Cardiovascular diseases

Preventive cardiology: a practical manual. Catriona Jennings, Alison Mead, Jennifer Jones, et al. Oxford: Oxford Medical Press, 2009 (xvi + 218 pp). ISBN: 978 0 19 923630 5. While cardiovascular disease (CVD) remains the predominant cause of death in our society, books on the topic will continue to find interest in the market, particularly those on preventive cardiology. Relatively few books on prevention, however, are written for health professionals by health professionals. Preventive cardiology: a practical manual, by a group of seven authors, addresses cardiovascular risk management and lifestyle factor assessment and application, for the benefit of and use by health professionals. The authors include representatives of nursing, dietetics, physiotherapy, physical activity and cardiology, so Preventive cardiology provides a uniquely holistic overview. With this multidisciplinary approach, the authors deal with both the assessment of risk factors and the application of findings in the management of patients with cardiovascular risk factors. One of the strengths of this book is its fundamental family-oriented approach. In a clear and concise manner, the authors address the main issues of identifying and treating patients with CVD risk factors, and provide a guide for health professionals in their work of identifying, assessing, treating and managing patients/clients at high risk, and steering them and their families through appropriate programs. The book covers all the usual topics of diet, smoking cessation, risk assessment, physical activity, identification of asymptomatic patients, blood pressure, lipid and glucose management, compliance, and so on. More importantly, it aims to assist the health professional team in getting such vital information lucidly and comprehensively across to patients and their families in a way that is most likely to be of practical benefit. The book comes in a pocket-sized format for easy access, and can be regarded as a ready companion and consistent helper for the cardiovascular professional.

Ian R Hamilton-Craig

The relationship between drug dose and clinical outcome has not been established for many medications used to treat chronic disease. Evidence is emerging that chronic diseases can be treated effectively with low doses. Adverse drug reactions account for significant morbidity and mortality and are generally dose related. Optimal drug dose — the best balance of benefit and risk — varies between individuals and may change over time. When treating chronic disease it is important to establish and maintain the optimal dose for each patient by close clinical monitoring.

Simon B Dimmitt MB BS, BMedSc(Hons), FRACP · Hans G Stampfer MB BS, FRANZCP

To the Editor: A recent article in the Journal describes, again, barriers to implementation of cardiometabolic monitoring among patients prescribed antipsychotic drugs.1 The cardiac health of patients with psychosis is not routinely assessed at first presentation for mental health services, adverse side effects of antipsychotic drugs are not systematically monitored, and patients with treatable risk factors for heart disease are not identified.2 We propose a practical solution to the seemingly intractable problem of implementing guidelines for cardiometabolic monitoring — change the delivery system. We have employed a general nurse to conduct cardiometabolic monitoring in a pilot study at the Recovery And Prevention of Psychosis Service (RAPPS), a first-episode psychosis service in Melbourne. All 15 eligible patients had their height, weight, blood pressure, waist circumference, fasting total cholesterol, high- and low-density lipoprotein cholesterol, triglycerides and glucose assessed according to national guidelines3 within 1 month of entry to the service, in the hospital, as an outpatient, or in the patient’s home; 14/15 blood samples were taken while the patient was fasting. Very early monitoring (within 7 days of first exposure to antipsychotics) was not implemented for four patients because they were inpatients and judged by ward staff as too unwell to be approached by a general nurse. Future follow-ups will be conducted at 3, 6, 12 and 18 months. Abnormal findings are referred to the treating psychiatrist, who is responsible for ensuring the patient receives appropriate follow-up. A general nurse can implement clinical guidelines, but this initiative requires substantial planning and ongoing management. Systematic identification of all patients eligible for monitoring requires identification of all pathways into the relevant mental health service, so as to begin monitoring at, or very close to, the point of first exposure to antipsychotics; management tools to track patients over time; and a clinical pathway to track test results and ensure appropriate medical interventions occur when required. Failure to implement prescribed monitoring guidelines is important because individuals with schizophrenia have a 20% shorter life expectancy than individuals in the general community.4 Side effects of antipsychotic drugs may include dramatic weight gain and elevations in serum cholesterol and glucose levels, which exacerbate the risk for cardiovascular disease. Most early deaths among individuals with schizophrenia are due to cardiovascular disease.5 Failure to monitor cardiovascular health and the adverse side effects of antipsychotic drugs is an important, life-shortening, failure of care. A simple solution to a complex problem exists if an effective delivery system is used.

Debra L Foley · Katherine I Morley · Karyn E Carroll · John Moran · Patrick D McGorry · Brendan P Murphy

In reply: Foley and colleagues rightly point out that a way to improve the cardiometabolic health of patients with psychosis is to change the way that mental health services are delivered. Although barriers to monitoring exist at the level of the patient, the illness, and the service,1 by focusing too narrowly on the barriers presented by patients, a blaming culture can be perpetuated. If blame is to be attributed, it should be directed towards inflexible services with a medieval belief in separating mental and physical health care. A number of centres in Australia have started to innovate in service delivery, with structured physical health clinics running in parallel to, and integrated with, mental health clinical programs. Our own centre, the Concord Centre for Cardiometabolic Health in Psychosis (ccCHIP), has been developed to take the notion of integrated care a step further — to actually treat the cardiometabolic abnormalities present. Our model involves a multidisciplinary team comprising psychiatrists, endocrinologists, and dietitians. However, we believe the potential for broader multidisciplinary input exists, including nurses, pharmacists, psychologists, occupational therapists, social workers and the patient’s general practitioner. It is our philosophy that although detection is the first step to improving the parlous outcomes for our patients, without active intervention, these poor outcomes are unlikely to improve. Recently, we received funding from the New South Wales Department of Health to develop a more comprehensive plan for education and training, including the production of a manual, to help psychiatric services in NSW develop their own monitoring and intervention services, using ccCHIP as their resource base. This initiative points to the need for government involvement to support these initiatives. Finally, it is apposite that Foley and colleagues write from the perspective of an early psychosis service — we believe that early detection and intervention for psychosis should be for physical as well as mental health issues.2

Timothy J R Lambert

We have a tool for absolute risk assessment — now we need a robust implementation program In March 2009, the National Vascular Disease Prevention Alliance (NVDPA), a consortium of Diabetes Australia, Kidney Health Australia, the National Heart Foundation of Australia, and the National Stroke Foundation, released evidence-based guidelines for assessing absolute cardiovascular risk.1 The guidelines are for use by health professionals who assess patients’ cardiovascular risk, primarily general practitioners. The risk charts that accompany the guidelines differ somewhat from the New Zealand risk charts,2 which are commonly used in Australia. Both the Australian and NZ charts are based on the Framingham Heart Study.3 The Australian cardiovascular risk charts are separated at the broader level into people with and without diabetes, rather than into men and women. In addition, systolic, but not diastolic, blood pressure is included because it is the stronger determinant of future events. The charts extend to upper cut-off points of 179 mmHg for systolic blood pressure and 7.5 mmol/L for total cholesterol level, respectively. The NVDPA guidelines also have an online risk calculator (http://www.cvdcheck.org.au). The new NVDPA guidelines and charts have the advantage of taking into account other drivers of practice in Australia, such as the Royal Australian College of General Practitioners’ Guidelines for preventive activities in general practice,4 and eligibility for Pharmaceutical Benefits Scheme subsidies for statins. Absolute risk assessment maximises the effectiveness of prediction of risk of future cardiovascular disease (CVD) events in people apparently free of such disease. This is because the underlying equations acknowledge fundamental epidemiological principles: risk depends on the range of independent risk factors and, for biomedical factors, risk typically increases in a log–linear manner above ideal levels (systolic blood pressure and total cholesterol level, 115 mmHg and 3.8 mmol/L, respectively).5 The present, somewhat arbitrary, definitions of hypertension and hypercholesterolaemia as ≥ 140/90 mmHg and ≥ 5.5 mmol/L, respectively, are fundamentally flawed, and most people who have CVD events have a clustering of risk factors with only modest abnormalities. If relative risk reduction with an intervention is relatively constant (the usual case), use of the intervention in those at higher absolute risk leads to greater absolute risk reduction and net benefit, thus also maximising cost-effectiveness. All absolute risk tools share some problems. As they are derived from large population studies, they are better at rank-ordering risk in subgroups and less precise in an individual. However, individual risk assessment may be refined (particularly in those initially assessed to be at intermediate risk) by measuring biomarkers or by imaging,6 and probably more so in the future, as more evidence becomes available. Other factors that might also be added to future algorithms include anthropometric measures (of these, waist circumference or waist : hip ratio appears more predictive than body mass index), a family history of premature atherosclerotic disease, and measures of socioeconomic deprivation.7 The NVDPA guidelines acknowledge that the Framingham risk equation may underestimate risk if these factors are present. The major determinant of CVD risk is increasing age, and it is also likely that equations specific for various age groups will become available. Particularly among younger people, this will improve identification of those with greater modifiable risk. Ideally, risk equations should be developed and validated in the local population. In Australia, algorithms for the general population have been developed from the Busselton8 and Dubbo9 studies. These are important contributions, although the relatively narrow endpoint (in Busselton) and the cohort age (in Dubbo) limit their application. How best can the NVDPA tools be used by practising clinicians? The first step is to identify high-risk groups. These include people with one or more of the following: prior CVD events, peripheral arterial disease, diabetes and age ≥ 60 years, chronic kidney disease, and familial hypercholesterolaemia. Such people should be treated accordingly and do not need absolute risk assessment. In all others, absolute risk assessments should commence at age 45 years, or 35 years for Aboriginal and Torres Strait Islander people, and be repeated at intervals reflecting the initial level of risk.1 An example of how to incorporate absolute cardiovascular risk assessment into management is given in the Box. What we now need is a robust implementation program. This makes economic sense. Recently, the National Health Service Health Check program was released in the United Kingdom.10 Everyone between 40 and 74 years, not already diagnosed with heart disease, stroke or kidney disease, will be invited, once every 5 years, to have their risk assessed using an absolute risk tool, and given support and advice to help them reduce or manage their risk. Analyses showed that this program would be very cost-effective compared with other accepted health interventions. The modelled cost-effectiveness ratio of this UK program is only £2480 per quality-adjusted life-year gained. Presently, in Australia, a Medicare item number supports a single health check for those aged 45–49 years. Although cost-effectiveness analyses are sensitive to the local health care system, the UK data strongly suggest that the current Medicare item number could be expanded, and other systems-based approaches implemented, to ensure that ongoing primary care risk assessments are supported, and that people at higher risk receive lifestyle and appropriate medical management. Implementation would be most likely to be effective if decision-support tools and recall mechanisms were used and incorporated into prescribing linked to electronic health records. Accompanying materials that appropriately communicate concepts of risk to patients would also be useful. The NVDPA is now developing a single CVD risk-management guide that will integrate the various specific risk-factor guides and make it easier to manage patients according to their absolute risk status. Absolute risk assessment does not replace the need to base all approaches to CVD prevention on lifestyle change. Studies have clearly shown the value of this, whether or not individuals are receiving blood-pressure or lipid-lowering therapies.11 However, absolute risk assessment leaves behind time-hallowed approaches based on individual risk factors, treated in silos, and often “dichotomised” to be regarded as “normal” or “abnormal”. It moves us forward to a more rational and effective paradigm for preventing our major health problem. How to incorporate absolute risk assessment into management using the Australian cardiovascular risk charts (the “People without diabetes” section of the charts is reproduced below) Example: Two women with similar risk profiles, but different ages Both women are smokers, without diabetes, with systolic blood pressure, 140 mmHg; total cholesterol : high-density lipoprotein cholesterol (TC : HDL) ratio, 7.2 mmol/L; and body mass index, 27 kg/m2. A is 46 years old and estimated to have a low risk (5%–9%) of developing cardiovascular disease (CVD) within 5 years. However, if she continues to smoke and to have a high TC : HDL ratio, she will place herself at high risk of prematurely developing CVD as she gets older. The chart can be used to demonstrate this to her. The priority intervention should be lifestyle advice, including smoking cessation, physical activity and healthy eating. B is 66 years old and estimated to be at high risk (20%–24%) of having a CVD event within 5 years. As a high priority, she should receive advice about smoking cessation and other lifestyle changes, as well as statin therapy. How to use the risk chart 1. Identify the chart relating to the person’s sex, diabetes status, smoking history and age. The charts should be used for all adults aged 45–74 years (and all Aboriginal and Torres Strait Islander adults aged 35 years or older) without known history of CVD or already known to be at high risk. 2. Within the chart, choose the cell nearest to the person’s age, systolic blood pressure (SBP) and total cholesterol (TC):HDL ratio. For example, the lower left cell contains all non-smokers without diabetes who are 35–44 years and have a TC:HDL ratio of less than 4.5 and a SBP of less than 130 mm Hg. 3. The colour of the cell that the person falls into provides their 5-year absolute cardiovascular risk level (see legend above for risk category). People who fall exactly on a threshold between cells are placed in the cell indicating higher risk. Charts are based on the NVDPA’s Guidelines for the assessment of absolute cardiovascular disease risk and adapted with permission from New Zealand Guidelines Group. New Zealand Cardiovascular Guidelines Handbook: A Summary Resource for Primary Care Practitioners. Second edition. Wellington, NZ: 2009. www.nzgg.org.nz. These charts are taken from Absolute cardiovascular disease risk assessment – quick reference guide for health professionals. © 2009 National Heart Foundation of Australia. Reproduced with permission. No further reproduction is allowed.

Andrew M Tonkin MD, FRACP, FCSANZ · Andrew N Boyden MPH, FRACGP · Stephen Colagiuri FRACP

A systematic, integrated national approach is needed to implement 2006 Australian guidelines for management of acute coronary syndromes (ACS). Clinical outcomes can be improved by closing the current gaps between evidence and practice. In 2007, the National Heart Foundation of Australia, the Cardiac Society of Australia and New Zealand, and the Australasian College for Emergency Medicine held a national forum to identify current gaps in ACS management and priority strategies to improve outcomes. Consensus recommendations were based on evidence and expert opinion. Prompt reperfusion for patients with ST-segment-elevation myocardial infarction should be ensured by establishing protocols for single-call activation of primary percutaneous coronary intervention, or, where unavailable, enabling health care workers to initiate thrombolysis. Accuracy of risk stratification of non-ST-segment-elevation ACS (NSTEACS) should be improved using clinical pathways that integrate ambulance, medical and nursing care. Rates of early invasive management for patients with high-risk NSTEACS should be increased using efficient systems for transfer to revascularisation facilities. All patients with an ACS should be referred to rehabilitation and secondary prevention programs, including alternative models of care where appropriate. Equal access to recommended care for all Australians with an ACS — including those in rural, remote and Aboriginal and Torres Strait Islander communities — should be achieved by improving workforce capacity in under-resourced regions and ensuring access to third-generation fibrinolytic agents, defibrillation, timely essential pathology tests and invasive revascularisation facilities. National standards for data collection and clinical outcomes should be established, and performance should be monitored.

on behalf of the National Heart Foundation ACS Implementation and Advocacy Working Group

A 49-year-old man presented with verapamil toxicity complicated by hypotension and a junctional rhythm, in the context of deliberate self-poisoning with multiple drugs. The patient’s hypotension normalised following the early use of high-dose insulin euglycaemic therapy (HIET), without the need for additional vasopressors; it recurred when HIET was prematurely stopped, and again stabilised when HIET was recommenced. Consideration should be given to the early use of HIET in treating severe calcium channel blocker toxicity, rather than as a last resort after other therapies have failed. (MJA 2009; 191: 350-352) Clinical recordA 49-year-old man presented to a peripheral hospital emergency department 1–1.5 h after deliberately ingesting multiple medications: verapamil (unknown amount), controlled-release morphine sulfate (20 × 30 mg), diazepam (50 × 5 mg) and tramadol (15 × 200 mg). He was a smoker with a history of depression, ethanol misuse, chronic back pain, hypertension and a previous instance of deliberate self-poisoning with multiple drugs. At initial assessment, the patient’s vital signs were: temperature, 36.8°C; pulse, 84 beats/min; respiratory rate, 19 breaths/min; blood pressure (BP), 115/80 mmHg; oxygen saturation, 95% on room air; and Glasgow Coma Scale score, 14/15. He was drowsy, disorientated to time, and had 2 mm pupils that were equal and reactive. He had ataxia, dysarthria and was generally weak. His breath ethanol concentration was 0.172 mg%. Thirty minutes later, the patient was hypotensive (BP, 85/45 mmHg; pulse, 72 beats/min). He was treated with oxygen, 2 L intravenous (IV) 0.9% saline, a naloxone IV infusion (400 μg/h), and 10 mL IV 10% calcium gluconate. He was transferred to a tertiary referral centre and, on arrival (at 2.25 h after initial presentation), his BP was 85/45 mmHg, pulse was 64 beats/min, and an electrocardiogram (ECG) showed a junctional rhythm. Rapid sequence intubation (with propofol 40 mg + 20 mg IV and suxamethonium 100 mg IV) was performed for airway protection and ongoing management of haemodynamic instability, while metaraminol IV boluses (total, 0.7 mg) were administered. Activated charcoal (50 g) was given, and sedation was maintained with a propofol infusion. The patient remained hypotensive (BP, 75/45 mmHg; pulse, 56 beats/min) after intubation, so high-dose insulin euglycaemic therapy (HIET) was commenced at 3.5 hours after presentation. He was given dextrose (50 mL 50% glucose) and a 30 IU short-acting insulin IV bolus (~ 0.5 IU/kg), followed by a further bolus of 50 mL 50% glucose and a short-acting insulin IV infusion (30 IU/h) (Box 1). His BP improved to 110/70 mmHg at 4 hours, with a pulse of 82 beats/min and sinus rhythm on ECG, and he remained stable during transfer to the intensive care unit (ICU). The insulin infusion was abruptly stopped 5.5 hours after presentation, on arrival in the ICU. The patient’s hypotension subsequently recurred (systolic BP, 70 mmHg; pulse, 75 beats/min), prompting administration of 500 mL IV Gelofusine (a colloidal plasma volume substitute; B. Braun, Sydney, NSW) and commencement of an adrenaline IV infusion (20 μg/min). The insulin infusion (30 IU/h) was restarted at 8.5 hours, and his BP again stabilised (Box 1). The propofol IV infusion was gradually increased from 50 mg/h to 150 mg/h between 5.5 hours and 11.5 hours after presentation, and a noradrenaline IV infusion was commenced at 9.5 hours to maintain normotension. At 15.5 hours, pulmonary artery catheter measurements showed a high cardiac index (5.1 L/min/m2; reference range [RR], 2.5–4.0 L/min/m2) and a low systemic vascular resistance index (1047 dynes·s/cm5/m2; RR, 1900–2400 dynes·s/cm5/m2); the patient’s pulse was 85 beats/min and BP was 140/60 mmHg. HIET was continued and the patient remained haemodynamically stable. Adrenaline and noradrenaline were weaned off (at 17.5 hours and 23.5 hours, respectively), despite the propofol infusion rate being increased to 500 mg/h at 18.5 hours. Once sedation was withdrawn, the patient was extubated at 26.5 hours. Insulin was weaned over 5 h and discontinued at 30.5 hours; dextrose was stopped 1 h later. The patient was transferred to the observation ward and discharged well later that day, after psychiatric clearance. During treatment with HIET, the patient’s blood glucose levels were checked hourly and ranged from 6.6 mmol/L to 13.2 mmol/L (RR, 3.5–5.5 mmol/L). He received about 25 g/h of dextrose (mostly as 50% dextrose infusions). Potassium and magnesium levels were also serially monitored; the minimum potassium level was 2.7 mmol/L (RR, 3.5–5.0 mmol/L) at 8.75 hours, and the magnesium level troughed at 0.5 mmol/L (RR, 0.75–1.05 mmol/L) at 15 hours. These were corrected with a total of 200 mmol of potassium chloride and 20 mmol magnesium chloride. DiscussionHIET is an increasingly accepted therapy for calcium channel blocker (CCB) toxicity, but reports of its use are limited and it remains controversial. Indeed, the scarcity of severe CCB poisoning cases means that a randomised controlled trial of HIET may not be feasible.1 Treating clinicians who seek advice from clinical toxicologists are often hesitant about the high doses required and the potential for adverse effects. Such hesitancy is potentially harmful, as a hypotensive patient with a CCB overdose who otherwise appears well is at risk of abrupt lethal cardiovascular collapse.1 HIET is traditionally recommended after other therapies have failed.2,3 This case report aims to raise awareness of HIET for the treatment of CCB toxicity and supports its early use, rather than as a last resort.4 Verapamil binds the alpha-1 subunit of L-type calcium channels, preventing the intracellular influx of calcium.5 These channels are functionally important in cardiac myocytes, vascular smooth muscle cells, and islet beta cells.5 Verapamil’s cardiac toxicity results from excessive negative inotropy, negative chronotropy and negative dromotropy, characterised by myocardial depression, sinus bradycardia, and atrioventricular node blockade.4 Vascular smooth muscle tone is impaired, resulting in decreased afterload, systemic hypotension, and coronary vasodilation.5 Less well known are the metabolic effects of CCBs such as verapamil. Under the stress of the drug-induced shock state, the cardiac myocytes shift from using free fatty acids, their favoured “resting state” energy substrate, to carbohydrates.3,4 CCB toxicity also impairs the uptake of glucose and free fatty acids by cardiac myocytes3,4 and inhibits calcium-dependent mitochondrial activity required for glucose catabolism.3,4 Furthermore, insulin release is dependent on calcium influx into islet beta cells through L-type calcium channels.3,4 Thus, CCB toxicity can cause hypoinsulinaemia,3,4 which, in conjunction with CCB-induced insulin resistance, may lead to hyperglycaemia and a ketoacidotic state.6 Atropine, calcium boluses and infusions, glucagon, inotropes, vasopressors, and cardiac pacing have all been advocated for managing CCB toxicity, despite questionable efficacy.3,4,7-9 For instance, the evidence for glucagon is limited to small, non-blinded animal studies where no survival benefit or improvement in mean arterial pressure was shown, although heart rate improved in some cases.7 Rarely, heroic measures such as extracorporeal circulatory support and intra-aortic balloon counterpulsation have been successfully employed.5,10 HIET was first used to treat verapamil toxicity in humans in 1993, with a favourable outcome.6 Since then, in addition to animal studies, there have been nearly 70 cases reporting the beneficial use of HIET in humans, with an overall survival rate of 85%.8 However, to our knowledge, use of HIET in humans before the administration of glucagon or vasopressors has only been reported once.6 There have been some reports of HIET failure in treating CCB toxicity, although the dosing of insulin was low or uncertain, or it was used late.6,8 Early use of HIET may be more effective than HIET rescue therapy, as CCB-induced insulin resistance is greatest in the first 24 hours2 and the maximal haemodynamic benefit of HIET may not occur immediately.6 HIET may allow the heart to overcome metabolic starvation in CCB toxicity, which compounds the direct CCB impairment of myocardial contractility.3,4 Insulin increases glucose and lactate uptake by myocardial cells and improves function without increased oxygen demand.11,12 It also induces pyruvate dehydrogenase, hastening myocardial lactate oxidation, and helps clear the cytosol of glycolytic byproducts that impair calcium handling and cause diastolic dysfunction.3 Insulin promotes excitation–contraction coupling and contractility because enhanced glycolysis promotes increased sarcoplasmic reticulum-associated calcium ATPase activity and increased cytoplasmic calcium concentrations, and promotes calcium entrance into mitochondria and sarcolemma.3 HIET may be best used adjunctively with other measures such as catecholamines, for two reasons. First, insulin-mediated inotropy is not catecholamine-mediated, and is not affected by β blockers.3 Second, although insulin appears to improve myocardial contractility, it has no chronotropic effect and may cause vasodilation.3,8 HIET is safe, and adverse events are predictable, uncommon, and easily managed.2,8 The maximum safe dose of insulin is unknown, but loading doses of 0.5–1.0 IU/kg followed by infusions of 0.1–2.5 IU/kg/h are typically used.8 Interestingly, neither the inadvertent administration of a 1000 IU insulin loading dose for verapamil toxicity13 nor treatment of toxic cardiogenic shock for 2 days with a 6 IU/kg/h insulin infusion had any adverse effects.14 Adverse effects of HIET include hypoglycaemia, hypokalaemia, hypomagnesaemia, and hypophosphataemia.2,6,8 Although these are rarely clinically significant, they necessitate careful monitoring. Hypoglycaemia (blood glucose < 3.3 mmol/L) occurred in 16% of 55 published cases,8 and no cases of hypoglycaemia within 24 hours of CCB overdose were noted in Greene and colleagues’ series of seven cases.2 Greene et al also reported a mean dextrose requirement of 0.05 g/kg/h (range, 0–0.17 g/kg/h), although the mean blood glucose level exceeded the euglycaemic range.2 Some cases of severe CCB toxicity in patients presenting with hyperglycaemia do not require any additional glucose administration despite high-dose insulin therapy,15 and hypoglycaemia may be more likely in milder cases without marked hypotension.8 In addition, hypokalaemia (potassium < 3.5 mmol/L) was noted in only two patients in Greene et al’s small series, with a minimum potassium level of 2.8 mmol/L.2 Excessive correction of hypokalaemia should be avoided, because it reflects the intracellular shift of potassium from the extracellular compartment due to the action of insulin, rather than a potassium-depleted state.4 Interestingly, hypokalaemia in HIET may augment myocardial contractility by enhancing calcium entry during systole, and increased intracellular potassium may have a membrane-stabilising effect in excitable cells.4,6 In conclusion, we advocate consideration of the early use of HIET (as detailed in Box 2) for the prevention and treatment of life-threatening complications from potentially lethal CCB overdoses. HIET is safe, inexpensive and freely available, and suitable for use even in remote settings before transfer to a referral centre. 1 Early changes in the patient’s systolic blood pressure (SBP) and heart rate, relative to treatment with high-dose insulin and adrenaline infusions Following administration of a 0.5 IU/kg short-acting insulin bolus 3.5 hours after presentation, a short-acting insulin intravenous infusion (0.5 IU/kg/h) was commenced (black line), and the patient’s blood pressure improved. The infusion was abruptly discontinued 2 hours later and the patient again became hypotensive. This resolved following commencement of an adrenaline infusion (20 μg/min) (grey arrow), and the insulin infusion (0.5 IU/kg/h) was restarted 8.5 hours after presentation (black arrow). 2 Recommended high-dose insulin euglycaemic therapy protocol,3,4,9 based on the clinical experience of the Western Australian Toxicology Service, published case reports, reviews and animal studies Commence therapy with: Glucose 25 g (50 mL of 50% solution) IV bolus, unless marked hyperglycaemia (blood glucose > 22 mmol/L) is present Short-acting insulin 1 IU/kg bolus to maximally saturate insulin receptors Continue therapy with: Short-acting insulin infusion starting at 0.5 IU/kg/h and titrated every 30 min to a maximum of 5 IU/kg/h* Dextrose 25 g/h IV infusion titrated to maintain euglycaemia (blood glucose, 5.5–14 mmol/L); central venous access may be required to allow use of concentrated solutions (eg, 50% dextrose) and limit excess volume administration Monitor: Glucose — every 20 min for first hour, then every 1 h Potassium — replace only if < 2.5 mmol/L and there is a source of potassium loss Therapeutic end points: Improvement in myocardial ejection fraction (> 50%); increased BP (systolic BP > 90 mmHg in adults) Adequate heart rate (> 60 beats/min) Resolution of acidaemia; euglycaemia; adequate urine output (1–2 mL/kg/h) Reversal of cardiac conduction abnormalities (QRS interval < 120 ms) Improved mentation Therapy is weaned after the withdrawal of other vasopressors, as cardiotoxicity resolves. Dextrose may be required after cessation of insulin. IV = intravenous. BP = blood pressure. * The maximum safe and effective rate of infusion is unknown but may be even higher than 5 IU/kg/h. In animal studies, insulin infusions as high as 10 IU/kg/h have been safely used.11

Christopher P Nickson MB ChB, DTMH, GCertClinTox · Mark Little FACEM, DTMH, MPHTM

To the Editor: The ASPREE (ASPirin in Reducing Events in the Elderly) study may provide useful data on the benefits and risks of aspirin therapy in patients aged ≥ 70 years, as described by Woods and colleagues.1 However, the decision to allow general practitioner co-investigators to “help decide whether the patient is a suitable candidate for the placebo-controlled trial” introduces a source of selection bias that may limit the generalisability of the results. Without pre-specified objective selection criteria, it is likely that primary-prevention patients assessed by GP co-investigators as being at high vascular risk will be excluded because the GPs believe they should be taking antiplatelet agents. Similarly, those at low risk may be thought inappropriate participants because the risks of random allocation to this therapy might outweigh the perceived benefits, as has been shown in previous meta-analyses.2,3 ASPREE may end up with a disproportionate number of intermediate-risk patients. In the case of diabetes, a recent observational study from our group highlighted patients with diabetes and retinopathy and those taking a sulfonylurea as being at increased risk of complicated peptic ulcer disease.4 By contrast, we did not find that aspirin use, positive serological results for Helicobacter pylori, or the interaction of these two factors predicted complicated peptic ulcer disease. If GP co-investigators were aware of these findings, they might also influence the screening and recruitment of patients with diabetes to ASPREE. According to the trial registration details (ISRCTN83772183), patients with diabetes were eligible for recruitment to ASPREE from late February 2009, even though the trial started 6 years ago.5 Given this delayed eligibility, the fact that a substantial proportion of patients with diabetes older than 70 years will already have vascular disease, and the expected total sample size of 19 000,1 the trial might include fewer than 1000 patients with diabetes and thus have insufficient statistical power to assess the risks and benefits of aspirin for primary prevention in this important subgroup. We question why subjective assessment forms part of patient selection for a potentially important study such as ASPREE, and also what steps the investigators are taking to determine whether the sample they recruit is representative. In addition, details of planned statistical analyses involving diabetic participants in this non-superiority trial would be reassuring.

Timothy M E Davis · Brett A Sillars · Wendy A Davis

In reply: Recruitment to clinical trials through general practice is representative of the population, as a high proportion of all Australians regularly attend their general practitioners.1 GP co-investigators are appropriate to decide whether their patients are suitable for the ASPREE (ASPirin in Reducing Events in the Elderly) study because their assessment includes objective inclusion and exclusion criteria that must be satisfied before enrolment in the study (clinical trial registration number ISRCTN83772183),2 as well as patient-specific potential risks with using aspirin, and known medical factors likely to influence patient survival during the trial. These include the risk of complicated peptic ulcer disease in patients with diabetes treated with a sulfonylurea.3 GP co-investigators support participation in ASPREE by eligible patients because of aspirin’s therapeutic equipoise for primary prevention in older patients4 and in those with diabetes.5 Because of age alone, ASPREE participants will be at least at intermediate risk of cardiovascular disease and also at increased risk of bleeding. Determining the aspirin balance underpins the importance of collecting more data in older people, who have been under-represented in previous primary prevention trials. ASPREE is a superiority trial with pre-specified subgroup analyses, including for the subgroup with diabetes.2 The study is powered to address the primary question reliably in the total cohort rather than subgroups. To date, fewer than 500 participants have been randomly allocated, with recruitment slowed subject to National Institutes of Health funding deliberations. Recruitment will be reinvigorated in late 2009, and will continue to include people with diabetes.

Robyn L Woods · Mark R Nelson · Andrew M Tonkin · Christopher M Reid

How you can use the evidence to improve your patients’ outcomes The most recent edition of Heart Foundation guidelines for the management of hypertension is an evidence-based and practical guide for doctors.1 It is self-evident that clinical guidelines need to be used by doctors if they are to improve population health outcomes. Despite publication of multiple editions of the hypertension guidelines, blood pressure (BP) control in Australia is less than ideal.2 The reasons for this are varied, and include health system, doctor and patient factors.3 Here, I outline simple but effective strategies for addressing some of the doctor factors associated with lack of BP control (Box), based on the Heart Foundation guidelines and supplemented by research conducted in Australian general practice. These strategies should help protect patients from stroke, myocardial infarction and other major organ damage, and are all practical in the general practice setting. Although they will not lead to universal control (because other factors are at play), they should help protect against therapeutic inertia and doctors’ doubts about their own self-efficacy — issues that may adversely affect patient health. Get blood pressure measurements from a variety of sources. When doctors measure BP, the measurements they record may differ from the true values, because of measurement error, “white coat effect”, poor technique, single measurements, observer error, and data misinterpretation.4 These problems can be addressed, to some degree, in a variety of ways. One approach is to have someone else, or something else, record BP for adult patients. In clinical practice, BP should be measured repeatedly (and preferably by a nurse) — three times, 5 minutes apart, and the last two measurements averaged. The process can be automated with some oscillometric devices, which further reduces bias.4 Away from the practice, the patient can record their BP on a validated,5 regularly serviced machine that they have been taught to use, or they can have their BP recorded by an ambulatory BP monitor. The latter are superior predictors of hard clinical endpoints compared with clinical measurements.6 Specific advice about technique for patients (as well as clinicians) is covered in the chapter of the Heart Foundation guidelines entitled “Measuring blood pressure”.1 Repeated measurements help reduce measurement error and variability, but they need to be interpreted logically. Suitable home BP monitoring can be achieved by asking the patient to measure BP in the morning and evening, to do so twice on each occasion (2 minutes apart after sitting quietly for 5 minutes), and to record the second measurement in a spreadsheet or diary for use at their next appointment. Interpreting the data can be as simple as highlighting elevated measurements, calculating the percentage of elevated systolic and diastolic measurements, or averaging the measurements. The goal is all or nearly all measurements (or average BP) at or below target levels. When interpreting the data, remember that cut-points are lower for recordings made away from the practice; for example, 135/85 mmHg is the cut-point for BP measured away from the practice in patients with uncomplicated hypertension. Act on absolute risk. In cases where repeated measurements of elevated BP are recorded in at-risk individuals, general practitioners may still not initiate or intensify BP management. Barriers to initiation or adjustment of drug therapy include: clinical uncertainty about underlying true BP and distrust of the technology used to measure BP; distrust of the evidence underpinning the recommendations for management of hypertension; a perceived increased rate of adverse events associated with drug therapy among older patients; perceived patient attitudes towards drug therapy or the need for it; a lack of internal motivation on the part of the practitioner; and health system issues such as lack of time in consultations. The decision to initiate treatment of elevated BP should not be based on BP alone (unless it is very high). An absolute cardiovascular disease risk score should be used, such as the recently released Australian cardiovascular risk charts, that now include risk for Aboriginal and Torres Strait Islander peoples.7,8 This is a more holistic approach than use of a single risk factor — it integrates all risk factors and thus more accurately identifies at-risk individuals. In primary prevention, population risk calculators are required as doctors cannot reliably estimate absolute risk.9 Patients with mildly elevated BP, who are at low absolute risk, do not require drug therapy but still need action on lifestyle factors that affect BP (eg, alcohol intake, diet, overweight/obesity, and physical inactivity). Don’t neglect behavioural factors. GPs recognise that behavioural factors underlie elevated BP and mitigate against effective BP control, but may feel that they have limited influence on their patients’ lifestyle. However, brief advice from a GP is the most cost-effective intervention for smoking cessation.10 Also, walking is a simple, free, all-year activity that GPs can recommend. For overweight patients, caloric restriction can be recommended and, for all patients, recommendations that can be considered include moderation of alcohol intake (do not recommend alcohol to non-drinkers), restriction of salt intake (by reading and interpreting processed food labels), and consumption of fruit and vegetables (two serves of fruit and five serves of vegetables per day). Advice should be supplemented with appropriate referrals (eg, to a dietitian). Accept that most patients will need more than one drug. Most patients will need more than one drug to control their BP.11 This is exacerbated by the need to manage the clustering of risk factors and multiple morbidity, which is common among patients, and especially older patients, with high blood pressure. These factors drive a high evidence-based pill count, which should be distinguished from unnecessary polypharmacy. Thus, the need for two or more drugs to effectively manage hypertension should be communicated to patients from the outset. Follow the guideline recommendations for combinations of drugs. Ways to deal with the necessary polypharmacy in managing high BP in at-risk individuals include: minimising side effects by starting with low doses (especially in older patients and patients with renal impairment), using low-dose combinations, discontinuing ineffective drugs, avoiding agents contraindicated for other conditions that are present, and monitoring for adverse outcomes such as renal impairment; minimising cost by using fixed-dose combinations, generics, agents with a larger number of daily doses dispensed, and drugs listed on the Pharmaceutical Benefits Scheme (avoiding “brand premiums”); increasing adherence by using combination therapies (especially those that allow within-combination dose adjustments); and reducing polypharmacy across morbidities by choosing antihypertensive agents that are indicated for other diseases that are present. Treat to goal. Once treatment of high BP has been moved to an absolute risk basis, the goals are logically reduced to lower levels for those individuals who are at high absolute risk. For example, the guidelines recommend lower BP targets for increasing levels of proteinuria in patients with chronic kidney disease.1 These patients will require greater individual risk factor reduction to reach low risk than patients who are at intermediate risk. This means more drugs, higher doses, higher costs, and greater difficulty in reaching therapeutic targets. In cases where the goal is not being reached, assessing for adherence to drug therapy is important — especially during the initiation of drug therapy. Participants in the Second Australian National Blood Pressure Study who answered yes to the question “Did you ever forget to take your medication?” were significantly more likely to experience a cardiovascular event or death than those who answered no.12 Strategies for dealing with necessary polypharmacy will also help reach the goals of target BP and adherence to drug therapy. The five ways together. Combining these strategies will help to improve BP control via an evidence-based chain of action: obtaining BP measurements systematically, in and away from the general practice setting; stratifying patients according to absolute risk, and acting on risk; considering behavioural measures for all patients; and utilising drugs (usually two or more) for patients who are at high risk, to reach recommended, targeted goals. Simple evidence-based strategies for managing high blood pressure in general practice Get blood pressure measurements from a variety of sources Act on absolute risk Don’t neglect behavioural factors Accept that most patients will need more than one drug Treat to goal

Mark R Nelson MB BS(Hons), FRACGP, PhD

To the Editor: We concur wholeheartedly with Gill and colleagues1 in support of recognising obesity as a public health issue, and we dispute claims that the current problem of obesity is being exaggerated. Gill and colleagues point out that obesity trends have climbed over decades, and state that 6%–8% of Australian school children are affected.1 While this is a substantial burden of over a quarter of a million children, we also consider that restricting definitions of obese to arbitrary cutoff points may underestimate the problem, given that the entire distribution of childhood weight is increasing, not just the extreme group classified as obese. Adiposity is related to cardiovascular outcomes such as myocardial infarction and stroke in a (curvi)linear fashion. Defining obesity by arbitrary cutoff points is vulnerable to differences between sexes, ethnicity and age, and limits our understanding of obesity-related diseases. It is well known that cardiovascular risk factors cluster, particularly the adiposity-driven components of the so-called metabolic syndrome. In the Western Australian Pregnancy Cohort (Raine) Study, we have used cluster analysis to identify a group of children at risk of future cardiovascular disease with features of the metabolic syndrome.2 The differences in characteristics are shown in the Box. The “high risk” and “low risk” cluster groups differ widely in terms of not only body mass index, the most widely used measure of obesity, but also waist circumference (a measure of central adiposity), insulin resistance, blood pressure, and levels of triglycerides, high-density lipoprotein cholesterol, total cholesterol (data not shown) and low-density lipoprotein cholesterol (data not shown). Not only the conventionally used 95% confidence intervals, but also the 99% confidence intervals do not overlap for any of these intermediate cardiovascular risk factors. We found that 29% of children were in the high-risk cluster at the age of 14 years2 and a similar analysis suggested that even at age 8 years, 25% of children were at increased risk of future obesity, cardiovascular disease and diabetes.3 C-reactive protein (CRP) level is known to be associated with future cardiovascular diseases in adults,4 and with an adverse metabolic profile in children.5 The “high risk” children had significantly higher CRP levels at the age of 14 years than their low-risk counterparts. Certainly, the magnitude of this problem, affecting up to a third of our youth, needs to be addressed by government and health-planning bodies. We suggest our approach of cluster analysis will help identify earlier those children at substantially increased risk of cardiovascular and other adiposity-related disorders in Australia. Features of the cluster groups with respect to components of the metabolic syndrome, showing 99% CIs* BMI = body mass index. HOMA = homeostatic model assessment (for quantifying insulin resistance). SBP = systolic blood pressure. HDL = high-density lipoprotein cholesterol. * From Huang et al.2 Reprinted with permission from the American Diabetes Association.

Rae-Chi Huang · Fiona J Stanley · Lawrence J Beilin

To the Editor: There is a substantial volume of evidence from a range of national and state-based surveys illustrating increases in the rates of obesity and overweight among Australian children over the past two decades,1 concurring with trends observed in most developed countries.2 The recent article by Gill and colleagues highlighted questions that have been raised publicly regarding the extent and impact of levels of obesity and overweight among Australian children, including whether trends have been exaggerated.1 To examine these issues using the latest data available, we present data from the three most recent national surveys in which weight and height of Australian children were measured: the Australian Health and Fitness Survey (1985),3 the National Nutrition Survey (1995),4 and the Australian National Children’s Nutrition and Physical Activity Survey (2007).5 We examined overweight and obesity levels among young Australians from comparable age groups at three time points over more than 20 years, using the same internationally accepted definitions of childhood overweight and obesity. For 1985 and 1995 data, we used the figures reported by Magarey et al in 2001,6 which compared results from the 1985 and 1995 surveys using new standard international definitions to classify overweight and obesity among Australian children and adolescents.7 We calculated body mass index for the 2007 Australian National Children’s Nutrition and Physical Activity Survey using the raw data file obtained through the Australian Social Science Data Archive,8 categorising children as overweight or obese based on the same international definitions used by Magarey et al.6 We based our calculations on the age group common to each of the three surveys: 7–15-year-olds. As shown in the Box, the prevalence of overweight and obesity in boys aged 7–15 years has risen from 11.0% (95% CI, 10.99%–11.01%) in 1985 to 20.0% (95% CI, 19.97%–20.03%) in 1995 and 23.7% (95% CI, 23.68%–23.72%) in 2007. In 7–15-year-old girls, the prevalence of overweight and obesity has increased from 12.2% (95% CI, 12.19%–12.21%) in 1985 to 21.5% (95% CI, 21.47%–21.53%) in 1995 and 25.8% (95% CI, 25.78%–25.82%) in 2007. While data from additional time points are required to map national trends more comprehensively, our analysis clearly indicates an upward trend in overweight and obesity levels in both boys and girls aged 7–15 years between 1985, 1995 and 2007. This trend is cause for alarm, given the widely recognised body of evidence on the significant short-term and long-term consequences of childhood obesity.9 Prevalence of overweight and obesity in Australian children aged 7–15 years, 1985–2007 * Data weighted for age, sex and region with the weighting variable in the raw data file obtained from the Australian Social Science Data Archive.8

Lyn M Roberts · Tessa R Letcher · Alexandra A Gason · Tim Lobstein

To the Editor: Davis and colleagues stated that the Framingham and United Kingdom Prospective Diabetes Study (UKPDS) cardiovascular risk equations are not suitable for predicting risk in an Australian population with type 2 diabetes.1 If confirmed, this would be extremely disappointing. However, before accepting this conclusion the following important considerations should be noted. Davis noted that the Fremantle Diabetes Study (FDS) patient group differed significantly from the UKPDS baseline group (eg, 38% of the FDS patients were aged outside the validated age range of the risk engine [25–65 years] and were assessed by non-validated extrapolation). Similarly, it cannot be assumed that the FDS group is representative of patients in general practice and hospital diabetes clinics around Australia. Moreover, it would be interesting to know how well the engine performs in FDS patients in the age group in which it was validated (ie, patients diagnosed with diabetes at age 25–65 years). It is likely that the low rate of cardiovascular events in the FDS (4.8% with at least one myocardial infarction, and 2.9% with at least one stroke)1 affects the accuracy of the results obtained with the UKPDS risk engine. The Framingham risk score has already been found to vary considerably in accuracy between populations, with predicted-to-observed ratios ranging from underprediction of 0.43 to overprediction of 2.87.2 Further, the UKPDS risk engine recently overestimated the risk of cardiovascular disease events in a UK general practice population.3 In purely pragmatic terms, most patients with type 2 diabetes aged over 50 years are at “high risk” for cardiovascular events (cardiovascular risk of more than 20% over 10 years),4 and the UKPDS risk engine is unlikely to influence prescribing practice significantly. However, we have found the engine to be a useful educational tool for explaining risk to patients. Even if the UKPDS risk engine is not optimally calibrated, the FDS analysis revealed that the coronary heart disease risk equation had modest discrimination (area under the receiver operating characteristic curve [AUC], 0.68), and the stroke risk equation had good discrimination (AUC ≥ 0.86),1 identifying those at highest risk. We believe that, rather than being irrelevant in Australians, the UKPDS risk engine continues to identify those at highest risk for cardiovascular events, operates well within its validated age group, and provides a motivational tool for encouraging changes in patient behaviour. Until a large dataset is pooled from various Australian studies, we believe the UKPDS risk engine should not be discarded.

Roland W McCallum · John R Burgess · Timothy M Greenaway

In reply: We thank McCallum and colleagues for their comments. In relation to their specific points: The Fremantle Diabetes Study (FDS) cohort is representative and drawn from a typical Australian urban centre.1 The 488 cardiovascular disease-free FDS participants with type 2 diabetes who were aged 25–65 years at both diagnosis and study entry had 22 coronary heart disease (CHD) events compared with 72 predicted, with a similar area under the receiver operating characteristic curve (AUC) to that for all 791 patients who were included in the analysis2 (0.66 v 0.68). Calibration indicated significant discrepancies between predicted and actual outcomes (P ≤ 0.02), and positive predictive values were low (≤ 3.5%). Therefore, restricting our patient sample to a “UKPDS” cohort did not alter our conclusions. We agree that the low observed CHD event rate in the FDS compared with that predicted by the UKPDS risk engine undermines its validity in Australians with type 2 diabetes. There was a similarly low CHD event rate in the FIELD study, which included many Australasians.3 Contemporary diabetes care clearly differs from that during the Framingham Study and UKPDS. Although the study cited by McCallum and colleagues, in a UK general practice population, is not strictly comparable to our study, it also found that the UKPDS cardiovascular disease risk engine performed only moderately (AUC, 0.72).4 Accurate risk prediction should be a basis for cost-effective care. We have developed an FDS risk calculator which should improve clinical management for Australians with diabetes.5

Wendy A Davis · Stephen Colagiuri · Timothy M E Davis

Implementing existing knowledge about cardiac rehabilitation (CR) and heart failure management could markedly reduce mortality after acute coronary syndromes and revascularisation therapy. Contemporary CR and secondary prevention programs are cost-effective, safe and beneficial for patients of all ages, leading to improved survival, fewer revascularisation procedures and reduced rehospitalisation. Despite the proven benefits attributed to these secondary prevention interventions, they are not well attended by patients. Modern programs must be flexible, culturally safe, multifaceted and integrated with the patient’s primary health care provider to achieve optimal and sustainable benefits for most patients.

Tom G Briffa PhD · Leigh Kinsman RN, MSc · Andrew J Maiorana MSc, PhD · Robert Zecchin RN, MN · Julie Redfern BSc, BAppSc(Physio)(Hons), PhD · Patricia M Davidson RN, PhD · Glenn Paull RN, CCUCert, BN(Hons) · Amanda Nagle PhD · A Robert Denniss FRACP, FAHA, FCSANZ

To the Editor: A 71-year-old man presented with a firm erythematous painful swelling over the sternoclavicular region. He had undergone coronary artery bypass grafting (CABG) 18 months earlier. A chest x-ray showed the presence of sternal wires and mediastinal clips from the surgery, and pleural thickening in the right costophrenic angle. There were no focal abnormalities seen on the x-ray when compared with pre-CABG radiographs. A computed tomography scan of the chest showed a destructive lesion of the manubrium, with an associated soft tissue mass extending into the pectoralis muscle and anterior mediastinum. A sternal suture was noted within the lesion, and a separate surgical clip was identified in the suprasternal notch region (Box, A). Surgical exploration of the sternotomy wound revealed tumour in the muscle around the proximal sternum, with bone destruction. Histopathological examination of the tumour confirmed the presence of an osteosarcoma (Box, B). (A section of normal trabecular bone [Box, C] is shown for comparison.) There have been few reported cases of primary sternal tumours. To our knowledge, primary osteosarcoma arising contiguous to a surgical suture has never been reported. It is unknown why the osteosarcoma originated in the part of the sternum that contained the sternal suture rather than originating de novo in another part of the bony skeleton. Chronic localised sternal inflammation or mechanical irritation of the proximal sternum by the suture may have been contributory factors in triggering carcinogenesis in this uncharacteristic site.1 However, the effect of trauma and mechanical stimulation on development of primary cancers and their metastases has never been proven. Patients who present with bony tumours frequently have a history of previous trauma to the area where the tumour develops. While there have been numerous reports suggesting some relationship between trauma/chronic inflammation and oncogenesis,1-5 there is no evidence that a single incident of trauma can cause cancer. The combination of trauma, in-situ metal and malignancy after CABG is rare, and there are currently no grounds for suspecting a direct relationship between them. A: Computed tomography scan of the chest showing a destructive lesion in the cortex of the manubrium. A sternal suture, surgical clip and soft tissue mass are visible within the tumour (A = anterior, R = right). B: Histopathological section of osteosarcoma of the sternum. Pleomorphic and hyperchromatic cells are present in a disorganised immature bone matrix (osteoid) (haematoxylin and eosin stain; original magnification, × 20). C: Histopathological section showing normal trabecular bone of the sternum (haematoxylin and eosin stain; original magnification, × 2.5).

Laurence Weinberg · Joseph Mathew

To the Editor: I read with interest the article by Medi and colleagues,1 but note that the authors do not mention the effect of supraventricular tachycardia on atrial natriuretic peptide — a hormone that causes vasodilation and renal excretion of sodium and water. Plasma levels of atrial natriuretic peptide increase markedly during supraventricular tachycardia.2 Pacing studies reveal that release of atrial natriuretic peptide occurs when the heart rate is greater than 120 beats/min.3 The resultant diuresis would lead to an urge to urinate and, in a prolonged episode of tachycardia, to polyuria.4,5

Weekitt Kittisupamongkol

Objective: To determine the incidence of coronary heart disease (CHD) events in an urban Aboriginal population.Design, setting and participants: Cohort study of 906 Aboriginal people without CHD from 998 who had undergone risk-factor assessment in the Perth Aboriginal Atherosclerosis Risk Study (PAARS) in 1998–1999. PAARS cohort data were electronically linked to a range of databases that included Western Australian hospital morbidity data and death registry data. We analysed data from January 1980 to December 2006 to identify previous admissions for CHD from 1980 to baseline (1998–1999) and new events from baseline to 2006.Main outcome measure: First CHD event (hospital admission or death).Results: There were 891 linked records for the 906 participants without previous CHD. The event rate was 12.6/1000 person-years (95% CI, 10.2–15.6/1000 person-years). Annual CHD event rates ranged from 8 to 18/1000 person-years. After adjustment for age (sex was not associated with the risk factors assessed), factors associated with risk of a CHD event in the PAARS cohort were a history of diabetes, overweight or obesity (indicated by body mass index), smoking, and hypertension, but not waist circumference. People with these risk factors were 1.9–2.7 times more likely to experience a CHD event. Compared with previously published information from a remote Aboriginal community in the Northern Territory, the incidence of CHD events among urban-dwelling Aboriginal people was not significantly different (P > 0.05 overall and for subgroups defined by age and sex).Conclusions: City-dwelling Aboriginal Australians have an incidence of CHD events comparable to that of Aboriginal people living in remote northern Australia.

Pamela J Bradshaw PhD · Helman S Alfonso MSc, PhD · Judith C Finn RN, MEdStud, PhD · Julie Owen DipT, MPHC, PhD · Peter L Thompson MD, FRACP, MBA

Objective: To describe baseline characteristics, operative events and late mortality among Indigenous Australians undergoing cardiac surgery.Design, setting and participants: Prospective study of consecutive patients undergoing cardiac surgery at Flinders Medical Centre in Adelaide between January 2000 and December 2005.Main outcome measures: Operative (30-day) mortality and late mortality after cardiac surgery.Results: Of 2635 patients undergoing cardiac surgery, 283 (10.7%) were Indigenous. Indigenous patients were substantially younger than non-Indigenous patients (mean, 47 [SD, 14] years v 65 [SD, 12] years; P = 0.001) and were more likely to have diabetes (39.6% v 27.3%; P = 0.001), renal dysfunction (3.2% v 1.2%; P = 0.009), and valvular surgery (53.0% v 23.1%; P < 0.001). There was a non-significant trend toward excess operative mortality in Indigenous patients (Indigenous 2.5% v non-Indigenous 1.3%; hazard ratio [HR], 1.67 [95% CI, 0.74–3.75]). But in the under-55-years age cohort, the difference between the two groups was highly significant (Indigenous 3.3% v non-Indigenous 0.4%; HR, 7.99 [95% CI, 1.66–38.50]), even after adjustment for euroSCORE (the European System for Cardiac Operative Risk Evaluation). Survival at 1 and 5 years was 94.0% and 80.6%, respectively, for Indigenous patients compared with 96.7% and 87.7%, respectively, for non-Indigenous patients. There was an excess in euroSCORE-adjusted mortality in the Indigenous cohort overall (HR, 1.46 [95% CI, 1.03–2.07]) that strengthened when restricted to the under-55-years cohort (HR, 6.9 [95% CI, 1.42–33.5]).Conclusion: Indigenous Australians present for cardiac surgery nearly 20 years earlier than non-Indigenous Australians and experience excess age-stratified operative and late mortality.

Sam J Lehman MB BS, FRACP · Robert A Baker PhD · Philip E Aylward MB BS, FRACP, PhD · John L Knight MB BS, FRACS · Derek P Chew MB BS, MPH, FRACP

Do you have patients who could benefit from therapeutic pacing and defibrillator devices? In recent years, management of chronic heart failure has advanced considerably, especially the optimisation of key pharmacological strategies (angiotensin-converting enzyme inhibitors, β-blockers) and multimodal management. In parallel, there has been a quieter revolution: the use of therapeutic pacing and defibrillator devices in patients with heart failure has moved from experimental and clinical research to everyday clinical practice. Milestones include landmark trials establishing the definitive mortality benefit of implantable defibrillators in ischaemic cardiomyopathy,1 the clinical utility of electronically synchronising contraction of both ventricles,2 and mortality benefits of cardiac resynchronisation therapy (CRT).3 Nonetheless, therapeutic pacing and defibrillator devices appear to be underutilised,4 perhaps due to lack of awareness of their clinical benefits and concerns regarding cost. What are the established modalities? Sudden cardiac death is a significant risk in patients with impaired left ventricular function. The use of implantable cardioverter defibrillators (ICDs) is established in primary and secondary prevention of sudden cardiac death in chronic heart failure — large randomised controlled studies have demonstrated a significant mortality benefit.1,5 American6 and Australian7 guidelines for heart failure management state that an ICD may be used after cardiac arrest, ventricular tachycardia or ventricular fibrillation; ≥ 40 days after myocardial infarction in patients with New York Heart Association (NYHA) class I, II or III symptoms and left ventricular ejection fraction (LVEF) ≤ 30%; and in patients with ischaemic or non-ischaemic cardiomyopathy, NYHA class II or III symptoms and LVEF ≤ 35%. Newer “risk stratifiers” are being explored to better identify patients likely to benefit from ICD therapy.8 The implantation procedure for an ICD is identical, in principle, to that of a pacemaker, with some exceptions: the lead is larger (thus stiffer), so care is required during its manipulation within the heart; the battery is larger, so it requires careful positioning to avoid skin erosion; and testing of the device involves inducing ventricular fibrillation to ensure adequate sensing of arrhythmia and an adequate safety margin in terms of the threshold of defibrillation. Also, the sophisticated programming of ICD therapy requires a cardiac electrophysiologist. ICDs can be programmed to treat ventricular arrhythmias with either antitachycardia pacing (which is painless) or shock therapy. After the patient experiences their initial therapy, which unfortunately may involve a potentially distressing shock while the patient is conscious, individualised adjustments may be needed. Despite the survival benefit associated with ICDs, their impact on quality of life is uncertain. In contrast to other heart failure therapies, ICDs do not improve cardiac function. They would not be expected to improve a patient’s exercise capacity or ability to perform activities of daily living. Also, implantation can be associated with various immediate and late complications, including device infection, failure and inappropriate discharge.9 The failing heart is frequently characterised by abnormalities of mechanical synchrony, often reflected by abnormalities of electrical conduction. Based on adverse consequences of ventricular dyssynchrony in heart failure, researchers have sought to resynchronise the failing myocardium. One approach, CRT, involves pacing both ventricles in a coordinated manner to restore the normal physiological chronology of left- and right-sided contraction. Ventricular dyssynchrony can be crudely detected on an electrocardiogram by QRS prolongation.10 Epidemiologically, QRS prolongation has been associated with worsening of clinical outcomes in patients with heart failure. Echocardiography has been proposed as a better tool for evaluating mechanical dyssynchrony.11 The implantation of a CRT device extends the standard pacemaker or ICD implantation procedure by placement of a left ventricular pacing lead. This requires specialised sheaths to access the coronary sinus, angiographic identification of an appropriate lateral branch, and careful positioning of the lead. Several factors determine the ideal position for the lead, including proximity to the lateral wall at a position furthest from the right ventricular lead, stability of lead placement, presence of viable myocardium that can be captured by pacing at the site, and avoidance of diaphragmatic pacing. The procedure requires an experienced operator and a service that can optimise programming. CRT has undergone considerable evaluation and, according to American and Australian guidelines, it is indicated in patients with NYHA class III or IV symptoms, LVEF ≤ 35% and QRS duration on electrocardiogram > 120 ms.6,7 More than 4000 patients have been evaluated in randomised single- or double-blind controlled trials of CRT in heart failure and, in systolic heart failure, CRT has consistently been associated with improved patient wellbeing and ventricular systolic function, and reduced recurrent hospitalisation for heart failure. Meta-analyses and a stand-alone study have shown reduced all-cause mortality with CRT.3,12 These benefits add to those of standard drug therapies for systolic heart failure, and may be further enhanced by use of a defibrillator. Indeed, most CRT devices used in Australia include a defibrillator function. Ideally, patients should be in sinus rhythm for maximum benefits from this therapy. Some evidence suggests that CRT is also beneficial in patients with atrial fibrillation, and that this cohort may be better optimised with atrioventricular node ablation.13 However, current Australian Government Department of Health and Ageing guidelines do not support the use of these devices in patients with atrial fibrillation.14 In addition, not all patients who meet the criteria for CRT benefit from the therapy. There is a 20%–30% “non-response rate”, in that patients do not feel better or ventricular function does not improve.14 The reason for this is elusive, but improved evaluation of dyssynchrony, using measures more sophisticated than QRS duration (eg, echocardiography, magnetic resonance imaging), may reduce the non-response rate, and CRT trials that base entry criteria on results of imaging alone are underway. Nonetheless, CRT has gained popularity in recent years, particularly for patients who remain severely symptomatic despite drug therapy. What other modalities are being evaluated? Cardiac contractility modulation (a new form of electrical therapy) is currently being evaluated in patients with heart failure. A recent clinical study demonstrated improved exercise tolerance and quality of life,15 but these data need to be confirmed in large, randomised controlled studies. Ventricular pacing alone has also been trialled, but can result in deleterious mechanical effects. In patients with impaired left ventricular function, right ventricular pacing can cause further deterioration.16 Adverse effects may be minimised by pacing the right ventricular outflow tract or high septum rather than the apex.17 Perhaps more importantly, atrioventricular synchrony can be maintained, and many pacemakers allow minimisation of ventricular pacing by various programmable algorithms. What is needed now? Over the past decade, many pacing therapies have been rigorously evaluated in patients with chronic heart failure, and there are now proven indications for their application in clinical practice. The clinical outcomes, potential problems and costs of CRT, ICD and right-sided pacing are summarised in the Box. Doctors should be aware of these therapies and consider referring individual patients who meet the criteria for their use. Comparison of some features of pacing modalities for chronic heart failure and comorbid arrhythmias Cardiac resynchronisation therapy Implantable cardioverter defibrillator Right-sided pacing Clinical outcomes Decreased mortality, morbidity and hospitalisation Improved exercise tolerance, quality of life, NYHA class Decreased mortality Decreased incidence of sudden cardiac death No proven benefit in chronic heart failure Potential problems Relatively high non-response rate Procedural complications (early and late) Uncertain quality-of-life benefits Inappropriate discharge Procedural complications (early and late) Worsening left ventricular function in systolic chronic heart failure in certain modalities Cost14 High: public hospitals, $21 075; private hospitals, $59 100* High: public hospitals, $14 975; private hospitals, $45 100† Relatively low NYHA = New York Heart Association. RA = right atrial. RV = right ventricular. LV = left ventricular. * Costs for cardiac resynchronisation therapy include: (public hospitals) generator, $17 000; RA lead, $475; RV lead, $1500; LV lead, $2100; and (private hospitals) generator, $44 500; RA lead, $1350; RV lead, $8750; LV lead, $4500. † Costs for implantable cardioverter defibrillator include: (public hospitals) generator, $13 000; RA lead, $475; RV lead, $1500; and (private hospitals) generator, $35 000; RA lead, $1350; RV lead, $8750.

Henry Krum MB BS, PhD, FRACP · Prashanthan Sanders MB BS(Hons), PhD

Objective: To evaluate current evidence in support of therapies for preventing and treating cardiogenic shock (CS) after acute myocardial infarction that can be initiated in hospitals without invasive cardiac facilities.Study design: Systematic review.Data sources: MEDLINE and PubMed were searched from January 1985 to May 2008 using the MeSH terms “myocardial infarction”, “thrombolytic therapy”, “shock, cardiogenic”, “angioplasty, transluminal, percutaneous coronary”, “intra-aortic balloon pumping” and “platelet aggregation inhibitors”. Additional keyword and reference list searches were performed. Articles in English relating to adults were included.Study selection: Meta-analyses and comparative studies were included if they reported mortality or prevention of CS as an endpoint. In total, 35 articles were analysed (four meta-analyses, eight randomised controlled trials and 23 cohort studies).Data extraction: Studies were summarised by the first author and the level of evidence graded. Each study was checked by the second author and consensus was reached about inclusion and levels of evidence.Data synthesis: In the management and prevention of CS, the following are supported by high-level evidence: prehospital thrombolysis, transfer for emergency revascularisation (patients aged < 75 years) and thrombolysis for older patients (patients aged ≥ 75 years). In established CS, evidence supporting inhospital thrombolysis and intra-aortic balloon pump use in patients aged < 75 years and emergency revascularisation in older patients is limited to subgroup analyses and observational studies.Conclusions: In regional centres, prevention of CS is achieved with early fibrinolysis, preferably before hospital arrival. Patients of all ages should be considered for thrombolysis, early transfer for coronary revascularisation, and intra-aortic balloon pump insertion unless contraindicated. Glycoprotein inhibitors have no role in the management of CS in non-tertiary hospitals.

Enda O’Connor MRCPI, FJFICM · John F Fraser FRCA, FFARCSI, FJFICM

Clinical record A 68-year-old man presented to our general district hospital in December 2006 with the chief complaint of sore throat, which had started abruptly 2 hours earlier. The pain was described as intense with a stabbing character. He reported minimal improvement after being given 10 mg of morphine subcutaneously. The patient did not report experiencing any cardiac or pulmonary discomfort, and he had no pertinent past medical history. His family history included one sister who had died of a ruptured aortic aneurysm. The patient was a non-smoker and denied any recent medication use. Physical examination showed that the patient’s vital signs were stable, with a normal level of consciousness, a regular pulse of 61 beats/min, and a blood pressure equal at both arms of around 115/70 mmHg. He was slightly tachypnoeic and diaphoretic. An ear, nose and throat examination did not provide any diagnostic clues as to the cause of the pharyngeal pain. Findings of a cardiovascular examination were normal apart from an audible right carotid artery bruit. No other physical abnormalities were detected. Results of laboratory tests were unremarkable, except for a markedly elevated d-dimer level (8.41 mg/L; upper limit of normal, 0.50 mg/L). Routine chest radiography was suggestive of mediastinal widening (Figure A). On the basis of these findings, a thoracic computed tomography scan was performed, which showed a 5.4 cm dissecting ascending aortic aneurysm (Figure B). The dissection involved the aortic root, ascending part of the aorta and aortic arch, and propagated into the right brachiocephalic trunk and left common carotid artery (Figure C). Transthoracic echocardiography additionally showed the presence of a bicuspid aortic valve with moderate grade 2/4 aortic insufficiency. Thoracic aortic dissection was diagnosed, classified as a Stanford type A dissection, given the involvement of the ascending aorta. A congenital bicuspid aortic valve and an ascending aortic aneurysm were predisposing factors for aortic dissection. The patient successfully underwent emergency surgery with graft replacement of the aortic valve and the dissected aortic segment. A: Chest x-ray showing mediastinal widening. The upper normal mediastinal width is defined as a mediastinum to chest-width ratio of over 0.25, measured at the level of the aortic arch (illustrated by the length of the solid line); this is noticeably exceeded in our patient (dashed line). B: Computed tomography scan showing an aneurysmatic dilatation of the ascending aorta with a classical dissection flap (black arrowhead) separating a true and false lumen. C: Propagation of the dissection process into the supra-aortic vessels (white arrows). The clinical presentation in our case was rather trivial, but the combined results from two basic investigations — an elevated d-dimer level and an abnormal chest x-ray — heightened our clinical suspicion for aortic dissection and led us to perform aortic imaging. Thoracic aortic dissection generally results from a laceration of the intimal lining of the aorta. This allows blood leakage into the aortic wall resulting in a propagating separation of the aortic media, thereby creating a false blood-filled lumen.1 Hence, the major criterion for definitive diagnosis of aortic dissection includes visualisation of a so-called intimomedial flap that divides the aorta into a true and a false lumen. Several aortic imaging techniques can be used for this purpose, of which contrast-enhanced computed tomography (CT) and transoesophageal echocardiography (TOE) are the most feasible to perform in an emergency department setting.1,2 Moreover, these investigations help to localise the dissection, thereby allowing appropriate classification. Currently, the Stanford classification of aortic dissection is the most widely adopted system.1,2 This system has the virtue of merely dividing aortic dissection into two subtypes, depending on whether the ascending aorta is involved (type A) or not (type B).1,2 While the definitive diagnosis of aortic dissection is usually straightforward, making the initial clinical diagnosis can be extremely challenging. Aortic dissection is associated with a dramatic rate of misdiagnosis and delayed recognition.3 This is no doubt partially explained by the highly variable clinical presentation of the condition. Our case is a striking illustration of why acute aortic dissection is colourfully called a “clinical chameleon”.1 Although most patients with aortic dissection present with severe chest or back pain (Box 1), the pain can be variably localised to the neck, jaw or throat.4 Throat pain occurs most often in cases of a dissection of the aortic arch, particularly when the supra-aortic vessels are involved. Our patient complained only of a sore throat, and denied having thoracic pain. Only two similar cases have been previously reported.5,6 Moreover, findings on physical examination can be very subtle.1 Classical signs consistent with the diagnosis of thoracic aortic dissection, such as an aortic insufficiency murmur or decreased femoral arterial pulsation, were not present in our patient. According to the International Registry of Acute Aortic Dissection,7 these so-called typical findings are infrequently detected during physical examination (Box 1). In our case, the only notable features of the physical examination were diaphoresis and a right carotid artery murmur. The latter was presumably the result of propagation of the dissection into the right brachiocephalic trunk. Because symptoms and signs of aortic dissection can be diverse and sometimes treacherously trivial, the initial diagnostic suspicion might rely on abnormalities observed during the basal diagnostic work-up. This routinely consists of laboratory testing with d-dimer analysis and chest radiography. d-dimer analysis has only recently come to the fore, with several studies focusing on the stringent association between the d-dimer level and aortic dissection.3,8,9 The pathophysiological mechanism for this relationship is well explained by the release of tissue factor from the dissected aortic wall. This sets off a cascade of events — activation of the extrinsic coagulation system, generation of fibrin, and secondary fibrinolysis with d-dimer formation.8 The d-dimer assay is reported to have an excellent sensitivity and negative predictive value for aortic dissection (Box 1). The quoted sensitivity is equal for both types of dissection, although absolute d-dimer values tend to be higher in type A aortic dissections as they are usually more extended.10 Given its high sensitivity and negative predictive value, d-dimer testing is an attractive tool for the diagnostic work-up of aortic dissection, particularly in the setting of a low pretest probability for aortic dissection. In such cases, a normal d-dimer result can reliably exclude the presence of aortic dissection, hence obviating the need for further investigations.9,10 Besides elevation of the d-dimer level, the clinical suspicion for aortic dissection should also be heightened if the chest radiograph is abnormal (Box 1). Mediastinal widening (relative mediastinum to chest-width ratio > 0.25;11 Figure A) is the most common radiographic finding in aortic dissection.7 Of note, absolute estimations of the mediastinal width are practically inaccurate, as these measurements are influenced by the distance between the roentgenographic source and the thorax.12 It is worth mentioning that one in three patients with aortic dissection has a normal chest x-ray.11 Thus, relying on chest radiography alone as the initial diagnostic modality is inefficient as it clearly carries a high risk of misdiagnosis. When readily available, contrast-enhanced CT and TOE are the preferred imaging modalities in an acute care setting. Both investigations have a comparable diagnostic accuracy and allow a definitive diagnosis of aortic dissection to be established.1,2 However, the diagnosis must first be suspected before it can be confirmed — this case serves as a reminder of this life-threatening condition’s wide variability in clinical presentation, and the need to maintain continuing vigilance. 1 Clinical and basic diagnostic features of thoracic aortic dissection, and percentages of patients presenting with these features who are subsequently diagnosed with Stanford type A or B aortic dissection1,2 Stanford classification Features Type A* Type B† Clinical symptoms and signs7 Presence of any pain 94% > 95% Retrosternal pain 71% 44% Interscapular pain 33% 41% Back pain 47% 64% Abdominal pain 22% 43% Blood pressure Hypotension or shock/tamponade < 25% < 5% Hypertension 35% 70% Aortic insufficiency murmur < 45% < 15% Decreased or absent peripheral pulsations < 20% < 10% Laboratory analysis8,9 d-dimer sensitivity (cutoff, 0.50 mg/L) > 95% > 95% d-dimer negative predictive value (cutoff, 0.10 mg/L) 100% Not reported Chest radiography7 Mediastinal widening 63% 56% Abnormal or blurred aortic contour 47% 53% Other radiographic features‡ < 25% < 25% * Dissection with involvement of the ascending aorta. † Dissection of the descending aorta without involvement of the ascending aorta. ‡ Such as displaced aorta, aortic calcification, tracheal displacement, pleural effusion. Lessons from practice Thoracic aortic dissection is characterised by a highly variable clinical picture, which has led to the condition being called a “clinical chameleon”. d-dimer testing can be of value in excluding aortic dissection. A normal chest x-ray does not rule out the possibility of aortic dissection. Advanced aortic imaging should be performed early in patients who have symptoms suggestive of aortic dissection in order to prevent misdiagnosis.

Sébastien Anguille MD · Aurélie M Derweduwen MD · Jeroen Lenz MD · Luc Vanuytsel MD, PhD · Frank J Cools MD

Clinical records Over the past 3 years, we have identified five cases of coronary syndromes attributable to a left subclavian stenosis proximal to a left internal mammary artery (LIMA) graft for coronary artery disease. All occurred in men aged between 56 and 73 years, presenting a median of 52 months (range, 26–138 months) after coronary artery bypass grafting. One patient presented with stable angina, three had unstable angina, and one had a non-ST elevation myocardial infarction. Arm claudication was present in one patient. Three of the five patients had an exercise or pharmacological stress test — all with anterior wall ischaemia. At cardiac catheterisation, the diagnosis was recognised by careful comparison of the pressure tracings in the subclavian artery and aorta. All patients had a significant pressure gradient across the subclavian stenosis (median, 35 mmHg; range, 20–85 mmHg), measured by a 5F or 6F diagnostic catheter, and a significant angiographic stenosis (median, 70%; range, 50%–80%). Non-invasive left arm blood pressure measured at the time of cardiac catheterisation was substantially lower than aortic pressure (> 20 mmHg difference in all patients). Retrograde flow up the LIMA graft during native left coronary angiography, a characteristic of subclavian steal, occurred in one of the five patients (Figure 1). All patients were treated with percutaneous stenting, using 9–10 mm balloon expandable stents, with successful abolition of the pressure gradient in the proximal subclavian artery (Figure 2). The difference in non-invasive blood pressures between the arms after stenting was less than 5 mmHg in all patients. All patients had relief of their angina symptoms over a median follow-up of 20 months (range, 5–29 months). 1 A: Subtracted angiogram showing the subclavian stenosis prior to the left internal mammary artery (LIMA) origin. B: Selective left coronary angiogram showing flow down the left anterior descending artery (LAD) (1) then retrograde up the LIMA (2 and 3). C: Diagram showing the relationship of the stenosis to the left vertebral and LIMA origins. 2: Angiograms of the left subclavian stenosis before (A) and after (B) stenting, showing the improvement in antegrade LIMA flow. The intra-arterial subclavian pressure tracings are shown below the angiograms. Before stenting (left) the pressure tracing is blunted, while after stenting (right), there is an improvement in blood pressure and normalisation of the arterial waveform. A potentially clinically significant stenosis in the subclavian or brachiocephalic arteries will produce a difference in systolic blood pressure between the right and left brachial arteries of 15–20 mmHg or more.1 Therefore, bilateral arm blood pressure measurements should be taken in symptomatic patients after coronary artery bypass using internal mammary artery grafts. Unfortunately, this simple non-invasive assessment is often overlooked, as it was in the patients reported here. A haphazard approach to catheterisation of the left internal mammary artery (LIMA) graft can also cause the diagnosis to be missed, as the catheter can often cross a significant subclavian stenosis. Meticulous comparison of the subclavian and aortic pressure tracings will identify the gradient and enable diagnosis. The difference in pressure between the arms may be reduced or absent in patients with significant bilateral subclavian and/or brachiocephalic disease, a scenario more likely in patients with extensive atherosclerotic peripheral vascular disease elsewhere.2 Coronary subclavian steal syndrome describes angina related to a subclavian stenosis with retrograde flow up the LIMA graft. This reverse LIMA flow results from lower vascular resistance and blood pressure in the arm compared with the myocardial territory supplied by the LIMA. However, steal with reverse LIMA flow is not an absolute requirement for angina. In our patients, none had angina precipitated by left arm activity that would uncover a latent steal syndrome. In many cases, subclavian stenosis behaves physiologically more like a very proximal LIMA stenosis. In this case, “LIMA-inflow syndrome” may be a more accurate term. Regardless of the semantics, this is a rare phenomenon that is reported in 0.1%–5.0% of patients after coronary artery bypass grafting.2-4 The differential diagnosis includes other diseases obstructing large arteries such as Takayasu’s arteritis (especially in young women), post-radiation arteritis, and giant cell arteritis (especially in older patients). The management of subclavian and brachiocephalic stenoses depends on the clinical presentation. All patients require medical therapy with intensive atherosclerosis risk factor reduction, as the 10-year total and cardiovascular mortality approaches 40%–50%.1 Asymptomatic individuals do not need intervention, so non-invasive imaging is unnecessary. In symptomatic patients, non-invasive imaging with contrast computed tomography or magnetic resonance or conventional angiography can confirm the diagnosis when an intervention is anticipated. Traditionally, symptomatic patients were treated with carotid-subclavian bypass. However, percutaneous angioplasty and stenting are increasingly used because of their lower morbidity and similar long-term results.2,5-8 The risk of stroke from stenting is low, and no higher than for surgical bypass.2,5-8 Post-procedural management includes treatment with aspirin for life and clopidogrel for at least 1 month. Clinical follow-up includes surveillance for recurrent symptoms with a difference in brachial blood pressures. Although the LIMA-inflow syndrome from subclavian stenosis is a rare cause of angina, it is easily identified non-invasively by comparing the brachial blood pressures in both arms. Advances in percutaneous stenting permit a relatively easy and durable treatment in a cardiac catheterisation laboratory. Lessons from practice Systolic blood pressure should be measured in both arms with a standard sphygmomanometer in all patients with past coronary artery bypass grafting and progressive angina or acute coronary syndromes. A difference in systolic blood pressure of greater than 15–20 mmHg between the right and left arms is strongly suggestive of subclavian stenosis. Asymptomatic subclavian stenosis does not require imaging or revascularisation, but does denote high cardiovascular risk warranting intensive risk factor reduction. Symptomatic subclavian stenosis can be successfully treated with percutaneous stenting.

Daniel Tsyvine MD · Maryanne Hartzell MD · Marc P Bonaca MD · Gerard Connors MB BS, FRACP · Scott Kinlay MB BS, PhD, FRACP

Supraventricular tachycardia (SVT) is a common cardiac rhythm disturbance; it usually presents with recurrent episodes of tachycardia, which often increase in frequency and severity with time. Although SVT is usually not life-threatening, many patients suffer recurrent symptoms that have a major impact on their quality of life. The uncertain and sporadic nature of episodes of tachycardia can cause considerable anxiety — many patients curtail their lifestyle as a result, and many prefer curative treatment. SVT often terminates before presentation, and episodes may be erroneously attributed to anxiety. Sudden-onset, rapid, regular palpitations characterise SVT and, in most patients, a diagnosis can be made with a high degree of certainty from patient history alone. Repeated attempts at electrocardiographic documentation of the arrhythmia may be unnecessary. Treatment of SVT may not be necessary when the episodes are infrequent and self-terminating, and produce minimal symptoms. When episodes of tachycardia occur frequently, are prolonged or are associated with symptoms that affect quality of life, catheter ablation is the first choice of treatment; it is a low-risk procedure with a high success rate. Long-term preventive pharmacotherapy is an alternative approach in some patients.

Caroline Medi BMed, FRACP · Jonathan M Kalman MB BS, PhD, FRACP · Saul B Freedman MB BS, PhD, FRACP

To the Editor: The author of “High levels of confusion for cholesterol awareness campaigns”1 identifies my comment as the source of her perplexity. My remark, which Hall quotes in relation to the “Test the Nation” campaign, was actually given in response to a question about the Pfizer-sponsored “National Cholesterol Awareness Campaign”, which ran simultaneously. It seemed too inconsequential to request correction of the relevant newspaper article,2 because public health guidelines differ in regard to the target population for lipid testing. My comment reflected conservative Australian guidelines.3 It is well known that other sources recommend more widespread testing of adults.4 Hall’s confusion was a rhetorical device to justify her discussion of “condition branding” and to “explore the motivations” of the campaigns. Hall’s article attacks two programs that promote diet and lifestyle management of cardiovascular risk. It also criticises pharmacological treatment, thus eliminating all available options to address this important problem. The article undermines the tenuous availability in Australia of plant sterol-containing products, such as yoghurt, but provides no alternative strategies. It fails to take responsibility for its potential negative impact on the implementation of nutritional and other life-saving interventions. It is disconcerting that such a negative article has emanated from a so-called Centre for Health Initiatives. The cholesterol awareness campaigns are likened to “an unnecessary focus on an unimportant health problem” and disparagingly compared with a program devoted to public awareness of fungal nail infections. Understandably, the latter led to professional irritation and frustration. By contrast, the formal involvement of the Royal Australian College of General Practitioners in the Test the Nation–National Cholesterol Education Program of Australia (NCEPA) represents an effort to ensure that the initiative was justified, that the content was relevant, and that the logistics were attuned to primary care practice. The participation of professional organisations reinforced the quality, relevance and independence of the information provided. The dietary advice that was distributed by the NCEPA was widely acclaimed. Dyslipidaemia accounts for 49% of the attributable risk of coronary heart disease.4 Full implementation of risk factor guidelines could massively reduce cardiovascular disease,5 but public and professional adherence to guidelines is suboptimal.6 Chen and colleagues report that, in addition to those with diabetes or coronary heart disease, over 700 000 Australians are at high risk,7 but most Australians are unaware of the consequences. It seems extraordinary that anyone with a professed interest in public health could be so opposed to public education about risk factor management. Consequently, Hall’s article itself generates further confusion. The health sector is in the process of responding to calls for greater independence from commercial interests. Both cholesterol programs illustrate the implementation of many of the suggested changes. Unfortunately, Hall’s article suggests an open-ended list of demands that will be impossible to satisfy. Calls for further change need to be more constructive and clearly enunciate realistic proposals, supported by evidence that the net impact on Australian health care has been (or will be) beneficial. The article implies restrictions that would be impractical in other sectors. Standards for the interaction between industry and the health sector should be an example to emulate, rather than a soft target that loses step with normal practice.

David R Sullivan