Guidelines for the management of atrial fibrillation released

Guidelines for the management of atrial fibrillation (AF) have been released by the European Society of Cardiology (ESC).

The 2016 Atrial Fibrillation Guidelines, created around state-of-the-art research and evidence, were released earlier this week at the ESC Congress in Rome.

AF remains one of the major causes of stroke, heart failure, sudden death and cardiovascular morbidity in the world, with emerging evidence offering innovative approaches to its diagnosis and management.

The guidelines list recommendations for diagnosis, general management, stroke prevention, rate control and rhythm control of AF.

Catheter ablation, which has now become a common treatment for recurrent AF, is also discussed as a possible treatment within the guidelines. In general, it should be used as second-line treatment after failure of or intolerance to antiarrhythmic drug therapy. In such patients, when performed in experienced centres by adequately trained teams, catheter ablation is more effective than antiarrhythmic drug therapy.

Other guideline recommendations for the management of AF include:

Opportunistic screening for AF is recommended by pulse taking or ECG rhythm strip in patients over the age of 65
The proposal of lifestyle changes to all suitable AF patients to make their management more effective
The use of the CHA₂DS₂-VAS_c score to predict stroke risk, and initiation of oral anticoagulation when score is 2 or more for males, or 2 or more for females
The avoidance of combinations of oral anticoagulants and platelet inhibitors in AF patients without another indication for platelet inhibition
The selection of antiarrhythmic drugs based on the presence of co-morbidities, cardiovascular risk, potential for proarrhythmia, extracardiac toxic effects, patient preference and symptoms, and consideration of catheter or surgical ablation when antiarrhythmic drugs fail
Moderate regular physical activity is recommended to prevent AF, while athletes should be counselled that long-lasting, more intense sports participation can promote AF

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[Perspectives] Shengshou Hu: leader of cardiac surgery and health reform in China

“Wise man finds pleasure in streams”, says an old Chinese saying. Being at one with water has always been part of Chinese cardiac surgeon Shengshou Hu’s life, from the wide waters of the Yangtze river to the swimming pool close to his professional home today in Beijing, where he is President of Fuwai Hospital, affiliated with the Chinese Academy of Medical Sciences. “As a young man, swimming across the Yangtze river with its strong currents seemed a good metaphor for life, and even today I find swimming a good time for reflection and relaxation, especially after surgery”, he says.

Cardiac machines linked to infection

Health departments around the country are contacting open heart surgery patients who may have been exposed to a rare infection that can be found in some heater-cooler units used in surgery.

According to international reports the design and manufacture of some heart bypass heater-cooler units made by Sorin have made them susceptible to harbouring the rare bacterium mycobacterium chimaera.

M. chimaera infections in cardiac surgery patients overseas have been linked to the heater-cooler units made by medical equipment manufacturer Sorin. It is thought that the units were contaminated during their manufacture.

It’s a common bacterium that occurs naturally in the environment and only causes rare infection. The infections tend to be slow to develop (it can take from several months to over a year for an infection to develop) and often affect people with compromised immune systems.

There has been one reported possible patient infection following an open cardiac surgery in 2015.

According to a statement by the Therapeutic Goods Association: “These infections have been associated with the use of heater-cooler devices which are used within the operating theatre to control the temperature of blood diverted to cardio-pulmonary bypass machines. Heater-cooler devices contain water tanks that provide temperature-controlled water for the operation of the device. This water does not come in contact with the patient.”

The TGA says it’s monitoring the situation and has updated its advice for health facilities regarding how to manage devices that test positive for mycobacterium chimaera.

In NSW, the hospitals that have used the potentially contaminated machines are Prince of Wales, St George, Sydney Children’s Hospital and The Children’s Hospital at Westmead.

All machines have been cleaned or replaced and the risk to patients is low.

Related: Cheap way to cut infection risk

“The risk of infections to an individual patient is very small, but it’s important that we’ve alerted clinicians to the risk and put systems in place to reduce the risk further,” infectious disease specialist Dr Kate Clezy, from the NSW Clinical Excellence Commission, said in a statement.

In Victoria, Fairfax media reports that the bacterium has been detected in heater-cooler units at The Alfred, Austin and Cabrini hospitals in Melbourne.

“All the units were decommissioned and replaced once the test results were known,” a department spokesman said.

It’s believed doctors are checking patient records to see whether anyone has been harmed by the bacterium.

According to director of infectious diseases and microbiology at the Austin Hospital Professor Lindsay Grayson, there is about a 1 in 10 000 chance of the bacterium causing an infection.

“If you think about this, the chances of having a car accident are one in 4000, so it is very rare.”

He said the infection could be cured with surgery and use of specific antibiotics.

According to NSW Health, the signs of possible M. chimaera infection include:
fatigue
difficulty breathing
persistent cough or cough with blood
fever
night sweats
redness, heat, or pus at the surgical site
muscle pain
joint pain
abdominal pain
weight loss
nausea
vomiting

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Progress in the care of familial hypercholesterolaemia: 2016

Familial hypercholesterolaemia (FH) is the most common autosomal dominant condition.1 FH reduces the catabolism of low-density lipoprotein cholesterol (LDL-c) and increases rates of premature atherosclerotic cardiovascular disease (CVD). This review focuses on recent advances in the management of FH, and the implications for both primary and secondary care, noting that the majority of individuals with FH remain undiagnosed.2

FH was previously considered to have a prevalence of one in 500 in the general community, including in Australia.3 Recent evidence, however, suggests the prevalence is between one in 200 and one in 350, which equates to over 30 million people estimated to have FH worldwide.4,5 These prevalence figures relate to the general population, and while FH is present in all ethnic groups, communities with gene founder effects and high rates of consanguinity, such as the Afrikaans, Christian Lebanese and Québécois populations, have a higher prevalence of the condition.

Further, the prevalence of homozygous or compound heterozygous FH has been demonstrated to be at least three times more common than previously reported, with a prevalence of about one in 300 000 people in the Netherlands.4 The detection and management of individuals with homozygous FH has been described in a consensus report from the European Atherosclerosis Society.6 Homozygous FH is a very severe disorder, with untreated people often developing severe atherosclerotic CVD before 20 years of age. Such individuals often have LDL-c concentrations > 13 mmol/L and severe cutaneous and tendon xanthomata. While diet and statins are the mainstays of therapy, early intervention (before 8 years of age) with LDL apheresis or novel lipid-lowering medication, such as proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitors or microsomal triglyceride transfer protein inhibitors, is indicated. Patients with suspected homozygous FH should be referred to a specialist centre.6

Several recent international guidelines on the care of FH have been published.3,7–10 These have focused on early detection and treatment of individuals with FH. However, there is still no international consensus on the diagnostic criteria for FH, or on the utility of genetic testing. The Dutch Lipid Clinic Network criteria (DLCNC) are preferred for diagnosing FH in index cases in Australia (Box 1).2 The International FH Foundation guidance acknowledges geographical differences in care, and recognises the need for countries to individualise service delivery. CVD risk in FH is dependent on classic CVD risk factors. However, FH is appropriately excluded from general absolute CVD algorithms, since these underestimate the absolute risk in FH.

FH guidelines provide therapeutic goals, which vary depending on the specific absolute CVD risk for patients with FH. In adults, the general LDL-c goal is a least a 50% reduction in pre-therapy LDL-c levels, followed by a target of LDL-c < 2.5 mmol/L, or < 1.8 mmol/L in individuals with CVD or other major CVD risk factors; these international targets update those of previously published Australian FH recommendations.2,3,10 Currently only about 20% of individuals with FH attain an LDL-c level < 2.5 mmol/L.11

Detecting FH in children

The European Atherosclerosis Society published a guideline focusing on paediatric aspects of the diagnosis and treatment of children with FH in 2015.8 This guideline outlined the benefit of early treatment of children with FH using statins. There is a significant difference in the carotid intima medial thickness (a measure of subclinical atherosclerosis) in children with FH and their unaffected siblings by 7 years of age, with implications for the value of early treatment. Lifestyle modifications and statins from 8 years of age can reduce the progression of atherosclerosis to the same rate as unaffected siblings over a 10-year period.8 Early treatment of children improves CVD-free survival by 30 years of age (100%) compared with their untreated parents (93%; P = 0.002).8 While further long term data on statin use in children are required, there are 10-year follow up data for children who were initiated on pravastatin between the ages of 8 and 18 years, which demonstrate that statin therapy is safe and effective.12 Hence, the balance of risk and benefit suggests that use of statins in children with FH is safe and efficacious, at least in the short to intermediate term, with all recommendations appropriately requiring that potential toxicity and adverse events be closely monitored.

Childhood is the optimal period for detecting FH, as LDL-c concentration is a better discriminator between affected and unaffected individuals in this age group. After excluding secondary causes and optimising lifestyle and repeating fasting LDL-c on two occasions, a child is considered likely to have FH if they have:

an LDL-c level ≥ 5.0 mmol/L;
a family history of premature CVD and an LDL-c level ≥ 4.0 mmol/L; or
a first-degree relative with genetically confirmed FH and an LDL-c level ≥ 3.5 mmol/L.

Universal screening for FH in children has been demonstrated to be effective in Slovenia, but experience is limited elsewhere.13 The therapeutic targets for children are less aggressive than for adults: a reduction in LDL-c of over 50% in children aged 8–10 years and an LDL-c level < 3.5 mmol/L from the age of 10 years.8

Cascade screening

Recent reports from Western Australia confirm that cascade screening is efficacious and cost-effective.11,14 The genetic cascade screening and risk notification process followed in Western Australia is shown in Box 2.11 Cascade screening involves testing close relatives of individuals diagnosed with FH. The autosomal dominant inheritance suggests 50% of first-degree relatives would be expected to have FH. Two new cases of FH were found by cascade screening for each index case in WA.11 These individuals were younger and had less atherosclerotic CVD than index cases. Interestingly, about 50% were already on lipid-lowering therapy, but they were not treated to the recommended goals and further lipid reductions were achieved overall. Over 90% of patients were satisfied with the cascade screening process and care provided by this service .11 However, for individuals who have not had genetic testing performed, or for individuals with clinical FH in whom a mutation has not been identified, cascade screening should also be undertaken using LDL-c alone.

Although we have recently shown that genetic testing is cost-effective in the cascade screening setting ($4155 per life year saved),14 only a few centres in Australia have this facility and testing is currently not Medicare rebatable. However, combining increased awareness of the benefits of identifying people with FH with the reducing analytical costs may increase the use of genetic testing. This in turn could guide advocacy and lobbying Medicare to support genetic testing for FH.

Detecting FH in the community

A novel approach that utilises the community laboratory to augment the detection of FH has recently been tested in Australia. The community laboratory is well placed to perform opportunistic screening, since they perform large numbers of lipid profiles, the majority (> 90%) of which are requested by general practitioners.15 Clinical biochemists can append an interpretive comment to the lipid profile reports of individuals at high risk of FH based on their LDL-c results. These interpretive comments on high risk individuals (LDL-c ≥ 6.5 mmol/L) led to a significant additional reduction in LDL-c and increased referral to a specialist clinic.16 A phone call from the clinical biochemist to the requesting GP improved both the referral rate of high risk (LDL-c ≥ 6.5 mmol/L) individuals to a lipid specialist and the subsequent confirmation of phenotypic FH in 70% of those referred, with genetic testing identifying a mutation in 30% of individuals.17 There is a list of specialists with an interest in lipids on the Australian Atherosclerosis Society website (http://www.athero.org.au/fh/health-professionals/fh-specialists).

In Australia, GPs consider they are the best placed health professionals to detect and treat individuals with FH in the community.18 A large primary care FH detection program in a rural community demonstrated that using pathology and GP practice databases was the most successful method to systematically detect people with FH in the community.19 However, a survey of GPs uncovered some key knowledge deficits in the prevalence, inheritance and clinical features of FH, which would need to be addressed before GPs can effectively detect and treat individuals with FH in the community.18 A primary care-centred FH model of care for Australia has recently been proposed to assist GPs with FH detection and management, but this requires validation.20 The model of care includes an algorithm that is initiated when an individual is found to have an LDL-c level ≥ 5.0 mmol/L, which could be highlighted as at risk of FH by either a laboratory or the GP practice software.20,21 The doctor is then directed to calculate the likelihood of FH using the DLCNC. Patients found to have probable or definite FH are assessed for clinical complexity and considered for cascade testing. See the Appendix at mja.com.au for the algorithm and definition of complexity categories. FH-possible patients should be treated according to general cardiovascular disease prevention guidelines.

Molecular aspects

There have also been advances in molecular aspects of FH. A recent community-based study in the United States confirmed that among patients with hypercholesterolaemia, the presence of a mutation was independently predictive of CVD, underscoring the value of genetic testing.22 The mutation spectrum of FH was described in an Australian population and was found to be similar to that in Europe and the United Kingdom.23 Mutation detection yields in Australia are comparable with the international literature; for example, 70% of individuals identified with clinically definite FH (DLCNC score > 8) had an identifiable mutation, whereas only 30% of those with clinically probable FH had a mutation.23

Polygenic hypercholesterolaemia (multiple genetic variants that each cause a small increase in LDL-c but collectively have a major effect in elevating LDL-c levels) is one explanation for not identifying an FH mutation. An LDL-c gene score has been described to differentiate individuals with FH (lower score) from those with polygenic hypercholesterolaemia (higher score), but this requires validation.24 About 30% of individuals with clinical FH are likely to have polygenic hypercholesterolaemia, and cascade screening their family members may not be justified.25

A further possible explanation for failure to detect a mutation causative of FH in an individual with clinically definite FH may lie in the limitations of current analytical methods such as restricting analysis to panels of known mutations. Further, FH is genetically heterogeneous and there may be unknown alleles and loci that cause FH. Next generation sequencing is capable of sequencing the whole genome or targeted exomes rapidly at a relatively low cost, and may improve mutation detection and identify novel genes causing FH, but further experience with its precise value in a clinical setting is required. Whole exome sequencing was able to identify a mutation causing FH in 20% of a cohort of “mutation negative” but clinically definite FH patients.25 However, when applied to patients with hypercholesterolaemia in a primary care setting, pathogenic mutations were only detected in 2% of individuals, with uncertain or non-pathogenic variants detected in a further 1.4%.26

Cardiovascular risk assessment

Absolute CVD risk assessment, employing risk factor counting, should be performed as atherosclerotic CVD risk is variable in FH.10,27 This involves appraisal of classic CVD risk factors including, age, sex, hypertension, diabetes, chronic kidney disease and smoking. The prevalence of classic CVD risk factors among Western Australians with recently identified FH was 13% for hypertension, 3% for diabetes and 16% for smokers, all of which were amenable to clinical intervention.11

Other non-classic CVD risk factors are also important for individuals with FH, especially chronic kidney disease and elevated levels of lipoprotein(a).28 Lipoprotein(a) is a circulating lipoprotein consisting of an LDL particle with a covalently linked apolipoprotein A. Its plasma concentration is genetically determined and it is a causal risk factor for CVD in both the general population and FH patients.29,30 Lipoprotein(a) concentrations are not affected by diet or lowered by statins.31

Management and new therapies

The past 2 years have also seen the development of new treatments for FH, but lifestyle modifications and statins remain the cornerstones of therapy for FH. Ezetimibe has been demonstrated to reduce coronary events against a background of simvastatin in non-FH patients with established CVD.32 PCSK9 inhibitors have recently been approved to treat individuals with FH or atherosclerotic CVD not meeting current LDL-c targets in Europe and America. PCSK9 is a hepatic convertase that controls the degradation and hence the lifespan of the LDL receptor. PSCK9 is secreted by the hepatocyte and binds to the LDL receptor on the surface of the hepatocyte. The LDL receptor–PCSK9–LDL-c complex is then internalised via clathrin-dependent endocytosis, but the PSCK9 directs the LDL receptor towards lysosomal degradation instead of recycling it back to the hepatocyte surface.33 A recent meta-analysis of early PCSK9 inhibition trials involving over 10 000 patients demonstrated a 50% reduction in LDL-c, a 25% reduction in lipoprotein(a), and significant reductions in all-cause and cardiovascular mortality.34

The PCSK9 inhibitors alirocumab and evolocumab were approved by the European Medicines Agency in 2016 for homozygous and heterozygous FH and non-FH individuals unable to reach LDL-c targets, and for individuals with hypercholesterolemia who are statin intolerant. In the US, the Food and Drug Administration has approved alirocumab for heterozygous FH and individuals with atherosclerotic CVD who require additional reduction of LDL-c levels. Evolocumab and alirocumab have recently been approved by the Therapeutic Goods Administration in Australia for people with FH. Adverse events are generally similar to placebo, but reported side effects include influenza-like reaction, nasopharyngitis, myalgia and raised creatine kinase levels, and there have been reports of neurocognitive side effects (confusion, perception, memory and attention disturbances).34 The cost of these agents is likely to be the major limitation to their clinical use. The indications and use of lipoprotein apheresis and other novel therapies, including lomitapide, a microsomal triglyceride transfer protein inhibitor, and mipomersen (an antisense oligonucleotide that targets apolipoprotein B), have been recently reviewed.35

Despite the advances reviewed, the implementation and optimisation of models of care for FH remain a major challenge for preventive medicine. Areas of future research should focus on better approaches for detecting FH in the young and on enhancing the integration of care between GPs and specialists. The value of genetic testing and imaging of pre-clinical atherosclerosis in stratifying risk and personalising therapy merits particular attention. Further, with families now living in a global community, more efficient methods of communication and data sharing are required. This may be enabled by international Web-based registries.36 Care for people with FH needs to be incorporated into health policy and planning in all countries.10

Conclusion

There have been significant advances in the care of individuals with FH over the past 3 years. An integrated model of care has been proposed for primary care in Australia. Progress has also been made in the treatment of FH with the emergence of PCSK9 inhibitors capable of allowing more patients already on statins to attain therapeutic LDL-c targets and hence redressing the residual risk of atherosclerotic CVD. Future research is required in the areas of models of care, population science and epidemiology, basic science (including genetics), clinical trials, and patient-centric studies.37 Finally, the onus rests on all health care professionals to improve the care of families with FH, in order to save lives, relieve suffering and reduce health care expenditure.

Box 1 –
Dutch Lipid Clinic Network Criteria score for the diagnosis of familial hypercholesterolaemia (FH)2

Criteria

Score

Family history

First-degree relative with known premature coronary and/or vascular disease (men aged < 55 years, women aged < 60 years); or

First-degree relative with known LDL-c > 95th percentile for age and sex

First-degree relative with tendon xanthomas and/or arcus cornealis; or

Children aged < 18 years with LDL-c > 95th percentile for age and sex

Clinical history

Patient with premature coronary artery disease (ages as above)

Patient with premature cerebral or peripheral vascular disease (ages as above)

Physical examination

Tendon xanthomata

Arcus cornealis at age < 45 years

LDL-c

≥ 8.5 mmol/L

6.5–8.4 mmol/L

5.0–6.4 mmol/L

4.0–4.9 mmol/L

DNA analysis: functional mutation in the LDL receptor, apolipoprotein B or PCSK9 gene

Stratification

Definite FH

> 8

Probable FH

6–8

Possible FH

3–5

Unlikely FH

< 3

LDL-c = low-density lipoprotein cholesterol. PCSK9 = proprotein convertase subtilisin/kexin type 9.

Box 2 –
Protocol for genetic cascade screening in Western Australia*

* Family cascade screening process performed according to national guidelines2 after obtaining written consent from the index case.11 This was undertaken by a trained nurse who contacted the family members and obtained verbal consent to contact further family members, after providing counselling and offering specialist review as indicated.

[Editorial] Atrial fibrillation and stroke: unrecognised and undertreated

When did you or your primary care physician last palpate your wrist to check for a regular heart rate? This simple action, followed by an electrocardiogram if the heart rate is irregular, might be crucial in preventing death and disability from ischaemic stroke, heart failure, or myocardial infarction. In this week’s issue, we publish a clinical Series of three papers on atrial fibrillation ahead of the annual European Society of Cardiology (ESC) meeting held in Rome, Italy, Aug 27–31. Atrial fibrillation is estimated to affect 33 million people worldwide.

Remote Australians more likely to be hospitalised with heart-related issues

Patients from very remote Australia are nearly twice as likely to need a hospital for a heart-related event.

The Heart Foundation has released heart-related hospital admissions data maps, revealing huge gaps between city dwellers and those living in remote Australia.

Heart Foundation National Chief Executive Officer Adjunct Professor John Kelly said the maps bring together a national picture of hospital admission rates for the first time.

“Those regions that rate in the top hotspot areas are regions where a large proportion of residents are of significant disadvantage. This disadvantage includes a person’s access to education, employment, housing, transport, affordable healthy food and social support,” he said.

“This contrasts to areas with the lowest rates – particularly the northern suburbs of Sydney, where there is little disadvantage of the community.

“There is a five-fold difference of hospital admissions between Northern Territory Outback and the region with the lowest admission rates North Sydney & Hornsby, which highlights the association between remoteness, disadvantage and our heart health.”

The heart maps reinforce the knowledge that heart admissions are correlated with obesity, smoking and physical activity.

However Professor Kelly points out that the differences are not because people from disadvantaged areas make unhealthy choices.

“They are the result of a combination of social, economic and physical conditions, like a person’s access to education, employment, housing, transport, affordable healthy food, and social support,” he explained.

“These conditions shape matters such as people’s eating habits, participation in physical activity and their likelihood to see a doctor.

He said governments and health services need to work together to provide access and opportunities for people in more remote locations.

“Prevention programs work, simple early detection and heart health checks by doctors can help early identification of the risk factors and reduce hospital admissions.

“Health is a basic human right. It should not matter who you are, how much you earn or where you live,” he said.

Top 5 Regions for Heart-Related Hospital Admissions

Top 5 Regions with the lowest heart-related hospital admission rates

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Pitting and non-pitting oedema

The distinction is essential to determine aetiology and treatment

Oedema can be divided into two types: pitting and non-pitting. These types are relatively easy to distinguish clinically and the distinction is essential to determine aetiology and treatment.

Oedema is the swelling of soft tissue due to fluid accumulation. Pitting is demonstrated when pressure is applied to the oedematous area and an indentation remains in the soft tissue after the pressure is removed (Box 1 and Box 2). Moreover, mild pitting oedema is best identified by applying pressure over an area of bony prominence. Non-pitting oedema refers to the lack of persistent indentation in the oedematous soft tissue when pressure is removed.1

In addition to the differentiation of pitting and non-pitting oedema, the pattern of distribution is reflective of the underlying aetiology. With pitting oedema, there may be bilateral dependent oedema of the lower limbs, generalised oedema or localised oedema. Non-pitting oedema generally affects an isolated area, such as a limb. There are two ways of describing the severity of pitting oedema. Most commonly, in the setting of peripheral oedema, severity is graded by its proximal extent, so that oedema located above the knee is more severe than oedema presenting below the knee. The alternative approach is based on depth and duration of pitting after the release of pressure (Box 3).2

A number of factors3 can be considered to be major contributors to the development of oedema:

increased intravascular hydrostatic pressure;
reduced intravascular oncotic pressure;
increased blood vessel wall permeability;
obstructed fluid clearance in the lymphatic system; and
increased tissue oncotic pressure.

The underlying pathophysiology for oedema explains the reason for pitting and non-pitting. Oedema is the accumulation of fluid in the interstitium. In normal circumstances, there is a balance between fluid leaking from capillaries and drainage by the lymphatics.3 In the setting of increased intravascular hydrostatic pressure, reduced oncotic pressure or where there is increased vessel wall permeability, fluid leaks out of vessels into the interstitial space. When external pressure is applied, extracellular fluid is displaced with increased drainage through the lymphatic system, creating an indentation that is visible in the skin and is described as pitting. When pressure is removed, the fluid slowly returns and the indentation disappears (see the video at mja.com.au). Lymphoedema, which is the most common form of non-pitting oedema, occurs when fluid accumulates in the interstitial space as a result of a reduction in lymphatic drainage. The application of pressure does not result in an indentation as there is an inability to drain fluid through the damaged lymphatic system.4 An uncommon form of non-pitting oedema, myxoedema, can occur as a result of accumulation of hydrophilic molecules in the subcutaneous tissue.5

The differentiation between pitting and non-pitting oedema, in addition to the pattern of distribution, reflects different pathophysiology and may therefore be helpful in identifying the underlying aetiology. Pitting peripheral lower limb oedema resulting from raised hydrostatic pressure can occur in congestive cardiac failure, venous insufficiency and as a result of the use of a calcium channel blocker. Generalised oedema may be seen in kidney disease, where reduced intravascular oncotic pressure occurs through protein loss or where increased vascular volume occurs through sodium and fluid retention. Localised pitting oedema is likely related to a local inflammatory process resulting in increased vessel wall permeability. Non-pitting oedema of an isolated area is consistent with failure of lymphatic drainage, which may rarely have a primary (hypoplastic) aetiology or, more commonly, a secondary (obstructive) aetiology. Secondary causes include external compression from a tumour, involvement of lymph nodes in metastatic disease, and lymph vessel damage following radiotherapy or following lymph node resection. Myxoedema is associated with thyroid disease.5

The underlying aetiology will guide treatment options. In the setting of congestive cardiac failure, treatment would generally include fluid restriction and diuretics (including spironolactone). Compression bandaging and leg elevation are useful for oedema related to venous insufficiency. In the setting of oedema related to inflammation, a general approach would include applying ice and elevation in addition to treating the underlying cause of the inflammatory process. Lymphoedema may be detected using a perometer and managed with compression garments and manual lymph drainage. Myxoedema may resolve with treatment of the underlying thyroid condition.

Box 1 –
Pressure applied to an oedematous area to demonstrate pitting

Box 2 –
Indentation remaining in soft tissue after pressure to an oedematus area is removed

Box 3 –
Alternative approach for grading the severity of pitting oedema based on depth and duration of pitting after release of pressure

Severity

Description

Grade 1+

A pit of up to 2 mm that disappears immediately

Grade 2+

A pit of 2–4 mm that disappears in 10–15 seconds

Grade 3+

A pit of 4–6 mm that may last more than 1 minute

Grade 4+

A deep pit greater than 6 mm that may last as long as 2–5 minutes

Adapted from Guelph General Hospital Congestive Heart Failure Pathway.2

Variation in coronary angiography rates in Australia: correlations with socio-demographic, health service and disease burden indices

The known Angiography rates vary across Australia. Whether this variation is correlated with indices of socio-economic deprivation, chronic disease, acute coronary syndrome (ACS) incidence, or health service characteristics is uncertain.

The new Social disadvantage and remoteness were correlated with ACS incidence and mortality, but not with angiography rates. Private hospital cardiac admissions were strongly correlated with angiography rates; the relationship with public hospital cardiac admissions was less marked. Socio-economic indicators, regional location, and ACS and chronic disease burden were not significantly associated with angiography rates.

The implications A focus on clinical care standards and better health service distribution is needed to reduce the variation.

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 1 –
Socio-economic and health service characteristics, and age- and sex-standardised rates of death, diagnosis, and coronary procedures (per 100 000 population), by Medicare Locals stratified according to metropolitan, regional and rural locations, for the calendar year 2011

	Total	Metropolitan	Regional	Rural	P

Number	61	27	24	10
Socio-economic indicators
SEIFA score, mean (SD)	992 (42)	1022 (39)	976 (21)	955 (33)	0.001
Indigenous population, mean (SD)	3.9% (5.5)	1.1% (0.7)	3.1% (2.1)	13.2% (8.1)	0.001
Long term unemployed, mean (SD)	3.5% (1.4)	2.6% (1.1)	4.1% (1.0)	4.6% (1.5)	0.001
Private insurance, mean (SD)	44.3% (9.9)	51.7% (9.3)	40.8% (4.3)	33.0% (5.2)	0.001
Chronic health status indicators
Diabetes, mean (SD)	5.3% (1.0)	5.7% (1.1)	4.8% (0.7)	5.5% (0.9)	0.004
Hypertension, mean (SD)	10.2% (0.6)	10.2% (0.6)	10.3% (0.6)	10.1% (0.5)	0.994
Smokers, mean (SD)*	19.1% (3.6)	16.2% (2.9)	21.4% (1.8)	22.8% (1.5)	0.001
Obesity, mean (SD)*	28.3% (4.2)	25.5% (4.4)	30.6% (1.9)	31.4% (2.1)	0.001
Hypercholesterolaemia, mean (SD)	33.1% (1.7)	32.9% (1.4)	33.6% (1.8)	32.1% (2.2)	0.186
Chronic cardiovascular condition, mean rate (SD)*	88 (14)	81 (11)	91 (9)	102 (21)	< 0.001
Premature ischaemic heart disease, mean rate (SD)	28.4 (10.2)	22.9 (5.1)	27.6 (3.4)	45.3 (13.3)	< 0.001
Access and health workforce indicators
Delay in medical consultation because of cost, mean (SD)	14.6% (3.6)	13.2% (3.8)	15.3% (2.9)	16.8% (3.1)	0.006
Primary care physicians, mean rate (SD)	110.8 (17.4)	113.9 (22.1)	109.1 (10.8)	106.3 (15.8)	0.776
Specialist physicians, mean rate (SD)*	22.9 (21.6)	34.2 (26.7)	13.4 (6.5)	10.8 (6.4)	0.002
Health service provision indicators
Primary care health check, mean rate (SD)	4266 (1181)	4336 (1034)	4548 (1239)	3401 (1111)	0.032
Public cardiac admissions, mean rate (SD)	1684 (451)	1366 (274)	1826 (316)	2201 (479)	< 0.001
Private cardiac admissions, mean rate (SD)^†	752 (264)	861 (202)	717 (283)	527 (227)	0.021
All emergency department presentations, mean rate (SD)	30 881 (11 358)	24 939 (11 358)	32 400 (9837)	43 277 (17 082)	< 0.001
Likelihood of angiogram in suspected acute coronary syndrome, mean (SD)	40.6% (16.7)	49.2% (17.2)	30.9% (8.9)	41.4% (18.2)	< 0.001
Coronary events and procedures
Myocardial infarction, mean rate (SD)	250 (63)	225 (48)	250 (46)	316 (90)	0.003
Acute coronary syndrome, mean rate (SD)	419 (108)	375 (93)	423 (84)	532 (120)	< 0.001
Coronary angiography, mean rate (SD)	849 (236)	803 (167)	895 (300)	863 (218)	0.742
Percutaneous coronary intervention, mean rate (SD)	212 (47)	222 (38)	215 (58)	178 (23)	0.009
Coronary artery bypass surgery, mean rate (SD)	70 (15)	64 (13)	74 (15)	75 (18)	0.040
Revascularisation, mean rate (SD)	278 (49)	284 (41)	283 (61)	250 (25)	0.089
Premature ischaemic heart disease deaths, mean rate (SD)^‡	28.4 (10.2)	22.9 (5.1)	27.6 (3.4)	45.3 (13.3)	< 0.001
Premature cerebrovascular accident deaths, mean rate (SD)^‡	9.2 (2.4)	8.2 (1.6)	9.4 (1.7)	11.5 (3.7)	< 0.001
Total mortality, mean rate (SD)	88 (14)	81 (11)	91 (9)	102 (21)	< 0.001
Population, mean (SD)	296 666 (165 595)	414 767 (144 115)	232 023 (110 353)	132 939 (94 442)	< 0.001

SEIFA = Socio-Economic Indexes for Areas. * Estimates from modelled data: not available for three Medicare Locals (all rural). † Data not released for three Locals (one each for metropolitan, regional and rural). ‡ Annualised rates per 100 000 individuals for 2008–2011.

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*

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 3 –
Correlations between indicators of socio-economic status, health status, health workforce, health care access and clinical practice, and coronary angiography, acute coronary syndrome and mortality rates in Medicare Locals*

Coronary angiography rate

Acute coronary syndrome admission rate

Total mortality rate

Socio-economic indicators

SEIFA score

–0.11 (0.42)

–0.62 (< 0.001)

–0.54 (< 0.001)

Indigenous population^†

–0.08 (0.53)

0.53 (0.002)

0.30 (0.019)

Long term unemployed^†

–0.07 (0.62)

0.60 (< 0.001)

0.46 (0.002)

Private insurance^†

–0.15 (0.24)

–0.65 (< 0.001)

–0.62 (< 0.001)

Chronic health status indicators

Diabetes^†

–0.22 (0.10)

–0.05 (0.72)

0.001 (0.94)

Hypertension^†

–0.27 (0.03)

–0.17 (0.20)

0.16 (0.22)

Smokers^†

0.25 (0.05)

0.61 (< 0.001)

0.62 (< 0.001)

Obesity^†

0.15 (0.26)

0.51 < 0.001)

0.65 (< 0.001)

Hypercholesterolaemia^†

0.16 (0.23)

–0.39 (0.002)

–0.08 (0.54)

Chronic cardiovascular condition^†

–0.21 (0.12)

0.05 (0.70)

0.38 (0.003)

Premature ischaemic heart disease

0.13 (0.32)

0.59 (< 0.001)

0.58 (< 0.001)

Access and health workforce indicators

Delay in medical consultation because of cost^†

0.05 (0.69)

0.61 (< 0.001)

0.45 (< 0.001)

Primary care physicians

–0.07 (0.59)

–0.26 (0.04)

–0.39 (0.002)

Specialist physicians

0.12 (0.37)

–0.41 (0.002)

–0.47 (< 0.001)

Health service provision indicators

Primary care health check (45 years)

0.28 (0.03)

0.02 (0.88)

–0.12 (0.35)

Public cardiac admissions

0.30 (0.02)

0.65 (< 0.001)

0.49 (< 0.001)

Private cardiac admissions

0.44 (0.006)

–0.13 (0.32)

–0.42 (< 0.001)

Emergency presentations

0.14 (0.28)

0.47 (0.001)

0.35 (0.005)

Likelihood of angiogram in suspected acute coronary syndrome^†

0.06 (0.69)

–0.01 (0.96)

–0.40 (0.002)

SEIFA = Socio-Economic Indexes for Areas. * Expressed as correlation coefficient, with significance (P) in parentheses. † Correlation between percentage of population positive for indicator and angiography, acute coronary syndrome admissions and mortality rates.

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

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

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

Ensuring access to invasive care for all patients with acute coronary syndromes: beyond our reach?

We need to ensure that those who need care most receive it

Coronary artery disease (CAD) remains the leading cause of death and disability in Australia, with suspected acute coronary syndromes (ACS) being the most common reason for acute presentation to hospital.1 A substantial body of evidence supports the early use of invasive care — coronary angiography and, if appropriate, revascularisation (either by percutaneous coronary intervention [PCI] or coronary artery bypass grafting [CABG]) — in patients presenting with ST-elevation myocardial infarction to reduce mortality and re-infarction rates.2 Evidence and expert opinion also favour invasive management of patients with high risk, troponin-positive non-ST-elevation ACS (NSTEACS).3,4 In patients with stable CAD, there is no evidence for any benefit from invasive care if optimal medical therapy is administered.5 Access to invasive care should be in accordance with clinical need, and this is likely to be greater in populations with a higher prevalence of CAD, CAD-related deaths, and coronary risk factors.

In this issue of the MJA, a large ecological study encompassing the entire population of 61 (former) Medicare Locals and using information from several databases identified associations between socio-economic, geographic and chronic cardiovascular disease factors and ACS incidence and mortality rates.6 Chew and colleagues also examined whether rates of invasive care (coronary angiography being the key measure) were correlated with indicators of disease burden, access to care, and clinician practice.

The study had some limitations. Data were analysed and associations between different variables (presumed to be linear) defined at the population rather than at the individual level; data on private hospital admissions were missing for three of eight state or territory jurisdictions; rates of ACS, invasive care and CAD-related deaths were only adjusted for age and sex, not for other risk factors or measures of disease severity; the likelihood of a patient with suspected ACS receiving coronary angiography was based on a relatively small national snapshot audit (n = 4398) from 8 years ago;7 the timing of invasive care after the ACS event was not provided; and rates of non-invasive co-interventions for ACS were not included in the analysis.

Despite these limitations, some of the key findings are interesting. Rates of angiography and of ACS were only weakly correlated, with no correlation between ACS and PCI rates; these trends were most evident in non-metropolitan areas where CAD mortality was highest. While ACS rates varied 3.7-fold between Medicare Locals, angiography rates varied 5.3-fold. The strongest predictor of angiography being undertaken was admission as a cardiac patient to a private hospital (71 additional angiograms per 1000 admissions), despite lower rates of ACS among private patients, suggesting that many procedures were for non-ACS indications. Coronary revascularisation rates as a proportion of angiography rates varied between 17% and 61%; higher angiograms rates were associated with reduced likelihood that revascularisation followed. There was a reasonably strong positive association between rates of ACS and CABG, suggesting that less invasive PCI is more vulnerable to unwarranted use. Depressingly, the study also reconfirmed the higher ACS rates in non-metropolitan locations where the prevalence of smoking, obesity and chronic cardiovascular disease is higher.

The disparity between rates of invasive care and those of ACS and overall CAD burden probably means that some patients are receiving interventions they do not need, while, more worryingly, patients who have real need for them are missing out. Without data on clinical indications and criteria of appropriateness for individual patients, overuse cannot be distinguished from underuse. Nevertheless, such variations in invasive care, seemingly unexplained by variations in clinical indications, are of concern, especially as they have been documented since 2005.7–11

So why is universal access to invasive care according to need seemingly beyond our reach? It is not for want of trying on the part of national professional bodies that develop, disseminate and promote evidence-based recommendations and implementation frameworks.12 The answer lies with front line health care delivery systems. Cardiology service networks at the state level should collect data on ACS incidence and rates of invasive care in public and private facilities, identify locations where the mismatch is greatest, and seek to understand and mitigate the relevant factors. Networked, hub-and-spoke support systems of rapid diagnostic, referral and transfer procedures are needed, whereby patients with ACS presenting to any emergency centre have rapid access to invasive care in angiography-capable facilities, in accordance with clinical indications and socio-cultural context, and without logistical barriers.13,14 Hospitals should report on their provision of appropriate ACS care according to agreed care standards and data collection methods, for benchmarking against peers and sharing improvement strategies.15

Invasive care prevents about 10% of all CAD-related deaths, whereas medical treatments and reducing risk factors account for at least 80% of saved lives.16 As Chew and colleagues report, a higher probability of undergoing coronary angiography was associated with only a modest reduction in ACS mortality rates (three fewer deaths per 100 000 population for each 10 percentage point increase in likelihood of angiography). The maximal gain in lives saved after ACS onset will require optimisation of all care modalities along the entire patient trajectory. However, while non-invasive care is not consistently employed across Australia,7–10 differences in the use of invasive care are more marked and cannot be allowed to persist into the next decade.

Improving outcomes in coronary artery disease

Systems, procedures and policies are needed to further reduce the toll of cardiovascular disease

Although major advances have been made in many aspects of the treatment of heart disease, rates of mortality and morbidity from acute coronary syndromes (ACS) in Australia and New Zealand remain significant. The SNAPSHOT ACS study reported outcomes of patients presenting with ACS.1 The 18-month mortality for patients presenting with an ST-elevation myocardial infarction was 16.2%, 16.3% for those presenting with a non-ST-elevation myocardial infarction, and 6.8% for those with unstable angina. Although these outcomes are a substantial advance on historical data, there is still much room for improvement.2 It is therefore timely that the National Heart Foundation (NHF) and the Cardiac Society of Australia and New Zealand (CSANZ) have revised the Australian guidelines for the management of ACS (summarised in this issue of the MJA).3 The NHF, CSANZ and all involved should be congratulated on the development of these guidelines.

The revised ACS guidelines simplify the target time for myocardial reperfusion in patients presenting with an ST-elevation myocardial infarction. Primary percutaneous coronary intervention (PCI) should be performed within 120 minutes of first medical contact or within 90 minutes of presentation to a PCI-enabled hospital. Otherwise thrombolysis should be administered unless there are contraindications. Patients’ outcomes are maximised when the duration of myocardial ischaemia (ie, time from symptom onset to reperfusion) is minimised, with optimal outcomes occurring when this time is less than 120 minutes.4 Protocols to expedite thrombolysis or PCI are required to minimise treatment delays.5 Continuing public education programs are needed to raise awareness of the symptoms of a heart attack. Such campaigns have been shown to reduce Australian patients’ time to presentation.6 Pre-hospital electrocardiograms recorded by the ambulance service further reduce delays, and pre-hospital thrombolysis programs, especially for patients in remote locations, can significantly reduce ischaemia times, as reported by Khan and colleagues in this issue of the Journal.7 Additionally, the revised guidelines provide clinical assessment protocols to expedite troponin testing using highly sensitive assays to rule out myocardial infarction within 2 hours of presentation. This will particularly benefit compliance with the 4-hour National Emergency Access Target for presentations to emergency departments.8

In this issue of the Journal, May and colleagues indirectly address the appropriate use of coronary stenting (PCI) in patients with stable coronary artery disease.9 The DEFER study confirmed that subjective operator assessment of the severity of intermediate coronary artery lesions is a poor predictor of myocardial ischaemia as assessed by fractional flow reserve (FFR), an index of reduced myocardial perfusion.10 The FAME 2 trial demonstrated that the benefit of PCI in stable patients is confined to stenting lesions with an FFR < 0.80.11 FFR was used in 4.8% of coronary angiograms funded by Medicare in 2015. It is not known how many of these patients were investigated for stable coronary disease or whether these patients underwent pre-procedural stress testing as an alternative to FFR. PCI should be carefully targeted in stable coronary artery disease; it is of benefit when there is limiting angina due to a proximal coronary artery stenosis > 50%, a positive stress test demonstrating ischaemia in at least 10% of the myocardium, or an FFR < 0.80.12

Following a cardiac event, secondary prevention strategies improve outcomes.13 Secondary prevention is traditionally overseen in a cardiac rehabilitation program. Only a minority of patients attend such programs, and a significant number do not continue with guideline-recommended therapy and lifestyle modifications.14 New technologies including video conferencing and various apps may provide a mechanism to extend the reach of cardiac rehabilitation, as Gallagher and Neubeck note in this issue of the Journal.15 These technologies may enhance or replace traditional services. It is yet to be demonstrated that they will deliver on their promise. Strategies that enhance compliance with the Australian Commission on Safety and Quality in Health Care ACS standard are required.16

There is a need to enhance quality assurance by establishing registries to assess patient outcomes. The SNAPSHOT ACS study provided valuable insights into the nationwide treatment of ACS patients, and allowed the identification of treatment gaps and compliance with guidelines and standards. Such information is required to assess the impact of various treatment strategies and health care policies. The CSANZ has established the Australasian Cardiac Outcomes Registry (http://www.acor.net.au). Sustainable funding models need to be established to support the collection of risk-adjusted patient, procedural and device outcomes. It is incumbent on the cardiac community to ensure that systems, procedures and policies are developed to further reduce the toll of cardiovascular disease in an environment where outcomes are monitored and continuously assessed.