduced and survival benefit is
greater. When epicardial flow is restored within 30 minutes of occlusion
infarction can be aborted.
If flow is achieved within 3 hours, considerable myocardial
salvage can occur with beneficial effects on ventricular function and mortality
with additional long-term benefit from the presence of an open infarct related
artery (IRA). When reperfusion is achieved after 3 hours myocardial salvage is
progressively reduced and recovery of ventricular function is dependant on
established collateral flow. Beyond 6 hours myocardial salvage is minimal or
absent with the major benefit being that related to an open
IRA.3 Reperfusion can be achieved using a
strategy of fibrinolysis or primary PCI. Door to balloon times should be <90
minutes.1++A
Primary PCI vs fibrinolysisInfarct artery patency rates at 90 minutes with PCI are
superior to fibrinolysis (90% vs 60%). In a recent meta-analysis of 23 trials
comparing PCI to fibrinolysis (which included the SHOCK trial which compared
stabilisation with immediate revascularisation for cardiogenic
shock).4,5 PCI appeared superior in reducing
short-term mortality, reinfarction, and stroke. However, for patients presenting
very early after symptom onset the outcomes with fibrinolysis may be superior.
In the PRAGUE6 study for
patients randomised to receive streptokinase within 3 hours of symptom onset,
the 30-day mortality was similar to that with primary PCI. Theoretically, based
on the GUSTO-17 results, where patients treated
with tPA had a 1% absolute reduction in mortality compared with patients treated
with streptokinase, an accelerated tPA regimen could achieve a 1% lower
(absolute) mortality than PCI. In the CAPTIM8
study patients who received (pre-hospital) fibrinolysis within 2 hours of
symptom onset had improved outcomes compared with primary PCI. Thus for patients
presenting <3 hours after symptom onset fibrinolytic therapy may be the
treatment of choice for mortality reduction. For patients presenting >3 hours
and <12 hours after symptom onset primary PCI appears to be superior and is
the reperfusion therapy of choice.
The choice of strategy adopted at any given institution,
however, depends on a number of factors (Table 2).
Elderly patientsThe optimal reperfusion strategy in the elderly is not
defined.7,9 In a recent re-analysis of the
Fibrinolytic Trialists Enrollment Group overview of patients >75 years there
was a significant 15% relative reduction in mortality equating to 34 lives saved
per 1000 patients treated; larger than the 16 lives saved per 1000 in patients
aged <55 years.10 Although the risk of
intracranial haemorrhage increases with age, most elderly patients who suffer an
intracranial haemorrhage die (and are not counted in the mortality benefit) and
the risk of non-fatal strokes with major disability occurring is
small.10 In patients up to the age of 84 tPA
has been shown to be superior to streptokinase for reducing the composite of
mortality and non-fatal disabling
stroke.7
Choice of fibrinolyticIn the absence of contraindications (Table 3) a fibrin
specific agent (tPA, TNK, rPA (see Table 4) is most effective in patients <84
years,1++A7 or patients
previously administered streptokinase because of formation of antibodies and
concerns about lack of
efficacy.2++B11 Streptokinase
is cheaper but less effective than fibrin specific agents (Table 4). If cost is
an issue, streptokinase is a suitable alternative for some patients.
Streptokinase is a vasodilator and may cause hypotension in
10% of patients. This should be managed by head down tilting, with consideration
to giving iv sodium chloride 0.9% 250 mL boluses x 2-3. Allergic or febrile
reactions to streptokinase may also occur and should be treated with
hydrocortisone 100 mg iv and/or promethazine 12.5–25 mg iv stat. For
severe anaphylaxis adrenaline sc/iv should be administered (which is otherwise
absolutely contraindicated in the setting of an acute MI because of the risk of
VF).
If major haemorrhage occurs with either streptokinase or
tPA: apply local pressure and if appropriate consider reversing the effects of
heparin with protamine and administering 1–3 units fresh frozen
plasma.
MonitoringContinuous ECG monitoring should be performed during
infusion of fibrinolytic therapy and 12-lead ECGs should be recorded to give
assessment of ST segment recovery. These are recommended to be performed at 90
minutes and 3 hours after first starting the infusion of fibrinolytic
therapy.D4 To obtain a peak troponin level as a guide to
infarct size troponins should be measured at least twice in the 24 hours and at
24–36 hours CKMB should be measured at ≈24 hours to aid detection of
reinfarction as troponin T levels remain elevated for 10–14
days.D4
Adjunctive therapiesOxygen should be administered to keep the saturations around
96% (higher doses of oxygen increase afterload via arterial vasoconstriction.
Sublingual GTN and morphine should be administered for pain relief (observe BP
and RR) or fentanyl. IV antiemetics should be given with morphine
(metoclopramide 10 mg or cyclizine 25 mg).D4
AspirinAll patients should immediately receive aspirin
150–300 mg which should be chewed if enteric-coated and 75–150 mg
continued indefinitely (if there are no contraindications). This recommendation
is based on the collaborative meta-analysis of randomised trials of antiplatelet
therapy showing no relation of dose with
efficacy12 and information from other studies
showing increased bleeding with increasing aspirin
doses.1++A13
ClopidogrelAdministration of clopidogrel should be considered at
presentation in all patients with STEMI. For patients treated with fibrinolysis
who are <75 years it is recommended that a loading dose of 300 mg followed by
75 mg daily be given for 2 weeks.14 For
patients over 75 years receiving fibrinolysis or patients of any age not
receiving fibrinolysis, consideration should be give to commencing 75 mg of
clopidogrel at presentation and continued for 2
weeks.1++A15
For patients undergoing primary PCI clopidogrel can be given
(with a loading dose of 300 mg–600 mg) at presentation or after defining
the coronary anatomy and continued for up to 12 months depending on the type of
stent used.1+A
Clopidogrel is relatively expensive but several studies have
shown it to be cost effective.16–18 It is
not currently funded except for patients undergoing stenting.
Table 1. Risk stratification of STEMI patients
using the TIMI – STEMI risk
score2 (*Referenced
to average mortality [95% confidence intervals])
Table 2. Preferred reperfusion strategy for
STEMI
Table 3. Contraindications to
fibrinolysis
Table 4.
Fibrinolytic agents
*Bolus 15 mg infusion 0.75
mg/kg over 30 minutes (maximum 50 mg), then 0.5 mg/kg not to exceed 35 mg over
the next 60 minutes to an overall maximum of 100 mg
Antithrombotic therapyHeparinAdjunctive heparin therapy is recommended to be administered
immediately with tPA and as an option with streptokinase. (Some hospitals may
prefer not to use heparin with streptokinase particularly if patients are
elderly and/or have a small inferior MI).
The dose of heparin has recently been adjusted downwards
because of concerns about the risks of intracranial haemorrhage with
fibrinolytic therapy and a bolus of UFH of 60 units/kg (maximum 4000 units)
followed by an infusion of 12 units/kg/h (maximum 1000 units/h) with the
infusion rate adjusted according to the APTT at 3h and the heparin infusion
adjusted to achieve an APTT of 50-70sec is
used.1+A19 The infusion should
continue for 48 hours.
Enoxaparin is the preferred antithrombotic therapy with
fibrinolytic therapy. In the ExTRACT trial 30-day death in MI was reduced
by 17% with enoxaparin compared with unfractionated heparin (12.0% vs 9.9%)
p<0.0001 (Antman NEJM 2006). Major bleeding was increased by 0.7%
absolute in patients treated with enoxaparin (1.4% unfractionated heparin vs
2.1% enoxaparin) with similar rates of intracranial haemorrhage 0.7%
unfractionated heparin vs 0.8% enoxaparin. In patients *75 years the
absolute benefit of enoxaparin was similar to the benefit in younger patients
and major bleeding (2.9% vs 3.3%) and intracranial haemorrhage (1.7% vs 1.6%)
was similar in patients treated with unfractionated heparin and enoxaparin
respectively. In patients <75 years an IV bolus of 30mg followed by
1.0mg/kg 12 sc hourly should be given for at least 48 hours and is recommended
to be given through angiography if performed and until hospital discharge.
In patients *75 years the bolus should be omitted and 0.75mg given sc 12
hourly. For patients with creatinine clearance ≤30mls/min the dose
should be reduced to 1.0mg/kg once a day. It is noted that the IV bolus is
not registered in New Zealand but this can be given by a doctor.”
Glycoprotein IIb/IIIa inhibitorsThese are not recommended with fibrinolytic therapy. For PCI
and stenting abciximab is recommended.20
β-blockersIV β-blockers are recommended to be considered for
administration immediately or following initiation of fibrinolysis in patients
who are haemodynamically stable without heart failure (Killip III or IV) and
without contraindications (asthma, systolic BP <110 mmHg, heart rate <50
minutes, Mobitz Type II 2nd degree or
3rd degree heart
block)21 and oral therapy continued
indefinitely—e.g. metoprolol 5 mg IV bolus every 2 minutes up to 15 mg
followed 15 minutes later by 50 mg orally or atenolol 10 mg IV bolus followed 15
minutes later by 50 mg orally. For patients with heart failure it is recommended
that ß-blockers (carvedilol or metoprolol) be begun when the patient is
stable for 24-48
hours.1++A22,23
ACE inhibitorsAll patients with evidence of heart failure, anterior
infarction or a history of previous infarction should be considered to receive
oral ACE inhibitors beginning 2 hours after admission if the systolic BP is
>100mmHg usually commencing with a low dose of a short acting drug and then
increasing over several days to maximally tolerated
doses.1++A24,25 In all other
patients ACE inhibitors are recommended to be begun on day 1 and continued long
term.1++A
If a choice has to be made between β-blockers and ACE
inhibitors because of hypotension, ACE inhibitors are the preferred initial
therapy (because of their effect on remodelling). If patients are intolerant of
ACE inhibitors they should be started on an angiotensin receptor
blocker.26
Lipid modifying therapyInitiation of statin therapy should be begun in-hospital
(e.g. simvastatin 40 mg or atorvastatin 80 mg) with an aim to reduce the LDL to
1.6 mmol/L.1++A27-29
NitratesNitrates are appropriate for the control of angina and
hypertension.D4
Calcium channel blockersThere is no evidence that calcium antagonists improve
prognosis following myocardial infarction, but they can be used for symptomatic
angina in combination with a beta-blocker. Heart rate limiting calcium channel
blockers are preferred if patients cannot tolerate a beta-blocker e.g. verapamil
or diltiazem.1-B30
WarfarinPatients with pedunculated or mobile left ventricular
thrombus should be anticoagulated for 3-6 months with repeat echocardiography at
this time to determine if continuation of anticoagulation is appropriate.
Anticoagulation of patients with low ejection fractions and no LV thrombus is
controversial and treatment should be individualised. There is no need to
anticoagulate patients with transient AF (<24 hours). Anticoagulation and
rate control may be preferred for patients with AF and other risk factors (over
60, hypertension, diabetes, heart failure, EF ≤35%, prior thromboembolism,
persistent atrial thrombus) rather than anticoagulation for 3 weeks, and
cardioversion (or TOE guided), although for younger patients this may be
appropriate. Ongoing warfarinisation may still be appropriate for some patients
who are initially returned to sinus rhythm.1++A
Failed fibrinolysisIn patients with continuing ischaemia or haemodynamic
instability, after lytic therapy, rescue PCI should be undertaken as soon as
possible.D4 Lack of resolution of ST segment elevation by 30%
of baseline at 90 minutes is also considered to be indicative of failed
reperfusion but has less evidence for its support as an indication for rescue
PCI.
Stenting and adjunctive devices for PCIStenting is recommended. Drug eluting stents are indicated
in small vessels, long lesions, bifurcation or ostial lesions, bypass grafts and
patients with diabetes.1++A
Rotablation is recommended for fibrotic or heavy calcified
lesions that cannot be adequately dilated before stenting.D4
Distal protection devices are indicated for use in saphenous
vein grafts and where there is a high thrombus load.1++A Randomised trials are
testing these devices. Other approaches such as aspiration systems are also
being tested.
Facilitated PCIFacilitated PCI is defined as planned PCI soon after
fibrinolysis. A number of trials are investigating various fibrinolytic and
glycoprotein IIb/IIIa regimens. These approaches cannot be recommended at
present.
Angiography in patients who have received thrombolytic therapyThere are two approaches. One is ischaemia-driven if
ischaemic symptoms or ischaemic ECG changes occur despite medical therapy or
ischaemic changes occur during exercise stress testing or pharmacologic or
stress echo imaging. This is the most common approach in New Zealand.
The other approach is to perform angiography in all patients
who would be candidates for revascularisation. Routine angiography and PCI as
appropriate on significant stenoses may provide prognostic information and
enable patients to be discharged home early and reduce ischaemic events post
discharge.D4 This approach is supported by the GRACIA 1 trial
where an invasive strategy within 24 hours (median 16.7 hours) of thrombolysis,
compared with an ischaemia guided strategy resulted in a lower incidence (9% vs
21%) of the primary end-point of the combined rate of death, reinfarction or
revascularisation at 1 year and there was a trend for a reduction in death and
MI, 7% vs 12% (RR 0.59, 0.33–1.05).31
There are a number of ongoing trials evaluating the most appropriate timing for
angiography.
Surgical revascularisation (CABG)The success of PCI and fibrinolysis for STEMI has meant that
the need for urgent surgical reperfusion is limited to a very few select
circumstances although it may be used as the primary reperfusion strategy in
2-5% of patients with STEMI:
Diabetes mellitusDiabetics are a high-risk group and all patients with a
blood glucose >11 mol/L and a suspected or definite MI or unstable angina
with an Ischaemic ECG should be treated aggressively with an insulin, glucose
and potassium regimen.32 There are several
appropriate regimens. At this stage without a clear optimal strategy, local
units are advised to discuss this therapy with colleagues, and to institute a
local policy.1-A
Complications of myocardial infarctionThe majority of deaths in hospitalised patients with STEMI
are due to LV pump failure and mechanical complications. Compared to the
pre-reperfusion era, ventricular tachyarrhythmias are now less common.
Mechanical complicationsA number of mechanical complications may occur including
Mitral regurgitation, ventricular septal defect and free wall rupture—all
of which require urgent echocardiography, and may require urgent insertion of an
intra aortic balloon pump and often an urgent surgical consultation.
ArrhythmiasVentricular or atrial arrhythmias are frequent. Local CCUs
have standard protocols for treatment.
Ongoing ischaemiaIf patients have ongoing ischaemia (an ECG should be
obtained during symptoms to document the degree and extent of ischaemia)
expeditious angiography should be considered.
Other complicationsDelayed complications include post myocardial infarction
syndrome and Deep Vein Thrombosis/Pulmonary Embolism.
Cardiogenic shockThe presence of shock due to left ventricular dysfunction
following MI implies ischaemia/infarction of a large area of myocardium and is
associated with 70–80% in-hospital mortality. Shock is defined as
hypotension (BP ≤90 mmHg or requiring inotropes to keep the BP >90 mmHg
for 30 minutes) unresponsive to fluid loading and usually with associated
decreased tissue reperfusion and decreased urine output. The SHOCK trial has
shown that mortality is reduced to ~50% when aggressive support measures
including administration of fibrinolytic therapy, intra aortic balloon
counter-pulsation, mechanical ventilation and early revascularisation are
performed.5 In patients without important
comorbidity the interventional team, including an anaesthetist should be
contacted immediately and oxygen, appropriate ventilation and inotropic support
should be begun immediately and emergency angiography should be
undertaken.1++A For patients where PCI is not appropriate,
surgery should be
considered.1++A33
Heart failureFrusemide should be given to decrease breathlessness. All
patients should be placed on evidence based therapies including ACE
inhibitors,24
spironolactone34,35 and
β-blockers.22,23If patients are intolerant
of ACE inhibition an ARB should be prescribed.1++A Enoxaparin
50 mg/day should be given to prevent deep vein thrombosis and pulmonary
embolism.1+A Digoxin should be considered for patients in sinus
rhythm who continue to be symptomatic as it has been shown to decrease
rehospitalization.1+A36
Right ventricular infarctionRight ventricular infarction is usually diagnosed clinically
or by ST elevation in right precordial ECG leads or on echocardiography.
Patients may have raised jugular venous pressure, hypotension and clear lung
fields. It is important that all patients get adequate fluids—i.e. at
least 2 litres in the first 24 hours. If patients are hypotensive a fluid
challenge should be given—e.g. 200 mL of IV saline over 10–15
minutes. Swan Ganz catheterisation may help monitor volume
status.4D
ReinfarctionApproximately 2–6% of patients experience reinfarction
in hospital and this is associated with increased mortality and more frequent
heart failure, cardiogenic shock and ventricular arrhythmias. Urgent PCI should
be considered. In hospitals without PCI facilities readministration of a
fibrin-specific agent (50% of dose in first 24 hours) should be considered,
followed by urgent transfer for
PCI.1+A37
Testing for inducible ischaemiaAll patients who have not had angiography or have had
incomplete revascularisation should undergo testing for inducible
ischaemia—e.g. by treadmill, stress echo, or nuclear imaging prior to
hospital discharge.D4
EchocardiographyPre-discharge assessment of left ventricular function is
necessary to assess left ventricular function in all patients if this has not
been assessed by other means.D4
Holter monitoringRoutine Holter monitoring is not
recommended.D4
Resource availabilityIt is recognised that in New Zealand there are limitations
on resources. Pharmacoeconomic analyses are planned to determine the appropriate
levels of funding in New Zealand for patients with STEMI.
RehabilitationAll patients should be referred to the Rehabilitation
Service and be encouraged to attend rehabilitation programmes, to stop smoking,
undergo regular exercise, (30 minutes of brisk walking or equivalent on most
days of the week), to achieve ideal weight, and to have a cardioprotective diet,
and to aid compliance with medications.1++A
Advice about return to work and sexual activities should be
tailored to the individual patient. The National Heart Foundation of New Zealand
has several excellent patient information brochures. For driving guidelines,
refer to page 56 of the “Medical Aspects of Fitness to Drive” book
issued by the Land Transport Safety Authority.
ConclusionIt is very important that patients with STEMI receive some
form of reperfusion therapy as quickly as possible along with the other evidence
based therapies and that access across New Zealand be equitable, particularly
for Maori. These guidelines are the evidence base for best practice management
of patients with ST-elevation acute coronary syndromes.
Author information: ST-Elevation Acute
Coronary Syndrome Guidelines Group (refer to Appendix 1 below), nationwide; The
New Zealand Branch of The Cardiac Society of Australia and New Zealand,
Wellington.
Acknowledgement: We are extremely grateful
to Charlene Nell for secretarial assistance.
Correspondence: Professor Harvey White,
Green Lane Cardiovascular Service, Auckland City Hospital, Private Bag 92024,
Auckland 1030. Fax: (09) 630 9915; email HarveyW@adhb.govt.nz
Appendix 1. ST-Elevation Myocardial Infarction
Guidelines Group
Albert Ko Middlemore
Hospital, Auckland
Andrew Hamer Nelson
Marlborough Health Service, Nelson
Andrew Kerr Middlemore
Hospital, Auckland
Brandon Wong Whangarei
Hospital, Whangarei
Charles Renner Kew Hospital,
Invercargill
Cherian Sebastian Taranaki
Base Hospital
Cheuk-Kit Wong Dunedin
School of Medicine, Dunedin
Chris Ellis Green Lane
Cardiovascular Service, Auckland City Hospital
Chris Nunn Waikato Hospital,
Hamilton
Clyde Wade Waikato Hospital,
Hamilton
Elana Curtis Auckland (Maori
Advisory Group)
Euan G. Grigor The Old
Cottage Hospital (Lay Representative)
Gerry Wilkins Dunedin
Hospital, Dunedin (Cardiac Society Representative)
Guy Armstrong North Shore
Hospital, Auckland
Hamid Ikram Christchurch
Hospital, Christchurch
Hamish Hart North Shore
Hospital, Auckland
Harvey White Green Lane
Cardiovascular Service, Auckland City Hospital
Helen Williams Ministry of
Health Representative
Hitesh Patel North Shore
Hospital, Auckland
Ian Crozier Christchurch
Hospital, Christchurch
John Elliott Christchurch
Hospital, Christchurch (Heart Foundation Representative)
John French Green Lane
Cardiovascular Service, Auckland City Hospital
Laura Lambie Ministry of
Health, Wellington
Malcolm Abernathy Wakefield
Hospital, Wellington (Private Hospital Representative)
Mark Simmonds Wellington
Hospital, Wellington
Mark Webster Green Lane
Cardiovascular Service, Auckland City Hospital
Paul Tansor Midcentral,
Palmerston North
Penny Astridge Nelson
Marlborough Health Service, Nelson
Phil Matsis Wellington
Hospital, Wellington
Richard Luke Napier
Hospital, Napier
Stewart Mann Wellington
Hospital, Wellington
Younis Al-Khairulla Greymouth
Gerry Devlin Waikato Hospital, Hamilton
Appendix 2
Following
assessment of the level of evidence for individual papers, recommendations were
given a grade from A to D as below. This grading system departs from the
Scottish Intercollegiate Guidelines Network (SIGN) system which was derived
primarily for treatment guidelines and revises ranking according to therapy or
prognosis. Questions relating to prognosis were considered a feature of this
guideline to determine how to tailor cardiac rehabilitation services according
to individual patient needs. For further details on the SIGN system see
www.sign.ac.uk.
References:
This article has been corrected to reflect the
Erratum published 6 June 2008 at http://www.nzma.org.nz/journal/121-1275/3105
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