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Early management of unstable angina and non-ST-segment elevation myocardial infarction: summary of NICE guidance
  1. Huon H Gray1,
  2. Robert A Henderson2,
  3. Mark A de Belder3,
  4. S Richard Underwood4,
  5. A John Camm5 on behalf of the guideline development group (listed at the end)
  1. 1National Clinical Guideline Centre, London and Southampton University Hospital, Southampton, UK
  2. 2Nottingham University Hospitals, Nottingham, UK
  3. 3James Cook University, Middlesbrough, UK
  4. 4Royal Brompton Hospital, London, UK
  5. 5St George's Hospital, University of London, London, UK
  1. Correspondence to Prof Huon H Gray, Wessex Cardiac Unit, Southampton University Hospital, Southampton SO16 6YD, UK; huon{at}

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Acute coronary syndromes are due to rupture or erosion of an atherosclerotic coronary artery plaque with superimposed platelet aggregation and coronary thrombosis. Complete thrombotic occlusion of a coronary artery generally causes acute ST-elevation myocardial infarction (STEMI), whereas incomplete occlusion will usually cause some myocardial necrosis (as shown by a rise in a cardiac-specific serum biomarker such as troponin) and is termed ‘non-ST elevation myocardial infarction’ (NSTEMI). When myocardial ischaemia is present without evidence of myocardial necrosis the clinical syndrome is described as unstable angina (UA). Hospital Episodes Statistics data for England suggest that there may be as many as 100 000–150 000 admissions with UA or NSTEMI per year (Green S, Personal communication, 2010). Although very early mortality (first few days) is lower for NSTEMI than for STEMI, over a longer period (6 months) their risk of death is comparable.1

The recently published NICE clinical guideline on the early management of UA and NSTEMI (CG94) examines selected aspects of in-hospital management, including risk assessment and its impact on patient management, antiplatelet and antithrombin therapy, the role of coronary angiography, revascularisation and intra-aortic balloon counterpulsation, testing for myocardial ischaemia and left ventricular function, specialist versus non-specialist care, rehabilitation and discharge planning. Detailed discussion of the evidence for the guideline can be found in the full version (, accessed August 2010), and this article summarises the most important conclusions. CG94 assumes that a firm diagnosis of UA or NSTEMI has already been established, and the differentiation of cardiac from non-cardiac chest pain is dealt with in separate NICE guidance (, accessed August 2010).

Risk assessment

An appreciation of an individual's risk of an adverse outcome following UA or NSTEMI is important when assessing which treatment strategies are most appropriate. For instance, antithrombotic agents may reduce further ischaemic events, but increase bleeding complications, and this balance of benefit and risk and hence the cost-effectiveness of treatment is influenced by the underlying risk of adverse cardiovascular events. If an effective intervention has the same relative benefit across all risk groups, the absolute number of adverse events avoided will be greatest in those at the highest level of underlying risk, though the risk of bleeding or other complications may also increase with underlying risk. The inter-relationship of risk and outcome has left those managing patients with UA or NSTEMI with a dilemma: should they offer a particular cocktail of drugs, each with evidence of benefit, to an individual patient or will this benefit be offset by the associated complications?

Many individual factors predict adverse outcomes in patients with UA or NSTEMI (Box 1) but a single risk variable may not provide a reliable assessment of risk. For instance, serum troponin level (a highly sensitive and specific marker of myocardial injury) has been associated with an increased risk of future adverse cardiovascular events, but does not accurately measure risk in individual patients, particularly when used as a dichotomous variable (troponin ‘positive/negative’). In comparison with a well-validated risk scoring system (GRACE) that uses multiple risk components to predict mortality, a significant number of troponin-positive patients were found to be at low risk, and conversely, some troponin-negative patients were at high risk.2 The guideline development group (GDG) therefore recommended the use of a validated risk scoring system (such as GRACE (Global Registry of Acute Cardiac Events)) to determine risk in individual patients (Box 2).3 4 The outcome variable selected was 6-month mortality because the GRACE score predicts this outcome reliably across all patient groups with ACS and at all levels of underlying risk. The GRACE score is derived from a large cohort of unselected patients with ACS, it is available online (, accessed August 2010), is easy to use and its components are an effective tool in an unselected UK population.5

Box 1 Factors predicting adverse outcome in unstable angina/non-ST elevation myocardial infarction

  • Advancing age

  • Presence and severity of ECG changes of ischaemia

  • Magnitude of rise in biomarkers of myocardial injury (eg, serum troponin)

  • Left ventricular dysfunction

  • Cardiogenic shock

  • Increased heart rate

  • Arrhythmias (ventricular, atrial fibrillation)

  • Renal impairment

  • Diabetes mellitus

  • Anaemia

  • Cerebrovascular disease

  • Peripheral vascular disease

Box 2 Global Registry of Cardiac Events (GRACE) risk score for in-hospital death with range of scores for each parameter in parentheses

  • Age (0–100)

  • Killip class (see below) (0–59)

  • Heart rate (0–46)

  • Systolic blood pressure (58–0)

  • Serum creatinine (1–28)

  • ST-segment deviation (28)

  • Cardiac arrest at admission (39)

  • Elevated serum cardiac enzymes (14)

  • Total possible score =372 points

GRACE risk score for death at 6 months with range of scores for each parameter in parentheses

  • Age (0–100)

  • Killip class (0–44)

  • Heart rate (0–34)

  • SBP (40–0)

  • Serum creatinine (1–28)

  • ST-segment deviation (17)

  • Cardiac arrest at admission (30)

  • Elevated serum cardiac enzymes (13)

  • Total possible score =306 points

NB: GRACE uses eight variables to derive a GRACE score, with two separate predictive models for in-hospital, and 6-month, mortality.3 4 The numeric GRACE score (summation of the numbers assigned to each variable) for an individual patient differs depending on the predictive model being used. See, accessed August 2010.

Killip class is defined as (1) no evidence of heart failure; (2) mild–moderate heart failure (third heart sound, rales <one-third up lung fields, raised jugular venous pressure (JVP)); (3) overt pulmonary oedema; (4) cardiogenic shock.

A modified version of GRACE (mini-GRACE)i was used to risk-stratify a cohort of 64 312 patients with UA/NSTEMI from the Myocardial Ischaemia National Audit Project (MINAP). The patients were divided into quartiles of risk, and the two lower-risk categories were further divided into octiles of risk to define six risk groups (table 1). The GDG superimposed these risk groups (table 1) onto a plot of GRACE score against predicted 6-month mortality (‘GRACE curve’, figure 1) to illustrate the relationship between the GRACE score and the spectrum of risk in the MINAP population. Plotting 6-month mortality data from randomised clinical trials (RCTs) on the ‘GRACE curve’ then allowed identification of those risk groups for whom an intervention is likely to have significant benefit, those where benefit has not been demonstrated and others (usually those at highest risk) who fall outside the RCT data. Most RCTs recruited patients at low to intermediate risk and patients at higher risk have generally been excluded from the evidence base. It was estimated that this lack of a firm evidence base could apply to as many as 40–50% of patients included in the MINAP registry. This exercise allowed the GDG to vary their recommendations according to the underlying risk of adverse cardiovascular events, particular in the sections on antiplatelet and antithrombin therapy, and on coronary angiography. Recommendations for those patients at high risk, who fall outside the evidence derived from RCTs, were based on consensus and highlighted the importance of balancing the benefits and risks of an intervention, and the potential value of more research in this area.

Table 1

Risk category and corresponding 6-month mortality for the Myocardial Ischaemia National Audit Project (MINAP) population with unstable angina or non-ST elevation myocardial infarction (n=64 312)

Figure 1

The curve shows the relationship between Global Registry of Acute Cardiac Events (GRACE) score and predicted 6 month mortality. The long vertical lines show the guideline risk groups derived from the quartiles and octiles of risk in the Myocardial Ischaemia National Audit Project (MINAP) registry (table 1). The very high risk group includes approximately 50% of the United Kingdom (MINAP) population with non-ST elevation-acute coronary syndrome (NSTE-ACS) at highest risk; other risk groups each include approximately 12.5% of the ACS population. The squares show 6 month mortality for patients enrolled in the RITA-3 trial and managed by an initial conservative strategy (bars are 95% CI) and plotted by RITA-3 risk stratum (1–4b).6 RITA-3 patients are representative of patients at low and intermediate levels of risk. Patients in the very high risk group were generally excluded from RITA-3 and from other randomised trials referred to in the guideline.

Antiplatelet therapy

The guideline recommends that aspirin (300 mg loading dose) should be given to all patients with UA/NSTEMI and continued indefinitely.


Clopidogrel is a thienopyridine that blocks platelets by inhibition of the P2Y12 (adenosine diphosphate) receptor. The guideline updates a previous appraisal of clopidogrel (TA80, 2004) and recommends a loading dose of 300 mg for patients with a 6 month predicted mortality >1.5%, (ie, all but the lowest risk group) and maintenance treatment (usually 75 mg daily) for 12 months. Emerging evidence supports a higher loading dose (600 mg) if angiography/PCI is scheduled within 24 h of admission, but the evidence base was insufficient to make a firm recommendation and higher loading doses are currently unlicensed in the United Kingdom. Some patients, for instance those who have had drug-eluting stents as part of complex PCI procedures, may be advised to remain on a P2Y12 receptor antagonist indefinitely.

Glycoprotein IIb/IIIa inhibitors

Glycoprotein IIb/IIIa inhibitors (GPIs) inhibit the final common pathway of platelet aggregation (cross-bridging of platelets by fibrinogen binding to the GPIIb/IIIa receptor). GPIs include abciximab (a monoclonal antibody fragment), tirofiban (a peptidomimetic) and eptifibatide (a cyclic heptapeptide). All GPIs are administered by intravenous infusion in weight-adjusted doses. Early clinical trials assessed the use of GPIs in combination with aspirin and heparin, and these trials were reviewed by NICE in 2002 (TA47). Since then the use of clopidogrel has increased considerably, and CG94 reassesses the place of GPIs against background treatment with aspirin, clopidogrel and an antithrombin agent. RCTs in patients with UA/NSTEMI, who were mostly treated with clopidogrel (ACUITY, EARLY-ACS), demonstrate that routine use of a GPI reduces the risk of cardiac ischaemic events but increases the risk of bleeding.7 8 The data from these trials were included in a health economic analysis and after considering this evidence the GDG concluded that GPIs are likely to be cost-effective for those at intermediate or higher risk (predicted 6-month mortality >3.0%) who are scheduled to undergo early angiography. In addition, CG94 recommends that abciximab should be considered as an adjunct to PCI for these patients, when not receiving a GPI already. Clinical judgement remains important in determining whether a GPI should be offered, and in individual patients the potential for a reduction in ischaemic risk must be balanced against any increase in risk of bleeding.

Antithrombin therapy

Unfractionated (UFH) and low molecular weight (LMWH) heparins are indirect thrombin inhibitors that form complexes with antithrombin and inactivate thrombin and factor Xa (and to a lesser extent, factors XIIa, XIa and IXa). Randomised trials and economic evaluation have shown that enoxaparin (LMWH) is at least comparable to, and probably better than, UFH in the treatment of patients with UA/NSTEMI. Fondaparinux is a synthetic pentasaccharide and the first of a new class of synthetic antithrombotic agents.


Fondaparinux binds to antithrombin with greater affinity than either UFH or LMWH, and increases the ability of antithrombin to inactivate clotting factor Xa. It has 100% bioavailability after subcutaneous administration and has a half-life much longer than those of UFH or LMWH.

The OASIS-5 trial randomised over 20 000 patients with UA or NSTEMI to receive either fondaparinux or enoxaparin. Patients who had serum creatinine levels >265 μmol/l were excluded. At 9 days the composite end point of death, MI or refractory ischaemia was no different between the fondaparinux and enoxaparin groups, but fondaparinux was associated with a significantly lower rate of major bleeding. This difference occurred irrespective of whether a thienopyridine or GPI was administered or whether patients underwent PCI. The reduction in bleeding persisted to 180 days and was associated with a reduction in mortality in the fondaparinux group.9

Catheter thrombosis at the time of angiography was reported in a small number of cases (0.9% for the fondaparinux group versus 0.4% for the enoxaparin group). Unlike UFH and enoxaparin, fondaparinux does not inhibit the contact clotting activation pathway (involving clotting factors XII, XI) and this may explain this difference, which was not associated with any difference in clinical events between the two treatment groups. The authors of OASIS-5 observed that addition of conventional doses of UFH to fondaparinux at the time of PCI provided protection against catheter thrombus but did not increase the risk of major bleeding. It is therefore recommended that fondaparinux-treated patients should be given adjunctive UFH at the time of PCI.9

OASIS-5 confirmed the importance of bleeding as a predictor of adverse outcome and the need for clinicians to be aware of this association when patients with UA or NSTEMI are offered combinations of antiplatelet and antithrombin agents. Renal dysfunction is known to increase the risk of an adverse cardiovascular event and major bleeding, and OASIS-5 excluded people with creatinine >265 μmol/l. Nevertheless, an exploratory analysis of OASIS-5 indicated that the benefit of fondaparinux over enoxaparin was greatest in those with the worse renal function within the trial population (glomerular filtration rates <58 ml/min).10 It would therefore be illogical to use dose-adjusted enoxaparin as an alternative to fondaparinux for patients with greater degrees of renal impairment (who were excluded from OASIS-5), especially as such dose adjustment is often not undertaken appropriately in practice.11

Although the evidence for fondaparinux is derived from a single RCT (OASIS-5), this was a large study of high quality. Moreover, fondaparinux is given once daily and does not require weight adjustment, unlike enoxaparin, which requires twice-daily administration and is weight dependent. Economic modelling undertaken for this guideline found that fondaparinux was cost-saving and improved clinical outcome. The guideline therefore recommends a change from the current use of LMWH in favour of fondaparinux. If angiography is planned within 24 h of admission, UFH is recommended as an alternative to fondaparinux because it is likely to be given anyway during the procedure. UFH, with dose adjusted to clotting function, is recommended for patients with a serum creatinine >265 μmol/l.


Bivalirudin is a direct inhibitor of soluble and clot-bound thrombin. It has a rapid onset of action with a half-life of 25 min, and is given as an intravenous infusion. In current UK practice bivalirudin is used as an alternative to the combination of heparin and a GPI during PCI. Its licence requires concomitant treatment with clopidogrel. The benefit of bivalirudin is predicated on its ability to reduce bleeding in patients who undergo angiography and it has not been shown to reduce ischaemic risk in comparison with patients who are treated with heparin and a GPI.12 13 The guideline modelled various uses of bivalirudin and found significant uncertainty about its cost-effectiveness, but concluded that it could be considered as an alternative to the combination of heparin and a GPI for patients at intermediate or higher risk (predicted 6-month mortality >3.0%) who are scheduled for angiography within 24 h from admission. Bivalirudin was not recommended for patients already receiving fondaparinux because there are no data to support such a change in antithrombin treatment.

Early invasive versus conservative management

For PCI or coronary artery bypass grafting (CABG) to be considered as treatment options for UA or NSTEMI, coronary angiography has to be undertaken first to define the extent and severity of coronary disease. Angiography may be undertaken early, deferred until later, or undertaken selectively if the person has evidence of recurrent ischaemia despite appropriate drug treatment. Randomised trials in patients with UA or NSTEMI have compared a routine early invasive strategy (coronary angiography and revascularisation as clinically indicated) with a conservative strategy (medical treatment with coronary arteriography reserved for patients with recurrent spontaneous or inducible ischaemia). Comparison of the people enrolled in these trials with the unselected cohort of MINAP patients (n= 64 312) suggested that the trials had mainly enrolled people at low to intermediate levels of risk and people at the highest levels of risk were usually excluded. An early invasive strategy was found to reduce the risk of recurrent ischaemia and infarction, an effect that was greatest in people at higher risk of such events. Conversely, those at lowest risk are likely to have a similar outcome whether managed initially with an early invasive strategy or conservatively. These findings are supported by the recent TIMACS trial,14 which was not available for review in this guideline.

In the randomised trials, the time to coronary angiography in patients assigned to the early invasive strategy was up to a median of 4 days. The European Society of Cardiology (ESC) has recommended 'early angiography' within 72 h but the ESC guideline does not state whether this time period is from hospital admission or the decision to undertake angiography.15 The GDG acknowledged that the optimum timing of angiography is controversial and it can be argued that the earlier angiography is undertaken the earlier a decision about revascularisation can be made. Lay representatives on the GDG were also keen that angiography should be made available at the earliest opportunity, provided that expedited investigation is not associated with greater risk. As further evidence emerges it may be that a shorter recommended time limit can be more strongly supported.

Based on the risk assessment exercise and its use in placing clinical trials in a UK context CG94 recommends that clinicians should:

  • Offer coronary angiography (with follow-on PCI if indicated) within 96 h of first admission to patients at intermediate or higher risk (predicted 6-month mortality >3.0%) and no contraindications (such as active bleeding or comorbidity).

  • Perform angiography as soon as possible for patients who are clinically unstable or at high ischaemic risk.

  • Offer conservative management without early coronary angiography to patients with low risk (predicted 6-month mortality <3.0%).

  • Consider testing for myocardial ischaemia (stress electrocardiography, myocardial perfusion scintigraphy, magnetic resonance imaging, stress echocardiography) before discharge from hospital in those patients managed conservatively.

  • Offer coronary angiography (with follow-on PCI if indicated) to patients initially assessed to be at low risk if ischaemia develops or is demonstrated.


Trials comparing PCI and CABG have predominantly enrolled people with stable angina rather than ACS, and have generally not enrolled the elderly (>75–80 years) or those at highest risk. Interpretation of trials is also confounded by changes in surgical and interventional techniques, and adjunctive pharmacotherapy over time. The GDG concluded that the available evidence supports the use of both revascularisation strategies in patients with UA and NSTEMI, and that the choice should take account of the extent and severity of coronary disease, left ventricular function, the presence of comorbidity, the estimated risk of each procedure and patients' informed choice. Lay representatives on the GDG emphasised the importance of individuals being fully informed of the relative risks, benefits and differences between the two procedures to allow an informed choice. Clinicians on the group also highlighted the need for an appropriate consent process, and the value of multidisciplinary meetings to agree the most appropriate treatment strategy when both are feasible.

Intra-aortic balloon counterpulsation

Intra-aortic balloon counterpulsation (IABP) was first described in 196216 and has been used as a means of supporting the circulation, predominantly in those with failing left ventricles (particularly cardiogenic shock), or as an adjunct to cardiac surgery or high-risk coronary angioplasty. Use of IABP increases diastolic blood pressure (thereby improving coronary blood flow) and reduces left ventricular afterload (thereby increasing cardiac output). In 2007 The British Cardiovascular Intervention Society reported IABP use as an adjunct to coronary angioplasty (PCI) in 983 cases (1.7% of all PCI cases).17 There was insufficient evidence on which to base firm recommendations, but the GDG concluded that clinicians should consider use of IABP for patients with recurrent myocardial ischaemia despite medical treatment, and for those who are haemodynamically unstable before surgical or percutaneous revascularisation.

Testing for left ventricular function

There is extensive literature on the association between the degree of left ventricular impairment and clinical outcome. However, much of this evidence is derived from people with stable coronary disease, which may be less applicable early after ACS when myocardial function can be influenced by temporary stunning, left ventricular remodelling or the effects of medication. During admission with an ACS, some people have echocardiography as part of their assessment, some have left ventriculography at the time of coronary angiography and some have radionuclide imaging for the assessment of myocardial ischaemia. All these tests provide an assessment of left ventricular function and it is likely that only a minority of people with UA or NSTEMI do not have an opportunity for their left ventricular function to be recorded during their hospital admission or shortly thereafter. In a previous clinical guideline on secondary prevention, assessment of left ventricular function was recommended in all people after MI (NSTEMI and STEMI). CG94 recommends that assessment of left ventricular function be considered in all people with UA and NSTEMI so that specific treatment for it can be offered to improve symptoms and outcome. The results of the assessment of left ventricular function should be documented in the person's care record and communicated to the primary healthcare team.

Specialist care

The management of ACS has become more complex with a range of diagnostic and therapeutic options. Many of these options—for example, continuous cardiac rhythm monitoring and the administration of specialist drugs, require staff with specialist knowledge and skills. Certain interventions now considered standard practice, such as coronary angiography, can also only be delivered in specialist environments by specialist teams. On the other hand, many people, including the elderly, are admitted to general wards and managed by general medical or elderly care teams, with referrals to specialist care being dependent on local custom and practice.

Data from registries (MINAP, CRUSADE) suggest that differences in practice may exist, particularly with respect to the uptake of secondary prevention treatments, and the use of angiography, and that there may be gender and age-related bias.18 19 Adherence to best practice guidelines is known to affect outcome but varies between institutions and types of healthcare services. The GDG concluded that there was insufficient evidence to make specific recommendations about the systems of care in which people with UA or NSTEMI are managed. Nevertheless, care delivered by skilled staff in properly equipped settings is the preferred pathway and this was supported strongly by the patient representatives on the group.

Rehabilitation and discharge planning

In 2000 the National Service Framework for Coronary Heart Disease (, accessed August 2010) recommended that more than 85% of people discharged from hospital with a primary diagnosis of acute MI, or after coronary revascularisation, should be offered cardiac rehabilitation. However, <50% of such people currently attend comprehensive cardiac rehabilitation. Uptake is particularly poor among ethnic minorities, women, the elderly, those on low incomes, or people with physical or mental comorbidities. In 2007 NICE published guidance on secondary prevention following MI (, accessed August 2010), and recommended rehabilitation. The British Association for Cardiac Rehabilitation (2007) have identified standards and core components for its delivery (, accessed August 2010). The GDG agreed that good evidence exists for the cost-effectiveness of a comprehensive rehabilitation process following MI. The patient representatives on the GDG emphasised the importance of patient information and education before discharge from hospital, and the need for this to be comprehensive, yet in a form that is appropriate to the individual, taking account of ethnic, cultural, gender and psychological differences. The over-riding consideration should be to ensure that the process is continuous and that responsibility for delivery of the components of rehabilitation (education, information, psychosocial support, structured exercise, etc) should be clearly attributed.


CG94 provides a detailed analysis of data within its scope and those who are interested in the topics outlined above are encouraged to refer to the full guideline ( Fondaparinux is recommended over low molecular weight heparin, and angiography (with follow-on PCI at the same procedure where appropriate) should be undertaken earlier than is often the case at present. The importance of formal risk assessment is emphasised, and analysis of risk is used in the guideline to draw conclusions about choice of drug treatments, and whether conservative or invasive management of patients with unstable angina or NSTEMI is appropriate. Balancing the risks of a patient's underlying condition and comorbidity, and the potential for treatment benefit and treatment-related complications, is complex and often has to be undertaken in the absence of a clear evidence base. The recommendations made within the guideline, summarised in its key messages for implementation (see below) and management algorithm (figure 2), are intended to assist clinicians in their deliberations and discussions with patients, but are not a substitute for individualised clinical management.

Figure 2

Algorithm for the management of patients with unstable angina and non-ST elevation myocardial infarction.

Key messages of the guideline (key priorities for implementation)

  • As soon as the diagnosis is made, and aspirin and antithrombin treatment have been offered, formally assess individual risk of future adverse cardiovascular events using an established risk scoring system that predicts 6-month mortality (for example, Global Registry of Acute Cardiac Events (GRACE)).

  • Consider intravenous eptifibatide or tirofiban as part of the early management for patients who have an intermediate or higher risk of adverse cardiovascular events (predicted 6-month mortality >3.0%), and who are scheduled to undergo angiography within 96 h of hospital admission.

  • Offer coronary angiography (with follow-on PCI if indicated) within 96 h of first admission to hospital to patients who have an intermediate or higher risk of adverse cardiovascular events (predicted 6-month mortality >3.0%) if they have no contraindications to angiography (such as active bleeding or comorbidity). Perform angiography as soon as possible for patients who are clinically unstable or at high ischaemic risk.

  • When the place of revascularisation or the revascularisation strategy is unclear, resolve this by discussion involving an interventional cardiologist, cardiac surgeon and other healthcare professionals relevant to the needs of the patient. Discuss the choice of revascularisation strategy with the patient.

  • To detect and quantify inducible ischaemia, consider ischaemia testing before discharge for patients whose condition has been managed conservatively and who have not had coronary angiography.

  • Before discharge offer patients advice and information about:

    • Their diagnosis and arrangements for follow-up (in line with 'MI: secondary prevention', NICE clinical guideline 48);

    • Cardiac rehabilitation (in line with 'MI: secondary prevention', NICE clinical guideline 48);

    • Management of cardiovascular risk factors and drug treatment for secondary prevention (in line with 'MI: secondary prevention', NICE clinical guideline 48, and 'Lipid modification', NICE clinical guideline 67);

    • Lifestyle changes (in line with 'MI: secondary prevention', NICE clinical guideline 48);

    • Health education.


View Abstract


  • Full membership of the Guideline Development Group

    Professor John Camm (Chair)

    BHF Professor of Clinical Cardiology, St. George's Hospital, University of London

    Prof Huon Gray

    Clinical Advisor, National Clinical Guideline Centre (NCGC), London; Consultant Cardiologist, Southampton University Hospital

    Mr Sotiris Antoniou Principal Cardiac Pharmacist, Barts and the London NHS Trust and Lead Pharmacist for North East London Cardiac and Stroke Network

    Ms Lina Bakhshi

    Senior Information Scientist, NCGC

    Ms Jenny Cadman

    Cardiac Rehabilitation Service Manager, Senior Nurse in Cardiology,

    Luton and Dunstable

    Dr Emily Crowe

    Senior Research Fellow, NCGC (from May 2008)

    Dr Mark de Belder

    Consultant Cardiologist, James Cook University Hospital, Middlesbrough

    Dr Jose Diaz

    Research Fellow, NCGC (until May 2008)

    Mr David H Geldard

    Patient/Carer representative; Immediate Past President, Heart Care Partnership (UK)

    Dr Robert Henderson

    Consultant Cardiologist, Nottingham University Hospitals

    Professor Marjan Jahangiri

    Professor of Cardiac Surgery, St George's Hospital, University of London

    Ms Taryn Krause

    Senior Project Manager, NCGC (from November 2008)

    Miss Kate Lovibond

    Health Economist, NCGC

    Mr Gavin Maxwell

    Patient/Carer representative, Patient and Carer Network,

    Royal College of Physicians of London

    Dr Francis Morris

    Accident and Emergency Physician, Sheffield University Hospitals

    Mr Alun Roebuck

    Cardiology Nurse Consultant, Sunderland

    Ms Nicola Sloan

    Research Fellow, NCBC (July 2008-March 2009)

    Ms Claire Turner

    Senior Project Manager, NCBC (until November 2008)

    Professor S Richard Underwood

    Professor of Cardiac Imaging, Royal Brompton Hospital, London

    Mr Mark Whitbread

    Clinical Practice Manager/Senior Paramedic/Cardiac Lead Medical Directorate, London Ambulance Service NHS Trust.

  • Funding This work was undertaken by National Clinical Guideline Centre for Acute and Chronic Conditions which received funding from the National Institute for Health and Clinical Excellence. The views expressed in this publication are those of the authors and not necessarily those of the Institute.

  • Competing interests None.

  • Provenance and peer review Not commissioned; externally peer reviewed.

  • i See full guideline for details of the modification, which used surrogates of heart failure and renal impairment recorded in MINAP, for Killip class and creatinine recorded in GRACE. Adjustment resulted in risk stratification by mini-GRACE being very similar to that of the full GRACE score.

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