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Health services for Aboriginal and Torres Strait Islander people: handle with care

This special Indigenous health issue of the MJA features stories of successful health care services and programs for Aboriginal and Torres Strait Islander people. As we seek to build on the wealth of experience outlined, it is worth considering what these contributions have to tell us about the characteristics and value of effective Indigenous health services.

It is more than 40 years since the founders of the first Aboriginal health service recognised a need for “decent, accessible health services for the swelling and largely medically uninsured Aboriginal population of Redfern [New South Wales]” (http://www.naccho.org.au/about-us/naccho-history#communitycontrol). There are now about 150 Aboriginal community controlled health services (ACCHSs) in Australia: services that arise in, and are controlled by, individual local communities, and deliver holistic, comprehensive and culturally appropriate health care. Panaretto and colleagues (doi: 10.5694/mja13.00005) describe how these services have led the way in high-quality primary care, as well as enriching both the community and the health workforce.

With the ACCHS model setting the standard, the values of responding to community need, Indigenous leadership, cultural safety, meticulous data gathering to guide improvement, social advocacy and streamlining access have gradually been adopted in other health care settings. The progress of the Southern Queensland Centre of Excellence in Aboriginal and Torres Strait Islander Primary Health Care (a Queensland Health-owned service also known as Inala Indigenous Health Service), is an example (doi: 10.5694/mja14.00766). Among the hallmarks of the service’s vitality are its ever-increasing patient numbers, research output, building of community capacity, expansion into specialist and outreach services and multidisciplinary educational role.

The East Arnhem Scabies Control Program, described by Lokuge and colleagues (doi: 10.5694/mja14.00172), is a dramatic example of innovation inspired by local need. This part of Australia has the highest rates of crusted scabies in the world, and the program involved collaboration between two external organisations, an ACCHS and the Northern Territory Department of Health. Importantly, it was able to be integrated into existing health services and largely delivered by local health workers, using active case finding, ongoing cycles of treatment and regular long-term follow-up.

Mainstream health services are now beginning to take the lead from Indigenous-specific ones. For example, the repeated observation that Indigenous men and women with acute coronary syndromes are missing out on interventions and are at risk of poor outcomes inspired a working group from the National Heart Foundation of Australia to develop a framework to ensure that every Indigenous patient has access to appropriate care (doi: 10.5694/mja12.11175). The framework includes clinical pathways led by Indigenous cardiac coordinators, and it is already producing results.

There is growing evidence for the value of sound and accessible primary care for Indigenous Australians. A letter by Coffey and colleagues (doi: 10.5694/mja14.00057) highlights the significant progress towards closing the mortality gap between Indigenous and non-Indigenous Australians in the NT since 2000, temporally associated with investment in primary health care. A research report from Thomas and colleagues shows that patients with diabetes living in remote communities were more likely to avoid hospital admission if they accessed regular care at one of the remote clinics, saving both lives and money (doi: 10.5694/mja13.11316).

While the diversity of health services and the evidence of effectiveness is indeed something to celebrate, it is a fragile success. In their editorial, Murphy and Reath (doi: 10.5694/mja14.00632) highlight the need for sustained, long-term financial investment in primary health care services for Indigenous Australians and the uncertainty arising from changes to health care funding and Indigenous programs announced in the recent federal Budget (http://nacchocommunique.com/category/close-the-gap-program). The detail of how funding will be reallocated with the “rationalisation” of Indigenous programs has not yet fully emerged. Analysis indicates the cuts over 5 years include $165.8 million to Indigenous health programs, which will be added to the Medical Research Future Fund. New spending on Indigenous programs includes $44 million in 2017–18 for health as part of the Department of the Prime Minister and Cabinet Budget (Adjunct Associate Professor Lesley Russell, Menzies Centre for Health Policy, University of Sydney, NSW, personal communication).

Changes to primary care funding are of particular concern. Knowing, as they do, the importance of removing barriers to access, there is increasing public discussion that ACCHSs and large Aboriginal medical services will not pass on the proposed $7 copayment to patients (http://theage.com.au/act-news/health-service-facing-budget-blackhole-by-not-charging-copayment–20140527-zrpb7.html). This will result in a decrease in funding to services that provide vital programs and deliver high-quality outcomes. The government has stated that everyone should share the deficit burden, yet the copayment has only been targeted at general practitioners and not specialist consultations. Is this fair and equitable?

It seems ironic that this threat to access and resourcing has arisen just as it is emerging that our investment in primary care for Indigenous Australians has been well made. In an Australia where many Aboriginal and Torres Strait Islander people still face significant socioeconomic and health disadvantage, the need for “decent, accessible health services” is greater than ever.

A framework for overcoming disparities in management of acute coronary syndromes in the Australian Aboriginal and Torres Strait Islander population. A consensus statement from the National Heart Foundation of Australia

Cardiovascular disease, particularly coronary heart disease (CHD), is the major cause of premature death for Aboriginal and Torres Strait Islander peoples, accounting for 26% of all deaths.1 Cardiovascular disease is also a major contributor to the gaps in life expectancy between Indigenous and non-Indigenous Australians,2 with recent statistics suggesting that Australian Aboriginal and Torres Strait Islander men and women can expect to live 10.6 and 9.5 fewer years, respectively, than other Australians.3

Acute coronary syndromes (ACS) include a broad spectrum of clinical presentations including ST-elevation myocardial infarction (STEMI), non-STEMI and an accelerated pattern of angina without evidence of myonecrosis (unstable angina); the latter two are often grouped as non-ST-elevation acute coronary syndromes (NSTEACS). Current National Heart Foundation of Australia/Cardiac Society of Australia and New Zealand guidelines highlight the importance of effective systems of care in delivering optimal management of ACS.46

In 2006, the Australian Institute of Health and Welfare (AIHW) released a landmark report on access to ACS treatment by Aboriginal and Torres Strait Islander patients. The report found that, compared with other Australians, Indigenous Australians hospitalised with ACS had:

  • more than twice the rate of death from CHD
  • a 40% lower rate of being investigated by angiography
  • a 40% lower rate of percutaneous coronary intervention (PCI)
  • a 20% lower rate of coronary artery bypass graft (CABG) surgery.7

Further studies have indicated that, over and above inhospital treatment disparities for ACS, Aboriginal and Torres Strait Islander patients have greater mortality 6–12 months after a coronary event than non-Indigenous Australians, owing to suboptimal follow-up care.811 These disparities in outcomes underpin the development of this patient-oriented framework for the diagnosis and management of ACS in Aboriginal and Torres Strait Islander peoples. The process of developing the framework is described in Appendix 1.

Aboriginal and Torres Strait Islander people represent 2.5% of the Australian population,7 dispersed at varying density levels across urban, regional and remote locations. In 2006, almost one-third of the Indigenous population lived in major cities; 21% in inner regional areas; 22% in outer regional areas; 10% in remote areas; and 16% in very remote areas.12 While Aboriginal and Torres Strait Islander people make up a small proportion of the population in the large cities, there are higher population densities of Indigenous Australians in regional and remote communities — in the Torres Strait, 83% of the population is Torres Strait Islander; in the Northern Territory, 32% of the total population is Indigenous (> 75% in Arnhem Land); and in Central Australia, Aboriginal people make up 50% of the population.11,13 The diversity of this linguistic, cultural and geographic landscape provides many challenges to the delivery of appropriate cardiac services for these populations.

Patient pathways: barriers and enablers

It is a commonly held misconception that Aboriginal and Torres Strait Islander peoples living in urban centres have outcomes similar to the non-Indigenous urban population. There are a number of systemic issues that detrimentally affect the outcomes of all Indigenous Australians, although these issues are likely to be exacerbated by remoteness. Contributing to negative outcomes across the geographic spectrum are issues of fear, institutional racism,14 cultural misunderstandings, waiting times, transport issues, financial constraints and poor health literacy.

Generic pathways to timely diagnosis and management as recommended by best-practice guidelines for patients with ACS living in urban communities are shown in Appendix 2. The more complex pathway for those living in regional or remote communities is tracked in Appendix 3.

Key barriers contribute to the disparities in care and outcomes experienced by Aboriginal and Torres Strait Islander patients regardless of whether they follow a regional/remote or less convoluted urban pathway. These, along with key strategies for addressing them, are discussed below.

Early response and access

There is strong evidence that Aboriginal and Torres Strait Islander patients with a suspected heart attack may delay presentation to hospital.11 Urgent access to care is firstly dependent on patients and/or their families understanding the potentially serious nature of the situation and the need to seek medical help urgently.

Aboriginal and Torres Straits Islander peoples’ culture, spirituality and health literacy all play major roles in potential communication gaps, particularly in remote and isolated communities where English is likely to be a second language. Qualitative internal research undertaken by the Heart Foundation in 2010 identified factors linked with patient delay (unpublished report; Heart Foundation of Australia. Warning signs Aboriginal and Torres Strait Islander Research. Report of qualitative research. Melbourne: The Social Research Centre, 2010) for Aboriginal and Torres Strait Islander people with ACS, including limited knowledge of symptoms and a lack of awareness of the need for urgent treatment: the symptoms associated with ACS are often not acted on until they are unbearable. Other factors contributing to delay include:15,16

  • competing personal and family demands that may be seen as higher priorities than the individual’s own health (eg, caring for family members, and cultural or community events)
  • cultural beliefs
  • fear of hospitals, which may be perceived as places to go to die or as being unfriendly to Aboriginal and Torres Strait Islander patients based on previous personal or family encounters
  • lack of available or affordable transport
  • lack of communication options for calling for assistance
  • long distance to the nearest hospital
  • lack of understanding of the diagnostic and treatment pathways, and inability to have family involvement in decision making
  • going to the nearest Aboriginal community controlled health service before going to hospital or calling an ambulance
  • inappropriate triage at first contact between a health service provider and patient due to inadequate understanding of the symptoms and signs of ACS on the part of the health care provider.

To overcome these barriers, health care providers must look at effective strategies to improve Aboriginal and Torres Strait Islander peoples’ understanding of the warning signs of a heart attack. This requires the development and provision of culturally appropriate health education through community and primary health care networks, including media organisations. Such programs must not only improve understanding of the warning signs of heart attack within local communities, but also advise how to access immediate help and provide information about the patient journey so that patients and their families understand what might happen once they seek help, and can make informed decisions about treatment. In an urban setting, this includes culturally specific education around the triple zero (000) emergency service and the availability and potential cost of the ambulance service.

Minimising delay: pre-tertiary pathways

Beyond health education and basic access to emergency services, patients require access to timely and effective treatment through a system of care that supports early diagnosis and is responsive to patient need, including digital 12-lead electrocardiogram capability, point-of-care pathology testing and, where relevant, prehospital fibrinolysis.

It is essential that centres providing initial care for patients with suspected ACS are part of a clinical network for the provision of cardiac care, and are appropriately equipped to follow up-to-date evidence-based protocols17 (Appendix 4). For urban populations, tertiary “receiving” hospitals need to develop formalised networks with smaller secondary “referring” hospitals that provide initial triage, as well as with the local ambulance services. In regional and remote settings where patient transfer times to centres with PCI capability are greater than 1 hour, it is essential that there is a formalised “designated provider clinical network” of cardiac care providers — essentially a mechanism for providing or obtaining expert clinical advice at short notice — that includes appropriate infrastructure and treatment and transfer protocols.18,19

NSTEACS

All patients with NSTEACS should have their risk of adverse clinical outcomes assessed to direct management decisions.4 Patients identified as being at high risk should be treated with dual antiplatelet therapy and an antithrombin agent, and arrangements should be made for coronary angiography and (where indicated) revascularisation as soon as possible. Regional and remote communities have the added difficulty of seeking distant, expert medical advice with appropriate and timely transfers to facilities that have at least full diagnostic and risk stratification capability. NSTEACS patients stratified as intermediate risk or high risk are best managed within a structured clinical pathway,4 as ad hoc management can lead to delays in seeking advice and the potential for inappropriate and/or conflicting advice, as well as inefficient use of emergency medical transport services.

Early reperfusion for STEMI

The initial diagnosis, treatment and subsequent outcomes for patients experiencing STEMI are determined by the patient’s location, the level of medical expertise of the first emergency medical contact, and the infrastructure available. Patients with STEMI who present within 12 hours of the onset of ischaemic symptoms should have reperfusion therapy implemented as soon as possible, using either fibrinolytic therapy or PCI.4

Urban and some inner regional populations often have direct access or immediate access through interhospital transfer to primary PCI facilities with first emergency medical contact to PCI delays of less than 90 minutes. Where such access exists, clearly, primary PCI is the preferred modality for reperfusion. Patients in other inner regional, most outer regional and all remote areas will not have such access and require early fibrinolysis (door-to-needle time of less than 30 minutes4) with immediate or early transfer (within 24–48 hours) to a tertiary cardiac facility with revascularisation capability (PCI and/or CABG surgery). For most patients in non-urban settings, the local hospital emergency department will be the most appropriate facility for early STEMI diagnosis and fibrinolysis. However, where inherent delays between first emergency medical contact and access to any facility capable of delivering reperfusion therapy exceed 60 minutes, routine access to prehospital fibrinolysis is strongly recommended.

There are essential infrastructure and standards requirements for prehospital fibrinolysis, either in an ambulance or a remote health clinic (Appendix 5). Currently, in the Northern Territory, remote health clinics provide prehospital fibrinolysis without a doctor being present, and several state ambulance services are effectively providing prehospital fibrinolysis via intensive care paramedics.20

Designated provider clinical networks should be configured to reduce the number of medical transport legs and time delays to tertiary care (including bed access block) to a minimum, given that remote area patients will often unavoidably require up to three transfers (Appendix 3) over very long distances. Historically, this has resulted in tertiary access delays of 5 days or more (own unpublished data; M K I, 2012).

Hospital treatment

As highlighted in the 2006 AIHW and subsequent reports, the inhospital disparities in ACS care experienced by Aboriginal and Torres Strait Islander peoples warrant special consideration by health service providers.7,18

It is well documented that Aboriginal and Torres Strait Islander people suffering from ACS are less likely to undergo angiography in hospital and receive PCI or CABG surgery than non-Indigenous patients.7 Although there has been no extensive study of why these disparities exist, potential reasons include:18

  • poor health literacy and understanding of invasive procedures
  • inadequate cultural competence of health care providers and hospitals
  • bias favouring conservative management based on perceptions of more comorbidities among Aboriginal and Torres Strait Islander patients and lower compliance with medications
  • disengagement of family members in the decision-making process10
  • delayed patient transfer to hospitals with PCI facilities compounded by the complexity of the patient journey (highlighted in Appendix 3) in requiring multiple transfers
  • patient choice.

Difficulties in transferring patients to hospitals with revascularisation facilities may be overcome with improved communication to enhance uptake of these crucial interventions. Patients frequently have a poor understanding and fear of these procedures, and studies indicate that they often feel disengaged from medical staff.8 The support of Indigenous cardiac coordinators (described below) is important in this process.

Other key strategies for improvement, involving Aboriginal health practitioners (where access is available), general hospital staff, retrieval services and the state health departments, include:

  • establishing a coordinated transfer system as part of the overall designated provider clinical network (fewer steps in the patient pathway will reduce the number of transfers and inherent delays)
  • providing a system that allows a family member to accompany the patient throughout the continuum of care
  • developing a patient care plan in conjunction with the patient and his or her family, with involvement of the hospital Aboriginal liaison officer (ALO) and interpreters as needed
  • commencing patient education in hospital using culturally appropriate educational tools, so that both the patient and his or her family are fully informed of the clinical process and timelines for returning home
  • ensuring financial and social support to facilitate transfer to other hospitals, even in the urban environment.

Discharge against medical advice

Aboriginal and Torres Strait Islander patients have a much higher rate than other patients of discharge from hospital against medical advice, which increases with remoteness.21 This reflects problems in communication and a lack of engagement with and respect for Aboriginal and Torres Strait Islander patients and their families that contributes significantly to a fear of hospitals and invasive procedures. A lack of culturally competent health care providers accentuates this problem.

Aboriginal and Torres Strait Islander patients and their families need considerable explanation of their diagnosis and proposed procedures to minimise the risk of discharge against medical advice. Patients who have had PCI procedures or CABG surgery should be encouraged to become patient advocates and discuss their story with other patients and family members.

In the urban environment, language is usually not presumed to be an issue (although literacy levels may be22), but for patients referred from regional and remote settings English is likely to be a second language, resulting in additional communication barriers.18 It is essential that interpreters are made available on request and that considerably more time is set aside for discussions with Aboriginal and Torres Strait Islander patients and their families than might be expected for non-Indigenous patients.

Follow-up care, cardiac rehabilitation and secondary prevention

Proven short- and long-term health benefits and reductions in mortality form the basis for recommendations that all patients with ACS be referred for appropriate cardiac rehabilitation.23,24 Unfortunately, rates of participation in cardiac rehabilitation programs by Aboriginal and Torres Strait Islander peoples are extremely low due to extended family responsibilities, sociocultural inappropriateness of programs, poor understanding of cardiac rehabilitation, the connection between colonialism and health services, heart health messages in the media and the younger age of the affected Indigenous population.25

Patients returning home after ACS must have an understanding of their medical condition, and require education regarding medication use, wound care (in the event of recent surgery), risk factor modification, potentially reduced functional capacity, and prognosis. Therefore, patient education must be commenced while in hospital and include culturally appropriate education tools26 and the development of an individualised care plan that provides the basis of the outpatient and maintenance cardiac rehabilitation programs after patients return to their communities (Appendix 6).

The care plan is essential in providing support to the local medical officer and clinics regarding a patient’s:

  • medications
  • targeted program for outpatient and maintenance cardiac rehabilitation
  • overall prognosis
  • returning to work and personal independence issues (eg, driving).

This requires the treating hospital to have a comprehensive understanding of the services available on the patient’s return home as well as his or her risk-factor profile, home circumstances (specifically, family support, occupation and capacity to return to work) and education and literacy levels. To improve outcomes it is also important to assess the patient’s and family’s understanding of the importance of ongoing cardiac rehabilitation and adherence to an individualised, formalised care plan.

The care plan should be developed with the patient and his or her family in liaison with the Indigenous cardiac coordinator. At discharge, the plan should be forwarded to the appropriate cardiac rehabilitation services nearest to the patient’s home. Follow-up care and outpatient and ongoing maintenance programs should include the elements highlighted in Appendix 7. Appendix 8 outlines key considerations in planning cardiac rehabilitation programs for Indigenous patients, as recommended by National Health and Medical Research Council guidelines.26

The longer-term maintenance of secondary prevention strategies is perhaps the most important element of postacute care for Aboriginal and Torres Strait Islander patients after an ACS, as ineffective strategies result in poorer long-term outcomes among Indigenous patients even when short-term hospital outcomes are similar.11,27 Cardiac coordinators are required to facilitate regular appointments for general and specialist review and investigation (including echocardiography when necessary). In addition, regular coordinated outreach clinics are required to service Aboriginal and Torres Strait Islander populations in urban, regional and remote areas because of inherent difficulties in attending hospital outpatient clinics and private cardiology practices.

Pathway coordination

The ACS continuum-of-care pathway needs coordination, enabling timely access to investigation and treatment and making efficient use of the resources available within that clinical network. Appropriate infrastructure, protocols and policies that are specific to each designated provider clinical network provide the framework for investigations and decision making28 (for requirements, see Appendix 4). However, there is also a need to coordinate patient and escort transfers for coronary procedures and the return home.

Indigenous cardiac coordinators have been trialled in the Northern Territory and at Flinders Medical Centre in South Australia, with significant improvements in patient flow, attendance for procedures and revascularisation rates (unpublished report; Heart Foundation of Australia; as above). Coordinators receive support from ALOs or interpreters as appropriate, as well as administrative support — a key factor in the success of the network. The Indigenous cardiac coordinators:

  • review patients and have contact with their families within 24 hours of hospital admission
  • monitor and coordinate patients’ progress before and after diagnosis, including procedures and clinical reviews up to 3 months after an event
  • liaise with cardiologists, remote health clinics and general practitioners
  • coordinate transfers of Indigenous cardiac patients, with the relevant patient information, between hospitals, health clinics and other relevant agencies
  • assess patients returning from tertiary services, including clinical assessment and consideration of social issues
  • ensure cultural factors are considered when organising patients’ appointments.

The success of the designated provider clinical network requires coordination of patient information from all elements of the network. Electronic transfer of patient records, including referrals, discharge information (to the local medical officer and local cardiac rehabilitation service or equivalents), medications and follow-up care plans, needs to be incorporated, and the development of electronic records will contribute significantly to this process.

Conclusion

To improve the quality of care across the health care continuum for Aboriginal and Torres Strait Islander patients with ACS, a properly structured and clearly defined patient-oriented clinical pathway (comprising adequate human, pharmacological and equipment resources) is essential for the delivery of evidence-based, high-quality care. The generic ACS management framework outlined is designed to provide guidance to policymakers, health planners and health care providers on the establishment of jurisdiction-specific designated provider clinical networks that significantly reduce inappropriate delays to treatment and enhance the uptake of medical services.

Coordinated pathways of care — involving Indigenous cardiac coordinators, facilitated by designated provider clinical networks and supported by ALOs — ensure the following for all Aboriginal and Torres Strait Islander patients, regardless of where they live:

  • availability of culturally appropriate information regarding warning signs
  • appropriate inhospital treatment
  • individualised inpatient care plans developed jointly with the patient and his or her family
  • education involving culturally appropriate tools within the hospital setting and inclusion of families, with support from ALOs and interpreters as appropriate
  • adequate follow-up care, secondary prevention programs and specific outpatient cardiac rehabilitation programs.

As the designated provider clinical networks need to be specific for each jurisdiction, they must be developed in collaboration with all involved in the patient pathway. This includes discussions and coordination with patients, families, Aboriginal health practitioners, primary care teams, retrieval services, emergency and cardiology services and health educators. The system should provide adequate cultural support throughout the process so that patients and families are engaged and adequately informed. Although cost-effectiveness has not been investigated in this consensus statement, the recommended framework should offer greater efficiencies in the use of existing resources.

With the advent of the ACS National Goal (announced by the Australian Commission on Safety and Quality in Health Care) and the recently funded Lighthouse Hospital initiative, improved data collection for monitoring effectiveness (including uptake and outcomes) is essential for the successful ongoing management and modification of the networks. The data from the designated provider clinical networks will also provide a more complete understanding of the issues confronting Indigenous patients. However, any delays in establishing the networks will only maintain the current disparities in service delivery and gaps in life expectancy. Therefore, the current lack of data should not delay the establishment of these networks.

With great power comes great responsibility

To the Editor: In October 2013, the Australian Broadcasting Corporation television program Catalyst featured a two-part documentary series entitled Heart of the matter. The first episode questioned the role of dietary saturated fat in the development of heart disease, and the second debated the use of
3-hydroxy-3-methylglutaryl coenzyme
A (HMG-CoA) reductase inhibitors (statins) as a suitable treatment for hypercholesterolaemia.1

Justin Coleman, a general practitioner and senior lecturer in medicine at Griffith University, provided an excellent summary of the two episodes, highlighting the bias of several of the medical experts featured in the program.2 Coleman drew particular attention to their undisclosed conflicts of interest, describing one expert as having his own commercial line of alternative treatments for heart disease. The views portrayed in the program could not have been published in any reputable medical journal without adequate disclosure of the experts’ conflicts of interest. So why should this be allowed on television, when the audience is potentially so much larger and more impressionable?

Perhaps the worst of the views aired was from an expert who suggested that starting statins means weighing up the risk of getting diabetes as a trade-off
for preventing a cardiovascular event. Such an opinion shows ignorance of international standards for scientific evidence — pitting the weak observational data suggesting a slight increase in risk of diabetes among statin users3 against the overwhelmingly strong evidence from multiple randomised controlled trials demonstrating the benefits of statins when used for secondary prevention after an acute coronary syndrome.4 Why are television stations allowed
to broadcast material on so-called scientific programs that includes
such misleading statements?

This program significantly hinders progress in tackling problems such as non-adherence with evidence-based medicines after acute coronary syndromes. It has been demonstrated that patients who stop taking their medications after myocardial infarction have a 10% higher chance of dying within 1 year.5 Resolving this problem requires patient education and empowerment, and a strong doctor–patient relationship — a relationship that is, unfortunately, often tested
by skewed views from the media.

Age, CKD and other kidney messages

Chronic kidney disease in the elderly is common, potentially harmful and amenable to nuanced management

Every March for the past 8 years, the International Society of Nephrology (ISN) and the International Federation of Kidney Foundations have jointly organised World Kidney Day (WKD; http://www.worldkidneyday.org). The purpose of WKD is to increase the awareness of kidney disease among politicians, the general public, general practitioners, physicians, nephrologists and other health care workers. WKD has been taken up with gusto in an increasing number of countries around the world, including Australia, and it is evident that the messages are being heard and to some extent have influenced policy. This year’s WKD will be held on 13 March, around the theme of “Chronic kidney disease (CKD) and aging”. Is this a message as substantive as those of previous WKDs?

Previous messages have been standouts. In 2007, the message was that kidney disease is common (affecting 10% of adults worldwide), harmful (not only from complications of CKD and end-stage kidney disease [ESKD], but also from a substantially increased risk of premature death, especially from cardiovascular causes) and treatable.1 In 2009 and 2010, the nexus between kidney disease and hypertension and diabetes, respectively, was stressed. Hypertension is a major risk factor for CKD and a key therapeutic target.2 The prediction that there will be 1.5 billion hypertensive people on our planet by 20252 is indeed a sobering one! Diabetes, especially type 2, is now the commonest cause of CKD and ESKD in most countries3 — and things are only going to get worse before they get better. By 2025, there will be almost 400 million people worldwide with type 2 diabetes3 and a similar number with impaired glucose tolerance, many of whom will go on to develop CKD. CKD, especially in the presence of proteinuria, is a principal risk factor for cardiovascular disease.4 Cardiovascular risk rises proportionally as kidney function declines; for example, Stage 3 CKD independently carries an almost 50% increased risk of cardiac death, a risk greater than that of diabetes or previous cardiovascular disease. Considering all stages of CKD together, there is a 100-fold greater chance of premature death (especially cardiovascular) than of developing ESKD. Importantly, interventions designed to slow CKD progression and reduce proteinuria appear also to reduce cardiovascular risk.

What began as a risky experiment about 50 years ago has now become routine practice in more than 80 countries around the world; there is no doubt at all that renal transplantation is the best way to replace kidney function in patients with ESKD.5 But, currently, only 10% of global need for kidney transplantation is met, restricted by economic considerations, insufficient donors, too small a trained workforce, immunological barriers and ethical considerations.5 Last year’s WKD focused on acute kidney failure (AKF). The prevalence of AKF is increasing worldwide and most cases are preventable,6 yet prevention and dialytic support during AKF are pipedreams for many countries. In response, the ISN has launched an ambitious program called “0 by 25” with the lofty aim that by 2025 no one should die of untreated AKF in the poorest parts of Africa, Asia and South America.

So is 2014’s WKD message as weighty as its antecedents (Box)? The latest message concerns CKD and ageing.7 Just like the body that surrounds them, kidneys age; a contemporary question is whether this ageing represents progressive CKD. Another key question is whether the automatic reporting of estimated glomerular filtration rate (eGFR) has spawned an epidemic of worried but well elderly people. The answer to the second question is yes and no. Otherwise healthy elderly people with a mild reduction in eGFR are likely to see out their years without any increased risk. However, whatever the cause of impaired eGFR, especially in the presence of proteinuria and with a rate of decline more rapid than expected for age alone, there will be increased risk.8 Despite their age, elderly patients with CKD will benefit from therapies aimed at slowing disease progression, better controlling metabolic derangements, reducing cardiovascular complications and allowing informed choices about ESKD therapy. That greater life expectancy does not necessarily equate with increased years of good health probably applies more to patients with CKD than any other ageing population. But treatment of selected older patients can increase survival, whether that treatment is conservative, dialytic or by transplantation. Older patients have less chance of undergoing transplantation, usually because of their comorbidities, but they can respond well, and various strategies (such as use of marginal and older donors) have increased the donor pool. Older patients with limited comorbidities can do well on dialysis, with improved survival; yet those with comorbidities may do better with non-dialytic, conservative therapy. So messages about CKD are just as important for older patients, and their wise application among older patients may do more for global health than among younger age groups.

What should developed countries be doing to lessen the global burden of kidney disease? Many developed countries must focus on their own groups at high risk of kidney disease, such as the Aboriginal population in Australia. In addition, they can play a key role in helping low-to-middle income countries tackle their kidney disease burden. The ISN directs a large proportion of its budget and efforts towards transformational capacity-building programs, including its Fellowship,9 Sister Renal Centre and other programs.10,11 By an increasing contribution to these programs, Australia can play a key role in the global response to kidney disease.

Important global messages* about kidney disease

2007

CKD is common, harmful and treatable

2009

Hypertension is a major risk factor for CKD

2010

Diabetes is a major risk factor for CKD

2011

CKD is a principal risk factor for cardiovascular disease

2012

Transplantation is the best therapy for ESKD, but is in short supply

2013

AKF is common and preventable

2014

CKD in the elderly is common, and amenable to discerning management


* Messages of World Kidney Day. CKD = chronic kidney disease.
ESKD = end-stage kidney disease. AKF = acute kidney failure.

Renal sympathetic denervation for resistant hypertension in a patient with a single kidney

To the Editor: We report a case
of successful renal sympathetic denervation (RSD) treatment for resistant hypertension in a patient with a single kidney.13 RSD is performed via femoral arterial access, using a radiofrequency ablation catheter to deliver energy
to the renal artery wall. When delivering RSD to a single kidney, potential renal artery vascular complications can have a significant negative impact on a patient’s renal function, compared with patients with two functioning kidneys.

Our patient was a 71-year-old man with resistant hypertension for many years. He had a congenitally absent left kidney. He was on
five antihypertensive agents: candesartan/hydrochlorothiazide
32/12.5 mg daily, lercanidipine 20 mg daily, atenolol 50 mg daily, moxonidine 0.4 mg daily and prazosin 0.5 mg twice daily. Despite this, his blood pressure was poorly controlled, with systolic blood pressure readings frequently above 200 mmHg. Renal ultrasound demonstrated a normal right kidney with normal renal artery, and the
left kidney could not be identified.
A computed tomography renal angiogram confirmed a single right renal artery with no plaque or stenosis. Other secondary causes
of hypertension had been excluded. Given refractory hypertension on medical therapy and suitable anatomy on imaging, the patient underwent RSD treatment to his right renal artery in 2012. Because
of its exceptional length, 12 ablations were delivered along
the artery.

On the day of the procedure, the patient’s sitting blood pressure was 180/76 mmHg. At 1-year follow-up, his sitting blood pressure was 155/66 mmHg. To date, our patient has benefited from sustained blood pressure reduction after RSD, with maintenance of his renal function (Box). He has continued on the same oral antihypertensive regimen.

To our knowledge, this is the second report of RSD for resistant hypertension in a patient with a single kidney.4 The previous report was limited by a follow-up period of only 3 months.4 The success of our case demonstrates the role of RSD
as an effective and well tolerated treatment for resistant hypertension, with an enduring result up to 12 months, even in patients with a single kidney, when it is performed at an expert centre.

Blood pressure and renal function immediately before renal sympathetic denervation (RSD) and at follow-up


eGFR = estimated glomerular filtration rate.

The cat and the nap

A patient’s apnoea is discovered by his “owner”

We report the case of a 72-year-old man who presented to his general practitioner with cat scratch — not cat-scratch disease, but trauma to the face and nose caused by repeated savage night-time attacks perpetrated by none other than his trusty loyal cat. The patient had a history of stable coronary artery disease, type 2 diabetes mellitus, diabetic neuropathy and hypertension.

Why the cat would be doing this puzzled his GP, who concluded that perhaps the cat was witnessing something which it deemed required intervention. The GP subsequently requested overnight polysomnographic assessment. This revealed moderate obstructive sleep apnoea (OSA) with an apnoea–hypopnoea index of 30, and bradycardia with 7-second cardiac pauses. Although 7-second cardiac pauses do not normally require cardiopulmonary resuscitation, the patient’s cat rushed in, knowing no better, to perform C(at)PR. Biting the nose that sneezes at you is not normally a recipe for success, but in this case it appears that the patient has had nine lives thanks to his cat. Happily, at routine follow-up after starting treatment with continuous positive airway pressure, the patient reported that the cat was no longer traumatising his face.

It is not unusual in a patient with these comorbidities to have both OSA and bradycardia with cardiac pauses,1 but what makes the case fascinating is the fact that sleep apnoea can trigger cardiac pauses.1 This raises the possibility of a unifying hypothesis — the cat was responding to and intervening in the patient’s apnoeic and asystolic episodes.

OSA has been causally related to cardiac arrhythmias and sudden cardiac death. Several mechanisms seem to underpin the association between OSA and cardiac arrhythmias,2 including intermittent hypoxia associated with autonomic nervous system activation, alteration in myocardial excitability, recurrent arousals with sympathetic activation and increased negative intrathoracic pressure which may mechanically stretch myocardial walls. There is a high prevalence of OSA in patients with cardiac arrhythmias.

So it appears that this cat, although unable to identify the exact cause of the apnoeic and asystolic episodes, was aware of the patient’s ill health and impending doom. Perhaps we should not be surprised by this, given the anecdotal stories that appear in the popular press from time to time — for example, stories of cats being “aware” of a woman’s pregnancy.

How could this all work? Animals live in a sensory world that is very different to our primarily visual world. While dogs have been shown to be able to detect various forms of human cancers,35 cats can detect smells and vapours that humans cannot detect.

In times of economic austerity, at least in Europe, let us commend this “natural” intervention. We hope that guideline groups will take note of this case and recommend the prescription of felines to patients at risk of OSA rather than home oximetry.

Tachycardia of unknown Origin

This is the first published case of onset of tachycardia despite triple rate-controlling medication during a rugby league match. The case highlights the importance of a thorough history to exclude Origin-induced tachycardia.

Clinical record

A 40-year-old Queensland man on continuous telemetry for decompensated idiopathic dilated cardiomyopathy following explantation of an infected implantable cardiodefibrillator was noted to have abnormal tracing (Box) between 19:00 and 22:00 on 4 July 2012. The patient was well, symptom-free and in excellent spirits. His medication included digoxin 250 μg daily, amiodarone 200 mg daily and bisoprolol 7.5 mg daily, with a resting heart rate of 60 beats per minute.

Telemetry showed asymptomatic variable persistent sinus tachycardia over a 3-hour period on the previous evening.

Further history revealed that the patient had been watching the deciding match of the annual State of Origin rugby league series between Queensland and New South Wales on television. The Box shows the onset of the tachycardia at the start of the match coverage at 19:00, with a second peak at kick-off (20:15). The recorded rhythm was sinus with left bundle branch block (QRS duration, 140 ms). The sinus tachycardia persisted throughout the first half until the half-time interlude, when normocardia resumed. The tachycardia reoccurred at the start of the second half, reaching a peak in the dying minutes of the game, when the patient’s home state, Queensland, scored a field goal at 75 minutes — followed by a missed long-range field goal by the NSW halfback in the final minute of the game — securing victory by one point for Queensland (21:55).

Discussion

This case illustrates a sustained run of tachycardia in a continuously monitored inpatient with cardiomyopathy, which terminated itself after trying circumstances and which occurred despite multiple rate-limiting medications.

Had the patient’s defibrillator still been in place, it mercifully would not have been activated, as his defibrillation threshold was set at 180 beats per minute. Origin-induced tachycardia should be a differential diagnosis for asymptomatic sinus tachycardia in passionate Queensland rugby league supporters, whose only cure when watching televised coverage is to turn off their televisions.

Cardiac telemetry trace

Sotalol-associated cardiogenic shock in a patient with asymptomatic transient rate-related cardiomyopathy

To the Editor: An 80 kg, 73-year-old man with type 2 diabetes managed with gliclazide and metformin was discharged on a dose of 40 mg twice daily of sotalol and a therapeutic dose
of warfarin after an admission for
atrial flutter. Transoesophageal echocardiography during his admission showed normal left ventricular (LV) size with mild to moderate global systolic dysfunction and moderate mitral incompetence.

Two weeks later, he developed generalised weakness, malaise, diaphoresis, nausea and dull left-sided chest pain, progressing to severe shock within 45 minutes of onset, evident on arrival at a hospital emergency department. Two hours before onset, he had taken a planned increase in his oral dose of sotalol to 80 mg.

His systolic blood pressure was 74 mmHg without evidence of respiratory compromise. Results of an arterial blood gas analysis were consistent with severe tissue hypoperfusion. Electrocardiography showed a sinus rhythm of 60 beats
per minute, normal conduction, a lengthened QTc interval (510 ms), and anterolateral T-wave inversion without ST-segment abnormalities. Results of bedside ultrasonography suggested global LV dysfunction.

The patient was given 2 litres of fluids and high doses of noradrenaline and adrenaline intravenously, but his condition did not improve. Intravenous calcium chloride (10 mmol) and glucagon (2 mg) restored his blood pressure to 120/70 mmHg, maintained with adrenaline (5 μg/min) alone. The initial relative bradycardia, prolonged QTc interval and response to calcium and glucagon were consistent with cardiogenic shock secondary to sotalol therapy. Other investigations excluded circulatory, cardiac, pulmonary, infective and drug causes of sudden cardiovascular collapse. The patient’s initial mild to moderate LV systolic dysfunction abated after adequate rate control, consistent
with a transient rate-related cardiomyopathy. Echocardiography showed normal LV function 2 months after discharge.

This is the first reported case of acute cardiogenic shock associated with low-dose sotalol alone (note that therapeutic doses range up to 640 mg/day). Cardiogenic shock has been reported in a patient taking a combination of sotalol and diltiazem,1 and in another patient taking digoxin, sotalol and verapamil.2 I have seen a similar case of reversible life-threatening cardiovascular collapse after sotalol (40 mg) was given orally to a 26-year-old with known atrial fibrillation. In that case, non-compliance with digoxin therapy resulted in an unrecognised rate-related cardiomyopathy.

As with all β-blockers, the official prescribing information for sotalol
in 2013 cautions about use in patients with known LV dysfunction, but does not warn of the risk of
life-threatening cardiogenic shock.
It is contraindicated only in “uncontrolled congestive heart failure”. “Hypo-tension” is considered a side effect.3

Research is indicated to determine whether rate-related cardiomyopathy is an independent risk factor for sotalol-induced cardiogenic shock and/or sudden death. Prescribing information for commencing sotalol or increasing the dose may need to be amended to warn of the risk of cardiogenic shock in this subset of patients.

Arrhythmia management distilled

The authors of this book work in Australia, the United Kingdom and Canada, and are well known to and respected by many Australian cardiologists working in the field of cardiac arrhythmia. The first edition was published in 2010. In view of the rapid advances in arrhythmia management, particularly the new medication and guidelines for management of atrial fibrillation (AF), as well as in catheter ablation, the authors considered a second edition warranted.

The target audience includes general practitioners, nurses, medical students, technicians and cardiology trainees. The layout is as simple as possible for a very complex subject. As is to be expected, because of its prevalence, AF is given prominence. The use of two important guidelines for assessing risk of thromboembolism and bleeding in patients with AF is emphasised: the CHA2DS2-VASc (congestive heart failure, hypertension, age >75 years [doubled], diabetes mellitus, stroke [doubled], vascular disease, age 65–74 years, sex category) score; and the HAS-BLED (hypertension, abnormal renal/liver function, stroke, bleeding history or predisposition, labile international normalised ratio, elderly, drugs/alcohol concomitantly) score.

Some antiarrhythmic drugs mentioned are unavailable in Australia, and the newer oral anticoagulants currently have only limited availability here. Hence, it is a little difficult to strictly follow the European and North American guidelines.

The vast majority of the information provided is correct; however, there are a few points with which I disagree. For example, lidocaine (lignocaine) is stated as having only minor negative inotropy, but experiments by Professor Robert McRitchie (personal communication) have shown it to be one of the most powerful negative inotropes of all antiarrhythmics.

In my opinion, the book is a concentrated distillation of the major points in arrhythmia management, and is potentially very useful for the target audience; it is certainly good value for money.

Acute coronary syndrome care across Australia and New Zealand: the SNAPSHOT ACS study

Despite well developed guidelines for managing acute coronary syndrome (ACS),1-6 local registries in Australia and New Zealand have demonstrated incomplete implementation of evidence-based recommendations,7-10 with variations in care appearing to correlate with differences in clinical outcomes. Geographical challenges, patient characteristics (including cultural diversity), health workforce and the health policy environment are likely factors affecting the optimal translation of this evidence base into timely, effective and risk-appropriate ACS care.11,12

Audits of hospitalisation for ACS in New Zealand have been crucial in defining treatment and resource gaps in practice.9,13 In Australia, registries have included relatively few patients from regional and remote centres.7 However, health service design and workforce provision have been found to be associated with variations in clinical outcomes in Australia.14 Hence, gaining a binational perspective from multiple health services of current ACS management is an essential step in health services redesign. The SNAPSHOT ACS study sought to inform these efforts by documenting care and outcomes among patients with suspected ACS through a comprehensive audit encompassing all hospitals and jurisdictions in Australia and New Zealand.

Methods

Study design and organisation

The SNAPSHOT ACS study was a prospective audit of the care provided to consecutive patients admitted with suspected ACS during a 2-week period in Australia and New Zealand. The study was designed by a binational academic network of clinicians and researchers, and managed by a steering committee with key stakeholder representation. It was developed as a collaborative quality improvement initiative between the Cardiac Society of Australia and New Zealand, the Heart Foundation of Australia, the Australian Commission on Safety and Quality in Health Care, the George Institute for Global Health, and health networks or state governments in New South Wales, Queensland, Victoria, South Australia and Western Australia (Appendix 1). The national organisations provided endorsement, in-kind resources and seed funding for central study management. State governments and health networks provided study coordinators to engage facilities, educate staff and assist with gaining ethics committee approval and data collection. The George Institute built the online database and coordinated data management.

All hospitals (public or private, metropolitan or rural) receiving patients with suspected ACS were identified through public records and health networks and approached about participating. Although sites were given training and support with data entry, each hospital’s participation was discretionary and resourced locally. Written study protocols were provided to all participating sites, and state-based education forums were held to standardise recruitment and data collection. Results were fed back to each site, benchmarked against the relevant state or territory and national aggregate at the end of the audit.

In Australia, ethics approval for opt-out consent was granted in all but two sites in Victoria, where opt-in consent was implemented. In New Zealand, expedited review by the National Multicentre Ethics Committee concluded that this was an audit of health service delivery, and a consent waiver was applied. In Australia, a consent waiver was applied to all inhospital deaths among patients with suspected ACS.

Patient eligibility and classification

Patients were eligible for inclusion if they were admitted for suspected or confirmed ACS between 14 and 27 May 2012 (inclusive). Consecutive first admissions within the audit window were included. Patients were tracked for the duration of the acute care episode, including all transfers between hospitals.

Patients were classified by primary discharge diagnosis into the following groups:

  • ST-segment-elevation myocardial infarction/left bundle branch block (STEMI/LBBB): patients with ST-segment elevation or LBBB on an electrocardiogram (ECG) at any time during the admission, with elevation of cardiac biomarkers (except where the patient died before biomarkers were measured).
  • Non-STEMI (NSTEMI): patients with evidence of biomarker elevation, with or without ECG changes consistent with ischaemia.
  • Unstable angina: recorded separately but combined with “likely ischaemic chest pain” for analysis.
  • Likely ischaemic chest pain: patients for whom the diagnosis remained uncertain in the absence of definitive ECG changes and/or biomarker elevation, but who received inhospital coronary revascularisation with either percutaneous coronary intervention (PCI) or coronary artery bypass grafting (CABG).
  • Unlikely ischaemic chest pain: extracted from the medical record, reflecting local clinician determination.
  • Other diagnosis: patients for whom a clear alternative primary diagnosis emerged, or where evidence of myonecrosis was considered secondary to another disease process (eg, pulmonary embolus).

Patient risk, inhospital care and events

Using a common case-record form with standardised completion note, data collection focused on patients’ presenting characteristics, including clinical variables enabling calculation of the Global Registry of Acute Coronary Events (GRACE) risk score, as well as logistical details of patient presentation and transfers between hospitals.15 Care provided across all institutions involved in acute care was documented, focusing on therapies recommended by published guidelines and inhospital events. Each participating hospital was also asked to complete a survey describing local resources, including cardiac investigation and management capabilities and workforce characteristics.

Inhospital events were defined as shown in Box 1. Reporting of clinical events relied on local documentation using the standardised completion note. Formal adjudication of events was not possible, but monitoring of 2%–5% of all case-record forms for data accuracy and quality was performed during and in the weeks after enrolment by coordinators across all jurisdictions.

Statistical analysis

Patient demographic and clinical characteristics, and rates of interhospital transfer, investigations, invasive procedures, provision of guideline-recommended therapies to patients surviving to hospital discharge, and inhospital events are presented as standard descriptive statistics stratified by discharge diagnosis, Australian Institute of Health and Welfare hospital classification, and health jurisdiction (Australian states or territories and New Zealand).4,5 Due to small sample sizes, the two tiers of medium regional hospital classification were combined, as were the other smaller hospital classifications. Private hospitals were considered as a separate group. These criteria were also applied to New Zealand hospitals. For stratification by jurisdiction, the Australian Capital Territory was combined with NSW, and Tasmania with the Northern Territory.

Dichotomous variables are reported as numbers and percentages and compared using the χ2 test. Continuous variables are reported as medians and interquartile ranges (IQRs) and compared using the Kruskal–Wallis test.

Propensity score-adjusted estimates of the influence of hospital classification and health jurisdiction on provision of angiography, provision of four or five guideline-recommended medications at discharge, referral to cardiac rehabilitation, and major adverse cardiac events (MACE) were generated using logistic regression modelling, stratified by discharge diagnosis. Assessment of angiography and MACE used all patients, while evaluation of rehabilitation referral and discharge medications was confined to patients with a discharge diagnosis of ACS. Propensity scores using age, sex, GRACE score, diagnostic group, heart failure at presentation, renal impairment, diabetes, hypertension, nursing home residence, dementia or cognitive impairment, private insurance, and primary language other than English were constructed for the likelihood of living in each jurisdiction and presenting to a hospital of each classification. Each model included the hospital classifications and jurisdictions as indicator variables, as well as their respective propensity scores, when reporting the jurisdiction or hospital estimates. Interaction terms of each jurisdiction and hospital classification were explored for significance, but no interactions were found. Given the observational and hypothesis-generating nature of these analyses, no adjustment of significance levels was undertaken.

Analyses were performed using Stata 11.2 (StataCorp), and P < 0.05 was considered statistically significant.

Results

Participating hospitals

Of 525 hospitals approached to participate, 478 gained ethics approval, and 435 provided site survey data describing their local resources. Within the 2-week enrolment period, 286 hospitals enrolled 4398 patients with suspected or confirmed ACS. Hospitals not enrolling patients were smaller centres and did not treat patients with suspected ACS during the audit window.

Most patients (65.7%; 2891/4398) presented to principal referral hospitals or hospitals in major cities (7.7%; 337/4398), while 7.3% (319/4398) presented to private hospitals. In terms of cardiac services available at the first presenting hospital, 79.7% of patients (3415/4283) presented where fibrinolysis could be administered, and 59.0% (2528/4283) presented to hospitals capable of providing primary PCI. Only 1.4% of patients (59/4283) presented to hospitals with no reperfusion therapy for STEMI. A quarter of patients (25.9%; 1138/4398) required transfer to at least one other hospital.

The distribution of hospital types by jurisdiction was comparable, except for Victoria, where a selective hospital recruitment strategy operated and there were fewer small regional hospitals (Box 2). Patient characteristics by health jurisdiction and hospital classification are presented in Appendix 2 and Appendix 3, respectively.

Patients with ACS

The risk profile of enrolled patients was high, with a median GRACE risk score of 119 (IQR, 96–144) across the entire population, and 138 (IQR, 114–161) among those with a discharge diagnosis of myocardial infarction (MI), including STEMI and NSTEMI.

Of the 4398 patients, 252 (5.7%) were Indigenous, Pacific Islander or Maori, and 165 (3.8%) were Asian. A primary language other than English was spoken by 294 patients (6.7%). Patient characteristics by discharge diagnosis are shown in Box 3. Among the 837 patients who were discharged with a diagnosis other than ACS, 317 (37.9%) had a troponin level above the local upper reference limit.

Provision of ACS care

Among the 421 patients with a discharge diagnosis of STEMI/LBBB, 106 (25.2%) received fibrinolytic therapy, 163 (38.7%) received primary PCI, and 152 (36.1%) received no reperfusion therapy. Of 1436 patients with STEMI or NSTEMI, coronary angiography was performed in 1019 (71.0%), PCI in 610 (42.5%), and CABG in 116 (8.1%). Reduced provision of invasive management with increasing risk was evident (GRACE score < 100, 90.1% v 101–150, 81.3% v 151–200, 49.4% v > 200, 36.1%; P < 0.001).

Guideline-recommended investigations and therapies were provided less frequently to patients presenting to non-principal referral hospitals, regardless of patient transfers (Box 4). Similar heterogeneity in the provision of care was observed when the results were stratified by jurisdiction (Appendix 4). Variation in the timeliness of care was also evident across jurisdictions; this was most marked in the median time to angiography and, to a lesser extent, in the overall length of stay (Appendix 5).

Inhospital events

Among the patients diagnosed with MI, the inhospital mortality rate was 4.5% (65/1436) and recurrent MI rate was 5.1% (73/1436). Inhospital adverse clinical events were highest among patients with STEMI/LBBB (Box 5). Inhospital mortality and recurrent cardiac failure were frequent among patients discharged with a diagnosis thought not to be ACS. Box 6 shows substantial heterogeneity in clinical events between hospital classifications, in all patients and in those discharged with a diagnosis of ACS.

Adjusted analyses

The propensity-adjusted odds ratios and confidence intervals describing the likelihood of undergoing inpatient angiography, receiving four or five guideline-recommended medications at discharge, receiving referral to rehabilitation, and experiencing inhospital MACE are shown in Box 7. There was a consistently lower likelihood of receiving guideline-recommended medications among patients originally presenting to non-principal referral hospitals. Patients in private hospitals were significantly more likely to undergo angiography, but not necessarily to receive guideline-recommended medications or rehabilitation referral. There was more variation in the occurrence of inhospital MACE at the health jurisdiction level than between hospital types.

Discussion

Optimising patient outcomes after MI through standardisation of care has emerged as a major near-term goal in the health agenda of Australia and New Zealand.17 Through the most representative assessment of ACS health service resources, clinical care provision and outcomes yet conducted in Australasia, this study provides unique insights into the challenges of providing timely and effective ACS care. These include the complexity of patient comorbidities, which brings the logistical challenges of providing timely invasive management to many patients in regional, remote and outer metropolitan centres into sharp focus.11,12

Translating evidence into practice requires a sophisticated understanding of determinants of care provision at the patient, clinical service and health policy level. Variations in clinical decision making, service availability and health policy represent potential targets for improving translation of the ACS evidence base and outcomes. An integrated approach to health service design is paramount to meeting the needs of our culturally diverse and geographically dispersed communities.

The efficient management of patients presenting with suspected ACS remains challenging. More sensitive markers of myonecrosis, such as high-sensitivity troponin assays, have not simplified this.18 This is demonstrated in our study by the substantial proportion of patients with suspected ACS who had elevated troponin levels, but in whom further investigations confirmed a final diagnosis other than ACS.19,20 Nevertheless, our data demonstrate high rates of inhospital events among such patients, as has been observed by others;21,22 yet the current evidence informing their management is very limited.

Similarly, our data demonstrate the substantial burden of clinical complexity among ACS patients, with relatively high prevalences of comorbidities including prior major bleeding events, cerebrovascular disease, cognitive impairment and concurrent malignancy.23 This complexity underscores the everyday challenges in applying the evidence among patients with typical ACS presentations. Reduced application of evidence-based therapies among patients with increased comorbidities has been found in other studies.24,25 Objective risk stratification that balances the benefits of evidence-based therapies against the risks associated with comorbidities may help narrow the evidence–practice gap for ACS patients with comorbidities.26

Our study highlights the potential for variation in care attributable to jurisdictional and geographical differences. The challenge of providing timely access to invasive management, not only in rural areas but also in the growing outer suburbs of cities, is highlighted by the fact that 26% of all ACS patients in our study required transfer. Attempts to improve consistency and quality of care, such as through clinical guidelines and clinical standards,17 need to consider the significant issues of transfer and coordination of care, particularly outside metropolitan areas, if such initiatives are to be effective and cost-effective.

In combination, these observations call for judicious and validated approaches to the development and implementation of clinical standards and performance measures that take these diagnostic and therapeutic complexities into account.

The broad hospital recruitment approach, consecutive patient enrolment, and high inhospital event rates in our study underscore the importance of representative patient inclusion when evaluating practice and outcomes.27 For the effective integration of clinical guidelines, clinical standards and performance measures into everyday care, the real challenge is to develop mechanisms to acquire and feed back such data on a routine and sustainable basis.28 The SNAPSHOT ACS study was the culmination of significant efforts to engage with national agencies and professional bodies, while implementation depended on the jurisdictional health networks. However, the study also required local hospital commitment to data collection and entry, an enormous unresourced effort that is difficult to quantify but attests to the dedication of health care providers to the quality of ACS care and outcomes. Future attempts to understand the lingering evidence–practice gaps will need to consider such resourcing issues carefully. Nevertheless, this study is unique in its ability to gain insights into the provision of care across multiple levels of decision making. Effectively delivering these insights to key decisionmakers at clinical, health service and health policy levels to enable the design and implementation of fully integrated approaches to ACS care remains the “translational” promise of this initiative.

1 Definitions of inhospital events

Inhospital mortality: included any-cause mortality

New or recurrent myocardial infarction (MI): recurrent chest pain lasting ≥ 30 minutes and ≥ 2 mm of ST-segment elevation within 18 hours of presentation, the development of a new left bundle branch block pattern or new Q waves or the following biomarker patterns: a rise in creatine kinase (CK) level to > 2 × upper reference limit (URL) and > 50% above previous baseline level; or CK-MB > 50% above prior level or troponin > 20% above previous baseline level

New MI after percutaneous coronary intervention: a rise in CK, CK-MB or troponin level to > 3 × URL if not previously elevated, or > 50% and > 20% rise above previous levels of CK-MB and troponin, respectively, if previously elevated

New MI after coronary artery bypass grafting: a rise in CK or CK-MB level to > 10 × and > 5 × URL, respectively, if not previously elevated, or a > 50% rise above previous level if elevated, or a 10-fold elevation in troponin level

Major bleeding: an event requiring a blood transfusion or involving a fall in haemoglobin level of > 4 g/dL

Stroke: a new neurological event involving single vascular territory, confirmed with neurological imaging

Cardiac arrest: sudden loss of cardiac function with loss of consciousness and spontaneous breathing

Worsening congestive heart failure: deterioration in Killip classification of one or more grades at any time during hospitalisation

Major adverse cardiac event: the occurrence of any one of the above events

2 Characteristics of hospitals enrolling patients with suspected or confirmed acute coronary syndrome (ACS), by health jurisdiction

 

Total

NZ

NSW/ACT

Queensland

Victoria

WA

SA

NT/Tas

P

No. of patients with suspected or confirmed ACS

4398

1007

1140

695

726

354

362

114

 

Estimated rate of admission for suspected ACS (per 100 000/year)

420

588

380

398

336

381

553

397

 

No. of hospitals participating

435

39

130

121

46

53

39

6

 

No. of hospitals enrolling patients

286

35

91

61

41

21

32

5

 

Principal referral*

88 (30.8%)

9 (25.7%)

29 (31.9%)

17 (27.9%)

19 (46.3%)

5 (23.8%)

5 (15.6%)

4 (80.0%)

< 0.001

Large, major cities*

19 (6.6%)

4 (11.4%)

7 (7.7%)

2 (3.3%)

2 (4.9%)

3 (14.3%)

1 (3.1%)

0

 

Large, regional towns*

19 (6.6%)

3 (8.6%)

4 (4.4%)

2 (3.3%)

6 (14.6%)

3 (14.3%)

0

1 (20.0%)

 

Medium, regional towns*

56 (19.6%)

8 (22.9%)

20 (22.0%)

10 (16.4%)

7 (17.1%)

0

11 (34.4%)

0

 

Small, other*

81 (28.3%)

11 (31.4%)

29 (31.9%)

20 (32.8%)

2 (4.9%)

6 (28.6%)

13 (40.6%)

0

 

Private*

23 (8.0%)

0

2 (2.2%)

10 (16.4%)

5 (12.2%)

4 (19.0%)

2 (6.3%)

0

 

Onsite cardiac intensive care*†

188 (65.7%)

29 (82.9%)

58 (63.7%)

43 (70.5%)

29 (70.7%)

13 (61.9%)

11 (34.4%)

5 (100%)

0.001

Onsite echocardiography service*

144 (50.3%)

24 (68.6%)

40 (44.0%)

28 (45.9%)

25 (61.0%)

11 (52.4%)

12 (37.5%)

4 (80.0%)

0.07

Onsite PCI service*

80 (28.0%)

10 (28.6%)

22 (24.2%)

16 (26.2%)

16 (39.0%)

7 (33.3%)

7 (21.9%)

2 (40.0%)

0.61

Onsite cardiac surgical service*

53 (18.5%)

5 (14.3%)

15 (16.5%)

11 (18.0%)

10 (24.4%)

5 (23.8%)

5 (15.6%)

2 (40.0%)

0.72


NZ = New Zealand. NSW = New South Wales. ACT = Australian Capital Territory. WA = Western Australia. SA = South Australia. NT = Northern Territory. Tas = Tasmania. PCI = percutaneous coronary intervention. * Percentages use number of enrolling hospitals in each jurisdiction as the denominator. † Dedicated higher cardiac acuity area such as intensive care, coronary care, high-dependency unit or integrated cardiac unit.

3 Characteristics of patients, by clinical diagnosis at time of discharge

 

Total

STEMI/LBBB

NSTEMI

Unstable angina/likely ischaemic chest pain

Unlikely ischaemic chest pain

Other diagnosis*

P

No. of patients

4398

421

1015

929

1196

837

 

Age in years, mean (SD)

66.5 (14.6)

65.6 (14.4)

71.2 (13.2)

68.1 (12.9)

62.1 (14.9)

65.8 (15.7)

0.001

Female

1771 (40.3%)

119 (28.3%)

376 (37.0%)

343 (36.9%)

567 (47.4%)

366 (43.7%)

< 0.001

Median creatinine level, µmol/L (25th–75th percentile)

84 (70–104)

89 (73–106)

89 (74–113)

86 (71–106)

78 (66–93)

85 (68–110)

< 0.001

Killip Class II–IV at presentation

599 (13.6%)

81 (19.2%)

206 (20.3%)

78 (8.4%)

69 (5.8%)

165 (19.7%)

< 0.001

Presentation with cardiac arrest

78 (1.8%)

35 (8.3%)

12 (1.2%)

4 (0.4%)

3 (0.3%)

24 (2.9%)

< 0.001

Median GRACE risk score (25th–75th percentile)

119 (96–144)

140 (118–165)

137 (114–159)

115 (96–136)

101 (80–122)

120 (94–147)

0.001

Diabetes

1115 (25.4%)

83 (19.7%)

314 (30.9%)

289 (31.1%)

217 (18.1%)

212 (25.3%)

< 0.001

Hypertension

2785 (63.3%)

229 (54.4%)

699 (68.9%)

677 (72.9%)

672 (56.2%)

508 (60.7%)

< 0.001

Dyslipidaemia

2391 (54.4%)

192 (45.6%)

588 (57.9%)

618 (66.5%)

578 (48.3%)

415 (49.6%)

< 0.001

Current smoker

800 (18.2%)

130 (30.9%)

175 (17.2%)

134 (14.4%)

218 (18.2%)

143 (17.1%)

< 0.001

Prior myocardial infarction

1195 (27.2%)

75 (17.8%)

345 (34.0%)

335 (36.1%)

250 (20.9%)

190 (22.7%)

< 0.001

Prior PCI

892 (20.3%)

48 (11.4%)

184 (18.1%)

308 (33.2%)

199 (16.6%)

153 (18.3%)

< 0.001

Prior CABG

466 (10.6%)

21 (5.0%)

135 (13.3%)

133 (14.3%)

88 (7.4%)

89 (10.6%)

< 0.001

Prior atrial fibrillation

667 (15.2%)

31 (7.4%)

174 (17.1%)

126 (13.6%)

144 (12.0%)

192 (22.9%)

< 0.001

Known PAD

267 (6.1%)

22 (5.2%)

91 (9.0%)

67 (7.2%)

41 (3.4%)

46 (5.5%)

< 0.001

Prior TIA or CVA

454 (10.3%)

23 (5.5%)

144 (14.2%)

108 (11.6%)

93 (7.8%)

86 (10.3%)

< 0.001

Prior admission for major bleeding or transfusion

107 (2.4%)

10 (2.4%)

26 (2.6%)

20 (2.2%)

25 (2.1%)

26 (3.1%)

0.63

Active cancer limiting life expectancy

106 (2.4%)

8 (1.9%)

27 (2.7%)

21 (2.3%)

26 (2.2%)

24 (2.9%)

0.76

Cognitive impairment or dementia

149 (3.4%)

11 (2.6%)

42 (4.1%)

27 (2.9%)

38 (3.2%)

31 (3.7%)

0.46

Nursing home resident

116 (2.6%)

13 (3.1%)

33 (3.3%)

28 (3.0%)

12 (1.0%)

30 (3.6%)

0.001


STEMI/LBBB = ST-segment elevation myocardial infarction/left bundle branch block. NSTEMI = non-STEMI. GRACE = Global Registry of Acute Coronary Events. PCI = percutaneous coronary intervention. CABG = coronary artery grafting. PAD = peripheral artery disease. TIA = transient ischaemic attack. CVA = cerebrovascular accident. * Includes secondary myonecrosis.

4 Provision of (A) investigations and revascularisation and (B) guideline-recommended therapies, among patients with a discharge diagnosis of acute coronary syndrome, by enrolling hospital classification*


PCI = percutaneous coronary intervention. CABG = coronary artery grafting. * n refers to number of patients.

5 Inhospital clinical events, by principal diagnosis at time of discharge*


MI = myocardial infarction. CHF = congestive heart failure. MACE = major adverse cardiac events. STEMI/LBBB = ST-segment elevation myocardial infarction/left bundle branch block. NSTEMI = non-STEMI.
* All comparisons of outcomes between diagnostic categories are significant (P < 0.001). n refers to number of patients.

6 Inhospital clinical events among (A) all patients and (B) patients with a discharge diagnosis of acute coronary syndrome, by enrolling hospital classification


MI = myocardial infarction. CHF = congestive heart failure. MACE = major adverse cardiac events. * n refers to number of patients.

7 Adjusted odds ratios* for likelihood of (A) provision of angiography, (B) provision of four or five guideline-recommended medications at discharge, (C) referral to cardiac rehabilitation, and (D) inhospital major adverse cardiac events, by hospital classification and health jurisdiction


* Principal referral hospitals and State D are the referent categories for hospital classification and health jurisdiction, respectively. Bars indicate 95% confidence intervals, which have been produced using the floating absolute risk method.16