Dr Alan Begg summarises SIGN recommendations for the immediate assessment, management, and discharge arrangements for people with acute coronary syndrome

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Read this article to learn more about:

  • assessment, diagnosis, and need for prompt transfer of patients to an appropriate centre
  • the management of ACS in the first 12 hours and up to and beyond hospital discharge
  • therapeutic and pharmacological interventions for ACS.

Key points

GP commissioning messages

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Box 1: NICE Accreditation Mark

NICE accreditation mark

SIGN Guideline 148 on Acute coronary syndrome has been awarded the NICE Accreditation Mark.

Coronary heart disease (CHD) remains a significant cause of mortality and morbidity in Scotland. In 2012, it accounted for 16% of all male deaths and 11% in women, as well as 17% and 9% of premature deaths in males and females, respectively. Patients with acute coronary syndrome (ACS) continue to have poor outcomes although the overall age–sex standardised mortality rates for myocardial infarction (MI) halved in Scotland between 2004 and 2013. This death rate, however, has fallen more slowly in women so that in 2014, cardiovascular disease (CVD) remained the leading cause of death in women but not in men.1

The original SIGN guideline on acute coronary syndrome was published in 2007 and updated in 2013. The latest version, SIGN 148, was released in April 2016 and has been awarded the NICE Accreditation Mark (see Box 1, below).1,2 In SIGN 148, text and recommendations are reproduced verbatim from SIGN 93 with no reappraisal of the original supporting evidence1 if no evidence was identified by the current guideline development group to support an update.

The guideline concentrates on the management of ACS in the first 12 hours and up to hospital discharge and only recommendations on dual antiplatelet therapy are made for the long term.1

Public education campaigns recommend the public to dial 999 if they develop severe chest pains suggestive of a suspected heart attack.3 The guideline refers to the pre-hospital management where appropriate but it does not make recommendations for the pre-hospital management by ambulance service personnel. Patients with ACS still do however present to primary care or the out-of-hours service, therefore the recommendations in the guideline remain relevant to primary care and general practice. One of the key aspects of the updated guideline is clarification on therapeutic recommendations and, specifically, on the use of dual antiplatelet drugs and the use of the newer drugs ticagrelor and prasugrel.


Acute coronary syndrome encompasses a spectrum of CHD from unstable angina to transmural MI, but all are due to the formation of thrombus on an inflamed and complicated atheromatous plaque. The definition and management depends on the specific characteristics of each element of the triad of clinical presentation, electrocardiogram (ECG) changes, and biochemical markers.

SIGN 148 focuses on how to manage unstable angina and spontaneous type 1 MI (see definition below). The evidence cannot be extrapolated to other types of MI; indeed, in some situations to do so may be harmful.

Definition of type 1: spontaneous myocardial infarction

The definition of type 1: spontaneous myocardial infarction quoted in SIGN 148 is:1,4'Spontaneous MI related to atherosclerotic plaque rupture, ulceration, fissuring, erosion, or dissection with resulting intramural thrombus in one or more of the coronary arteries leading to decreased myocardial blood flow or distal platelet emboli with ensuing myocyte necrosis. The patient may have severe underlying coronary artery disease (CAD) but on occasion non-obstructive or no CAD.'

Clinical presentation and immediate assessment

In patients presenting with likely ACS, no single sign or symptom taken in isolation has been found to be discriminatory but clinical risk factors should be considered together when assessing the likelihood of myocardial ischaemia. The diagnosis and management of a patient with suspected ACS requires a detailed clinical assessment and the recording of a 12-lead electrocardiogram (ECG).1

The recommendation is that this assessment should be done by an appropriate healthcare professional as soon as the patient presents. Best practice points suggest that repeat ECGs should be performed if there is diagnostic uncertainty, a change in the patient's clinical condition, and also prior to discharge. Patients with persisting bundle branch block or ST-segment change should be given a copy of their ECG in order to assist future clinical management in case they present again with suspected ACS.1

Patients with known CHD should follow the published British Heart Foundation (BHF) advice on the self-management of angina:5

  • stop what you are doing and sit down
  • take glyceryl trinitrate (GTN) spray or tablets
  • take a second dose if the pain does not ease within a few minutes
  • call 999 immediately if the pain does not ease within a few minutes after a second dose.

Biochemical diagnosis

The diagnosis of MI depends on the measurement of a rise and/or fall in cardiac troponin concentration but this should not be relied on in isolation. High-sensitivity cardiac troponin assays seem to improve diagnostic accuracy for MI but there is insufficient evidence to suggest that they improve patient outcomes; however, their use permits the use of lower diagnostic thresholds than with standard assays and allows earlier testing, which may reduce unnecessary hospital admissions, the time taken for test results, and consequently the anxiety felt by patients and carers.

Combining high sensitivity troponin assays with sex-specific diagnostic thresholds has been shown to improve the diagnosis of myocardial infarction in women, and so could lead to more effective identification of women at high risk of reinfarction and death.1

Clinicians should be aware that elevated troponin concentrations can occur in patients without myocardial injury due to ACS, so the advice from the guideline group is that troponin levels should not be interpreted in isolation but in the context of the clinical presentation of the patient.1

The guideline recommends that:1

  • troponin concentration should be measured:
    • at presentation to guide management and treatment
    • 12 hours after the onset of symptoms to establish a diagnosis of MI
  • measurement with a high-sensitivity assay at presentation and at 3 hours after presentation should be considered as an alternative to rule out an MI
  • sex-specific thresholds should be used for the diagnosis of MI.

Initial management (first 12 hours)

There is retrospective evidence that patients are more likely to receive appropriate evidence-based therapies when treated within a specialist cardiology service and this is more relevant in the context of the increased role of invasive coronary angiography and revascularisation.1

Cardiac monitoring and oxygen therapy

Patients with ACS should receive continuous cardiac rhythm monitoring to facilitate the prompt recognition and treatment of cardiac arrest. There is however no evidence that the routine administration of oxygen to all patients with ACS improves clinical outcome or reduces the infarct size.1

Therapeutic recommendations Antiplatelet therapy

SIGN 148 makes the following recommendations about antiplatelet therapy:1

  • if there are ischaemic ECG changes or there is elevation of cardiac troponin, loading doses of 300 mg aspirin plus 180 mg ticagrelor should be given immediately
  • aspirin and a loading dose of 60 mg prasugrel may be considered for people undergoing percutaneous coronary intervention (PCI)
  • A 300 mg loading dose of clopidogrel should be considered as an alternative to ticagrelor or prasugrel if the bleeding risks of those two agents outweigh their benefits (i.e. in reducing recurrent atherothrombotic events).

Anticoagulant therapy

Fondaparinux or low molecular weight heparin should be given immediately in ACS if there are ischaemic ECG changes or elevation of cardiac markers. People with ST-segment-elevation acute coronary syndrome (STEACS) should be given fondaparinux immediately if they are not receiving reperfusion therapy.

It is suggested that anticoagulation therapy should be continued for 8 days, or until hospital discharge or coronary revascularisation.

Beta blockers

The early benefits of beta blockade therapy were shown before the widespread use of thrombolytic therapy, but a recommendation is however made to consider intravenous and oral beta blockade immediately in patients with ACS if there is no bradycardia, hypotension, or clinical evidence of heart failure.

Glycaemic control

On the basis of the DIGAMI 1 and 2 trials,6,7 patients with diabetes or who have a high blood sugar (>11 mmol/l) should on confirmation of ACS receive immediate blood glucose control aiming for a glucose concentration of 7.0 to 10.9 mmol/l; however, initiating this approach should not delay time-dependent interventions such as primary PCI.

Coronary intervention

The revascularisation approach to the management of patients with acute ACS depends on whether or not there is elevation of the ST segment. In STEACS, primary PCI is superior to thrombolysis and local protocols are required to ensure immediate primary PCI in an interventional centre. Thrombolytic therapy should be given either pre-hospital or on admission if primary PCI cannot be given within 120 minutes of ECG diagnosis. A fibrin-specific agent that can be given as a bolus, such as tissue plasminogen activator (alteplase), should be the thrombolytic therapy of choice to help reduce treatment delays. Rescue PCI should be considered for those who fail to reperfuse if they present within 6 hours of symptom onset.1

Patients who have multi-vessel disease and present with STEACS are at higher risk of future events compared with those who have single-vessel disease. Possible treatment strategies are culprit-only PCI or complete revascularisation with multi-vessel PCI. The SIGN guideline development group was of the opinion that there was insufficient evidence to support a recommendation on the ideal approach and that clinical judgment was important to identify patients at low risk of complications from complete revascularisation.1

The recommendation for early coronary angiography and revascularisation in patients with non-STEACS (NSTEACS) is based on the TACTIC-TIMI-18 and FRISC II trials.8,9 People assessed to be at medium to high risk of early recurrent cardiovascular events in the short term (6–12 months) should undergo early intervention. On the basis of greater generalisability and accuracy, the use of the global registry of acute coronary events (GRACE) score for risk stratification is favoured in patients with ACS.1

Using the radial artery route for vascular access is preferred to the femoral one because it reduces the risk of major adverse cardiovascular events and associated major bleeding. Slightly longer procedure times with the radial arterial route were noted to be of no clinical relevance.1

Coronary artery bypass grafting

Both PCI and coronary artery bypass grafting (CABG) are options for treating patients with obstructive coronary disease, including people with ACS. The decision on the approach to be taken will depend on the balance of benefit and risk in specific subgroups of patients, taking into account patient preferences, comorbidities, disease complexity, and local expertise, and will involve a multidisciplinary team approach.1 On cost effective comparisons, PCI is unlikely to be cost effective compared with CABG because of the need for repeat revascularisation over time with PCI. The guideline suggests that CABG should be considered in people who are not at high surgical risk with:1

  • diabetes mellitus
  • left main-stem disease
  • multivessel disease.

Pharmacological intervention

Long-term pharmacological therapy following discharge, which is of particular interest to primary care, was beyond the scope of this guideline; recommendations are, however, made for therapies beyond the first 12 hours after an episode of ACS, which do have a relevance for the long term.


All patients should be maintained on long-term aspirin following ACS. The suggested dose is 75 mg rather than the 75 to 150 mg range suggested in the previous guideline.

Dual antiplatelet therapy

SIGN 148 recommends dual antiplatelet therapy for 6 months, with longer durations for people at higher risk of atherothrombotic events in relation to the bleeding risk and shorter durations where the risks of bleeding outweigh the risks of atherothrombotic events. The guideline does point out that there is a lack of contemporary evidence for the optimal duration of dual therapy for those patients who do not undergo PCI.1


In view of the higher bleeding risk, the oral anticoagulants rivaroxaban, apixaban, or dabigatran should not be offered in addition to dual antiplatelet therapy. In one systematic review, although there was a small reduction in major adverse cardiovascular events (hazard ratio [HR] 0.87), the HR of clinically significant bleeding was 2.34.1,10

Statin therapy

Long-term statin therapy should be started prior to hospital discharge.1

Beta-blocker therapy

Beta-blocker therapy after ACS should be maintained long term. A meta-analysis showed after an MI a 23% relative risk reduction (RRR) in total mortality and a 32% RRR in sudden death for those taking long-term beta blockers.1,11

The CAPRICORN trial reported positive results associated with beta blocker use specifically in patients with low ejection fraction following MI, and that delayed and cautious up titration resulted in 3% absolute RR (23% RRR) in all-cause mortality compared with placebo.1


A best-practice point suggests the use of nitrates to relieve cardiac pain due to continuing ischaemia or to treat heart failure. Rate-limiting calcium channel blocking drugs have not been shown to reduce mortality or reinfarction rates.

Angiotensin-converting enzyme inhibitors

Those with unstable angina and MI should be commenced on long-term angiotensin-converting enzyme inhibitor (ACEI) therapy and for the latter group this should be within the first 36 hours. Angiotensin receptor blockers (ARBs) are useful alternatives if there is ACEI intolerance after an MI but only if the MI is complicated by left ventricular dysfunction (HF-REF) or heart failure. In head-to-head trials between and ACEI and ARB, not all trials have consistently shown noninferiority for the ARB compared with the ACEI.1

Mineralocorticoid receptor antagonists

In patients post MI complicated by reduced ejection fraction (<40%) and in the presence of clinical features of heart failure or diabetes, long-term eplenerone therapy should be commenced.1

Patient information

Identifying and addressing psychological distress early can reduce morbidity, and standardised screening tools such as the Hospital Anxiety and Depression (HAD) Scale should be used to identify those most at risk.12 Interventions should identify and address health beliefs and cardiac misconceptions and this phase of the rehabilitation process should form part of a menu-driven cardiac rehabilitation programme and patient pathway.13

In order to understand the information needs of patients, carers, and families after an ACS event, the patient and lay representatives on the guideline group identified the key information that was required at different stages of the patient journey. The Scottish health charity, Chest Heart and Stroke Scotland (CHSS) works in the community to improve the quality of life for patients with heart disease. Their health information team distributes a range of constantly updated booklets and factsheets throughout Scotland for these patients.14 Demand for patient information is high; the CHSS booklet Heart Attack: a guide to your recovery is one of their most popular booklets with over 4000 distributed in the last year.15


The management of heart disease remains a significant component of a primary care workload. Within scheduled and out-of-hours care, patients can present with chest pain suggestive of ACS and in some areas, especially more remote and rural areas, GPs may be part of the emergency response in conjunction with the ambulance service. Although the acute management of ACS has become more specialised, those working in primary care need to be knowledgeable about the presentation of ACS, the initial management, and the need for prompt transfer to an appropriate centre. Those involved in the commissioning of care need to be aware of and ensure that all patients in their area receive the best up-to-date, evidence-based management. The primary care team has an important role to play in ensuring the appropriate cardiac rehabilitation, long-term monitoring, and therapeutic management as well as psychosocial care of the patient, carers, and family.

Conflict of interest

The author is a trustee of CHSS.

Key points

Coronary heart disease (CHD) remains a significant cause of mortality and morbidity in Scotland. In 2012, it accounted for 16% of all male deaths and 11% in women, as well as 17% and 9% of premature deaths in males and females, respectively. Patients with acute coronary syndrome (ACS) continue to have poor outcomes although the overall age–sex standardised mortality rates for myocardial infarction (MI) halved in Scotland between 2004 and 2013. This death rate, however, has fallen more slowly in women so that in 2014, cardiovascular disease (CVD) remained the leading cause of death in women but not in men.1

The original SIGN guideline on acute coronary syndrome was published in 2007 and updated in 2013. The latest version, SIGN 148, was released in April 2016 and has been awarded the NICE Accreditation Mark (see Box 1, below).1,2 In SIGN 148, text and recommendations are reproduced verbatim from SIGN 93 with no reappraisal of the original supporting evidence1 if no evidence was identified by the current guideline development group to support an update.

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GP commissioning messages 

written by Dr David Jenner, GP, Cullompton, Devon

  • SIGN 148 was developed for use in Scotland but commissioners in England and Wales can use this guidance to inform their local commissioning intentions
  • Initial suspected ACS should be investigated with an ECG and a troponin T test:
    • SIGN 148 recommends a high-sensitivity assay is used at baseline and 3 hours providing more rapid confirmation than the standard 12-hour troponin test
  • In England and Wales, NICE guidance differs from the recommendations in SIGN 148 on initial dual pharmacological therapy with aspirin and ticagrelor—CCGs should make local decisions on this issue with the involvement of local specialist teams
  • Commissioners should agree quality standards for intra-hospital care with local trusts and specify required interventions to be completed before discharge
  • Commissioners will need to ensure that acute PCIs are available for raised ST segment MI in specialist centres where possible or, if unavailable, thrombolysis within 120 minutes of ECG diagnosis
  • Cardiac rehabilitation and post-discharge support is an important intervention to be commissioned to ensure patents receive optimal secondary prevention.

ECG=electrocardiogram; PCIs=percutaneous coronary interventions; MI=myocardial infarction

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  1. Scottish Intercollegiate Guidelines Network. Acute coronary syndrome. SIGN 148. Edinburgh: SIGN, 2016. Available at: www.sign.ac.uk/guidelines/fulltext/148
  2. Scottish Intercollegiate Guidelines Network.Acute coronary syndromes. SIGN 93. Edinburgh: SIGN, 2007.
  3. British Heart Foundation website. Heart attack. www.bhf.org.uk/heart-health/conditions/heart-attack (accessed 5 July 2016).
  4. Thygesen K, Alpert J, Jaffe A et al: the Writing Group on behalf of the Joint ESC/ACCF/AHA/WHF Task Force for the Universal Definition of Myocardial Infarction. Third universal definition of myocardial infarction. J Am Coll Cardiol 2012; 60 (16): 1581–1598.
  5. British Heart Foundation website. Angina. www.bhf.org.uk/hearthealth/conditions/angina (accessed 5 July 2016).
  6. Malmberg K, Rydén L, Efendic S et al on behalf of the DIGAMI study group. Randomized trial of insulin-glucose infusion followed by subcutaneous insulin treatment in diabetic patients with acute myocardial infarction (DIGAMI study): effects on mortality at 1 year. J Am Coll Cardiol 1995; 26 (1): 57–65.
  7. Malmberg K, Norhammar A, Wedel H, Rydén L. Glycolmetabolic state at admission: important risk marker of mortality in conventionally treated patients with diabetes mellitus and acute myocardial infarction: long-term results from the Diabetes and Insulin-Glucose Infusion in Acute Myocardial Infarction (DIGAMI) study. Circulation 1999; 99 (20): 2626–2632.
  8. Lagerqvist B, Diderholm E, Lindahl B et al. FRISC score for selection of patients for an early invasive treatment strategy in unstable coronary artery disease. Heart 2005; 91 (8): 1047–1052.
  9. Januzzi J, Buros J, Cannon C on behalf of the Tactics TIMI 18 Investigators. Peripheral arterial disease, acute coronary syndromes, and early invasive management: the TACTICS TIMI 18 trial. Clin Cardiol 2005; 28 (5): 238–242.
  10. Douxfils J, Buckinx F, Mullier F et al. Dabigatran etexilate and risk of myocardial infarction, other cardiovascular events, major bleeding, and all-cause mortality: a systematic review and meta-analysis of randomized controlled trials. J Am Heart Assoc 2014; 3: e000515. doi: 10.1161/JAHA.113.000515.
  11. Freemantle N, Cleland J, Young P et al. Beta blockade after myocardial infarction: systematic review and meta regression analysis. BMJ 1999: 318 (7200): 1730–1737.
  12. Zigmond A, Snaith R. The hospital anxiety and depression scale. Acta Psychiatr Scand 1983; 67 (6): 361–370.
  13. Begg A. New SIGN guideline underlines importance of cardiac rehabilitation. Guidelines in Practice, April 2002. Available at: www.guidelinesinpractice.co.uk/apr_02_begg_sign_apr02
  14. Chest Heart and Stroke Scotland website. Coming to terms with a heart attack. www.chss.org.uk/heart-information-and-support/about-your-heart-condition/common-heart-conditions/heart-attack/coming-to-terms-with-a-heart-attack/ (accessed 5 July 2016).
  15. Chest, Heart and Stroke Scotland. Heart attack: a guide to your recovery. CHSS, 2013. Available at: www.chss.org.uk/documents/2014/01/heart-attack-guiderecovery.pdfG