Cardiovascular diseases

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

Ian Hamilton-Craig Chairman, MEDPED-FH Australia, North Adelaide Heart Centre, 80 Brougham Place, North Adelaide SA 5006. IhcATsahc.com.au To the Editor: In their editorial, Burnett and colleagues correctly emphasise the importance and cost-effectiveness of cascade family screening in the early diagnosis of familial hypercholesterolaemia (FH) among relatives of known cases. They point out that Australia does not have “a national program for detecting the vast majority of patients with FH in our community . . .”.1 Such an approach has been advocated since the 1980s by the international MEDPED-FH project, initiated in Utah to raise public and professional awareness of the need to detect and treat FH at an early age (MEDPED-FH stands for Make Early Diagnosis to Prevent Early Deaths in Familial Hypercholesterolaemia).2 Since then, the project has spread to over 30 countries, including Australia, and has over 25 000 patients with FH registered worldwide.3 In Australia, the MEDPED-FH program has registered about 700 patients with FH, about 2% of the estimated 33 000 patients overall.4 This proportion is similar to registrations in many other countries (including the US). Only the Netherlands, Denmark and Finland, where government-financed screening programs are in place, have higher proportions of registrations, with 10%–50% of patients with FH registered with MEDPED-FH. Also, in these countries, DNA detection of low-density lipoprotein cholesterol receptor gene mutations is used routinely for the diagnosis of FH. At present in Australia, nurse practitioners are performing FH cascade screening in collaboration with MEDPED-FH physicians in each capital city, supported by Pfizer Australia. Further work on FH is being carried out by Associate Professor David Sullivan and colleagues in Sydney, supported by the Western and Central Sydney Area Health Services. In addition, the Cardiac Society of Australia and New Zealand has established a working party to investigate cardiac genetic disorders, including FH, and is involved in further education among cardiologists regarding screening, diagnosis and treatment of FH. But these efforts are not enough. I support Burnett and colleagues in recommending the establishment of a nationwide screening program for FH, and also recommend that DNA diagnosis be incorporated as an essential component. There is a definite cost benefit of early detection and treatment with statins of patients with FH.

Ian Hamilton-Craig

John R Burnett,* David Ravine,† Frank M van Bockxmeer,‡ Gerald F Watts§ * Medical Biochemist, Department of Core Clinical Pathology and Biochemistry [corresponding author]; † Medical Geneticist, Medical Genetics Unit; ‡ Director, Cardiovascular Genetics Laboratory; § Physician, Department of Internal Medicine, Royal Perth Hospital, GPO Box X2213, Perth, WA 6847. john.burnettAThealth.wa.gov.au In reply: The international MEDPED-FH project has made a major contribution towards introducing family-based cascade screening into the Australian health care system. Although these achievements are important, we agree with Hamilton-Craig’s view that they are dwarfed by the magnitude of what now has to be done to deliver to all at-risk relatives the health gains that can be achieved by a proactive program of population screening. The risk of familial hypercholesterolaemia (FH) for a first-degree relative of an affected index case is 250 times greater than the risk for a member of the general population. The relative cost-efficiency of family-based cascade genetic screening is high, compared with population-wide screening for a dominantly inherited disorder.1,2 We disagree with Hamilton-Craig that DNA diagnosis is an essential component of an effective screening program. Among FH-affected families, biochemical testing has a sensitivity of 95%, and a specificity of 96%.3 The additional diagnostic gain from DNA testing in the context of screening relatives at 50% prior risk is marginal, although of use in determining with certainty whether or not a relative has inherited the family-specific trait. FH offers a paradigm of best clinical practice for improving health care outcomes for a widening range of “monogenic” disorders with complications that can be avoided or reduced by focused health care provision. The time has come when physicians, cardiologists, paediatricians, biochemists, geneticists, public health physicians, general practitioners and those administering the funding of health care delivery in Australia come together and formulate the changes necessary to allow cascade genetic screening for FH to become part of routine health care.

John R Burnett · David Ravine · Frank M van Bockxmeer · Gerald F Watts

Six patients being evaluated for phaeochromocytoma had misleading investigative findings: all initially had raised urinary catecholamine levels, and five had adrenal masses on imaging studies. Adrenalectomy in these five patients revealed only one pathologically confirmed phaeochromocytoma. Tricyclic antidepressant use produced misleading elevations in urinary catecholamine levels in three patients. 24-hour urine studies should be performed at least twice, after eliminating confounding factors (stressors, medications). Clinical recordThe details of six patients treated in the period April 1999 – October 2003 by members of the Section of Endocrine Surgery of the Royal Australasian College of Surgeons are outlined in Box 1. In all patients, clinical suspicion of phaeochromocytoma was raised by the presence of hypertension, paroxysmal symptoms, or both. Twenty-four-hour urinary catecholamine levels were found to be elevated, although in Patients 1–5 these abnormalities were confined to one or two analytes only. In all except Patient 2, adrenal lesions were discovered on imaging, with large haemorrhagic masses detected in patients with an acute presentation (Patients 5 and 6). Patients with abnormalities on computed tomography (CT) underwent surgery. In Patients 1, 3, and 4, the excised tissues were found to be pathologically normal or to show mild enlargement (benign). In Patients 5 and 6, blood clot and necrotic tissue comprised the bulk of the specimens (Box 2), with a phaeochromocytoma discovered in the latter patient. Of note, Patients 1–3 were receiving tricyclic antidepressants for non-standard uses that did not include the treatment of major depression. DiscussionFalse positive biochemical test results for phaeochromocytoma are common and present particular problems because of the low prevalence of the disease. The reported incidence of phaeochromocytoma is 2–8 per million people annually, accounting for less than 0.2% of all patients with hypertension.1 Despite the fact that phaeochromocytoma is a rare cause of hypertension, the diagnosis merits consideration in a potentially large group of patients for two reasons. Firstly, although the disease is frequently fatal if unrecognised, surgical removal is highly effective, achieving cure in greater than 90% of cases.2 Secondly, because no array of clinical indicators has proven to reliably include or exclude phaeochromocytoma,3 physicians must maintain a high level of suspicion and consider biochemical testing in patients at risk. The pretest probability for phaeochromocytoma is close to 0.5% (1 in 200 patients tested) in the presence of hypertension and suggestive symptoms.4 Assuming a specificity of 85% for biochemical testing, 30 false positive results are generated for every one patient with phaeochromocytoma identified.5 Fortunately, most false positive tests can be unmasked with careful additional investigation and/or the elimination of factors known to confound biochemical tests for levels of catecholamines and their metabolites. The misleading elevations in urinary noradrenaline levels in Patients 1–3 can be ascribed to their taking tricyclic antidepressants. Medications and conditions that may result in raised levels of plasma and/or urine catecholamines and their metabolites, and result in false positive test results for phaeochromocytoma, are listed in Box 3. Among these drugs, tricyclic antidepressants and phenoxybenzamine have been the most frequently implicated, together accounting for more than 40% of medication-associated false positive results in a recent large study.6 In Patients 3 and 4, false positive biochemical findings led to the identification of small (1.5 cm) adrenal masses on CT scanning, both of which were found, on histopathological examination, to be benign. Clinically unapparent adrenal masses (“incidentalomas”) are found in 2.1% of subjects at autopsy and in 1%–4% of abdominal imaging studies. Most of these masses are benign, hormonally inactive tumours that do not require surgical management.7 Phaeochromocytomas presenting with acute haemorrhage at presentation have been reported previously,8,9 with haemorrhagic tumours often losing characteristic imaging appearances and functional markers. Tumour necrosis may initially result in massive catecholamine release, followed by failure to demonstrate excess catecholamine levels, as was seen in Patient 6. Mildly elevated urinary catecholamine levels may also be seen as a consequence of hyperadrenergia from an acute stress response at the time of haemorrhage into a non-phaeochromocytoma lesion, as occurred in Patient 5. Role of biochemical testingAlthough measurement of plasma free metanephrine levels has been recently advocated by some groups, 24-hour urinary catecholamine levels and total metanephrine level have consistently proven to be the most specific tests available for the diagnosis of phaeochromocytoma.5,10 Elevations in the level of one or more of these analytes (above the 95% reference range designated as the upper limit of normal by laboratories) are common in patients with paroxysmal symptoms or poorly controlled hypertension not due to phaeochromocytoma. Thus, we recommend that higher cut-off values, roughly two times the upper limit of normal for most laboratories, be used to identify patients suitable for further workup. Repeat biochemical testing 6 weeks after stopping drugs likely to confound the results is ideal, and tests performed during major physical or psychological stress should be interpreted with extreme caution (if performed at all). It is important to note that alterations in plasma catecholamine levels may be caused not only by medications, but also by the underlying diseases being treated (eg, major depression in the case of tricyclic antidepressants or severe heart disease in the case of β-blockers).11-13 All patients should undergo at least two 24-hour urine collections for measuring levels of catecholamines and their metabolites. Clonidine suppression testing — the measurement of plasma free normetanephrine before and after the oral administration of 0.3 mg clonidine — is highly sensitive and specific, and may be a useful adjunct in patients with more than one prior set of equivocal tests.6 Role of imagingWhether imaging studies (both anatomical and functional) play a role in diagnosing phaeochromocytoma, as opposed to only localising tumours already diagnosed biochemically, remains controversial. In the patients described above, 131I‑metaiodobenzylguanidine scanning yielded true negative results in Patients 1–3, consistent with its known high specificity.4 However, current evidence suggests that, when appropriate biochemical tests are used, little discriminatory value is to be gained from imaging,14 and our experience illustrates how incidental radiographic findings may lead to unnecessary surgery. 1 Summary of the clinical records of six patients investigated for phaeochromocytoma Patient age/sex Presentation Blood pressure (mmHg) Medications 24-h Urinary catecholamine levels (nmol/d or μmol/d)* Radiological investigation† Surgical findings/ Clinical course Pathology Patient 1 49/M Weight loss (5 kg in 3 months), paroxysmal anxiety attacks, drenching sweats, chronic right flank pain 124/80 Clomipramine, 50 mg/day (anxiety) Adrenaline, 91/84 Noradrenaline, 860/1224 CT: 3 x 6-cm mass abutting upper pole of right kidney MIBG: negative Lobulated upper pole of kidney due to right renal artery branch running within posterior cleft Normal adrenal tissue Patient 2 41/M Migraines, chronic back pain, worsening hypertension, palpitations 145/85 Amitriptyline, 150 mg/day (migraine prophylaxis); amlodipine, 5 mg/day; ramipril, 5 mg/day; indapamide, 2.5 mg/day Adrenaline, 7/12 Noradrenaline, 485/1295 CT: No abnormalities MIBG: No abnormalities Normal findings on repeat urine studies after stopping amitriptyline — Patient 3 64/M Metastatic prostate cancer, poorly controlled hypertension 180/95 Imipramine, 100 mg/day (neuropathic pain); nifedipine, 180 mg/day; ramipril, 5 mg/day; chlorothiazide, 1000 mg/day Adrenaline, 115/99 Noradrenaline, 1070/1130 VMA, 33/38 CT: 1.5-cm left adrenal mass MIBG: negative Small left adrenal mass, macroscopically consistent with an adenoma Benign adrenal adenoma Patient 4 76/F Chronic hypertension, 15-month history of paroxysmal nausea and vomiting 144/80 Captopril, 25 mg/day Adrenaline, 65/129 Noradrenaline, 371/451 Dopamine, 1.55/2.02 CT: 1.5-cm left adrenal mass Smooth lesion palpable within left adrenal gland Enlarged adrenal gland (10.2 g; reference, 4 g) with thickened cortex but normal medulla Patient 5 75/M Sudden onset of intense back and left loin pain, chronic hypertension, weight loss (22 kg in 6 months), atrial fibrillation, diabetes, polymyalgia rheumatica 150/90 Warfarin, 5 mg/day; captopril, 25 mg/day; digoxin, 0.25 mg/day; isosorbide mononitrate, 60 mg/day; verapamil, 240 mg/day; prednisone, 5 mg/day; metformin, 2 g/day; rosiglitazone, 4 mg/day; thyroxine, 0.125 mg/day Adrenaline, 250 Noradrenaline, 720 Metanephrine, 1.68 Normetanephrine, 2.49 CT: 12-cm heterogeneous left adrenal mass (Box 2) Large blood clot with associated desmoplastic reaction occupying most of left adrenal gland Myelolipoma with haemorrhagic fat necrosis Patient 6 58/M Acute abdominal pain and hypertension, otherwise healthy 210/95 — Adrenaline, 2426/51 Noradrenaline, 18 370/464 Metanephrine, 13.3/0.8 Normetanephrine, 35.5/3.6 CT: 5-cm haemorrhagic left adrenal mass MRI (2 weeks after presentation): subacute haemorrhage into area without any distinct adrenal mass 12-cm dumbbell-shaped mass 3-cm phaeochromo-cytoma, large organising blood clot and necrotic tissue * Values separated by a forward slash represent separate collections, with abnormal values in bold. Reference ranges: adrenaline, < 100 nmol/d; noradrenaline, < 680 nmol/d; metanephrine, < 2.1 μmol/d; normetanephrine, < 5.6 μmol/d; VMA (vanillylmandelic acid), < 40 nmol/d; dopamine, < 3.0 μmol/d. †CT = computed tomography; MIBG = 131I-metaiodobenzylguanidine scanning; MRI = magnetic resonance imaging. 2 Computed tomography image of the haemorrhagic left adrenal mass in Patient 5 3 Medications and conditions that may cause false positive results of biochemical tests for phaeochromocytoma Medication or condition Test(s) confounded Tricyclic antidepressants Urinary catecholamines and metanephrines, plasma free metanephrines Clozapine Urinary catecholamines and metanephrines Phenoxybenzamine Plasma free metanephrines Calcium channel blockers Plasma noradrenaline, urinary noradrenaline, urinary adrenaline β-adrenergic blockers Urinary catecholamines and metanephrines, plasma free metanephrines (minor effect) α1-adrenergic blockers Urinary noradrenaline Sympathomimetics Urinary catecholamines and metanephrines, plasma free metanephrines Buspirone Urinary metanephrines Major physical or psychological stress* Urinary catecholamines and metanephrines, plasma free metanephrines * Hypoglycaemia, hypoxia, hypovolaemia, stroke, surgery, myocardial infarction, heart failure, severe pain, depression, panic disorder, sleep apnoea.

Jane L Harding MB BS · Michael W Yeh MD · Leigh W Delbridge MD, FRACS · Stan B Sidhu MB BS, FRACS · Bruce G Robinson MD, FRACP

An 81-year-old woman was fitted with a single-chamber pacemaker for atrial fibrillation and symptomatic bradycardia (Microny SR 2425T, Pacesetter, Sylmar, Calif, USA; silicone lead 1402 T, Siemens, Sylmar, Calif, USA). Seven years later, she presented with fatigue and presyncope of 1 week’s duration. She had also noticed contractions of the pectoral muscles on the left side of the chest. An electrocardiogram (Box 1) showed evidence of ventricular undersensing and non-capture, and a chest x-ray (Box 2) revealed complete fracture of the pacemaker lead. The pacemaker was replaced, and a new lead implanted using the cephalic vein cutdown approach. The patient’s medical record indicated that, 8 months previously, when she developed a cough, a chest x-ray had been performed by her physician. At around the same time, a routine check of the function of her pacemaker indicated that it was functioning normally. Re-examination of the x-ray revealed signs of lead erosion (Box 3) which had gone unnoticed. Thus, despite significant damage to the lead, pacemaker function may be unaffected. Friction of the lead, most often against the clavicle and the first rib (known as subclavian crush) can damage the lead. The incidence of fracture of pacemaker leads is about 1.0%–2.5% and increases with the age of the lead.1 A way of avoiding this complication is to introduce the lead into the axillary or cephalic vein rather than via subclavian vein puncture.2,3 Routine chest x-rays should be performed to monitor the condition of pacemaker leads, especially where they cross the clavicle. We recommend an annual chest x-ray for pacemaker-dependent patients. This may identify lead damage that may not be apparent during a standard pacemaker check, and thus, potentially, avoid syncope or sudden death. 1 Electrocardiogram on admission showing pacing spikes with evidence of ventricular undersensing and non-capture 2 Chest x-ray on admission showing complete section of the pacemaker lead at the level of the clavicle 3 Chest x-ray performed 8 months before admission, showing evidence of lead damage that went unnoticed

Stephane L Noble MD · Haran Burri MD · Henri Sunthorn MD

We still have no national program for detecting this potentially lethal disorder In 1985, Brown and Goldstein were awarded the Nobel Prize in Physiology and Medicine for unravelling the regulation of cholesterol metabolism in man. A key feature of their work was the elucidation of the molecular mechanism for autosomal dominant familial hypercholesterolaemia (FH), a potentially lethal disorder caused by defective endocytosis of low-density lipoprotein (LDL) cholesterol by its receptor (LDLR).1 This, in turn, led to the development of “statin” drugs, which potently lower plasma LDL cholesterol and reduce coronary heart disease (CHD) mortality. But, 20 years later, what have we achieved in detecting and treating FH? FH is characterised by lifelong marked hypercholesterolaemia (LDL cholesterol > 5 mmol/L) that leads to tissue cholesterol deposition — in such forms as tendinous xanthomata (particularly involving the Achilles), corneal arcus and palpebral xanthomas — and greatly increased risk of fatal CHD.2 Unfortunately, most people with FH are at present undiagnosed or only diagnosed after their first coronary event. We estimate that, of the roughly 40 000 cases of FH in Australia, about 20% are diagnosed and less than 10% are being adequately treated. Atherosclerosis in FH begins in early childhood. Children with FH are known to have endothelial dysfunction (the earliest phase of atherosclerosis) and increased carotid intima media thickness (CIMT), both surrogate markers of cardiovascular disease.3,4 Carotid atherosclerosis in FH rapidly progresses during childhood, at a rate proportional to plasma LDL cholesterol levels.4 FH typically involves mutations in the LDLR gene, with homozygotes having a more severe phenotype that heterozygotes. To date, about 1000 mutations have been identified in the LDLR gene (www.ucl.ac.uk/fh), most being unique, which makes the search for an unknown mutation challenging and expensive. Although heterozygous FH affects about 1 in 500 people overall,2 it occurs much more frequently in some populations such as Afrikaners, Christian Lebanese and French Canadians2 because of “founder” effects that occur when a few members of a population migrate and start a new colony. FH can be caused by mutations in genes other than LDLR. A mutation in the apolipoprotein B gene (APOB) may result in a clinical and biochemical picture that is indistinguishable from classic FH, although cholesterol levels are generally not as elevated and tendon xanthomas are less common.5 An autosomal recessive form of FH has also been described.6 The clinical picture of this condition is similar to that of homozygous FH, although it is generally less severe and more variable, with greater responsiveness to therapy. Except in “founder” populations, homozygosity for any of these conditions is exceedingly rare (about 1/1 000 000 people), and, without special intervention, such as LDL aphaeresis and liver transplantation, is typically lethal at an early age. Early statin treatment in children with FH improves endothelial function.3 A recent 2-year randomised controlled trial of pravastatin treatment (40 mg daily) in 214 children aged 8–18 years with FH showed regression of carotid atherosclerosis with no adverse effects on growth, sexual maturation, hormone concentrations, or serum liver and muscle enzyme levels.7 Despite this, the long-term safety and efficacy of statin use in children with FH is yet to be established. The Atorvastatin versus Simvastatin on Atherosclerosis Progression trial compared the effect of “aggressive” lipid-lowering treatment in FH with “conventional” lipid-lowering therapy.8 Over 2 years, LDL cholesterol lowering by high-dose atorvastatin resulted in regression of CIMT, whereas reduction with conventional-dose simvastatin did not. Moreover, the change in CIMT was proportional to the reduction in LDL cholesterol. These results support the concept that intensive lowering of LDL cholesterol levels in patients with CHD is beneficial. Although heterozygous FH patients are responsive to statins, additional treatment in combination with statins (for example, statin plus cholestyramine) is often required to achieve the desired LDL-cholesterol-lowering target.9 Moreover, combination therapy often permits use of a lower statin dose, which can benefit patients in whom adverse effects have occurred. Ezetimibe, a new drug that specifically inhibits intestinal cholesterol absorption alone, can reduce plasma LDL cholesterol concentrations by about 18%. Used in combination with a statin, it can achieve a further 25% reduction in LDL cholesterol levels over statin alone, by reducing both cholesterol supply to the liver and cholesterol biosynthesis.10 The long-term effects of ezetimibe on FH cardiovascular morbidity and mortality are unknown. The most cost-effective strategy for finding subjects with FH is to screen close relatives of patients already diagnosed with FH. Screening involves measurement of plasma LDL cholesterol, combined with either a clinical examination and family history or molecular genetic testing.11 Children born to an affected parent have a one in two risk of inheriting FH, and should be screened, at least biochemically, after the age of 2–3 years, when a cholesterol-lowering diet can be safely implemented.12 It is important to appreciate that a normal lipid profile does not rule out heterozygosity for an FH-causing mutation, particularly in early childhood.13 International experience shows that a family screening program must incorporate ethically acceptable protocols for approaching and interacting with relatives, follow-up communication with family members and their health care practitioners, as well as access to genetic counselling services, if required. Despite all these advances, it remains a tragedy that after 20 years of burgeoning knowledge about FH and the parallel development of powerful cholesterol-lowering drugs, Australia does not have a national program for detecting the vast majority of patients with FH in our community, let alone diminishing their risk of CHD.

John R Burnett MD, PhD, FRCPA · David Ravine DM, FRACP, FRCPA · Frank M van Bockxmeer BSc(Hons), PhD · Gerald F Watts DSc, MD, FRACP

Scott Kinlay Director, Vascular Medicine and Endovascular Therapy, Veterans Affairs Medical Center and Brigham and Women’s Hospital, 75 Francis Street, Boston, MA 02115, USA. skinlayATpartners.org To the Editor: Wang and Hoy1 deserve much credit for highlighting yet again the poor state of health of Indigenous Australians. However, their conclusion that the Framingham equation underestimated risk and that better prediction equations are needed may miss the point. The Framingham equations work well in other populations if the aim is to rank groups of individuals into higher or lower risk categories. Box 4 in the article by Wang and Hoy shows that they do this pretty well across increasing age groups. Framingham equations fall down when they are used to estimate absolute risk in populations whose coronary heart disease (CHD) rates are different from those in the Framingham study. Some years ago, we showed that adjusting the Framingham risk estimates in line with the overall incidence of CHD in the population modestly improved their performance.2 This is all very nice, but is better risk estimation the solution? We don’t estimate risk in other high-risk groups (eg, patients with CHD), because all are at high risk and all need risk factor reduction. A brief look at the risk factor profile in Box 2 of Wang and Hoy’s article reveals an alarming picture of uncontrolled CHD risk factors in a relatively young population (average age, 33–36 years). Cigarette smoking, dyslipidaemia, diabetes and overweight prevail. Perhaps, rather than concentrating on quantifying the exact risk in such a high-risk population, we should look at the reasons for the high rates of risk factors. What motivates some Indigenous people to smoke more, be more overweight and have a higher incidence of dyslipidaemia and diabetes than other Australians?3,4 Do they feel disenfranchised when governments infer they are “dirty” by tying financial aid to face-washing?5 Do they have attractive employment opportunities? Do they have enough sense of control over their lives to reduce their need to indulge in cigarettes and other short-term pleasures? Are there adequate supplies of healthy foods that they like? These factors may differ, as some rural Abori-ginal communities have much lower rates of smoking, overweight and diabetes6 than others. Exploring these issues will aid preventive methods aimed at the whole community. In the meantime, I would suggest that the Framingham equation does rank members of this community — into modest, high, and very high risk (the average 45–54-year-old has a 20% risk of a CHD event over 10 years1). This may help guide the medical treatment of risk factors and the pursuit of the medical model of prevention while social changes dictated by Aboriginal communities take effect.

Scott Kinlay

In reply: We agree with Kinlay that it is important to prevent risk factors at the population level (a population strategy). However, there is also a need to properly identify high-risk individuals who require immediate medical intervention (a high-risk strategy) and to understand the full spectrum of factors that determine such risk. The primary focus of our study was to assess whether the widely used Framingham risk functions were applicable to Aboriginal people in remote communities. Our data show that the Framingham functions significantly underestimated the risk of coronary heart disease (CHD). 1 The high CHD risk in Aboriginal people cannot be fully explained by traditional risk factors. Some major risk factors such as abnormal total cholesterol level and obesity in the study population are actually not as prevalent as those in the general Australian population. 2 Evaluation of traditional risk factors and identification of novel factors in this population are useful for the development of intervention strat-egies. Novel factors such as infection, inflammation, albuminuria and low birthweight have been suggested as predictors of CHD risk in this population. 3,4 Kinlay suggests that Framingham functions should be used to predict CHD risk in Aboriginal people. We disagree. Guidelines for the management of Aboriginal people need to recognise the serious underestimation of risk that the Framingham formulas provide. We agree that some high-risk groups, such as patients with established CHD, do not need additional risk estimates. With our current knowledge, however, we can not say whether the whole Aboriginal community should be treated as a very high-risk population.

Zhiqiang Wang · Wendy E Hoy

Dx/Rx: valvular heart disease. Dennis A Tighe, Theo E Meyer, Gerard P Aurigemma. Boston: Jones and Bartlett, 2005 (xi + 175pp). ISBN 0 7637 2385 1 This well presented pocket manual is part of the Dx/Rx Cardiology series. Written by clinicians from the Division of Cardiovascular Medicine at the University of Massachusetts Medical School, USA, it succeeds in providing, to quote the editor, “a clinical, concise and practical resource…” with which to approach cardiac valve disorders. Their aetiology, pathophysiology, natural history, clinical presentation and physical examination are discussed, followed by the diagnostic evaluation required and the suggested therapy — whether medical, interventional or surgical. The text is presented in a bullet-point format, aided by tables and figures throughout. Pertinent references are provided at the end of each chapter. Unfortunately, however, there are no illustrations of the various valvular abnormalities, which would have been helpful. The manual is more relevant to an adult population, although providing a considerable amount of information on congenital abnormalities of the valves. Aortic and mitral valve disease is reviewed in great detail with particular attention given to acquired valvular disease, especially rheumatic fever. Attention is also given to the less common disorders affecting the tricuspid and pulmonary valves. There is an excellent chapter on prosthetic valves, describing the types used, their specific clinical findings and the details of their assessment and follow-up requirements. Details of anticoagulation for mechanical valves are provided, including a special reference to difficulties associated with pregnancy. Homografts and autografts are briefly described. Infective endocarditis is referred to, where appropriate, throughout the text. Although aimed at postgraduate students, the manual may be a helpful resource for the busy clinician, whether general physician or family practitioner, as well as the practising cardiologist, for whom there is detailed information available related to less commonly used investigations, such as Doppler echocardiography to determine valve orifice size. While one could take issue with specific comments or details provided, I do think this well written manual achieves its goal. It may prove invaluable in the consulting room and may also become a welcome guide for interns, residents and registrars working in busy hospital settings. Within its small size, it contains a considerable amount of up-to-date information, clearly and concisely presented. Samuel MenahemCardiologist Monash Medical Centre and Royal Children’s Hospital, Melbourne, VIC

Samuel Menahem

Dx/Rx: heart failure. Theo E Meyer, Dennis A Tighe. Boston: Jones and Bartlett, 2005 (ix + 100pp). ISBN 0 7637 2309 6 This 100-page monograph on the diagnosis and management of heart failure, authored by two clinicians from the University of Massachusetts Medical School, USA, strikes a very good balance between the theoretical and practical aspects of this condition. An extremely well written, compact manual, it covers all aspects of heart failure in five sections. An introduction that deals with definition, classification, risk factors, prevalence and prognosis is followed by sections on the pathophysiology, clinical presentation, assessment and management of heart failure. Throughout the book, excellent tables and diagrams complement the text. I found the section about assessment very informative and thought the part on management contained useful practical information about the roles of different pharmacological and non-pharmacological agents used in the treatment of heart failure. Important results from various health failure trials are incorporated in a practical fashion, although in a book of this small size they cannot be presented or discussed in detail. I would highly recommend this book to all doctors who deal with patients who have heart failure, and am looking forward to reading other books in the Dx/Rx Cardiology series. Jitendra K VohraCardiologist Royal Melbourne Hospital, Melbourne, VIC

Jitendra K Vohra

Demands for efficiency should not be met at the expense of equity Despite countless reports over decades about the health disadvantages of Indigenous Australians, attention has only recently been turned to remedying disparities in the provision and quality of health care. A report in this issue of the Journal by Coory and Walsh about access to coronary procedures (page 507)1 adds to a growing body of evidence that Indigenous Australians do not receive the same level of care as other Australians.2-4 How might clinicians be contributing inadvertently to this “treatment gap”? And how can they remedy it? The responsibility for reducing ethnic disparities rests primarily with the health care system and its providers. Clinical decisions are based on imperfect information. To each clinical encounter, doctors bring prior beliefs about the likely nature of the condition. These beliefs differ according to the patient’s age, sex, socioeconomic status and ethnicity. They influence diagnosis, investigations and treatment. With identical descriptions of pain, a doctor is more likely to diagnose cardiac ischaemia in an elderly, sedentary, obese man than in a young, active woman of normal weight. Such stereotyping is helpful — and, indeed, promotes efficient practice — when it is based on epidemiology, statistical likelihood and best evidence. However, when incorrect, inappropriate and often implicit beliefs about the behaviour or health of a particular group are applied to individuals, stereotyping can be harmful. Uncertainty increases with patients who speak a different language or belong to a different cultural group. This, in turn, can lead to unhelpful, even harmful stereotyping. The experience of an Aboriginal politician who recently underwent emergency surgery demonstrates this. “I have had problems with my stomach and my abdomen for years. They were saying it was a problem with my kidneys and now that I have had this surgery on my bowels, they have found out that my kidneys are perfect,” she said. “So when I have gone to doctors complaining about illness over many years, I suppose they have taken my genetic heritage as a Tiwi Islander and thought it was renal.”5 Delays in diagnosis and treatment caused by such stereotyping might be partly responsible for Indigenous Australians’ poorer health outcomes. In the United States, concerns about the quality of health care received by racial and ethnic minorities compared with white Americans prompted Congress to request an investigation by the Institute of Medicine (IOM). Their landmark report, Unequal treatment: confronting racial and ethnic disparities in health care, found convincing evidence that racial and ethnic disparities exist across a wide range of conditions and health services and are associated with poorer outcomes.6 The report made several recommendations relevant to Australia, including cross-cultural training, use of interpreter services, and training more health care providers from ethnic and racial minority backgrounds.6 However, this might not suffice. Doctors who treat black Americans are less likely than those who treat white Americans to be “board certified” (ie, fully qualified) specialists. They are also more likely to report difficulty in arranging access to consultants, diagnostic imaging, and non-emergency hospital admission.7 In other words, doctors who treat black patients have less power, fewer resources, and possibly less training than doctors who treat whites. Is this also true in Australia? The IOM report defined disparities as racial or ethnic differences in the quality of health care not due to clinical need, patient preference or appropriateness of intervention.6 In Australia, these three factors have repeatedly been suggested as reasons for the treatment gap. Coory and Walsh suggest that the prevalence and severity of comorbidities may have a major impact on lower rates of coronary procedures and make providers question the appropriateness of such interventions.1 They note that selection favours lower-risk patients. However, even after controlling for the presence of comorbidities, Indigenous Australians still had significantly fewer interventions. With respect to patient preference, some commentators have suggested that, because Aboriginal people treated for chronic kidney disease fare poorly, they prefer not to be treated,8 but this hypothesis is contradicted by growing community activism to secure dialysis services in remote areas.9,10 A crucial issue is the increasing conflict between “efficiency” and equity. With increasing demands on health services, doctors attempt to maximise efficient use of scarce resources. Based on the mantra of “evidence-based medicine”, doctors perform more selective procedures and strive for lower rates of complications. A recent editorial suggested that people who cannot stop smoking should be excluded from a range of therapeutic interventions because of their higher risk of postoperative complications.11 Similar exclusions could also be applied to other groups, such as obese people. While this approach might increase “efficiency”, applying such standard criteria would greatly reduce Indigenous Australians’ access to beneficial interventions. Perhaps a higher complication rate is acceptable in the overall context of Indigenous Australians’ relative need for health care. Recovery from postoperative complications might be preferable to death without surgery. The responsibility for reducing ethnic disparities rests primarily with the health care system and its providers. System-level changes are clearly required, such as adequate funding for primary care, an adequate Indigenous health workforce, and improvements in the interface between primary care and specialist services.1,6,12 Clinicians have a central role to play in advocating for such changes. Because patients should be part of the solution, the IOM report recommends the development of appropriate education for patients in areas such as when and how to access health care, and how to participate effectively in clinical decision-making.6 However, most patients, in particular Indigenous Australian patients, are relatively powerless compared with doctors and “the system”. In Australia, the political debate about Indigenous health and development is framed in terms of “mutual obligation”. If we clinicians and researchers are to fulfil our obligation, we must first understand how we might inadvertently be contributing to the problem and then take steps to bridge the treatment gap.

Joan Cunningham ScD · Alan Cass PhD, FRACP · Peter C Arnold BSc, MB BCh, BA