These clinical guidelines have been developed to assist in managing patients presenting with chest pain suspected to be caused by an acute coronary syndrome (ACS) and those with confirmed ACS. The development of these guidelines has been informed by reviews of the literature dealing with key aspects of chest pain assessment and ACS care, as well as broad consultation with local opinion leaders, stakeholder groups and the public. The recommendations focus on the core clinical and system-based components of care most associated with improved clinical outcomes. As such, these guidelines should be read in conjunction with the Acute coronary syndromes clinical care standard, developed by the Australian Commission on Safety and Quality in Health Care,1 and the Australian acute coronary syndromes capability framework, developed by the National Heart Foundation of Australia (NHFA).2 Guidance regarding both the strength of evidence supporting the recommendations and their potential impact on outcomes is provided to assist in informing clinical practice.3,4 Additional guidance regarding the timing and considerations informing the use of therapies and management strategies is given in the accompanying practice advice. A full version of the NHFA and Cardiac Society of Australia and New Zealand (CSANZ) Australian clinical guidelines for the management of acute coronary syndromes 2016 is available at: http://heartfoundation.org.au/for-professionals/clinical-information/acute-coronary-syndromes.

Methods

The NHFA, in partnership with the CSANZ, has undertaken an update to the NHFA/CSANZ Guidelines for the management of acute coronary syndromes 2006 and addenda of 2007 and 2011.5–7 The updated guideline will provide a synthesis of current evidence-based guidance for health professionals caring for patients with ACS.

The ACS Guideline Development Working Group comprised an Executive and the four writing groups of which it had oversight, covering the topics of chest pain, ST segment elevation myocardial infarction (STEMI), non-ST segment elevation ACS (NSTEACS) and secondary prevention. In addition, a Reference Group included representatives from stakeholder groups, potential endorsing organisations and regional experts. The Working Group comprised a broad mix of health professionals, including a general practitioner, general physician, cardiac surgeon, consumer representative, pathologist, ambulance service representative, cardiologists, emergency physicians, exercise physiologists and cardiac nurses.

The Working Group consulted state-based cardiac clinical networks and the Reference Group on the scope determination for the updated guideline. Based on this consultation, the expert Working Group generated clinical questions to inform the literature search of evidence required for the guideline’s development. The separate writing groups reviewed and graded the evidence, generated and graded recommendations, and produced draft sections for the four topic areas. The Executive group provided oversight for this process and approved the final document.

A draft of the guideline was open for a 30-day period of public consultation in April 2016 to capture stakeholder views and aid engagement with the guideline once completed. Attention has been paid to ensuring appropriate governance processes were in place, to ensure transparency, minimise bias, manage conflict of interest and limit other influences during guideline development.

Key evidence-based recommendations

Each recommendation is presented with a Grading of Recommendations Assessment, Development and Evaluation (GRADE) strength of recommendation (Appendix 1) and a National Health and Medical Research Council level of evidence (Level) (Appendix 2). Practice points (PPs) are also provided.

Assessment of possible cardiac causes of chest pain

• It is recommended that a patient with acute chest pain or other symptoms suggestive of an ACS receives a 12-lead electrocardiogram (ECG), and this ECG is assessed for signs of myocardial ischaemia by an ECG-experienced clinician within 10 minutes of first acute clinical contact.8 GRADE: Strong; Level: IIIC

  • PP: Oxygen supplementation. The routine use of oxygen therapy among patients with a blood oxygen saturation (SaO₂) level > 93% is not recommended, but its use when the SaO₂ is below this level is advocated, despite the absence of clinical data.9,10 However, care should be exercised in patients with chronic obstructive pulmonary disease where the target SaO₂ level is to be 88–92%.

  • PP: Initial aspirin therapy. In all patients with possible ACS and without contraindications, aspirin (300 mg orally, dissolved or chewed) should be given as soon as possible after presentation. Additional antiplatelet and anticoagulation therapy, or other therapies such as β-blockers, should not be given to patients without a confirmed or probable diagnosis of ACS.

• A patient presenting with acute chest pain or other symptoms suggestive of an ACS should receive care guided by an evidence-based Suspected ACS Assessment Protocol (Suspected ACS-AP) that includes formal risk stratification.11 GRADE: Strong; Level: IA

  • PP: Selecting and implementing a Suspected ACS-AP. For hospitals using sensitive or highly sensitive troponin assays, the ADAPT or modified ADAPT protocol, respectively, identifies low risk patients (< 1% major adverse cardiac events [MACE] at 30 days) on the basis of negative troponin test results at both 0 and 2 hours, a Thrombolysis in Myocardial Infarction (TIMI) risk score of 0 (ADAPT) or 0 or 1 (modified ADAPT), and no ischaemic changes on ECG at both 0 and 2 hours.12,13

• Using serial sampling, cardiac-specific troponin levels should be measured at hospital presentation and at clearly defined periods after presentation using a validated Suspected ACS-AP in patients with symptoms of possible ACS.14 GRADE: Strong; Level: IA

  • PP: Timing of troponin testing. Most patients with an underlying diagnosis of acute myocardial infarction (AMI) have elevated troponin levels within 3–6 hours of symptom onset, although some assays may not show elevated levels for up to 12 hours (Box 1). Validated rapid rule-in and rule-out algorithms for AMI incorporated into Suspected ACS-APs and/or using highly sensitive troponin assays may reduce the serial testing time to 1–2 hours after presentation.18,19,21,24,25 Incorporating sensitive or highly sensitive troponin assay results into the ADAPT or modified ADAPT protocol, respectively, allows early (2 hours after emergency department presentation) risk stratification.12,13

• Non-invasive objective testing is recommended in intermediate risk patients, as defined by a validated Suspected ACS-AP, with normal serial troponin and ECG testing and who remain symptom free.26 GRADE: Weak; Level: IA

  • PP: Timing of testing. High risk patients require further objective testing during the index admission (Box 2). Intermediate risk patients may be safely accelerated for early inpatient testing or discharged for outpatient testing, ideally within 7 days but acceptable up to 14 days after presentation. Investigation before discharge from the emergency department is desirable among patients with characteristics associated with significant failure to re-attend for medical review, given the higher rates of MACE in such patients.27

• Patients in whom no further objective testing for coronary artery disease is recommended are those at low risk, as defined by a validated Suspected ACS-AP: age < 40 years, symptoms atypical for angina, in the absence of known coronary artery disease, with normal troponin and ECG testing and who remain symptom free.26 GRADE: Weak; Level: III-3C

Diagnostic issues, risk stratification and acute management of ACS

• The routine use of validated risk stratification tools for ischaemic and bleeding events (eg, GRACE score for ischaemic risk and CRUSADE score for bleeding risk) may assist in patient-centric clinical decision making in regards to ACS care.28–30 GRADE: Weak; Level: IIIB

  • PP: Choice of risk score. For ischaemic risk, the GRACE risk score is superior to the TIMI risk score in terms of discriminating between high risk and intermediate or low risk patients.28 However, estimating risk of death or recurrent myocardial infarction (MI) for an individual patient depends on local validation. For bleeding risk, the CRUSADE risk score is preferred, although it has limited validation in the Australian setting.31

Acute reperfusion and invasive management strategies for ACS

• For patients with STEMI presenting within 12 hours of symptom onset, and in the absence of advanced age, frailty and comorbidities that influence the individual’s overall survival, emergency reperfusion therapy with either primary percutaneous coronary intervention (PCI) or fibrinolytic therapy is recommended.32,33 GRADE: Strong; Level: IA

  • PP: ECG interpretation. In situations where expertise in ECG interpretation may not be available, an electronic algorithm for ECG interpretation (coupled with review by an expert) can assist in diagnosing STEMI. Local or state care pathways should incorporate means for allowing expert ECG reading within 10 minutes of first contact, integrated with clinical decision making to enable timely reperfusion.

• Primary PCI is preferred for reperfusion therapy in patients with STEMI if it can be performed within 90 minutes of first medical contact; otherwise, fibrinolytic therapy is preferred for those without contraindications.34–36 GRADE: Strong; Level: IA

  • PP: Strategies for reducing the time to reperfusion therapy. Coordinated protocols with planned decision making that incorporates ambulance services and paramedics, first-responder primary care physicians, and emergency and cardiology departments are critical for achieving acceptable reperfusion times. Strategies need to be tailored to the local community and the distribution of emergency services. Strategies that effectively shorten the time to reperfusion include: developing hospital networks with pre-determined management pathways for reperfusion; pre-hospital ECG and single call catheter laboratory activation; pre-hospital fibrinolytic therapy administered by suitably trained clinicians (eg, paramedics); the bypassing, where appropriate, of non-PCI-capable hospitals; and bypassing the emergency department on arrival in PCI-capable centres. Furthermore, an established capability for timely expert consultation for complex clinical scenarios is highly desirable. In the context of a system-based approach to reperfusion, the capacity for continuous audit and feedback is also advocated.

• Among patients treated with fibrinolytic therapy who are not in a PCI-capable hospital, early or immediate transfer to a PCI-capable hospital for angiography, and PCI if indicated, within 24 hours is recommended.37 GRADE: Weak; Level: IIA

• Among patients treated with fibrinolytic therapy, for those with ≤ 50% ST recovery at 60–90 minutes and/or with haemodynamic instability, immediate transfer for angiography with a view to rescue angioplasty is recommended.38 GRADE: Strong; Level: IB

  • PP: Hospital networks. Systems of care should be developed to provide advice and enable, when appropriate, immediate or early transfer for angiography of patients treated with fibrinolytic therapy who are not in a PCI-capable hospital.

• Among high and very high risk patients with NSTEACS (except type 2 MI [secondary to ischaemia due to either increased oxygen demand or decreased supply]), a strategy of angiography with coronary revascularisation (PCI or coronary artery bypass grafting [CABG]), where appropriate, is recommended.39 GRADE: Strong; Level: IA

  • PP: Mode of revascularisation. Patient comorbidities, fitness for major surgery and coronary anatomy are the main determinants. Urgent revascularisation with CABG may be indicated for patients with failed PCI, cardiogenic shock or mechanical defects resulting from MI (eg, septal, papillary muscle or free-wall rupture). A combined Heart Team approach may provide the best consensus decision about the care of an individual patient.

  • PP: Invasive management for type 2 MI. Type 2 MI remains a challenging diagnosis, and no trials have examined the benefits of a routine invasive strategy in patients with type 2 MI. In the absence of any trial evidence, angiography with a view to revascularisation may be considered if there is ongoing ischaemia or haemodynamic compromise despite adequate treatment of the underlying acute medical problem that provoked the type 2 MI.

• Patients with NSTEACS who have no recurrent symptoms and no risk criteria are considered at low risk of ischaemic events and can be managed with a selective invasive strategy guided by provocative testing for inducible ischaemia.39 GRADE: Strong; Level: IA

• Very high risk patients: Among patients with NSTEACS with very high risk criteria (ongoing ischaemia, haemodynamic compromise, arrhythmias, mechanical complications of MI, acute heart failure, recurrent dynamic or widespread ST segment and/or T wave changes on ECG; Box 3), an immediate invasive strategy is recommended (ie, within 2 hours of admission).40 GRADE: Strong; Level: IIC

• High risk patients: In the absence of very high risk criteria, for patients with NSTEACS with high risk criteria (GRACE score > 140, dynamic ST segment and/or T wave changes on ECG or rise and/or fall in troponin compatible with MI; Box 3), an early invasive strategy is recommended (ie, within 24 hours of admission).40 GRADE: Weak; Level: IC

• Intermediate risk patients: In the absence of high risk criteria, for patients with NSTEACS with intermediate risk criteria (such as recurrent symptoms or substantial inducible ischaemia on provocative testing; Box 3), an invasive strategy is recommended (ie, within 72 hours of admission).40–42 GRADE: Weak; Level: IIC

Pharmacology for ACS

• Aspirin 300 mg orally (dissolved or chewed) initially, followed by 100–150 mg/day, is recommended for all patients with ACS, in the absence of hypersensitivity.43 GRADE: Strong; Level: IA

• Among patients with confirmed ACS at intermediate to very high risk of recurrent ischaemic events, use of a P2Y₁₂ inhibitor (ticagrelor 180 mg orally, then 90 mg twice a day; or prasugrel 60 mg orally, then 10 mg daily; or clopidogrel 300–600 mg orally, then 75 mg daily) is recommended in addition to aspirin (ticagrelor or prasugrel preferred; see below).44–47 GRADE: Strong; Level: IA

  • PP: Choosing between P2Y₁₂ inhibitors. Given their superior efficacy, ticagrelor and prasugrel are the preferred first-line P2Y₁₂ inhibitors. Use of ticagrelor is advised for a broad spectrum of patients with STEMI or NSTEACS who are at intermediate to high risk of an ischaemic event, in the absence of atrioventricular conduction disorders (second and third degree atrioventricular block) and asthma or chronic obstructive pulmonary disease. Prasugrel may be considered for patients who have not received a P2Y₁₂ antagonist and in whom PCI is planned, but it should not be used for patients > 75 years of age, of low bodyweight (< 60 kg) or with a history of transient ischaemic attack or stroke. Use of either prasugrel or ticagrelor, rather than clopidogrel, is also recommended for patients who have experienced recurrent events while taking clopidogrel or who have experienced stent thrombosis. Clopidogrel is recommended for patients who cannot receive ticagrelor or prasugrel, as an adjunctive agent with fibrinolytic therapy or for those requiring oral anticoagulation (refer to relevant prescribing information documentation). Ticagrelor or clopidogrel should be commenced soon after diagnosis, but due consideration should be given to ischaemic and bleeding risks, the likelihood of need for CABG (more likely in patients with extensive ECG changes, ongoing ischaemia or haemodynamic instability) and the delay to angiography. Prasugrel should be commenced immediately after diagnosis among patients undergoing primary PCI for STEMI, or after the coronary anatomy is known among those undergoing urgent PCI. Initiation of prasugrel before coronary angiography outside the context of primary PCI is not recommended.

  • PP: Combination of P2Y₁₂ inhibition with long term anticoagulation. Among patients with an indication for oral anticoagulation, a careful assessment of thrombotic and bleeding risks is required, using CHA₂DS₂-VASc and HAS-BLED scores, respectively. The following advice is based on consensus opinion. In patients with a strong indication for long term anticoagulation (ie, mechanical heart valves, atrial fibrillation with CHA₂DS₂-VASc score ≥ 2), the anticoagulant should be continued at a reduced dose, and clopidogrel, rather than ticagrelor or prasugrel, should be used for these patients. The duration of triple therapy (ie, aspirin, clopidogrel and oral anticoagulation) should be determined by the bleeding risk.

• Intravenous glycoprotein IIb/IIIa inhibition in combination with heparin is recommended at the time of PCI among patients with high risk clinical and angiographic characteristics or for treating thrombotic complications among patients with ACS.48 GRADE: Strong; Level: IB

• Either unfractionated heparin or enoxaparin is recommended in patients with ACS at intermediate to high risk of ischaemic events.49,50 GRADE: Strong; Level: IA

  • PP: Choosing between indirect thrombin inhibitors. Enoxaparin may be preferred over unfractionated heparin as it does not require monitoring of partial thromboplastin time and is simpler to administer. Swapping between enoxaparin and unfractionated heparin has been shown to increase bleeding risk and is not recommended.

• Bivalirudin (0.75 mg/kg intravenously with 1.75 mg/kg/h infusion) may be considered as an alternative to glycoprotein IIb/IIIa inhibition and heparin among patients with ACS undergoing PCI with clinical features associated with an increased risk of bleeding events.51 GRADE: Weak; Level: IIB

Discharge management and secondary prevention

• Aspirin (100–150 mg/day) should be continued indefinitely unless it is not tolerated or an indication for anticoagulation becomes apparent.43 GRADE: Strong; Level: IA

• Clopidogrel should be prescribed if aspirin is contraindicated or not tolerated. GRADE: Strong; Level: IA

• Dual antiplatelet therapy with aspirin and a P2Y₁₂ inhibitor (clopidogrel or ticagrelor) should be prescribed for up to 12 months in patients with ACS, regardless of whether coronary revascularisation was performed. The use of prasugrel for up to 12 months should be confined to patients receiving PCI. GRADE: Strong; Level: IA

• Consider continuation of dual antiplatelet therapy beyond 12 months if ischaemic risks outweigh the bleeding risk of P2Y₁₂ inhibitor therapy; conversely, consider discontinuation if bleeding risk outweighs ischaemic risks.52 GRADE: Weak; Level: IIC

• Initiate and continue indefinitely, the highest tolerated dose of an HMG-CoA (3-hydroxy-3-methylglutaryl-coenzyme A) reductase inhibitor (statin) for a patient following hospitalisation with ACS, unless contraindicated or there is a history of intolerance.53 GRADE: Strong; Level: IA

  • PP: Target cholesterol levels. There is additional benefit from progressive lowering of cholesterol levels, with no apparent lower limit. Within the context of an individualised care plan, a target low density lipoprotein cholesterol level of less than 1.8 mmol/L is suggested in the first instance.

• Initiate treatment with vasodilatory β-blockers in patients with reduced left ventricular systolic function (left ventricular ejection fraction ≤ 40%) unless contraindicated.54 GRADE: Strong; Level: IIA

• Initiate and continue angiotensin-converting enzyme inhibitors (or angiotensin receptor blockers) in patients with evidence of heart failure, left ventricular systolic dysfunction, diabetes, anterior MI or co-existent hypertension.55 GRADE: Strong; Level: IA

• Attendance at cardiac rehabilitation or undertaking a structured secondary prevention service is recommended for all patients hospitalised with ACS.56,57 GRADE: Strong; Level: IA

  • PP: Individualisation of cardiac rehabilitation or secondary prevention service referral. A wide variety of prevention programs improve health outcomes in patients with coronary disease. After discharge from hospital, patients with ACS and, where appropriate, their companion(s) should be referred to an individualised preventive intervention according to their personal preference and values and the available resources. Services can be based in the hospital, primary care, the local community or the home.

System considerations

• Continuous audit and feedback systems, integrated with work routines and patient flows, are strongly advocated to support quality assurance initiatives and provide data confirming continued, cost-efficient improvement in patient outcomes as a result of new innovations in care.

The use of coronary pressure wires (or fractional flow reserve [FFR]) has been shown to reduce the frequency of major adverse cardiac events and of unnecessary stent procedures, and to lower treatment costs in both the public and private sectors in Australia.1–3 FFR is a tool for assessing physiological ischaemia in coronary artery stenosis, measuring pre- and post-stenosis pressures during adenosine-induced hyperaemia. Because it is evidence-based and quantifiable, it may be discussed during the upcoming Medicare reform. Data on its uptake across Australia, however, have not been published.

We examined trends in FFR use after its addition to the Medicare Benefits Schedule 10 years ago. We analysed Australian Government Department of Human Services data on Medicare items for coronary flow reserve, coronary angiography and percutaneous coronary angiography.

A total of 14 160 FFR services were processed by Medicare during the past 10 years. FFR use grew during this period, with a mean annual increase of 55%, from 131 services in 2007 to 3869 in 2015 (non-parametric analysis, P = 0.004). Time series analysis identified a Gompertz non-linear trend of FFR against time, indicating that national FFR use is continuing to increase, although growth began to slow in 2014. Further, FFR use increased on a population basis by an average of 45% each year, from 1 per 100 000 in 2007 to 16 per 100 000 in 2015, when these figures were highest in New South Wales (23 per 100 000) and Queensland (19 per 100 000) (Box).

The national rate of FFR per coronary angiogram increased from 0.02% in 2006 to 4.8% in 2015 (P = 0.004), when the highest rate was in NSW (5.8%). The rate of FFR per percutaneous coronary intervention (PCI) increased from 0.1% in 2006 to 19.2% in 2015 (P = 0.004), when the highest rate was in Queensland (26.6%). In 2015, there were 5.2 PCIs per FFR used; the rate was not related to the population size of the state or territory (Spearman non-parametric correlation, ρ_S = 0.07; P = 0.87) or to total PCI use (ρ_S = 0.12, P = 0.78). There was marked variation between states and territories (Box), highlighting heterogeneity across Australia in the use of FFR.

The data summarised in the Box allow operators and hospitals to compare their use of FFR with state and national averages, and they facilitate more standardised care across Australia. Barriers to the uptake of FFR include operator and centre experience, availability and cost. It has been suggested that FFR is discouraged by the lower remuneration received if stenting is not performed.4 From a national perspective, however, there is a mean saving of $1200 per patient in the public sector and $5000 per patient in the private sector when FFR makes stenting unnecessary,2 representing a total annual saving of $4 million.4

The use of FFR across Australia is heterogeneous, but it has grown over the past decade, both in absolute numbers and as proportions of coronary angiograms and PCI.

Managing coronary artery disease (CAD) with coronary angiography is informed by an extensive evidence base.1–5 Variation in the rates of coronary angiography has been described in Australia.6,7 This variation may be explained by heterogeneity in clinical need (ie, variations in disease incidence or prevalence), but differences unexplained by disease burden highlight inequities in access to health services, and differential over- and underuse of health care resources. These disparities are potentially targets for policy interventions that aim to improve population health and achieve a high quality health system.

Health care in Australia faces a combination of challenges. The geographic distribution of the population and substantial cultural diversity give rise to complexity in providing access to clinical expertise and procedures such as angiography. Clinical audits of acute coronary syndrome (ACS) practice have identified variations in applying components of care advocated in guidelines, particularly invasive management.8–12 Australia’s demography may contribute to heterogeneity in access to health services, differential clinical needs and variation in care. The relative contributions of demographic factors have implications both for national policy and for local efforts to re-design health services.

In our study we explored the associations of selected socio-economic, geographic, and chronic disease factors with ACS incidence and mortality rates, and examined whether rates of coronary angiography across the Australian population are correlated with indicators of disease burden, health access, and clinical activity.

Methods

Data sources

Socio-economic and health workforce data

Our analysis included data for the entire Australian population of about 23.5 million people. Between 2010 and 2015, federal government support for primary health care services was organised into 61 geographic divisions (Medicare Locals). Social, economic and health service characteristics of the Medicare Locals were obtained from a publicly accessible website that publishes age- and sex-standardised rates for these features, including the estimated proportions of privately insured residents and of Indigenous residents, based on data from the 2011 Australian census (conducted by the Australian Bureau of Statistics [ABS]).13 Data from the Socio-Economic Indexes for Areas (SEIFA),14 a relative measure of social and economic disadvantage (normalised to 1000; higher numbers denote more advantaged areas), were also used as a socio-economic indicator. Medical workforce data were drawn from the annual survey of the Australian Health Practitioner Registration Authority, which records the primary locations of practice and specialisations of all registered medical practitioners. Further, modelled rates of chronic cardiovascular conditions (prior myocardial infarction and angina, heart failure, stroke and rheumatic heart disease), estimates derived from the Australian Health Survey 2011–2013 (conducted by the ABS), were available for all but three Medicare Locals (Tasmania, Northern Territory, Australian Capital Territory).

As an indicator of local clinical practice in each region, the likelihood that a suspected ACS patient received coronary angiography, compared with the national average, was estimated from the SNAPSHOT ACS clinical audit.9,10

Rates of ACS, angiography, revascularisation and mortality

The National Hospital Morbidity Database (NHMD) was used to identify ACS separations (International Classification of Diseases, revision 10, Australian modification [ICD-10-AM] principal diagnosis codes I20 and I21) and catheter procedures during the calendar year 2011. Data on procedures undertaken as ambulatory care (eg, outpatient angiography) were obtained by the Australian Institute of Health and Welfare (AIHW) from the Medicare Benefits Schedule. The combined total rate of angiography is presented in this article. All cardiac-specific admissions were included in the analysis. Three of the eight state or territory jurisdictions did not report data for private hospital admissions, so that private hospital and total admissions were not available for three Medicare Locals (Tasmania, NT, ACT). Data on deaths attributed to CAD were drawn from the National Mortality Database (NMD).

Statistical analysis

Standardised age- and sex-specific rates — of ACS separations, inpatient and outpatient angiograms, percutaneous coronary interventions (PCI), coronary artery bypass graft (CABG) procedures, and CAD-related deaths of people aged 35 years or more grouped in 5-year age intervals (to 85 years or more) and by sex — were calculated by dividing by the corresponding Australian population figure (at 30 June 2001) for the relevant age and sex group, and expressed as numbers per 100 000 population.

Socio-economic data, health service information, procedure and ACS incidence, and mortality rates were stratified by geographic location of the Medicare Local as defined by the AIHW, and compared using Kruskal–Wallis tests. Univariate correlations between potential explanatory factors and rates of angiography, ACS and mortality were assessed using partial correlations; the strength of the adjusted correlation coefficient (CC) was defined as strong (> 0.70), moderate (0.50–0.69), or weak (0.30–0.49). Separate correlation plots of ACS v CAD mortality rates and of angiography v ACS rates were generated, and fitted linear predictions superimposed. To assess the potential overuse of angiography, the ratio of the numbers of coronary revascularisations to those of coronary angiograms was calculated for each Medicare Local, and plotted as a function of the rate of coronary angiography, using the fractional polynomial estimate.

Given the small numbers of Medicare Locals and the availability of earlier data to evaluate these relationships, a Bayesian linear regression approach was used (Appendix). All analyses were undertaken in Stata 14.0 (StataCorp); P < 0.05 was deemed statistically significant.

Ethics approval

This SNAPSHOT ACS study was conducted with local ethics approval for opt-out consent, except for two hospitals where opt-in consent was applied (lead ethics committee: Cancer Council NSW Human Research Ethics Committee; reference, 2011/06/334). The AIHW work program and any release of data from AIHW datasets are subject to the oversight of the AIHW Ethics Committee and handled in accordance with the AIHW Act 1987 (as amended), the Privacy Act 1988, and any terms and conditions set by data providers. Separate ethics committee approval is not required for the analysis of AIHW datasets that does not involve data linkage, and was thus not needed for our study.

Results

Characteristics of the Medicare Locals

Of the 61 Medicare Locals, 27 were categorised by AIHW criteria as metropolitan, 24 as regional and ten as rural. Regional and rural locations were significantly more disadvantaged than metropolitan areas, with higher proportions of the population on long term unemployment support, greater reported delays in seeking medical consultation because of the associated costs, and lower proportions of residents with private health insurance. Similarly, the prevalence of smoking, obesity and chronic cardiovascular disease was higher in regional and rural areas than in metropolitan areas. There was no difference in the rates of total hospital admissions by geographic location, but there was a significantly lower rate of private hospital cardiac admissions in non-metropolitan locations, where fewer private hospitals exist (Box 1).

ACS rates were higher in non-metropolitan areas, but this was not reflected in a significantly higher rate of coronary angiography. PCI rates were significantly lower in rural areas, while rates of CABG were significantly higher in non-metropolitan areas. Overall, there was no significant difference in the combined coronary revascularisation rates according to geographic location. Premature death from CAD and total mortality were higher in regional and rural areas. There were 3.7-fold (ACS), 5.3-fold (angiography), 2.2-fold (revascularisation) and 2.3-fold (CAD mortality) differences between the lowest and highest rates for individual Medicare Locals. Box 2 shows the variation in ACS, angiography, revascularisation, and mortality rates for each Medicare Local by SEIFA index score.

Correlation of socio-economic, chronic health and health service data with ACS admission mortality rates

The ACS admission rates for individual Medicare Locals were significantly correlated with all-cause mortality (CC, 0.52; P < 0.001). There were strong correlations between socio-economic measures and ACS admission rates and mortality (Box 3). Similarly, rates of smoking, obesity and chronic cardiovascular conditions were all correlated with mortality; smoking and obesity rates were also correlated with ACS admission rates. Strong negative correlations between the proportion of insured people in the Medicare Local and the ACS admission and all-cause mortality rates were also observed. Conversely, there were negative correlations between local availability of specialist physicians and ACS admissions and mortality, as well as positive correlations between delays in consultations and these outcomes. From a health service use perspective, emergency department and public hospital admission rates were correlated with ACS admission and mortality rates, while private hospital cardiac admission rates were negatively associated with total mortality. An increased likelihood of patients admitted with suspected ACS undergoing angiography was associated with lower mortality (Box 3).

An adjusted analysis of mortality was performed to explore relationships with the indicators SEIFA score, regional location, local cardiovascular health status (chronic cardiovascular conditions), ACS rates, workforce capacity (access to specialist physician care), and health service provision (cardiac admission rates to public and private hospitals). Rural location was associated with increased mortality (19 additional deaths [95% CI, 10–27] per 100 000 population). Interestingly, the likelihood of coronary angiography in the context of ACS appeared to be associated with a modest reduction in mortality rates (three fewer deaths [95% CI, 1–5] per 100 000 population for each 10 percentage point increase in the likelihood of angiography for a suspected ACS admission). After considering these two factors, socio-economic index, disease burden, health service indicators, and angiography rates were not significantly correlated with the Medicare Local CAD mortality rate.

Correlation of socio-economic status, chronic health status and health service with angiography rates

There was no correlation between measures of social disadvantage or health service availability and coronary angiography rates (Box 3). A positive correlation between all cardiac admissions and angiography rates was evident, particularly private hospital cardiac admissions. This correlation was weaker when analysis was restricted to public hospital admissions. The likelihood of angiography for acute patients was not correlated with the overall rate of angiography in Medicare Locals. There was a weak correlation between the rates of angiography and of ACS (CC, 0.31; P = 0.018), but no correlation with premature ischaemic heart disease deaths (CC, 0.13; P = 0.315) or total CAD mortality (CC, 0.06; P = 0.671) (Box 4).

In the adjusted model, private hospital cardiac admissions had a large influence on the angiography rate (71 additional angiograms [95% CI, 47–93] per 1000 admissions). The relationship between public hospital admission rates and the angiography rate was more modest (44 angiograms [95% CI, 25–63] per 1000 admissions). Socio-economic indicators, regional location, and background ACS or chronic disease rate burden were not significantly associated with angiography rates.

Progression from angiography to revascularisation

The angiography rate was correlated with those of PCI (CC, 0.54; P < 0.001), CABG surgery (CC, 0.44; P < 0.001) and any revascularisation (CC, 0.65; P < 0.001). Revascularisation rates as a proportion of angiography rates varied greatly (17–61%). There was a striking negative correlation between the angiography rate and the proportion of patients undergoing angiography who proceeded to any form of coronary revascularisation (CC, −0.71; P < 0.001) (Box 5). This was also seen with the individual modes of revascularisation (PCI: CC, −0.62; P < 0.001; CABG: CC, –0.62; P < 0.001). There was no correlation between PCI rates and the incidence of myocardial infarction (CC, −0.11; P = 0.402) or ACS (CC, −0.12; P = 0.345). However, rates of CABG were correlated with those of myocardial infarction (CC, 0.53; P < 0.001) and of ACS (CC, 0.45; P < 0.001).

Discussion

We observed that:

• increasing socio-economic disadvantage, rural location, and chronic disease burden were each correlated with rates of ACS and of total mortality;

• local availability of specialist physicians and admissions to private hospitals were negatively correlated with ACS admissions and mortality rates;

• there was no association between coronary angiography rates and the burden of chronic cardiovascular disease, and a modest positive association with ACS rates, but there was a positive association between angiography rates and those of cardiac admissions to private hospitals; and

• the rates of angiography and coronary revascularisation were correlated, but there was a negative correlation between the local angiography rates and the proportion of these procedures proceeding to revascularisation.

These findings suggest that health reforms aimed at the appropriate use of diagnostic coronary angiography may be required to improve consistency and equity of access, and consequently to deliver positive outcomes for the Australian community more efficiently.

As expected, a correlation between the incidence of ACS and CAD mortality was evident. Similarly, higher ACS rates in regional and rural locations were confirmed, as was the relationship between indicators of socio-economic disadvantage and chronic cardiac disease burden, and between disease incidence and outcomes. However, the distribution of acute care services was negatively correlated with the incidence of disease in the population. This geographic mismatch has also been described elsewhere, including the United States, and highlights the influence of factors such as funding and workforce proficiency in delivering services to non-metropolitan communities.15–17

A solid evidence base supports using coronary angiography, with subsequent revascularisation where deemed appropriate, in ACS patients with elevated troponin levels.18 However, the superiority of angiography and revascularisation to medical management of patients with stable CAD is less robust.5,19 This clinical evidence base contrasts strongly with several of our findings. Firstly, the indicator most associated with variation in angiography appeared to be cardiac admission rates to private hospitals, but an inverse correlation with ACS rates implies that these procedures are mainly being undertaken for indications other than ACS. Secondly, while angiography rates were correlated with revascularisation rates, neither angiography nor PCI rates (unlike the CABG rate) were correlated with that of ACS. Thirdly, angiography rates were negatively correlated with progression to revascularisation. These observations are inconsistent with the evidence base for invasive management for non-ACS indications, with private institutions accounting for a higher proportion of the variation. Computed tomography coronary angiography for investigating non-acute CAD may reduce the use of invasive angiography for this indication, but caution should be exercised, as there is ample evidence that all forms of cardiac testing tend to motivate further investigations.19,20

These comparisons suggest certain policy targets for improving the clinically appropriate application of coronary angiography. At the higher end of patient risk, the Australian Commission on Safety and Quality in Health Care has developed clinical care standards for the management of ACS.21 These standards may appropriately increase the use of angiography for ACS patients, for whom the benefits of invasive management have been established. Linking the funding of hospitals to ACS performance measures may be an approach for achieving changes in practice and outcomes. Further, resourcing and implementing clinical support networks that serve regional and remote areas (eg, telemedicine) would enable the appropriate selection of patients who would benefit most from being transferred for angiography and revascularisation, and this would also be an opportunity for improving access to angiography. While there is no current guidance on stable CAD in Australian, criteria for the appropriateness of angiography and revascularisation have been developed in the US.22 It is notable that re-imbursement by Medicare and Medicaid in the US for the costs of invasive procedures is now linked to these appropriateness criteria. It is suggested that funding linked to the appropriateness of care or the achievement of clinical care standards, and limiting re-imbursement for angiography in low value clinical situations, should be focuses of debate in any health care reform discussion in Australia.

Limitations

Given the ecological study design, pockets of excellence in care and outcomes probably exist but are obscured by data aggregation. Further, in view of the small number of Medicare Locals, a linear relationship between variables was assumed, although curvilinear relationships are possible. The small sample of the SNAPSHOT ACS study is acknowledged, with caution accordingly exercised when interpreting the association with mortality rates. While this relationship should be examined in larger studies, our finding is consistent with international large scale data.23 Similarly, we cannot fully exclude the possibility of under- (misclassification) or over-reporting (double counting secondary to inter-hospital transfers) of ACS admissions or procedures; systematic under-reporting is, however, unlikely, given the funding implications of these coding practices. Detailed interrogation of the system would require documentation of patient-level characteristics and care, combined with an evaluation of the health service infrastructure beyond the availability of catheter laboratories, extending to other modalities of cardiac investigation, such as computed tomography coronary angiography and functional imaging. Such information is not currently available in Australia.

Conclusion

Significant variation in providing coronary angiography, not related to clinical need, is evident across Australia. A greater focus on clinical care standards and better distribution of health services will be required if these disparities are to be reduced.

Box 2 –
Variation in angiography, revascularisation, acute coronary syndrome and mortality rates according to Socio-Economic Index for Australia score for the location of the Medicare Local*

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SEIFA = Socio-Economic Indexes for Areas score; a higher SEIFA value indicates lesser disadvantage. * The size of the symbol is proportional to the size of the population served by the Medicare Local.

Box 4 –
Correlation between acute coronary syndrome and mortality rates, angiography and acute coronary syndrome admissions rates, and angiography and mortality rates*

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ACS = acute coronary syndrome. * The size of the symbol is proportional to the size of the population served by the Medicare Local.

Box 5 –
Revascularisation rates as proportions of angiography rates in each Medicare Local,* with fractional polynomial estimate and 95% confidence band

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* The size of the symbol is proportional to the size of the population served by the Medicare Local.