Cardiovascular diseases

To the Editor: The recommendation for managing acute ST-segment-elevation myocardial infarction with percutaneous coronary intervention (PCI) is that the door-to-balloon inflation time should be 90 minutes. However, it can be up to 120 minutes, depending on when patients present to the emergency department (ED) after the onset of their symptoms.1 In such cases, an alternative immediate reperfusion strategy — fibrinolysis — should be considered. At first glance, a door-to-balloon time of 90 minutes seems readily achievable, but what if the patient presents after hours, or presents to a hospital without PCI facilities? The time required to refer the patient for PCI, organise ambulance transport and call in cardiac catheterisation laboratory staff can be considerable. In the PRAGUE-2 trial from the Czech Republic, the average door-to-balloon time was 97 minutes.2 The DANAMI-2 study from Denmark had a cohort of 27 080 patients and had door-to-balloon times of about 114 minutes for those patients transferred to another facility.3 The National Registry of Myocardial Infarction 4 investigators reported a median door-to-balloon time of 185 minutes for American patients transferred to centres capable of PCI, and a door-to-balloon time of less than 90 minutes for only 3% of patients.4 Doctors working in EDs without onsite access to PCI need to know the door-to-balloon times of the institutions to which they refer patients for PCI. Centres performing PCI may not be forthcoming with this information, as they have a vested interest in keeping their numbers up for PCI. Alternatively, this information may not be known to the clinician accepting the patient for PCI. In addition, doctors in EDs who opt to transfer their patients have the burden of organising transport for potentially unstable patients who may develop lethal arrythmias. As door-to-needle time for thrombolysis has become a clinical indicator for EDs, perhaps door-to-balloon times can be a clinical indicator for cardiac catheterisation laboratories. Finally, it is important to note that in some patients requiring urgent coronary artery reperfusion, the first electrocardiogram (ECG) is not diagnostic, so a more pragmatic indicator would be diagnostic ECG-to-balloon time. This would require an enforcement of the current recommendations for an ECG to be performed and critically reviewed shortly after a patient presents with symptoms suggestive of an acute coronary syndrome.

Jayantha I Weeraratne

In reply: We agree with the points highlighted by Weeraratne, and these have been broadly addressed within the new National Heart Foundation of Australia and Cardiac Society of Australia and New Zealand Guidelines for the management of acute coronary syndromes 2006.1 The guidelines emphasise the need for appropriate systems of care which are regionally based, have formal links with specialist centres, include appropriate monitoring, feedback and quality improvement components, and are sensitive to the cultural and personal beliefs and wishes of individual patients. Clinicians do need to know the achievable door-to-balloon times for primary percutaneous coronary intervention within their local contexts, and if there is any doubt about the timely availability of this treatment for patients with ST-segment-elevation myocardial infarction, the guidelines recommend that fibrinolysis be given promptly.

Philip Aylward · Constantine N Aroney

Objective: We aimed to assess the pattern of use of drug-eluting stents (DESs) in patients undergoing percutaneous coronary interventions (PCIs) in Victorian public hospitals.Design, setting and patients: Prospective study comparing the use of one or more DESs versus bare-metal stents (BMSs) only, in consecutive patients undergoing 2428 PCIs with stent implantation from 1 April 2004 to 31 December 2005 at seven Victorian public hospitals.Main outcome measures: Adherence to current Victorian Department of Human Services guidelines which recommend DES use in patients with high-risk features for restenosis (diabetes, small vessels, long lesions, in-stent restenotic lesions, chronic total occlusions and bifurcation lesions).Results: Of the 2428 PCIs performed, at least one DES was implanted in 1101 (45.3%) and BMSs only were implanted in 1327 (54.7%). In 87.7% (966/1101) of PCI with DESs, there was at least one criterion for high risk of restenosis. DESs were more likely to be used in patients with diabetes (risk ratio [RR], 2.45; 95% CI, 2.02–2.97), small vessels (RR, 3.35; 95%CI, 2.35–4.76), long lesions (RR, 3.87; 95% CI, 3.23–4.65), in-stent restenotic lesions (RR, 3.98; 95%CI, 2.67–6.06), chronic total occlusions (RR, 1.30; 95% CI, 0.51–2.88) and bifurcation lesions (RR, 2.23; 95%CI, 1.57–3.17). However, 66.2% (1608/2428) of all PCIs were in patients eligible for DESs according to Victorian guidelines, and in 39.9% (642/1608) of these PCIs, a BMS was used.Conclusion: In Victorian public hospitals, DESs have been largely reserved for patients at high risk of restenosis in accordance with Department of Human Services guidelines. However, many patients with high-risk criteria for restenosis did not receive DESs. Greater use of DESs in these patients may improve outcomes by reducing the need for repeat revascularisation.

on behalf of the Melbourne Interventional Group (MIG) investigators

Objective: To review the management of glycaemia, blood pressure and serum lipids in a hospital outpatient diabetes clinic, the director of which co-authored the current national diabetes management guidelines.Design: Retrospective audit.Setting: Outpatient diabetes clinic in a tertiary referral teaching hospital, Sydney, NSW.Study population: 96 patients with type 1 diabetes (mean age, 44.4 [SD, 12.8] years) and 509 patients with type 2 diabetes (mean age, 64.4 [SD, 12.0] years) attending the clinic in 2003, who had undergone formal review of complications.Main outcome measures: Weight, height, control and treatment of glycaemia, blood pressure and serum lipids, and prevalence of diabetic microvascular complications.Results: Glycated haemoglobin (HbA1c) was < 7% in 13% of type 1 and 30% of type 2 diabetes patients, and > 8% in 47% and 34%, respectively. 35% of patients with type 1 diabetes and 71% of patients with type 2 diabetes were treated with antihypertensive agents. Of these patients, 29% and 24%, respectively, had blood pressure readings ≤ 130/80 mmHg. Among patients not treated with hypertensive agents, blood pressure readings were ≤ 130/80 mmHg in 60% of type 1 and 38% of type 2 diabetes patients. About 30% of patients with type 1 diabetes and 50% of those with type 2 diabetes were being treated with lipid-lowering agents; of these, about 60% had low-density lipoprotein (LDL) cholesterol levels < 2.6 mmol/L. Among patients not treated with lipid-lowering agents, about 40% had LDL cholesterol levels < 2.6 mmol/L. Retinopathy was documented in 52% and 18%, and nephropathy in 9% and 36% of type 1 and type 2 diabetes patients, respectively.Conclusions: Despite the demonstrated benefits of tight glucose, blood pressure and lipid control in reducing the risk of macrovascular and microvascular complications in type 1 and type 2 diabetes, our results suggest that treatment targets are not being met in a large proportion of patients attending a tertiary referral hospital. Responsible practice suggests that treatment targets and the current means to achieve them should both be examined.

Wendy Bryant,* RN, CDE, GradDipDiabetesEdManagement · Jerry R Greenfield,* PhD, FRACP · Donald J Chisholm FRACP · Lesley V Campbell FRCP, FRACP

A 58-year-old man presented with a 1-month history of persistent nausea, vomiting, diarrhoea and fevers. He also reported worsening shortness of breath, lower extremity swelling, and a 4.5 kg weight loss. He was febrile and hypotensive, with pedal oedema and a soft diastolic murmur over the mitral area. A white cell count and chest x-ray were normal. A transthoracic echocardiogram, performed to assess cardiac function, showed a large, highly mobile left atrial mass prolapsing into the left ventricle (Box, A [arrowed]). At urgent surgery, an 8 cm left atrial myxoma arising from the interatrial septum was resected (Box, B). Histopathological examination showed dense colonies of yeast. Histoplasma capsulatum was grown from blood cultures and cultures of the surgical specimen (Box, C). HIV testing was negative. The patient made a full recovery after completing antifungal therapy. Infected left atrial myxoma is rare. We know of only one other reported case in which Histoplasma was the infective agent.1 A: Transthoracic echocardiogram B: Surgical specimen C: Microscopic view of Histoplasma capsulatum (Gomori methenamine silver stain)

Ahmed Awab MD · Mehdi Hamadani MD · Bhanu Sud MD · Gene W Voskuhl MD

To the Editor: The discussion of fibrinolysis in the recently published guidelines for the management of acute coronary syndromes 20061 is interesting. The recommendations clearly indicate that second-generation agents should be preferred to streptokinase in all circumstances. The guidelines reference the GUSTO-I trial data2 as the primary support for those recommendations. These data are, at best, debatable in terms of showing any benefit of front-loaded tissue plasminogen activator over streptokinase, and then only in limited circumstances (ie, patients aged less than 75 years with anterior infarcts and within 4 hours of the onset of symptoms).3,4 To my knowledge, there have been no head-to-head trials of this size of the other fibrinolytic agents discussed against streptokinase. Thus there is no justification for the blanket superiority that is accredited to these agents, both by implication and explicitly, in the guidelines. It is a matter of some concern that guidelines from such respected groups should make statements that will be used broadly by clinicians, but that go beyond the evidence base to which they refer. On the balance of information available there is no compelling case to relegate streptokinase from the front line.

Andrew J Bezzina

In reply: As Bezzina states, the GUSTO-I trial is the main source of evidence for the superiority of front-loaded alteplase (rt-PA) over streptokinase, showing a 1% absolute and 15% relative benefit.1 Subgroup analysis suggested that only certain groups benefited, but this is an inappropriate use of subgroups, and the result should be applied overall. A clear mechanistic reason for the advantage of rt-PA — greater 90-minute full coronary patency — has also been demonstrated.2 Meta-analyses of the percutaneous coronary intervention (PCI) trials in acute myocardial infarction have all shown benefit over fibrinolysis. However, the benefit of PCI is greater compared with streptokinase than with plasminogen activators.3 Although not providing a head-to-head comparison, these data also support the superiority of plasminogen activators over streptokinase. The second generation plasminogen activator studies have all compared these with the “gold standard” front-loaded rt-PA. These agents have been shown to not be inferior in relation to mortality,4,5 and tenecteplase showed a decrease in systemic bleeding.5 Administration as a bolus without the adverse reactions commonly seen with streptokinase (such as hypotension) make them much more convenient and safe, particularly in smaller institutions. In addition, streptokinase is an inappropriate choice in Indigenous patients because many have high levels of anti-streptokinase IgG and streptokinase resistance.6

Philip Aylward · Constantine N Aroney · Ken Hossack · Andrew M Tonkin

Objective: To evaluate the use of cardiovascular medications in patients with and without heart failure after myocardial infarction (MI).Design and setting: Multicentre study of drug therapy for patients with MI in 16 major metropolitan teaching hospitals in Australia over a 1-month period at each hospital in the period November 2004 – March 2005.Participants: 479 patients admitted consecutively to the individual hospitals.Main outcome measures: Proportion of patients with and without heart failure who were prescribed key cardiovascular medications after MI.Results: 116 of the 479 patients admitted for MI (24.2%) had heart failure at some point during their hospitalisation. Patients with heart failure were older (68 v 63 years; P < 0.05), more likely to be women (34% v 24%; P < 0.05) and a higher proportion had diabetes (26% v 21%). There was significantly reduced prescribing of β-blockers, clopidogrel and statins for patients with heart failure compared with those without heart failure. Mineralocorticoid receptor antagonist use was low (< 10%) in the former group.Conclusions: We found reduced prescribing of some prognostically relevant medications for patients with heart failure. For β-blockers, this may be explained by the greater clinical instability in patients with heart failure. Given the absolute benefit of drug therapy in patients with heart failure after MI, our findings suggest suboptimal prescribing in Australian teaching hospital practice.

Henry Krum MB BS, PhD, FRACP · Adam Meehan · John Varigos BSc(Hons) · Philippa R Loane BBiomedSc · Baki Billah PhD

William Heath was born on 23 July 1925 in Casterton, western Victoria. The eldest of seven children, he was educated by the nuns at the Convent of Mercy School in Casterton. Bill’s father died when he was 14, so at the age of 15 he commenced work as a clerk with the AMP Society, a relationship which continued throughout his life and culminated in the position of Chief Medical Officer of the AMP Society. At the age of 18, Bill joined the Royal Australian Air Force and trained as a pilot. After the war, he returned to AMP for a year before commencing a medical degree at the University of Melbourne. After graduating with honours in 1953, he completed his training at St Vincent’s Hospital, Melbourne. Awarded a National Heart Foundation Travelling Scholarship in 1961, Bill took his young family to the United States to work as a cardiovascular research fellow at Georgetown University in Washington, DC, from 1962 to 1964. Bill then returned to Melbourne and quickly established an extensive private practice in Collins Street. He was much sought after as a clinician, teacher and source of expert medicolegal opinion. He held many board appointments, including Medical Director of the Mercy Hospital, Chief Medical Officer at Munich Reinsurance Company, and Treasurer and Secretary of the Medical Defence Association of Victoria. Bill was Honorary Physician to Pope John Paul II, Queen Elizabeth II, the Duke of Kent, the Prince and Princess of Wales, and the Queen of Denmark and Prince Consort, during their respective visits to Victoria. A deeply religious and compassionate man, Bill worked tirelessly caring for the less fortunate in our community, looking after alcoholics, drug addicts, homeless people and many others. A man of great good humour, Bill held very definite and firm opinions about most matters and had a very select list of dislikes (with parking attendants and Mexican waves being near the top of the list). Bill was a keen traveller, a lover of good food and wine, and an enthusiastic supporter of various clubs, including the Essendon Football Club, the Melbourne Cricket Club and the Kooyong Lawn Tennis Club. His last 2 years were blighted by a very aggressive lymphoma, involving recurrent visits to hospital and the traumas of chemotherapy and septicaemia. He died on 22 October 2005. Bill will be remembered as an eminent cardiologist, a very fine doctor and a true gentleman. He is survived by his wife Ann and children Jane, Simon, Susan, John, David and Sarah.

Bernard S Gilligan

Accessible and culturally appropriate services are needed The National Heart Foundation of Australia and the World Health Organization recommend that all patients with cardiovascular disease are routinely referred to an appropriate cardiac rehabilitation program.1,2 Their recommendations are based on firm evidence that three-phase rehabilitation programs — inpatient, outpatient and maintenance — provide a range of short-term and long-term benefits to health and wellbeing. Key points for success Ensure that cultural competency is integral to the core business of an organisation and supported at all levels within the organisation (eg, employ Indigenous staff across the organisation, support cultural awareness training for non-Indigenous staff, ensure availability of and support for interpreters and cultural mentors). Involve Aboriginal health workers and family members in the care of Aboriginal and Torres Strait Islander patients and develop flexible approaches to raising awareness of the importance of cardiac rehabilitation. Ensure community involvement in planning, implementing and evaluating health promotion, including the development of culturally appropriate materials. Incorporate elements of cardiac rehabilitation and secondary prevention into existing activities or set up activities that draw on existing networks within the community. Develop and sustain partnerships between organisations (eg, a hospital providing outreach cardiac rehabilitation services through the local Aboriginal Community Controlled Health Service). Take the specific needs of Aboriginal and Torres Strait Islander patients into consideration in planning and delivering mainstream cardiac services and develop policies and procedures to address these needs (eg, identifying Aboriginal or Torres Strait Islander status, providing culturally appropriate information on hospital discharge). Develop a specialist education base for continuing training and support of all health professionals working in cardiac care, including Aboriginal health workers. Although the benefits of cardiac rehabilitation are clear, only a small proportion of the people in the general population who have experienced cardiac events attend programs.3 Aboriginal and Torres Strait Islander people are even less likely to participate in cardiac rehabilitation programs than non-Indigenous Australians,3-5 despite being twice as likely to die from cardiovascular disease.6 As there is little published literature specific to cardiac rehabilitation among Aboriginal and Torres Strait Islander peoples, the National Health and Medical Research Council convened a committee to investigate barriers to effective practice and develop guidance for health professionals working in the area. In November and December 2004, the committee conducted workshops, hosted by Aboriginal Community Controlled Health Services in Darwin, Townsville and Mt Druitt (Sydney). Indigenous health professionals and consumers were asked to share their stories and make suggestions about how cardiac rehabilitation services could be made more accessible. This information contributed to the development of a practical guide for health professionals — Strengthening cardiac rehabilitation and secondary prevention for Aboriginal and Torres Strait Islander peoples: a guide for health professionals.7 The guide was tested for suitability by potential users of the manual at a workshop held in Adelaide in June 2005 and was published in September 2005. Through the workshops, the following barriers to uptake of cardiac rehabilitation among Aboriginal and Torres Strait Islander people were identified. “Not enough black faces”: Aboriginal and Torres Strait Islander people are not sufficiently involved in planning, delivering and evaluating relevant health care services. Contributing to this is a lack of training, education and support for Aboriginal health workers. Communication and understanding: Cultural factors that are often not understood and therefore not taken into account in mainstream services include the diversity of Aboriginal and Torres Strait Islander peoples and culture; the complexity of Aboriginal law; the importance of family and community involvement; and a holistic view of health that includes the body, the land and spirituality. Continuity of care: The process of cardiac care usually involves many different settings and people. Lack of continuity and linkages between services, in particular between mainstream and Aboriginal and Torres Strait Islander services, mean that people can miss out on important aspects of care. This is made worse when people live in remote communities and have to travel long distances to access services. Taking the message back home: It can be difficult to maintain a healthy lifestyle back in the community, where adopting healthy behaviours may be less of a priority than meeting basic needs such as food and housing, expectations of health may be low, and there may be strong counteracting social pressures. Self-determination and control: Health intervention programs may be implemented without appropriate consultation and community involvement from the outset. Programs are unlikely to succeed unless they build on the leadership provided by the community and on real partnership with the local community. Addressing these barriers presents considerable challenges. No single solution can be applied, due to the diversity within the population, as well as the need to find approaches that are suitable to remote, rural and urban areas and that take into account cultural issues and staff availability. Multidisciplinary methods are therefore required2 that can be adapted to make use of the skills available in each setting while taking a standardised approach to supporting system change. The Indigenous health sector and Indigenous health professionals are best placed to provide cardiac rehabilitation to Aboriginal and Torres Strait Islander people and should be supported to do this. However, cardiac rehabilitation is more likely to comprise a combination of both Indigenous and mainstream services (ideally a team including an Aboriginal health worker and general practitioner, with other health professionals as required). Establishing and maintaining links between individuals and organisations involved in cardiac rehabilitation is therefore fundamental to improving outcomes. Such linkages support continuity and quality of care, broaden the capacity of the health organisation, increase access to resources and help to integrate mainstream and Indigenous health services, so that it is easier for patients to move between the two systems. At the centre of care are the patients themselves. Showing cultural respect, as well as learning from patients and their families, carers and the community, will increase understanding of how culturally competent health care can best be provided.8 For example, addressing chronic diseases together in an holistic way is more consistent with Aboriginal and Torres Strait Islander concepts of health and illness than considering single diseases or body parts. This approach can also better take into account the importance of spirituality to health and wellbeing, depression and other psychosocial factors increasing the risk of cardiovascular disease,9 and the cultural, environmental and historical risk conditions that place Aboriginal and Torres Strait Islander people at greater risk of the onset and complications of chronic diseases. There is considerable activity under way across Australia to improve the cardiovascular health of Aboriginal and Torres Strait Islander peoples. Systems are in place to assist health services to improve preventive and coordinated care for these patients10 and there is a growing knowledge base to support improved practice. However, continuing efforts are needed across all health care settings, at both individual and organisational levels, to implement sustainable changes that will ensure that appropriate cardiac rehabilitation services are available for Aboriginal and Torres Strait Islander Australians.

Noel E Hayman MB BS, MPH, FAFPHM · Mark Wenitong MB BS · Jenny A Zangger BA, DipApplSci · Elizabeth M Hall BSc

A recent review shows how much more we need to find out about this important problem Perioperative ischaemic cardiac events include myocardial infarction, cardiac arrest and cardiac death, and are estimated to occur in 2%–5% of patients over 40 years of age.1 Mortality rates associated with perioperative myocardial infarction and cardiac arrest may be as high as 25% and 65%, respectively.2,3 In the Australian context, precise data on the numbers of patients at risk are not available, but with more than 440 000 general anaesthetics performed annually, this is likely to be an issue facing many physicians. A recent narrative review of the problem is therefore of timely importance.1,4 What is the risk of perioperative myocardial infarction? As the review points out, perioperative myocardial infarction may be difficult to diagnose, and often unrecognised. Three studies were identified totalling 1309 patients, with myocardial infarction diagnosed by creatine kinase MB elevations with new Q waves, with or without autopsy or positive pyrophosphate scan evidence. Myocardial infarction was identified in 30 patients (2.3%); notably, more than half of these did not have symptoms or signs. Creatine kinase MB assays may result in false negative and positive results, and troponin assays — the biomarker currently used in the European Society of Cardiology and American Heart Association guidelines for diagnosis of myocardial infarction — are now preferred. However, in the perioperative setting, troponin elevation may also arise from non-cardiac causes such as pulmonary embolism and renal failure, and limitations exist in the specificity of individual assays.5 Further, the pathophysiology of perioperative ischaemic events may differ from the non-perioperative acute coronary syndromes, and these differences may affect risk prediction and treatment. Non-perioperative acute coronary ischaemia results from rupture of an often mild, non-obstructive atherosclerotic plaque and superimposed coronary thrombosis.6,7 Although such plaque rupture and thrombosis is also thought to occur perioperatively, there are other important influences. The perioperative state is associated with activation and release of multiple inflammatory mediators and cytokines, sympathetic nervous system activation and catecholamine release, hypercoagulability, and hypoxia. These contribute to both plaque rupture and thrombosis. Additionally, the perioperative stress state may contribute to increased myocardial oxygen demand, in the setting of reduced oxygen supply from blood loss, hypoxia, and other factors. This adverse environment may be present up to 3 days into the postoperative period.8 How can we assess this risk? Given this propensity for perioperative ischaemic events, individual preoperative risk assessment has been keenly pursued by surgeons and anaesthetists, often resulting in referral to a cardiologist. Two methods are commonly used: clinical assessment, and noninvasive testing. A number of clinical assessment tools have been advised, a commonly used one being the Lee index.9 This defines a number of features of patient history, physical examination, baseline investigations, and proposed surgical procedure. Based on the presence of one to five of these clinical characteristics, patients’ risk can be stratified from 0.4% to 5.4% likelihood of a major perioperative event.9 Noninvasive exercise or pharmacological stress testing, usually with echocardiographic or nuclear imaging, is generally reserved for those at higher risk. In Australia, dobutamine stress echocardiography is a commonly used technique, achieving sensitivity and specificity of 85% and 70%, respectively, for a positive test predicting perioperative events in a meta-analysis,10 with similar results for nuclear imaging techniques.10 However, the relatively modest sensitivity and specificity of these tests mean a number of high-risk patients will be missed, and many with high risk will not have an event. The advice to patients about their risk must also be tempered by whether the planned surgery is elective or should go ahead regardless of the risk. How can we manage this risk? Coronary angiography is often advised for patients assessed to be at higher risk, but there is uncertainty in how to respond to the finding of significant coronary artery disease. Revascularisation — either percutaneous or surgical — has been suggested for patients with high grade coronary stenosis, particularly for widespread disease.11 However, supportive data are scarce; several retrospective studies suggest benefit, but a large recent randomised trial in selected stable patients undergoing vascular surgery showed no improvement in outcomes, and possibly an increased risk of events.11,12 At a practical level, if revascularisation is performed, observational data support delaying non-cardiac operations for at least a month following revascularisation surgery.13 Following coronary stenting, a window of 6 weeks after bare metal stenting is suggested, to allow endothelialisation of the stent struts and reducing stent thrombosis,14 but also reducing the possibility of in-stent restenosis, occurring maximally at 3–6 months.15 There are as yet no comparative data following drug-eluting stents, although these appear less attractive, given that stent-strut endothelialisation takes longer, and combined antiplatelet therapy with aspirin and clopidogrel is likely to be needed for longer, further increasing perioperative bleeding risk if these agents are continued, and increasing the risk of acute stent thrombosis if they are stopped early to allow surgery.16 Perioperative coronary events: risk management strategies for those at increased risk Consider not performing surgery if elective Smoking cessation: can be advised for all patients β-Blockade: some evidence, but disputed Aspirin, nitrates, statins: little evidence Revascularisation: little evidence of benefit, some evidence of harm; a particular problem with drug-eluting stents Similar uncertainty surrounds pharmacological methods of perioperative risk reduction. β-Blockers, by reducing myocardial oxygen demand and blocking sympathetic and catecholamine responses, would seem a logical option. Their use is widely promoted, and included in the joint American College of Cardiology and American Heart Association guidelines for perioperative management.17 However, these recommendations are based largely on two randomised controlled trials: one, a small unblinded study,18 the second, a larger study, which showed no survival benefit for β-blockade assessed on an intention to treat basis.19,20 Further trials are currently underway.20 Use of aspirin or statins also seems appropriate, given their previous efficacy in prevention of non-perioperative events,21 but aspirin may increase the perioperative bleeding risk,22 and statins have not yet shown robust benefit, although this is likely an area for future investigation. How then, should the physician put together what is at times confusing information? Firstly, perioperative ischaemia is relatively common and often unrecognised. Clinical assessment and non-invasive imaging are useful, but far from perfect, in risk stratification. Stopping smoking before surgery is a useful intervention to reduce risk.23 Revascularisation, while often used for patients with angiographically important disease, has little evidence to support it, delays subsequent surgery, and has a number of associated problems. Lastly, while statins, aspirin and β-blockers may appear intuitive and are commonly used, there is likewise little evidence to support these approaches. The review by Devereaux et al1,4 is a timely reminder of how little is known about such an important problem, a call to obtain better data, and a suggestion to discuss the rationale for surgery and its possible attendant risks carefully with patients.

Harry C Lowe FRACP, PhD · Saul B Freedman FRACP, PhD

Summary of key recommendationsSystems of care for patients with acute coronary syndromesEffective systems of care are required to deliver optimal care for patients with acute coronary syndromes (ACS), particularly in rural and remote areas. Systems of care should be regionally based, and have formal links with specialist centres for consultation and acute interhospital transfer. Systems should include appropriate monitoring, feedback and quality improvement components. Clinical decisions about care and transfer should take into account patients’ cultural and personal beliefs and wishes. New acute coronary syndrome terminology and implications for diagnosisIt is important to establish an initial working diagnosis to guide clinical decision making. New definitions of myocardial infarction, based heavily on the presence of cardiac biomarkers, have implications for coding and epidemiological studies. However, clinically they do not influence the indications for ongoing prevention therapies. Use of the ACS Dataset (part of the National Health Data Dictionary) can facilitate the collection of data relating to the presentation and management of ACS that can be compared and collated within and between health care providers. Acute management of chest painPeople experiencing symptoms of an ACS should seek help promptly and activate emergency medical services. The most important initial need is access to a defibrillator to avoid early cardiac death resulting from reversible arrhythmias. Aspirin should be given early (ie, by emergency or ambulance personnel) unless already taken or contraindicated. Oxygen should be given, as well as glyceryl trinitrate and intravenous morphine as required. As a minimum, medical facilities receiving patients should be given warning of incoming patients in whom there is a high suspicion of an ACS — particularly ST-segment-elevation myocardial infarction (STEMI) — or whose condition is unstable. Where appropriate, a 12-lead electrocardiogram (ECG) should be taken en route and transmitted to a medical facility. Where formal protocols are in place, prehospital treatment (including fibrinolysis in appropriate cases) should be facilitated. InvestigationsThe ECG is the sole test required to select patients for emergency reperfusion (fibrinolytic therapy or direct percutaneous coronary intervention [PCI]). Patients with STEMI who present within 12 hours of the onset of ischaemic symptoms should have a reperfusion strategy implemented promptly. Patients with a suspected ACS without ST-segment elevation on ECG should undergo further observation and investigation to rule out other diagnoses, enable risk stratification and determine the most appropriate treatment strategy. Patients whose ECG and cardiac marker levels are normal after a suitable period of observation should, where practicable, undergo provocative testing (eg, stress test) before discharge. Management of patients with ST-segment-elevation myocardial infarctionAdjuvant therapy in association with reperfusionAll patients undergoing reperfusion therapy for STEMI (PCI or fibrinolysis) should be given aspirin and clopidogrel unless these are contraindicated. Antithrombin therapy should be given in combination with PCI or fibrinolytic therapy with fibrin-specific fibrinolytic agents, but antithrombin therapy in conjunction with streptokinase is optional. It is reasonable to use abciximab with primary PCI, but glycoprotein (GP) IIb/IIIa inhibitors should generally be avoided with full or reduced doses of fibrinolytic therapy. Choice of reperfusion strategyTime delay (both to first medical contact and potential PCI or fibrinolytic therapy) plays a major role in determining best management of STEMI. In general, PCI is the treatment of choice, providing it can be performed promptly by a qualified interventional cardiologist in an appropriate facility. In general, the maximum acceptable delay from presentation to balloon inflation is: 60 minutes if a patient presents within 1 hour of symptom onset; or 90 minutes if a patient presents later. Note: for patients who present late (between 3 and 12 hours after symptom onset) to a facility without PCI capability, it is appropriate to consider transfer for primary PCI if balloon inflation can be achieved within 2 hours (including transport time). All PCI facilities should be able to perform angioplasty within 90 minutes of patient presentation. Fibrinolysis should be considered early if PCI is not readily available, particularly in rural and remote areas. When there are major delays to hospitalisation (ie, more than 30 minutes), prehospital fibrinolysis should be considered. Reperfusion is not routinely recommended in patients who present more than 12 hours after symptom onset and who are asymptomatic and haemodynamically stable. Choice of fibrinolytic agentSecond-generation fibrin-specific fibrinolytic agents that are available as a bolus (ie, reteplase, tenecteplase) are the fibrinolytics of choice. These agents should be available at all centres where fibrinolysis may be required. Streptokinase is an inappropriate choice in Aboriginal and Torres Strait Islander patients, or in patients with previous exposure to the drug. Transfer after STEMIPatients who have had STEMI should be considered for early transfer to a tertiary cardiac centre with PCI facilities and links to cardiac surgical facilities. If immediate transfer is not possible, patients should be transferred or referred as soon as is practicable for assessment of need for revascularisation (through PCI or coronary artery bypass grafting). Management of patients with non-ST-segment-elevation acute coronary syndromesAll patients with non-ST-segment-elevation acute coronary syndromes (NSTEACS) should have their risk stratified to direct management decisions (see Risk stratification for stratification criteria). All patients with NSTEACS should be given aspirin, unless contraindicated. High-risk patients with NSTEACS should be treated with aggressive medical management (including aspirin, clopidogrel, unfractionated heparin or subcutaneous enoxaparin, intravenous tirofiban or eptifibatide and a β-blocker), and arrangements should be made for coronary angiography and revascularisation, except in those with severe comorbidities. Intermediate-risk patients with NSTEACS should undergo an accelerated diagnostic evaluation and further assessment to allow reclassification as low or high risk. Low-risk patients with NSTEACS, after an appropriate period of observation and assessment, may be discharged on upgraded medical therapy for outpatient follow-up. Long-term management after control of myocardial ischaemiaBefore discharge, patients with an ACS should be initiated on a medication regimen, including antiplatelet agent(s), β-blocker, angiotensin-converting enzyme inhibitor, statin and other therapies as appropriate. Implantable cardiac defibrillators should be considered in some patients who, despite optimal medical therapy, have persistently depressed left ventricular function more than 6 weeks after STEMI. Patients should be given advice on lifestyle changes that will reduce the risk of further coronary heart disease (CHD) events, including smoking cessation, nutrition, alcohol, physical activity and weight management as relevant. All patients should have access to, and be actively referred to, comprehensive ongoing prevention and cardiac rehabilitation services. All patients should be provided with a written action plan for chest pain. Depression and CHD frequently coexist, and in patients with CHD, the presence of depression is more likely to lead to poorer outcomes. Social isolation and lack of social support are also associated with worse outcomes. All patients with CHD should be assessed for depression and level of social support. Levels of evidence and grades of recommendationThe levels of evidence and grades of recommendations used in these guidelines are adapted from the National Health and Medical Research Council (NHMRC) levels of evidence for clinical interventions and the US National Institutes of Health clinical guidelines. These classifications allow the ability to differentiate between strengths of recommendations and the levels of evidence on which these are based, and allow a classification for recommendations based on panel consensus judgement. Levels of evidence and grades of recommendation used in these guidelines RCT = randomised controlled trial. * National Health and Medical Research Council. A guide to the development, implementation and evaluation of clinical practice guidelines. Canberra: NHMRC, 1999. † Adapted from: US National Institutes of Health. Clinical guidelines on the identification, evaluation, and treatment of overweight and obesity in adults: executive summary. Expert Panel on the Identification, Evaluation, and Treatment of Overweight in Adults. Am J Clin Nutr 1998; 68: 899-917. IntroductionAcute coronary syndromes (ACS) include “a broad spectrum of clinical presentations, spanning ST-segment-elevation myocardial infarction, through to an accelerated pattern of angina without evidence of myonecrosis”.1 Collectively, they represent one of the most common causes of acute medical admissions to Australian hospitals. The current guidelines for the management of both ST-segment-elevation ACS and non-ST-segment-elevation ACS have been developed by a joint working party of the National Heart Foundation of Australia (NHFA) and the Cardiac Society of Australia and New Zealand (CSANZ). The aim of these guidelines is to incorporate contemporary information on the diagnosis and management of ACS into a set of recommendations that defines the boundaries of highest quality care. The guidelines expand on previous guidelines2,3 by consolidating recommendations for the management of ST-segment-elevation myocardial infarction (STEMI), non-ST-segment-elevation myocardial infarction and unstable angina, as well as incorporating the newer developments that have arisen since the previous guidelines, Management of unstable angina — 20003 (and addenda, available at: http://www.heartfoundation.com.au) and Reperfusion therapy for acute myocardial infarction (2002).2 These new guidelines provide a general framework for appropriate practice, to be followed subject to clinical judgement in each individual patient. They are primarily for doctors in a hospital environment (emergency physicians, general physicians, rural doctors and cardiologists) who manage patients with ACS, but they also contain information relevant to general practitioners and others, including ambulance personnel. The guidelines are designed to provide information to assist decision making, and are based on the best information available up to September 2005. It should be understood that the context in which clinical trials are performed and the local environment in which practice is undertaken must always be considered when assessing the evidence base for guidelines and, at times, their local implementation. These new guidelines represent a local synthesis of the most recent evidence including recent international guidelines. Where relevant, the evidence has been interpreted with regard to the Australian context in which the guidelines will be implemented. Key recommendations are summarised at the beginning of these guidelines. Systems of care for patients with acute coronary syndromesThe ability to implement best-practice guidelines for the management of ACS will depend on local resources and systems of care. The following guidance is offered to assist practitioners and organisations in facilitating the most effective systems of care for the communities they serve. Effective management of ACS requires collaborative systems of care to ensure that patients have access to the services that they need in a timeframe commensurate with their clinical condition and the potential benefit of treatments available in larger or specialised centres. The guiding principles for developing these systems are equity of access, equity of care and evidence-based care, taking into account patients’ preferences. The systems of care should be regionally based, formal rather than ad-hoc, and should cover the continuum of care from the first point of presentation to a health professional to definitive care and rehabilitation. Responsibility for establishing these systems should be at board or executive level within health services. The systems of care should address: clinical issues such as consultation, treatment and acute inter-hospital transfer protocols (note that systems should enhance options for patients without disempowering decision making by appropriate local clinicians); education; and quality monitoring, such as time to specific treatments and outcomes. The structure of these systems will vary depending on the features of the region in which they are placed. In a metropolitan setting, a hospital without percutaneous coronary intervention (PCI) capabilities may have arrangements with a local PCI-capable facility for timely transfer of selected patients. In a rural or remote setting, the system is usually considerably more complex and involves general practitioners or community health centres, prehospital care providers, retrieval services (such as Careflight, Victorian Adult Emergency Retrieval and Coordination Service, Royal Flying Doctor Service), and regional and metropolitan referral hospitals. The systems should be tailored to a region’s needs. The key elements of successful systems include: clear lines of communication (eg, single points of contact for consultation or referral and coordination of acute interhospital transfers; the consultation component is particularly important as the benefits of some treatments for ACS are time-dependent, so early decision making is vital); clear triage protocols where appropriate, recognising the fact that the closest hospital may not be the most suitable in all cases (algorithms can be developed to guide decisions about the best primary destination for patients); effective and timely feedback (this should be two-way, and should address ways to improve the process as well as collecting outcomes information; the latter should be both specific for the patient referred and pooled so that trends in outcomes and issues for improvement can be identified); agreed treatment protocols, with processes to facilitate drug availability if required; agreed acute interhospital transfer protocols and processes; program quality monitoring, including analysis of adverse events and system breakdowns; identified leaders (these may be drawn from across the system, but leaders should jointly accept responsibility for monitoring the system, providing education and feedback, developing improvements to the system if required, facilitating arrangements with relevant extra-regional organisations and acting as public spokespeople for the system); and ownership of the established systems at a senior level within hospital or health service management. Taking patient preferences into accountOn occasion, the pathway of care may recommend that patients be transferred from their local community or region to a distant centre. There may be strong personal or cultural reasons that make this difficult or unacceptable for some patients. Every effort should be made to overcome these barriers by appropriate explanation and discussion, involvement of family and community members and preferential transfer to centres that have specific programs and resources for relevant cultural groups (eg, Aboriginal Liaison Officers). If the barriers to transfer cannot be overcome and the patient asserts his or her right to be treated more locally, the patient should have the best care that can be delivered in that setting. This includes consultation with specialists. Aboriginal and Torres Strait Islander peoplesAboriginal and Torres Strait Islander peoples have a high rate of ACS, and lower intervention rates and poorer outcomes than non-Indigenous people.4 The reasons for this are complex and include barriers to health care access and language and cultural differences. To optimise outcomes for Indigenous people, systems of care that recognise these factors are needed in both metropolitan and rural and remote areas. These might include: providing culturally appropriate education and information to Indigenous patients and their families through Aboriginal Health Workers and Hospital Liaison Officers; and facilitating interhospital transfer arrangements by involving the local Aboriginal health sector and metropolitan hospital Aboriginal Liaison Officers. Key messagesEffective systems of care are required to deliver optimal care for people with ACS, particularly in rural and remote areas. Systems of care should be regionally based, with formal links with specialist centres for consultation and acute interhospital transfer. Systems should include appropriate monitoring, feedback and quality improvement components. Clinical decisions about care and transfer should take into account patients’ cultural and personal beliefs and wishes.

Acute Coronary Syndrome Guidelines Working Group

To the Editor: Investigators in the recent Canberra Heart Study1 highlighted the importance of improving the detection of heart failure in the community, given the high proportion of people with preclinical disease. The accompanying editorial2 expressed concern about the lack of major Australian initiatives that focus on the prevention and treatment of this disease. We fully endorse the authors’ view that under-recognition and under-treatment of heart failure is an important national issue. While we support their call for sustained and adequately funded programs, we feel it is important to note that there are initiatives under way to attempt to improve the situation. The National Prescribing Service, the National Heart Foundation of Australia and the National Institute of Clinical Studies joined forces in 2004 to improve the diagnosis and management of heart failure in primary care. A national program, undertaken in partnership with 45 divisions of general practice, began in October 2004 and will conclude in early 2006. Nationally, the program provided newsletter materials to all general practitioners, pharmacists and physicians.4 In participating divisions, educational outreach visits and interactive small group meetings involved over 1600 GPs and local specialists in discussions of the role of echocardiography in diagnosis, and pharmacological and lifestyle management issues. Patient education materials were also widely disseminated.5 Outcomes of this large-scale quality improvement program are currently being evaluated, and results are expected to be available in early 2007. Other groups have also recognised heart failure as an important issue — for example, it is one of the featured conditions in the Department of Veterans’ Affairs Medicines Advice and Therapeutics Education Services program.6

Heather H Buchan MBChB, MSc, FAFPHM · Susan M Phillips DPhil · Lynn M Weekes BPharm, MSc, PhD · Judith M Mackson BPharm, MMedSci(ClinEpi) · Andrew N Boyden MB BS(Hons), MPH, FRACGP · Andrew M Tonkin MB BS, MD, FRACP

Recommendations for primary prevention in women need to be different The efficacy of low-dose aspirin for the secondary prevention of cardiovascular disease among men and women is established.1,2 However, the risk-to-benefit ratio for aspirin in primary prevention is much less clear.2,3 The National Heart Foundation has recommended that low-dose aspirin be considered for people without symptoms but at increased (> 1% annual) risk of a coronary heart disease event.4 This recommendation is based on earlier primary prevention trials, with over 55 000 participants, showing a significant 32% reduction in the risk of myocardial infarction, but no significant change in risk of stroke or cardiovascular death.3 However, women comprised only 20% of trial participants, and fewer than 180 of the 2402 cardiovascular events occurred in women.3,5 Until recently, there has been limited direct evidence for the efficacy of aspirin in primary prevention among women. The Women’s Health Study (see Box) not only addressed this important sex issue, but suggested a significant difference in the cardiovascular response to aspirin between women and men.5 In this study, confined to healthy women aged 45 years or older, aspirin prophylaxis did not lower the risk of a first major cardiovascular event (non-fatal myocardial infarction, non-fatal stroke, or death from cardiovascular causes) — the primary endpoint. However, it did significantly reduce the risk of all strokes by 17%, and ischaemic stroke by 24%, without affecting the risk of myocardial infarction or cardiovascular death.5 This differs from previous aggregate data derived from mostly middle-aged men, and confirmed by a recent sex-specific meta-analysis, which showed that aspirin therapy significantly reduced the risk of myocardial infarction but not ischaemic stroke in men.6 Are there any apparent reasons for the seemingly opposite results for stroke and myocardial infarction in men and women? One possibility is that aspirin lowered the risk of stroke in women, but not men, simply because women have a higher risk of stroke than myocardial infarction. For instance, the ratio of incident stroke to myocardial infarction was 1.4 : 1 among women in the placebo group of the Women’s Health Study, compared with 0.4 : 1 among men of a similar age in the placebo group of the Physicians’ Health Study (a randomised, double-blind, placebo-controlled trial examining whether low-dose aspirin [325 mg every second day] decreases cardiovascular mortality and whether b-carotene reduces the incidence of cancer).7 Conversely, the Women’s Health Study may have lacked statistical power with respect to the risk of myocardial infarction. The study enrolled a group of largely healthy women, 85% of whom had a 10-year Framingham coronary risk score of less than 5%. Women also have a lower age-adjusted incidence of coronary heart disease than men; the rate of myocardial infarction among women in the Women’s Health Study was 97.3 per 100 000 person-years, about one-fifth the rate of myocardial infarction among men in the Physicians’ Health Study.7 Women tend to develop heart disease between 10 and 15 years later than men. This may explain why consistent benefits of aspirin on all major cardiovascular endpoints, including myocardial infarction and stroke, were observed only among women aged 65 years or older in the Women’s Health Study.5 This subgroup comprised 10% of the study population, but accounted for nearly a third of all cardiovascular events. In this subgroup, aspirin, compared with placebo, led to 44 fewer myocardial infarctions, strokes, or deaths from cardiovascular causes, but also caused 16 more gastrointestinal haemorrhages requiring transfusion, emphasising again the importance of balancing benefits and risks.5 A recent overview has also suggested that the risk of gastrointestinal and other bleeding with aspirin use may increase with age, and that the true balance of risks and benefits in the healthy aged population has not yet been established by randomised trials.8 The 100 mg alternate-day dose of aspirin used in the Women’s Health Study is lower than doses employed in previous trials. However, this regimen of aspirin was sufficient to reduce the risk of ischaemic stroke, and hence is likely to be an adequate dose for cardiovascular prevention. Nonetheless, sex differences in salicylate metabolism, platelet responses, vascular reactivity, and the nature of atherosclerotic disease may well cause different biological responses between men and women.9-11 This further highlights the need for women to be well represented in cardiovascular trials. What are the clinical implications of the Women’s Health Study? Overall, this study indicates that clinicians should be very cautious about advising women under the age of 65 years to take low-dose aspirin for primary prevention unless their global risk score is high. Even the benefit of aspirin for prevention of stroke in women needs to be carefully weighed against the increased risk of bleeding complications, and the low risk of stroke and other major cardiovascular events among apparently healthy women. To put this into perspective, the absolute risk reduction with aspirin therapy was about two stroke events per 1000 women treated.5 Thus, as with men, any decision about the use of aspirin for primary prevention among women requires an assessment of the net absolute benefit of therapy in an individual, and such a decision should be made only in association with an overall program of lifestyle measures to reduce cardiovascular risk.2 Reflecting these developments, the National Heart Foundation of Australia has recently amended its position statement on aspirin for cardiovascular disease prevention.12 Summary of the Women’s Health Study5 A large randomised placebo-controlled trial of aspirin (100 mg on alternate days) for primary prevention among 38 876 initially healthy women, aged 45 years or older, followed for 10 years for the occurrence of a first major cardiovascular event (myocardial infarction, stroke, or death from cardiovascular causes). The study recruited healthy women, 85% of whom had a 10-year Framingham risk score of less than 5%. The 10-year absolute cardiovascular event rate was low, and among placebo recipients there were more strokes than myocardial infarctions (266 v 193). At the end of the trial, major cardiovascular events (the primary endpoint) occurred in a non-significant 9% fewer aspirin recipients than placebo recipients (2.4% v 2.6%; P = 0.13). With regard to secondary endpoints, there was a significant 17% reduction in the risk of stroke in the aspirin group (1.1% v 1.3% with placebo; P = 0.04), owing to a 24% reduction in risk of ischaemic stroke; the two groups did not differ significantly in their incidence of myocardial infarction or cardiovascular death. Subgroup analyses showed that aspirin significantly lowered the risk of major cardiovascular events, ischaemic stroke, and myocardial infarction among women 65 years of age or older (6.4% v 8.5% with placebo; P = 0.008). The aspirin group had a higher frequency of gastrointestinal bleeding (4.6% v 3.8% with placebo; P < 0.001), and a non-significant increase in risk of haemorrhagic stroke (0.26% v 0.21% with placebo; P = 0.31). Overall, this trial indicates that caution is necessary when advising apparently healthy women to take low-dose aspirin for cardiovascular disease prevention.

Joseph Hung MB BS, FRACP, FACC

Rheumatoid arthritis is associated with an increase in cardiovascular mortality and morbidity; this increase is independent of traditional cardiovascular risk factors. Effective treatment of rheumatoid arthritis with disease-modifying antirheumatic drugs appears to reduce cardiovascular mortality. The optimal approach to prevention of cardiovascular disease in rheumatoid arthritis is evolving, but will include a combination of: cardiovascular risk factor screening and management; effective and sustained control of joint and systemic inflammation; and a high index of suspicion for silent cardiac disease.

Sharon Van Doornum FRACP, GradDipClinEpi, MD · Garry L R Jennings MD, FRCP, FRACP, FAHA · Ian P Wicks

Sports participation among children is declining. Sport and physical activity are important in childhood for optimising bone mass and reducing obesity and insulin resistance. Physical activity reduces cardiovascular risk factors in adults, and can improve survival in patients with cardiac failure. Musculoskeletal injury is the most common complication of sports participation in adults — not cardiac events. Some of the decline in function which occurs with ageing can be positively affected by regular physical activity.

Carolyn R Broderick MB BS, FACSP, GDSSc · Gregory J Winter FACSP, FRACGP, MSpMed · Roger M Allan FRACP, FCSANZ, FACC

The Canberra Heart Study findings are a wake-up call to those unaware of the extent of the condition Chronic heart failure is a major and growing public health issue that affects all Western countries. Accordingly, many countries (eg, Scotland1 and Sweden2) systematically monitor its population prevalence and overall impact on the health care system. However, public awareness of the condition remains low.3 Unfortunately, in Australia, apart from sporadic initiatives such as the NSW Chronic Care Collaborative, heart failure remains the “Cinderella” of health issues — hardly registering on the radar of key health care providers, regulators, relevant government bodies and the general public. For example, less than one in five eligible patients receives specialist heart failure management after hospitalisation for acute heart failure.4 Undoubtedly this is at least partly explained by the fact that we do not know the true magnitude of the problem in Australia. It is time for us to recognise heart failure as a major public health issue that cripples hundreds of thousands of Australians and places a substantial burden on the health care system. . . . heart failure remains the “Cinderella” of health issues . . . The facts from overseas population studies are plain and startling. Depending on how the condition is defined, anywhere between 3% and 9% of the adult population has heart failure, and a similar proportion has “silent” left ventricular dysfunction.5 Moreover, the incidence of heart failure is still rising. Indeed, it is the only cardiovascular condition not to experience a substantial decline in both incidence and prevalence over the past 20 years (taking into account the progressive ageing of populations).1 There are several reasons for this increase. Firstly, the incidence of heart failure increases with advancing age. In Australia, the proportion of people aged over 65 years (in whom heart failure prevalence is > 10%) will double over the next 50 years.2 Secondly, improvements in diagnostic techniques such as echocardiography have enhanced the ability to make a definitive diagnosis. Thirdly, treatment of heart attack has improved to the extent that patients who previously died of large myocardial infarctions are now able to survive. Finally, heart failure treatments themselves are keeping patients alive for longer and thus contributing to an ever-expanding pool of affected Australians. Can overseas data on prevalence be extrapolated to the Australian population? While the answer to this question is a qualified “yes”, specific issues in Australia relating to treatment approaches, access to diagnostic and health care services and the ethnic mix of the population may affect prevalence figures.5 Moreover, given the public health importance and impact of heart failure, it would seem reasonable to develop an Australia-specific response based on known rather than speculative facts. Thus there is an urgent need for a large-scale, definitive, Australia-wide epidemiological study to ascertain aetiological factors, diagnostic approaches and management of this condition in the Australian community. In this context, the Canberra Heart Study,6 published in this issue of the Journal, is an excellent start in helping to determine the true magnitude of the heart failure problem in Australia. The findings of this well conducted community-based study are a wake-up call to those unaware of the extent of the condition. Not only were 6.3% of the population surveyed found to have overt symptomatic heart failure, but there was a high proportion of patients with subclinical heart failure (left ventricular dysfunction in the absence of symptoms).6 The study also noted a significant proportion of patients with so-called “preserved systolic function” heart failure (ie, symptoms of the condition but with preservation of systolic ventricular function and pointers on echocardiography to impaired relaxation of the ventricle during diastole). The Canberra Heart Study is not without some methodological problems (eg, a relatively small sample size, and thus few positive diagnoses for heart failure; under-participation of elderly women, who may well have added to the burden of diastolic heart failure). Moreover, as with any study of heart failure, the definition of the condition is always fraught with uncertainty, although it appears to have been quite reasonably addressed in this analysis. Complexity in diagnosing heart failure is one of the main reasons for under-recognition of the condition. Indeed, there is no single agreed definition, and the forthcoming update of the current National Heart Foundation/Cardiac Society of Australia and New Zealand guidelines on heart failure7 will propose a further modification to earlier definitions. Heart failure is a syndrome — a cluster of signs and symptoms that require detailed investigation before arriving at a presumptive diagnosis. There are no definitive tests to confirm the diagnosis. Furthermore, as presenting symptoms may be non-specific, heart failure can masquerade as, and be masked by, many other conditions, particularly in elderly people. A recent Australian analysis describing barriers to diagnosis and management of heart failure in the primary care setting points to some of the difficulties of making a definitive diagnosis.8 Nevertheless, it is important that a definitive diagnosis be made because, at least for systolic left ventricular dysfunction (whether symptomatic or not), appropriate management can have a great impact on disease progression, symptoms and survival. Heart failure management is complex, involving a multidisciplinary approach, polypharmacy in drug prescribing, and ancillary modalities that may include exercise, device therapies (eg, cardiac resynchronisation, implantable defibrillators) and surgical procedures. Early detection of subclinical heart failure (to prevent progression to symptomatic disease) and treatment of known risk factors will be major foci of research and clinical interest in the evolution of future heart failure management strategies. In summary, the authors of the Canberra Heart Study6 have done the Australian community a great service in providing epidemiological data to show that heart failure truly is a major public health issue in Australia. The problem requires the type of national response that has been initiated in other Western countries. This regional study should be regarded as the critical stimulus for a national study that would provide a broader, more detailed analysis of the epidemiology, health care burden and management of heart failure in Australia. Without this, Australia will continue to fall behind other Western countries in improving the nation’s health by focusing on prevention and treatment of this highly debilitating and deadly condition.

Henry Krum MB BS, PhD, FRACP · Simon Stewart PhD, FESC, FAHA

Objective: To estimate the prevalence of heart failure (HF) and left ventricular (LV) systolic dysfunction in a population-based sample of older Australians.Design, setting and participants: A cross-sectional survey of 2000 randomly selected residents of Canberra, aged 60–86 years, conducted between February 2002 and June 2003. Participants were assessed by history, physical examination by a cardiologist, and echocardiography.Main outcome measures: Age- and sex-specific prevalence rates of clinical HF and LV systolic dysfunction (defined as LV ejection fraction ≤ 50%).Results: Of 1846 people eligible for our study, 1388 (75%) agreed to participate and 1275 completed all investigations (mean age, 69.4 years; 50% men). In the study sample, 72 subjects (5.6%; 95% CI, 4.4%–7.1%) had clinical HF that had been previously diagnosed and was confirmed by our assessment. A further 0.6% (95% CI, 0.3%–1.2%) had undiagnosed clinical HF (ie, evidence of structural heart disease and symptoms/signs of cardiac insufficiency without a previous diagnosis of clinical HF). Thus, the overall prevalence of clinical HF in the sample was 6.3% (95% CI, 5.0%–7.7%). Clinical HF increased in prevalence with advancing age (a 4.4-fold increase from the 60–64-years age group to the 80–86-years age group; P < 0.0001). Of the 75 subjects (5.9%; 95% CI, 4.7%–7.3%) with LV systolic dysfunction, 44 (59%) were in the preclinical stage of disease.Conclusion: Diagnosed HF cases represent the “tip of the iceberg” for the national burden of HF and LV systolic dysfunction. Clinically identifiable HF cases can remain undiagnosed, and the majority of people with LV systolic dysfunction are in a preclinical stage of the disease.

Walter P Abhayaratna MB BS, FRACP · Niels G Becker BSc, MSc, PhD · Wayne T Smith BMed, MPH, PhD · Thomas H Marwick MB BS, PhD, FRACP · Ian M Jeffery MB BS, FRACP · Darryl A McGill MB BS, PhD, FRACP

Clinical record Computed tomography of the thorax showed bilateral pleural effusions (PE) and diffuse thickening of the oesophagus (O). An 84-year-old woman presented to the emergency department following the sudden onset of retrosternal chest pain with associated nausea and sweating. The pain was exacerbated by swallowing, but this symptom was not felt to be significant at the time. She had no past history of ischaemic heart disease or diabetes and did not smoke, but did have a weak family history of heart disease, and a personal history of mild hypercholesterolaemia and refractory hypertension despite aggressive medical management (baseline systolic blood pressure consistently 150–220 mmHg, according to previous medical records). An electrocardiogram (ECG) showed a left bundle branch block, with no previous ECG available for comparison. Acute myocardial infarction was diagnosed. However, coronary angiography showed no abnormalities, and serial measurements of serum troponin and creatine kinase levels failed to confirm an infarction. The next morning, the patient developed profound dysphagia and had an episode of haematemesis. Full blood examination showed normocytic anaemia (haemoglobin concentration, 70 g/L; reference range [RR], 115–165 g/L), with mean cell volume of 91 fL (RR, 78–99 fL), neutrophilia (12.7 × 109 cells/L [RR, 2.0–8.0 × 109 cells/L]), and platelet count in the RR (172 × 109 cells/L [RR, 150–450 × 109 cells/L]). She developed a cough, and a chest x-ray showed left lower lobe consolidation. Intravenous ceftriaxone therapy was begun to treat this. Computed tomography was arranged to investigate the oesophageal symptoms. This showed a diffusely thickened oesophagus from the thoracic inlet to the gastro-oesophageal junction, bilateral pleural effusions, and left lower lobe collapse and consolidation (Figure). Endoscopy showed blackened oesophageal mucosa with extensive mucosal bleeding. The procedure was abandoned because of these findings, and the patient was intubated and transferred to our tertiary referral centre for ongoing care. On arrival, chest x-ray showed progression of the pulmonary effusion, obscuring the entire left lung field. At bronchoscopy, a substantial volume of old clot was evacuated from the left bronchial tree. Repeat endoscopy again showed an extensive mucosal lesion. A percutaneous endoscopic gastrostomy (PEG) tube was placed, and a provisional diagnosis of malignancy was made (biopsies subsequently showing benign tissue only). The patient remained haemodynamically stable throughout, and was extubated 2 days later. She remained asymptomatic and was able to eat a full diet 6 days later. A final diagnosis was made of dissecting haematoma of the oesophagus. The patient remained in excellent health at follow-up a month later, at which time the PEG tube was removed without incident. Dissecting haematoma of the oesophagus is a rare, relatively benign condition that mimics much more common and serious illnesses.1 The onset of sudden severe retrosternal chest pain in an elderly person, who often has other cardiovascular risk factors, may lead to an erroneous diagnosis of cardiac pain. In some cases, subsequent thrombolytic treatment has led to fatalities. In others, the appearance of intramural thrombus on radiological or endoscopic views has been mistaken for advanced oesophageal malignancy or rupture.2,3 Lessons from practice Dissecting haematoma of the oesophagus should be included in the differential diagnosis in elderly patients presenting with cardiac-type chest pain, and oesophageal symptoms should be specifically sought in the history. The presence of oesophageal symptoms (dysphagia or odynophagia) in the context of cardiac-type chest pain should prompt investigation with appropriate imaging studies (barium swallow or computed tomography of the thorax before administration of fibrinolytic agents. Concern about dissecting haematoma of the oesophagus can be clarified rapidly with a water "sip test". The course of dissecting haematoma of the oesophagus is essentially benign if unnecessary intervention is avoided. Because of the rarity of dissecting haematoma of the oesophagus, diagnosis depends on an accurate history and a high index of suspicion. Those affected are usually women (relative risk, 1.8 — the inverse to the male bias in cardiovascular and malignant oesophageal disease),3 elderly (median age, 63 years),3 and not uncommonly taking anticoagulant or antiplatelet agents. Patients present with a variable combination of chest pain (usually sudden in onset and of short duration), haematemesis (mainly small volume and occurring after the pain), and dysphagia and/or odynophagia. In one meta-analysis, 99% of patients had at least one of these symptoms, and 32% had all three.3 In particular, the presence of dysphagia or odynophagia in a patient otherwise thought to have angina or myocardial infarction should prompt oesophageal imaging before administration of fibrinolytic agents. A simple test is to ask the patient to take a sip of water as part of the examination. If this exacerbates symptoms or unmasks new ones, a more specific focus on the possibility of oesophageal abnormality is warranted. Dissecting haematoma of the oesophagus has a typical appearance on imaging.4,5 Barium swallow shows a long, smooth tubular filling defect in the lumen of the oesophagus, sometimes with the dissection space filled with a stripe of contrast (the “double-barrelled oesophagus”). As the dissection most commonly occurs along the posterior wall, the lateral view is most useful. Computed tomography demonstrates an obliterated lumen with thickening of the wall. This extends over a long length of the oesophagus, and can mimic oesophageal rupture or extensive malignancy. The haematoma is large, fluctuant, and blue or purplish when viewed at endoscopy. Delayed endoscopy shows a long ulcer, where the overlying mucosa has sloughed, followed by rapid regeneration and an ultimately normal appearance.3 For a condition with such dramatic presentation, the natural history is refreshingly benign. The best intervention is non-intervention: the haematoma almost always resolves, and full oesophageal function is restored. Intravenous hydration, supplemented by parenteral or enteral nutrition in appropriate cases, is usually all that is needed. Anti-ulcer medications have no proven benefit.3 Surgery is indicated if there is uncontrolled arterial bleeding, or if the partial rupture has been converted to a full thickness tear through endoscopy.3 A further indication for surgery is a focus of infection within the false lumen, preventing healing. In two such cases, endoscopic division of the overlying mucosal flap resulted in complete resolution of fever, odynophagia and neutrophilia.1,6 Unfortunately, aggressive intervention has led to fatalities.3

Deborah H Amott MB BS(Hons) · Gavin M Wright FRACS

Objective: To compare changes in autonomic nervous activity in healthy senior individuals while walking with and without a dog, and during routine activities at home and periods of interacting with the dog at home.Design: Controlled crossover study.Participants and setting: 13 healthy volunteers (3 men, 10 women; mean age, 67.5 years) who walked in a park adjacent to Gunma University, Japan, and 4 volunteers among these who underwent monitoring in their own homes.Interventions: Heart rate variability was monitored continuously by means of a palm-sized electrocardiographic monitor (which facilitated spectral analysis of the RR interval) while participants walked for 30 minutes (first with, then without, the study dog, or vice versa); three participants underwent this intervention on 3 consecutive days. Four participants underwent continuous monitoring for 6 hours in their own homes, including two 30-minute periods of free interaction with the study dog.Main outcome measures: High frequency (HF) power values of heart rate variability, which is a measure of parasympathetic neural activity.Results: During dog-walking, HF power increased significantly (P < 0.01); this increase was sustained throughout each dog walk, and was more pronounced during succeeding dog walks. At home, HF power was 1.87 times greater when the dog was present, and 1.57 times greater (P < 0.01) than in the walking experiment.Conclusions: Walking a dog has potentially greater health benefits as a buffer against stress in senior citizens than walking without a dog; and, independent of actually walking, merely patting and talking to a dog also raises parasympathetic neural activity. Power spectral analysis of heart rate variability shows promise as a non-invasive approach to quantifying clinicophysiological research on human health benefits possibly derived from interaction with companion animals.

Masahiko Motooka MMS · Nell L Kennedy PhD · Hiroto Koike MD, PhD · Tomoyuki Yokoyama MD, PhD

To provide physical activity recommendations for people with cardiovascular disease, an Expert Working Group of the National Heart Foundation of Australia in late 2004 reviewed the evidence since the US Surgeon General’s Report: physical activity and health in 1996. The Expert Working Group recommends that: people with established clinically stable cardiovascular disease should aim, over time, to achieve 30 minutes or more of moderate intensity physical activity on most, if not all, days of the week; less intense and even shorter bouts of activity with more rest periods may suffice for those with advanced cardiovascular disease; and regular low-to-moderate level resistance activity, initially under the supervision of an exercise professional, is encouraged. Benefits from regular moderate physical activity for people with cardiovascular disease include augmented physiological functioning, lessening of cardiovascular symptoms, enhanced quality of life, improved coronary risk profile, superior muscle fitness and, for survivors of acute myocardial infarction, lower mortality. The greatest potential for benefit is in those people who were least active before beginning regular physical activity, and this benefit may be achieved even at relatively low levels of physical activity. Medical practitioners should routinely provide brief, appropriate advice on physical activity to people with well-compensated, clinically stable cardiovascular disease.

Tom G Briffa PhD · Andrew Maiorana PhD · Noella J Sheerin RN, BAppSc · Anthony G Stubbs · Brian F Oldenburg PhD · Neville L Sammel DDU, FRACP, FACC · Roger M Allan FRACP, FCSANZ, FACC

Physical activity can significantly reduce the risk of cardiovascular disease, diabetes, some forms of cancer, osteoporosis, obesity, falls and fractures, and some mental health problems. While the benefits of physical activity are clear, there is a slightly increased risk of sudden death while exercising (compared with while sedentary), especially in untrained people undertaking unaccustomed vigorous activity. Routine exercise testing yields a significant number of false-positive results, and has not been shown to prevent exercise-related acute cardiac events. There is no convincing evidence that exercise is itself associated with osteoarthritis, but significant joint injury which occurs during sport is associated with an increased risk of subsequent development of osteoarthritis.

Peter D Brukner MB BS, FACSP · Wendy J Brown BSc(Hons), MSc, PhD

Objective: To estimate the incremental effects on cost and quality of life of cardiac rehabilitation after an acute coronary syndrome.Design: Open randomised controlled trial with 1 year’s follow-up. Analysis was on an intention-to-treat basis.Setting: Two tertiary hospitals in Sydney.Intervention: 18 sessions of comprehensive exercise-based outpatient cardiac rehabilitation or conventional care as provided by the treating doctor.Participants: 113 patients aged 41–75 years who were self-caring and literate in English. Patients with uncompensated heart failure, uncontrolled arrhythmias, severe and symptomatic aortic stenosis or physical impairment were excluded.Main outcome measures: Costs (hospitalisations, medication use, outpatient visits, investigations, and personal expenses); and measures of quality of life. Incremental cost per quality-adjusted life year (QALY) saved at 1 year (this estimate combines within-study utility effects with reported 1-year risk of survival and treatment effects of rehabilitation on mortality). Sensitivity analyses around a base case estimate included alternative assumptions of no treatment effect on survival, 3 years of treatment effect on survival and variations in utility.Results: The estimated incremental cost per QALY saved for rehabilitation relative to standard care was $42 535 when modelling included the reported treatment effect on survival. This increased to $70 580 per QALY saved if treatment effect on survival was not included. The results were sensitive to variations in utility and ranged from $19 685 per QALY saved to rehabilitation not being cost-effective.Conclusions: The effects on quality of life tend to reinforce treatment advantages on survival for patients having postdischarge rehabilitation after an acute coronary syndrome. The estimated base case incremental cost per QALY saved is consistent with those historically accepted by decision making authorities such as the Pharmaceutical Benefits Advisory Committee.

Tom G Briffa PhD, MSc · Simon D Eckermann PhD(Ec), MSc, GradDipHEc · Alison D Griffiths BA Hons · Anthony C Keech MB BS, MScEpid, FRACP · Phillip J Harris MB BS, DPhil, FRACP · M Rose Heath RN · Saul B Freedman PhD, FRACP, FACC, FESC · Lana T Donaldson RN, MPH · N Kathryn Briffa BAppSc(Physio), PhD

Objectives: To compare the safety, effectiveness and cost-effectiveness of drug-eluting coronary stents used in Australia with bare-metal stents and determine whether the benefits are greater for high-risk subgroups.Data sources: MEDLINE, Pre-Medline, EMBASE, Current Contents, CINAHL and the Cochrane Library database were searched to identify eligible randomised controlled trials and systematic reviews published in English between January 1966 and June 2004.Study selection: Seven randomised controlled trials that assessed polymer-based paclitaxel- or sirolimus-eluting stents versus bare-metal stents in patients with coronary atherosclerosis and reported on stent thrombosis, mortality, myocardial infarction, coronary artery bypass grafting or target lesion revascularisation.Data extraction: Two independent reviewers appraised eligible studies and extracted data. Relative risks (RRs) were calculated for each outcome and pooled using the Mantel–Haenszel method.Data synthesis: Rates of stent thrombosis, mortality, myocardial infarction and bypass grafts did not differ by stent type. Drug-eluting stents (DESs) resulted in a 71%–80% lower risk of revascularisation at 12 months (RR 0.29 [95% CI, 0.20–0.43] for paclitaxel-eluting stents [n = 1593 patients]; RR 0.20 [95% CI, 0.13–0.29] for sirolimus-eluting stents [n = 1296 patients]). Similar benefits were seen in several high-risk subgroups of patients: those with diabetes, lesion length > 20 mm and target-vessel diameter ≤ 2.5 mm. The benefits of DESs in these high-risk groups over lower-risk groups were inconclusive because of low numbers. The cost per revascularisation avoided by using DESs was A$3750–$6100, with an estimated cost per quality-adjusted-life-year (QALY) gained of A$46 829–$76 467. In sensitivity analyses, estimates varied from DESs being cost-saving to costing an additional $314 385 per QALY gained.Conclusions: DESs are effective in reducing revascularisation. Estimates of cost-effectiveness are very sensitive to changes in estimates of their true effects in clinical practice, market price and the number of stents used per patient. Decisions to limit DESs to only patients at the highest risk of restenosis may improve their cost-effectiveness but will need to be reassessed when evidence is available to compare absolute benefits between patient groups.

Sarah J Lord MB BS, MS(Epi), FRACGP · Felicity Allen BVSc(Hons), MPH · Luke Marinovich BA(Hons) · David C Burgess BMed, FRACP · Kirsten Howard MAppSc(Biopharm), MPH, MHlthEcon · Richard King MB BS, FRACP · John J Atherton MB BS, PhD, FRACP

Hypertension Michael Schachter, David Monkman. Edinburgh: Churchill Livingstone, 2004 (v + 134pp). ISBN 044 307470 4. Hypertension is a short book aimed at primary care physicians and junior doctors. It provides a comprehensive summary of the major issues in the diagnosis and treatment of hypertension. Each volume of Churchill’s In clinical practice series is written by a specialist working with a primary care physician, and both authors of Hypertension have appropriate qualifications. The book is very topical, given the publication of hypertension guidelines by a number of national and international organisations in the past year, and the subsequent controversy about some of their recommendations. Differences in the guidelines are discussed and some of the authors’ own interpretations are provided. Opinion is clearly differentiated from evidence in the book. Importantly, several major hypertension trials have been published since the book was written, and the ASCOT (Anglo-Scandinavian Cardiac Outcomes Trial) results are soon to be published. This means that parts of the book will be out of date in a relatively short time. However, whether the results of these recent trials lead to changes in the recommended management of hypertension remains to be seen. The presentation and writing style are very user-friendly and I found this an enjoyable book to read. Important points are listed in italics in the margins. The table of antihypertensive drugs provides an easily accessible summary of doses, indications and side effects. The cost of the book seems reasonable. There are few who manage hypertension who would not glean some useful and practical information from this book. I would particularly recommend it to specialist physician trainees as well as primary care trainees. Roger PeverillCardiologist Monash University, Melbourne

Roger Peverill