Cardiovascular diseases

The concept of “first-responder” defibrillation is not being embraced The article in this issue of the Journal by Finn and Jacobs (page 470)1 challenges our professions to find better ways of dealing with sudden unexpected cardiac arrest in the nation’s hospitals — that is, in those places which should be best able to deal with it. Nurses, with a nursing perspective, wrote the article. It underscores the important role played by nurses, and the problem that needs to be addressed by nurses through their influence within our hospitals. Australia played a major role in initiating coronary care wards for managing ventricular fibrillation (VF) in the early stage of myocardial infarction, through the work of Desmond Julian at Sydney Hospital2 and Graeme Sloman at Royal Melbourne Hospital3 during 1961 and 1962. While now taken for granted, one is apt to forget how controversial this development initially was, and how poor the initial results were until nurses were permitted to use defibrillators and so shorten the time from cardiac arrest to termination of VF. At the time, physicians claimed the high ground — defibrillators were too dangerous to be entrusted to nurses — ignoring the fact that the first article on successful use of external defibrillators was written in 1960 by two engineers and one surgeon.4 Fortunately, reason and logic triumphed, and defibrillation became the most important priority for coronary care unit and intensive care unit nurses, with a doctor being summoned concurrently, and usually arriving in time to document return of consciousness and plan ongoing management. Such pioneering work was followed by the development of automatic internal and external defibrillators (AIDs and AEDs, respectively). These are able to sense and interpret VF, and will operate and deliver a shock only if VF is present. They are small and ubiquitous. The US Vice-President, Dick Cheney, has an implanted AID. Indeed, the man who is “a heartbeat behind” the world’s most powerful man is himself “a heartbeat behind” (obviously a number of heartbeats behind) the scrutiny of an automatic implanted defibrillator. Implantation is one mode of use for defibrillators in people at high personal risk of VF. Another mode is public access defibrillation, where AEDs are placed in public places, like fire extinguishers, for use by minimally trained or untrained people, who apply chest pads to an unconscious person and respond to voice prompts delivered by the device. Providing such devices in Chicago’s airport complexes (Box) has resulted in long-term, neurologically intact survival of 56% of sudden cardiac arrest victims, compared with no cases of neurologically intact survival before the devices were made available.5 One of us (C S D) is responsible for a national program,6 in which nearly 700 defibrillators have been installed in airports, train stations, and other busy public places across England. Early results suggest that 29 people have survived to hospital discharge after sudden cardiac arrest. The downside has been minimal, with no injury from use, and virtually no theft, misuse or vandalism. Other highly favourable experiences involving police and the community have recently been reported.7,8 What relevance does the community experience have for Australian hospitals? Finn and Jacobs have identified a number of anomalies. Certainly, AEDs are now available in many Australian hospitals, so that training for nurses in their use is easier, less formidable, and less costly. But most Australian hospitals (57%) still do not have these devices. In hospitals with any kind of defibrillator, 16% in Australia do not permit nurses to defibrillate; in those with AEDs, this figure is 9%. This practice persists despite the knowledge that survival decreases by 10% for each minute that passes after onset of VF until defibrillation is achieved — automatically by an implanted defibrillator, or with manual intervention after placement of pads by doctor, nurse — by anyone. It matters not who places the pads and pushes the button, but hospital procedures are often based on the view that it does. The outcome, demonstrated by hospital, national and published data, is that cardiac arrest is more successfully treated in Chicago or Heathrow airport, on an American Airlines or Qantas jet, or in a Boston post office, than in the vestibules, corridors or general wards of Australia’s premier hospitals. An example of the existing problem is shown in the Box, which contrasts the well signed, alarmed, and easily accessible defibrillator at O’Hare Airport with the unsigned, unalarmed, padlocked defibrillator in the corridor of a major Australian hospital. Providing a defibrillator in such a way is a contemptuous gesture to modern knowledge, and to pronouncements of the Australian Resuscitation Council, as described by Finn and Jacobs. This “AED in a cage” symbolises the problems exposed by Finn and Jacobs,1 and illustrates the 1960s view — that defibrillation is the preserve of the enlightened few with access to the key. We are not overly concerned with the issue raised by Finn and Jacobs in relation to CPR training for medical staff. Their survey was sent to directors of nursing and the replies reflect the nursing perspective, which may not include full knowledge of medical staff activities. Medical practitioners usually prefer to train themselves in resuscitation, and there are surely few who cannot initiate CPR or use a defibrillator, so the number of hospitals identified as offering CPR training to doctors may not be important. We are delighted to see how many hospitals train lay staff in resuscitation. Hopefully, the future will see more communication between doctors, nurses and lay staff at hospitals where issues of “turf”, keys, and locked cages can be resolved, and where the chain of survival can be initiated expeditiously wherever and whenever the need arises. Forty years ago, the Australian hospital system was slow to pick up on the inspirational but logical initiative of Julian, Gaston Bauer (who recruited Julian to Sydney Hospital and encouraged subsequent developments) and Sloman. It remains slow in throwing off the shackles of officialdom. Finn and Jacobs are to be complimented on their fine work. Two approaches to providing automatic external defibrillators (AEDs) One of the many AEDs deployed along a concourse of Chicago’s O’Hare Airport. The device is clearly signposted (not seen in picture), alarmed, and connected by automatic phone to the emergency medical centre. AED in a corridor of a major Australian hospital. There is no signposting, the case is locked and no advice is given on the location of the key.

Michael F O’Rourke AM, MD, FRACP · C Siân Davies MBE, RN

Objective:To describe the policy and practice relating to cardiopulmonary resuscitation (CPR) and defibrillation in cardiac arrest in Australian hospitals.Design:Cross-sectional postal survey conducted in December 2001, using a semi-structured, four-page questionnaire.Participants:Australian hospitals with more than 10 beds.Main outcome measures:Type of defibrillator; provision of CPR/defibrillation training for healthcare professionals; hospital policy as to who can use the defibrillator.Results:Of the 878 hospitals surveyed, 665 (76%) responded. All but one hospital indicated that CPR training was provided for nursing staff, with 12-monthly or more frequent updates; only 55% of hospitals (366) indicated that CPR training was provided for doctors. 21 of the 665 responding hospitals (3.2%) indicated that they did not have a defibrillator. 43% of hospitals had one or more defibrillators with shock advisory capacity (ie, automated external defibrillators [AEDs]). Of the 644 hospitals with defibrillators, 16% (101) indicated that registered nurses were not permitted to defibrillate; this included 9% of hospitals with AEDs.Conclusions:The importance of CPR in cardiac arrest has been accepted by Australian hospitals, but the overwhelming evidence that “time to defibrillation” is the single most important determinant of cardiac arrest outcome seems less accepted. All Australian hospitals should review their resuscitation policies and practices to reflect this fact, with defibrillation by nurses, who are usually first on the scene, providing the best opportunity to minimise time to defibrillation.

Judith C Finn PhD, RN · Ian G Jacobs PhD, RN

Clinical recordA 71-year-old white woman presented with increased shortness of breath over a 6-day period, followed by acute onset of severe back and interscapular pain. Her past medical history consisted of hypertension, type 2 diabetes, and a distant history of alveolar-cell carcinoma of the lung, with right lower lobectomy in 1974. Physical examination revealed an obese lady weighing 95 kg, with a blood pressure of 80/40 mmHg, pulse 110/min, and a respiratory rate of 36/min. The patient was afebrile, diaphoretic and restless. Her venous pressure was elevated. Chest examination showed reduced breath sounds at both lung bases. Heart sounds were dual with no murmurs. Electrocardiography showed sinus tachycardia, 110/min with an S wave in lead I, a Q wave in limb lead III, and T-wave inversion in limb lead III. Arterial blood analysis (inspired oxygen content of 21%) showed pH, 7.156; Pao2, 61 mmHg; Paco2, 52 mmHg; Sao2, 83%. The patient’s chest x-ray showed a widened mediastinum on a mobile supine film, and previous right lower lobectomy. The provisional diagnosis was aortic dissection. The patient was intubated and ventilated in the emergency room, then taken to the intensive care unit, where she was resuscitated with intravenous fluids (both crystalloid and colloid) and an infusion of adrenaline. Transoesophageal echocardiography showed a small left ventricle with hyperdynamic systolic function. The right ventricle was dilated, with poor systolic function. There was grade 2/4 tricuspid regurgitation, with an estimated right ventricular systolic pressure of 60 mmHg. There was grade 3/4 mitral regurgitation secondary to systolic anterior motion of the anterior mitral leaflet, and dynamic left ventricular outflow tract obstruction with a maximum gradient of 90 mmHg. Significant thrombus was seen in the proximal right and left pulmonary arteries (Box 1A). There was no evidence of aortic dissection and no pericardial effusion. Other laboratory results included elevated D dimer level of 2.93 mg/L (normal, < 0.28 mg/L), with normal serum creatine kinase and cardiac troponin I levels. The patient was given 7000 U of unfractionated heparin and thrombolysis with 40 mg of intravenous tenecteplase administered twice, but she remained profoundly hypotensive (BP, 78/47 mmHg). Surgical embolectomy was considered, but was declined due to the recently administered thrombolysis. A decision was made to take the patient to the cardiac catheterisation laboratory for an attempt at mechanical intervention. While the laboratory was being prepared, a pulmonary artery flotation catheter was passed from the right internal jugular vein into the main pulmonary artery. This resulted in significant clearance of the “saddle” embolism from the main pulmonary artery, as determined by transoesophageal echocardiography. The time from administration of thrombolysis to commencement of the interventional procedure was 55 minutes. The activated clotting time, measured when femoral access was obtained, was 352 seconds. The main pulmonary artery was accessed via the right femoral vein with a multipurpose catheter. As a rheolytic thrombectomy catheter and other commercial devices were not available, an Amplatz 0.035" wire was used to remove the multipurpose catheter and insert a 7 Fr long sheath and a pigtail catheter. With the pigtail catheter, the embolism was mechanically cleared from the main pulmonary artery. A pulmonary angiogram then showed extensive embolism in the left main pulmonary artery, extending into several lower lobe segmental arteries (Box 1B). The pigtail catheter was used to macerate this embolism. Once some blood flow had been restored, a snare was then made using an 0.025" wire, but attempts to snare the clot were not successful — the clot was pushed further into the segmental arteries. Nevertheless, fragmentation of the embolism and clearance of the main pulmonary artery and left pulmonary artery was achieved. A multipurpose catheter was then passed to the right pulmonary artery and the stiff wire was used to remove the multipurpose catheter and insert the 7 Fr long sheath and a pigtail catheter. Pulmonary angiography of the right lung showed the right main pulmonary artery to be clear of thrombus, which had lodged in the right segmental branches. At the completion of the intervention, the systemic blood pressure had stabilised (90/54 mmHg) and the pulmonary pressures were only moderately elevated (44/24 mmHg). Angiography showed that blood flow through the lungs had improved. Anticoagulation was continued with intravenous unfractionated heparin. The activated partial thromboplastin time 4 hours after the intervention was > 250 seconds. The following day the patient was extubated and discharged to the ward. Her dyspnoea and mobility gradually improved, and she was started on warfarin. Four days after the procedure, transthoracic echocardiography showed the right ventricle to be at the upper limit of normal in size, with normal systolic function. The right ventricular systolic pressure was estimated at 62 mmHg. Acute major pulmonary embolism is associated with right ventricular dysfunction and shock.1 This condition is frequently lethal, despite thrombolysis.1,2 Adjunctive catheter fragmentation may prevent death.1-3 However, commercial systems for fragmentation of thromboembolic material are not widely available, and reported experience with these techniques is limited. In cases of major pulmonary embolism, patients are at serious risk of death due to right ventricular failure within the first hour of onset.4 Survival depends on rapid recanalisation of the pulmonary arterial occlusion and reduction of the right ventricular afterload. According to the results from a multicentre registry, overall in-hospital mortality rate ranges from 25% for patients presenting with cardiogenic shock to 65% for patients undergoing cardiopulmonary resuscitation.2 Thrombolytic therapy is a useful adjunct to heparin in patients who have pulmonary embolism and who are haemodynamically unstable.5 Rapid improvement of right ventricular function and pulmonary perfusion, accomplished with thrombolytic therapy followed by heparin, may lead to a lower rate of death and recurrent pulmonary embolism.1,5 However, in severe cases, even high-dose thrombolytic therapy may not prevent death.2 Transvenous catheter embolectomy or open surgical embolectomy should be considered in patients for whom thrombolysis is contra-indicated or deemed unsuccessful.3,6 Greenfield et al introduced the first percutaneous catheter thrombectomy device, an aspiration catheter, in 1969.7 There are currently several catheter thrombectomy techniques: aspiration thrombectomy, fragmentation thrombectomy, and rheolytic thrombectomy.3,6-8 However, the commercial devices used in these procedures are not widely available, and there is limited experience reported with any of these techniques. This type of procedure is typically confined to major interventional laboratories with experienced operators. There are several reports of successful fragmentation of pulmonary emboli with improvised equipment in patients with shock.9 Our case is of particular interest, as thrombolysis had failed to improve the patient’s immediate clinical state. The use of a pulmonary flotation catheter to dislodge the embolism from the main pulmonary artery proved to be a useful temporising measure. This type of catheter is easily passed without the need for fluoroscopic control. In this situation, transoesophageal echocardiography proved pivotal in diagnosing the embolism rapidly, and in monitoring the response to therapeutic manoeuvres.10 Movement of the embolism from the main pulmonary artery was visualised in real time, which may be better achieved with transoesophageal rather than transthoracic imaging. Further mechanical fragmentation could then be achieved in the catheterisation laboratory. The technique consists of fragmentation of central emboli and dislocation of the fragments to the periphery, resulting in a relative gain of non-obstructed, cross-sectional artery area. Moreover, the increased total surface area of the fragments may ac-celerate the efficacy of concurrent thrombolysis. In summary, for patients with major pulmonary embolism for whom thrombolysis is contraindicated or unsuccessful, the passage of a pulmonary flotation catheter and improvised catheter fragmentation of thrombus may be considered if there is suitable access to an interventional laboratory and an experienced interventionist. Lessons from practice Transoesophageal echocardiography, although more invasive and technically more demanding than transthoracic echocardiography, can be very useful for diagnosing pulmonary embolism. It also provides valuable information about prognosis and response to therapy. Mechanical fragmentation and dispersion of embolism can be a successful adjunctive strategy for treating massive pulmonary embolism when response to thrombolysis is suboptimal. Mechanical fragmentation and dispersion of embolism can be achieved with improvised equipment that is available in most interventional catheterisation laboratories. Images of the embolism A: Pulmonary “saddle” embolism situated in the proximal main pulmonary artery, as shown by transoesophageal echocardiography. B: Pulmonary angiography, showing the fragmented embolism that was dispersed to the segmental pulmonary arteries.

Warong Lapanun MD, FRCPT · Darren L Walters MB BS, FRACP · John McCarthy MB BS, FJFICM · Darryl J Burstow MB BS, FRACP

Heart failure prevalence is increasing because of the ageing of the population and the longer survival of people experiencing myocardial infarction and heart failure. The lifetime risk of developing heart failure in Western countries is about 20%. The increasing prevalence of overweight, obesity and diabetes is likely to accelerate heart failure incidence. While there have been major advances in treating heart failure, a preventive approach promises greater benefit to a larger proportion of the community. The medical strategy for heart failure prevention, based on calculation of individual risk, is focused on the minority of individuals who exceed an arbitrary risk threshold. A public health strategy targeting the whole population offers a greater prospect of reducing the incidence of heart failure and other cardiovascular disease. A multitiered approach, encompassing environmental determinants of lifestyle, legislation, and education about healthy lifestyles throughout life, in addition to aggressive control of risk factors in high-risk individuals, is likely to have the greatest impact.

Duncan J Campbell FRACP, PhD

Ian G Jacobs,* James Tibballs,† Peter T Morley,† Jennifer Dennett,‡ Jeff Wassertheil,§ Vic Callanan,¶ John Hall** (ARC executive committee on behalf of the Australian Resuscitation Council) * Chairman, Australian Resuscitation Council, C/- Royal Australasian College of Surgeons, Spring Street, Melbourne, VIC 3000; † Physician, Intensive Care Unit, Royal Children’s Hospital, Melbourne, VIC; ‡ Nurse Unit Manager, Central Gippsland Health Service, Sale, VIC; § Director of Emergency Medicine, Peninsula Health, Frankston, VIC; ¶ Head, Anaesthesia, Townsville Hospital, Townsville, QLD; ** Superintendent, Divisional Office, Ambulance Service of NSW, Hurstville, NSW. ijacobsATcyllene.uwa.edu.au To the Editor: With the increasing availability of biphasic defibrillators for use in both the manual and shock-advisory modes, considerable confusion has developed as to the appropriate energy levels to be used with these devices. This confusion has arisen partly because of differing recommendations from manufacturers, partly as a result of limited clinical evidence and partly because of the clinical availability of both monophasic and biphasic defibrillators. The differences between these waveforms are the way energy is delivered. Biphasic energy is delivered in two directions, whereas monophasic energies are delivered in one direction. Recommendations of the International Liaison Committee on Resuscitation state that biphasic energies less than or equal to 200 J are as efficacious as escalating higher-energy monophasic shocks.1 Lower-energy biphasic shocks cause less myocardial injury and postresuscitation myocardial dysfunction, and so potentially improve the likelihood of survival.2 Faced with the lack of data with respect to biphasic energy levels, the Australian Resuscitation Council makes the following recommendations: 1. When using manual biphasic defibrillators, energy levels of 150 J should be used for defibrillating ventricular fibrillation and pulseless ventricular tachycardia in adults. The basis of this recommendation is as follows: one randomised controlled trial in people in out-of-hospital ventricular fibrillation compared monophasic and biphasic shocks delivered by automated external defibrillators (AEDs).3,4 This study showed that 150 J biphasic shocks achieved higher rates of defibrillation and return of spontaneous circulation than higher-energy (200 J/200 J/360 J) escalating monophasic shocks. No differences were observed in the proportion of patients discharged from hospital. As clinical superiority of one particular biphasic waveform over another has yet to be demonstrated, it is appropriate to recommend this single energy level to achieve a consistent approach. 2. Biphasic energy levels of 1–2 J/kg should be used for defibrillating ventricular fibrillation and pulseless ventricular tachycardia in children. The basis of this recommendation is as follows: extrapolation from adult data, supported by studies in “child” and “infant” animal models, suggests that the dose for biphasic shocks in children should be 1–2 J/kg (about half the monophasic dose). Higher doses (up to 4 J/kg) are not likely to be harmful and are more efficacious than equivalent monophasic shocks.5 Biphasic shocks may be delivered in a fixed dose of 50 J by an AED. The use of AEDs in children less than 1 year of age is not recommended, as in this situation these devices are unable to differentiate between shock-able and non-shockable rhythms (eg, ventricular fibrillation v pulseless electrical activity). Energy levels for AEDs when used in automatic mode have been pre-set by the manufacturer, and do not require an energy level to be set by the user.

Ian G Jacobs · James Tibballs · Peter T Morley · Jennifer Dennett · Jeff Wassertheil · Vic Callanan · John Hall

Referrals should be offered to all patients, and the individual needs of each patient considered Cardiac rehabilitation has progressed markedly since it was introduced into Australia by the National Heart Foundation in 1961. At that time, the focus was on restoration of a sense of wellbeing and encouraging return to work for survivors of acute myocardial infarction and other cardiac illness. The first cardiac rehabilitation programs in Europe and the United States involved mainly supervised, high-intensity exercise training with electrocardiographic monitoring. As data accumulated that similar benefits could be achieved from low, moderate and high levels of exercise intensity,1,2 an Australian hospital model evolved, based on group light exercise and patient education.3 Recognition that psychosocial factors (rather than heart disease) were the main causes of disability after a myocardial infarction led to greater emphasis on counselling, education and support. This led, in turn, to the development of a multidisciplinary team approach to cardiac rehabilitation, with the aim of focusing on and dealing with the range of factors influencing patients’ quality of life. As evidence from large clinical trials emerged showing that modifying risk factors through both pharmacological interventions and lifestyle change could significantly reduce mortality and morbidity, the aims of cardiac rehabilitation broadened to include preventing progression of cardiovascular disease. . . . a majority of eligible Australians are failing to achieve the potential gains available from our network of outpatient cardiac rehabilitation programs. By 1986, cardiac rehabilitation had advanced sufficiently for it to be seen as an important component of cardiac care. Dr William A Seldon, a cardiologist at St Vincent’s Hospital, Sydney, and the first Director of the National Heart Foundation Cardiac Rehabilitation Centre in Sydney, wrote in the Journal: It is not difficult to envisage that a failure to provide cardiac rehabilitation services to patients with myocardial infarction will be regarded as medical negligence in the not too distant future.4 Since then, there has been a progressive increase in the provision of such services throughout Australia. The National Heart Foundation’s 2001 Directory of Australian cardiac rehabilitation programs5 lists 265 hospital- and community-based out-patient programs, compared with only 26 in 1985.6 The growth and development of these programs in Australia over the past two decades has occurred alongside the publication of several evidence-based guidelines summarising the benefits of structured cardiac rehabilitation and secondary prevention programs.7-9 Defined benefits include reduced mortality and reduced risk of further cardiac events; improvements in physical and social functioning, risk factor profiles and quality of life; and reduced prevalence of depression. Despite the convincing evidence and the increased availability of cardiac rehabilitation programs, the report by Scott et al10 in this issue of the Journal (page 341) highlights suboptimal rates of referral to and utilisation of outpatient cardiac rehabilitation programs in Queensland: 29% of patients with cardiac diagnoses discharged from participating hospitals were referred to an outpatient cardiac rehabilitation program, while 49% of discharged patients were eligible for such a referral. Fewer than a third of patients referred completed the program. It was estimated that only 40% of available outpatient cardiac rehabilitation program places were fully utilised. Similarly, a study of data from the NSW Hunter Region Heart and Stroke Register11 identified that only 39% of the patients on the register who were eligible for outpatient cardiac rehabilitation were invited to attend. This figure is likely to be an overestimate, as only 62% of all discharged patients consented to be on the register. It is clear that a majority of eligible Australians are failing to achieve the potential gains available from our network of outpatient cardiac rehabilitation programs. This distressing failure reflects both a lack of initial referrals and a failure of patients to attend, despite having been referred. Key factors contributing to these deficiencies include the following: data have not been collected to establish cardiovascular health indicators for monitoring the proportion of patients entering and completing a cardiac rehabilitation program;12 routine referral, although recommended in Australia,8 is not standard practice; cardiac rehabilitation programs are not available or accessible to all patients, especially those in rural and remote areas;12 and cardiac rehabilitation programs are not sufficiently accessible and attractive to certain population groups, such as Indigenous people, older women, those unable to speak English, and the indigent.12 What strategies can be implemented to address these issues? System factors resulting in failure of referral should be investigated and rectified. It is well known that discharge planning and linkages between hospitals and primary care services are often poor or non-existent. In addition, the attitude of the treating physician is a major predictor of patient non-participation in cardiac rehabilitation.13 Scott et al found that patients having coronary revascularisation procedures were more likely to attend rehabilitation programs than those with acute coronary syndromes.10 Is it that some patients perceive a greater need for rehabilitation programs as part of the recovery process and that this need is also appreciated by their key healthcare providers? Patient “denial” of severity of illness and a history of depression have both been found to be significant predictors of participation,13 and may also account for the varying participation rates by diagnosis or procedure. Patient preferences for different program models and methods of delivery should be canvassed. Referrals should be offered to all patients, and the individual needs of each patient considered. Medical practitioners and healthcare authorities need to understand and accept that not all patients’ needs can be met by so-called “usual” medical care.

Stephen J Bunker PhD, RN · Alan J Goble MD, FRACP, FRCP

Objectives: To determine patient participation rates in outpatient cardiac rehabilitation (OCR) programs; ascertain the barriers to participation; and evaluate the quality of OCR programs. Design and setting: Retrospective cohort study of patient separations from selected public and private Queensland hospitals; questionnaire survey of hospitals and all registered OCR programs. Participants: Patients discharged with cardiac diagnoses between 1 July 1999 and 30 June 2000 from 31 hospitals (24 public; 7 private). Main outcome measures: Rates of referral of hospitalised patients to OCR programs; rates of program attendance and completion; barriers to OCR referral and attendance. Results: 15 186 patients were discharged with cardiac diagnoses from participating hospitals, of whom 4346 (29%) were referred to an OCR program after discharge, compared with an estimated 59% (8895/15 186) of patients who were eligible for such a program. Proportionately more patients were referred from secondary (38% [1720/4500]) and private (52% [2116/4031]; P < 0.001) hospitals than from tertiary (25% [2626/10 686]) and public (20% [2230/11 155]) hospitals. Patients undergoing coronary revascularisation procedures comprised 35% of discharges, but accounted for 56% of all program attendances. Fewer than a third of all referred patients completed OCR programs, and only 39% of available OCR program places were fully utilised. Catchment populations of programs with unused places had excess coronary mortality. Conclusion: There is significant underutilisation of facility-based OCR programs in Queensland. Procedures are required for identifying and referring eligible patients to existing programs and improving program compliance. Alternative OCR models are also required.

Ian A Scott FRACP, MHA, MEd · Kylie A Lindsay BN, GradCertManag · Hazel E Harden BSc

The foundation of treatment for patients with hypertension is ongoing use of lifestyle measures such as physical exercise, weight reduction, and salt restriction. There should be emphasis on reduction of total cardiovascular risk, including smoking cessation and achievement of goal blood pressures. There are now five classes of first-line blood-pressure-lowering drugs — diuretics, β-blockers, angiotensin-converting enzyme inhibitors, angiotensin receptor blockers and calcium antagonists. In most patients, the choice of drug will be guided by the clinical situation in the individual patient, including the presence of target organ damage, diabetes, established vascular or kidney disease, or other comorbidities. In the absence of such clinical indications, start drug therapy with a low-dose diuretic. Combination therapy will be needed in around two-thirds of patients, and a diuretic will normally form one element of most combinations, with the second or third drug coming from among the remaining four. Consider the use of fixed-dose combinations to improve adherence to therapy. Use long-acting, once-daily preparations.

John P Chalmers MD, FRACP · Leonard F Arnolda PhD, FRACP

Keith V Woollard Cardiologist, 34 Murdoch Drive, Murdoch, WA 6015. KeithWoollardATwacardiology.com.au To the Editor: The recent review of digoxin by Campbell and MacDonald1 pointed out that a serum digoxin level of over 1.0 ng/mL is associated with excess mortality. Indeed, higher blood levels (≥ 1.2 ng/mL) are associated with higher crude rates for all-cause hospitalisation, and for increased hospitalisation for worsening heart failure or suspected digoxin toxicity.2 The post hoc analysis of the DIG trial2 suggests that the optimal range is 0.5–0.8 ng/mL. I recently surveyed 31 private pathology laboratories across Australia to determine their recommendations about the therapeutic range of serum levels of digoxin. In summary, their recommendations ranged from a lower limit between 0.5 ng/mL and 1.0 ng/mL, and an upper limit between 1.6 ng/mL and 2.1 ng/mL. Twenty-six of the 31 suggested that values below 0.8 ng/mL were subtherapeutic. It is likely that many doctors will heed such advice and inappropriately increase the dose of digoxin in patients being treated for heart failure. It is possible that adverse effects will flow from current laboratory industry recommendations, and these should be revised.

Keith V Woollard

Objective: To measure the prevalence of untreated hypertension in Australian adults, and examine the associations with clinical and lifestyle factors.Design: AusDiab, a cross-sectional survey conducted between May 1999 and December 2000, involved participants from 42 randomly selected census districts throughout Australia.Participants: Of 20 347 eligible people aged ≥ 25 years who completed a household interview, 11 247 attended a physical examination (response rate, 55%).Main outcome measures: The prevalence of hypertension (blood pressure ≥ 140/90 mmHg or self-reported use of antihypertensive drugs) and its treatment; associations of clinical and lifestyle factors with the treatment of hypertension; and adequacy of treatment for primary and secondary prevention of cardiovascular disease.Results: The prevalence of hypertension was 28.6 per 100 (95% CI, 25.0–32.3), and the prevalence of untreated hypertension was 15.2 per 100 (95% CI, 13.2–17.2). Of those with untreated hypertension, 80.8% (95% CI, 74.7%–85.0%) had had a blood pressure check within the preceding 12 months. At least one modifiable lifestyle factor was present in 71.7% (95% CI, 68.5%–74.8%) of participants with untreated hypertension. Although lower risk clinical characteristics of younger age and lack of hyperlipidaemia were independently associated with untreated hypertension, 53.5% warranted treatment based on current cardiovascular disease prevention guidelines and multivariable absolute risk assessment.Conclusions: Considerable scope remains for reducing the burden of cardiovascular disease through lifestyle modification and rational treatment of hypertension.

Esther M Briganti MB BS, MClinEpi · John J McNeil MB BS, PhD · Jonathan E Shaw MD · Paul Z Zimmet MB BS, PhD · Steven J Chadban MB BS, PhD · Robert C Atkins MB BS, DSc · Timothy A Welborn MB BS, PhD

Objective: To describe the results of a program for detecting high cardiovascular risk in an urban Aboriginal community.Design: Cardiovascular risk assessment program conducted between January 1998 and October 1999. Participants completed a questionnaire and underwent a physical assessment and biochemical tests.Participants: 738 self-selected members of the Perth Aboriginal community (332 men, 406 women; age range, 18–79 years).Results: The participants represented approximately a fifth of the Perth Aboriginal population aged 25–64 years (those aged 18–24 years comprised < 5% of Aboriginals aged 15–24 years in Perth). Eighty-four per cent fell within National Heart Foundation “high risk” or “highest risk” categories for cardiovascular disease; 15% of men and 6% of women had an absolute risk of a cardiovascular event of over 15% within 10 years. A high proportion of participants reported diabetes, hypertension, smoking, overweight and obesity. A fasting plasma glucose level indicative of diabetes or impaired fasting glucose was found in 8.6% (95% CI, 6.2%–11%) of people not previously known to have diabetes. Obesity and smoking were twice as prevalent in study participants as in the general population. Less than a third of subjects with hypertension and diabetes had attained recommended target levels for blood pressure reduction or glycaemic control, and only a third of those at high risk and one in six of those at highest risk had attained recommended lipid-level targets.Conclusions: A cardiovascular risk assessment program with strong community support in an urban Aboriginal population can identify a significant number of people with high cardiovascular risk who are candidates for intensive risk-factor reduction strategies.

Peter L Thompson MD, FRACP · Pamela J Bradshaw RN, MSc · Margherita Veroni MSc · Edward T Wilkes BA

Secondary prevention Aspirin provides benefit in nearly all groups of patients with clinical manifestations of coronary heart disease. This includes patients with evolving acute myocardial infarction or after recovery from myocardial infarction, with unstable or stable angina, and those who undergo coronary artery bypass grafting or coronary angioplasty. Aspirin provides benefit in patients with peripheral arterial disease. This includes patients with acute or previous history of ischaemic stroke or transient ischaemic attack, those with lower limb arterial insufficiency, and those who undergo grafting or angioplasty of peripheral arterial vessels. Primary prevention People without symptoms but at increased risk of a coronary heart disease event (> 1% annual risk) may reduce this risk by taking low-dose aspirin. However, the decision to take aspirin requires detailed consideration of individual cardiovascular risk and the potential benefit versus harm of treatment, particularly bleeding. Aspirin should only be used to prevent a cardiovascular event in association with an overall program of lifestyle measures including healthy eating, cessation of smoking, control of blood pressure and regular physical activity. Aspirin for prevention Prevention benefits of aspirin in heart disease can be achieved with doses as low as 75–150 mg daily. Unwanted effects of aspirin include stomach upsets, activation of peptic ulcers, an increased tendency to bruising, allergic reactions and increased risk of major gastrointestinal and other bleeding, including intracranial haemorrhage. In general, the risk of bleeding increases with increasing dose of aspirin and when it is used in combination with non-steroidal anti-inflammatory drugs or oral anticoagulants.

for the Medical Issues Committee of the National Heart Foundation of Australia

Risk factors and diseases in developing countries are becoming "westernised" Cardiovascular disease is usually considered to be the scourge of wealthy countries. However, the recent World health report1 draws attention to the increasing importance of cardiovascular disease in developing countries. The report identifies principal risk factors and diseases in regions of the world divided into three categories: developed countries, developing countries with low mortality rates, and developing countries with high mortality rates. It is no surprise that the leading risk factors contributing to disease, disability and death in developed countries are tobacco consumption, high blood pressure, high cholesterol level, overweight, low fruit and vegetable intake, and physical inactivity (Box 1). Coronary heart disease is the leading cause of death and disability, and stroke ranks third. In developing countries with high mortality rates (eg, Nepal, Myanmar, the Maldives and numerous African countries), factors such as underweight and unsafe sexual practice are more important than risk factors for non-communicable diseases. Nevertheless, tobacco consumption, high blood pressure and high cholesterol levels are still responsible for substantial morbidity and mortality (Box 1). The five leading causes of death and disability in these countries are HIV/AIDS, lower respiratory tract infections, diarrhoeal diseases, childhood diseases and low birthweight — coronary heart disease ranks eighth. Countries between these two extremes have rapidly changing profiles. In these low-mortality developing countries (eg, Cambodia, China, and Fiji), "developed country" factors have already outstripped traditional "developing country" factors in terms of importance for overall disease, disability and death (Box 1). In these countries, the juxtaposition of underweight with overweight as the fourth and fifth leading risk factors, respectively, starkly exemplifies the "double burden of disease" they carry. Following an upsurge in "developed country" risk factors in these countries, stroke is now the second most important cause of disability and death, and coronary heart disease the sixth. Unfortunately, the health services of low-mortality developing countries have not been able to adjust quickly enough to these changing disease profiles. The lack of epidemiological data on diseases and risk factors has hampered appropriate health service development and responses. A number of Australian organisations, including the Institute for International Health (IIH) at the University of Sydney,2 are trying to address these issues, with a focus on our neighbours in Asia and the Pacific region. The IIH has recently introduced initiatives, involving data collection and analysis, as well as technology transfer and capacity development, with partners in China, India and Thailand.3,4 The IIH has also worked with Asia–Pacific partners in multicentre trials and epidemiological studies, including the Asia Pacific Cohort Studies Collaboration (APCSC). The APCSC is a collaborative project that seeks to pool data from existing longitudinal studies with information on cardiovascular disease in the region. The project database now has data on 659 000 adults in eight countries (Box 2), making it one of the largest medical studies ever, and certainly the largest in the Asia–Pacific region. The collaboration aims to produce reliable regional estimates of the excess risks for coronary heart disease, stroke, total cardiovascular disease and all-cause mortality associated with a number of risk factors, and to accurately compare risk-factor associations between ethnic groups, age-specific groups and the sexes. After several years of compiling data, obtaining cooperation of key individuals and devising appropriate methodology, initial reports from the APCSC have begun to appear.5-7 These reports underline the increasing importance of cardiovascular disease in the less developed parts of the region, and show that the risk factors applicable in Australia are just as important elsewhere. This is a crucial finding that has not previously been established with large numbers. For instance, the analyses show that people with diabetes are about twice as likely to die from heart disease or stroke, regardless of whether they live in Asia or Australasia.5 Increasing levels of obesity across the region will lead to a considerable increase in diabetes and its sequelae, such as cardiovascular disease. Further, the research shows that younger people with diabetes have much larger excess risks for cardiovascular disease than older people. Asia, with its predominantly young population, can thus expect an even greater increase in cardiovascular disease than that anticipated in Australia. The challenge now is to use the results from the APCSC, and other relevant studies, as a starting point for tackling the global problem of cardiovascular disease highlighted by the World health report.1 In developing countries, substantial health gains can be made for relatively modest expenditures. In human terms, this means that much ill-health and millions of premature deaths can be avoided. As far as cardiovascular disease is concerned, a necessary step will be to develop accurate risk algorithms, specific to local situations.8 These algorithms would help in developing treatment and prevention strategies to target overall risk. For example, strategies to reduce salt intake and lower cholesterol level have been shown to be very cost-effective.1 Blood-pressure-lowering drugs are likely to benefit not only people with hypertension, but also normotensive people at high risk of cardiovascular disease.9 The ultimate aim will be to develop strategies with maximum benefit for minimum cost. This is especially the case in developing countries, where the conflicting demands on a meagre pool of resources make the need for cheap, finely-targeted strategies absolutely crucial. 1: The 10 leading selected risk factors for death and disability, by type of country1 High-mortality developing countries Low-mortality developing countries Developed countries 1 Underweight Alcohol consumption Tobacco consumption 2 Unsafe sexual practices High blood pressure High blood pressure 3 Unsafe water, poor sanitation and poor hygiene Tobacco consumption Alcohol consumption 4 Indoor smoke from solid fuels Underweight High cholesterol level 5 Zinc deficiency Overweight Overweight 6 Iron deficiency High cholesterol level Low fruit and vegetable intake 7 Vitamin A deficiency Low fruit and vegetable intake Physical inactivity 8 High blood pressure Indoor smoke from solid fuels Illicit drug use 9 Tobacco consumption Iron deficiency Unsafe sexual practices 10 High cholesterol level Unsafe water, poor sanitation and poor hygiene Iron deficiency 2: Geographical distribution of studies presently included in the Asia Pacific Cohort Studies Collaboration

Mark Woodward · Michael A Reid

Heart failure Digoxin therapy has no effect on mortality in heart failure. Digoxin may be useful for maintaining clinical stability and exercise capacity in patients with symptomatic heart failure. Digoxin appears to be of most benefit in patients with severe heart failure, cardiomegaly and a third heart sound. Digoxin should be used as a second-line drug after diuretics, angiotensin-converting enzyme inhibitors and β-blockers in patients with congestive heart failure who are in sinus rhythm. Digoxin should be used as a first-line drug in patients with congestive heart failure who are in atrial fibrillation. Arrhythmias Digoxin has a limited, but useful, role, either alone or in combination with other agents such as β-blockers, diltiazem or verapamil, in achieving satisfactory resting ventricular rate control in patients with chronic atrial fibrillation. In patients who lead a predominantly sedentary lifestyle (perhaps particularly in those who are elderly), digoxin alone may be the agent of choice.

Terence J Campbell MD, FRACP, FACC · Peter S MacDonald FRACP, PhD

Pulmonary arterial hypertension (PAH) is a heterogeneous condition with a wide range of causes. The diagnosis is often delayed or missed. PAH is covert in its early stages, when its detection and treatment should have the most impact. Access in Australia to effective PAH therapies has lagged behind that in other affluent countries. New agents for PAH, now becoming available, improve ...

Anne M Keogh MD, FRACP · Keith D McNeil MB BS, FRACP · Trevor Williams MB BS, FRACP · Eli Gabbay MB BS, FRACP · Leslie G Cleland MD, FRACP

The findings of two major trials show that rhythm control is not necessarily superior to rate control There are two broad strategic options in managing recurrent or persistent atrial fibrillation (AF). They are: Rhythm control, in which treatment is directed toward restoring and maintaining sinus rhythm; and Rate control, in which AF is allowed to continue or recur unimpeded, and medications are given to control ventricular rate.1 It has been a widely held and natural assumption that rate control is inferior to rhythm control. Theoretically, the advantages of maintaining sinus rhythm should include fewer thromboembolic complications, reduced need for anticoagulation, and less cardiac failure. In short, fewer deaths and fewer symptoms. However, antiarrhythmic medications have only modest efficacy for preventing AF recurrences, both symptomatic and asymptomatic, so rate-controlling and anticoagulant drugs must also be used in many patients being treated primarily for rhythm control. Also, antiarrhythmic medications can have serious side effects, including life-threatening proarrhythmia and, in the case of the commonly used drug amiodarone, pulmonary fibrosis, thyroid dysfunction and hepatic toxicity. Until recently, few randomised trial data have been available to gauge the extent to which these practical deficiencies offset the potential benefits of rhythm control.2 Now, two major trials comparing the two treatment strategies have been published.3,4 The larger AFFIRM trial was conducted in North America, with all-cause mortality its primary endpoint.3 The smaller trial was conducted in the Netherlands, and had a composite primary endpoint which included heart failure, thromboembolism, bleeding, need for pacemaker implantation, death from cardiovascular causes, and other severe adverse effects of drugs.4 The primary finding in both trials was that rate control was not inferior to rhythm control, and that there were some trends towards superiority of rate control. In the AFFIRM trial, 5-year mortality was 21.3% for rate control versus 23.8% for rhythm control (P = 0.08). In the Dutch trial, the primary endpoint occurred in 17.2% (rate control) versus 22.6% (rhythm control), also narrowly failing to reach conventional significance. For the patient populations studied (minimally symptomatic; mean age, 69 ± 9 years; most with at least one prior episode of AF), these findings indicate that the benefits of the rhythm-control strategy do not, in general, outweigh the risks. What drugs were used? In AFFIRM, by physicians' choice, amiodarone was used in 38% of patients being treated for rhythm control initially, and in 63% at some time in the trial. Sotalol was used in 31% initially, and 41% at some time. Other drugs, including propafenone, procainamide, quinidine, flecainide, disopyramide, moricizine and dofetilide were each used in less than 10% of patients. In the Dutch trial, sotalol was used initially, but replaced (if AF recurred within six months) by propafenone or flecainide, and then, if necessary, by amiodarone. Warfarin treatment could be stopped at the physician's discretion when sinus rhythm had apparently been maintained for four weeks after cardioversion. The detailed outcomes quantify the impact of shortcomings of these antiarrhythmic agents. Sinus rhythm was present in 62.6% (AFFIRM) and 39% (Dutch), respectively, of patients being treated for rhythm control at the conclusion of the trials. The proportion of patients taking warfarin remained above 70% in the AFFIRM study, and above 86% in the Dutch trial. Most disappointingly, the strategy failed to reduce the rates of stroke, other thromboembolic complications, or haemorrhages compared with rate control (see Box). Of the 80 ischaemic strokes incurred in the AFFIRM trial's rhythm-control arm, 55% occurred after discontinuation of warfarin. A further 21% occurred during warfarin treatment, while patients' international normalised ratios (INR) were < 2.0. Only 31% had AF at the time of their stroke. These findings suggest that it may be unsafe to stop anticoagulation for AF patients treated with a rhythm-control strategy, unless there are no other risk factors for stroke (age > 60, previous stroke or transient ischaemic attack, hypertension, rheumatic valve disease, diabetes, cardiomyopathy, planned or recent cardioversion) and/or maintenance of sinus rhythm has been demonstrated not only by lack of symptoms, but also by appropriate ambulatory ("Holter") monitoring.1,5,6 The rate-control arms had significantly lower rates of severe adverse effects attributable to medications — effects such as torsade de pointes, resuscitated cardiac arrest due to bradycardia or pulseless electrical activity, and various non-cardiac adverse events (see Box). The incidence of congestive cardiac failure was non-significantly lower in the rate-control arms in both trials. In subgroup analyses of the AFFIRM trial, rate control had lower risk of death for patients older than 64 years, those without pre-existing congestive cardiac failure, and those with coronary artery disease. A trend in favour of rate control in patients with hypertension in the AFFIRM trial is supported by superiority (primary endpoint 17.3 % v 30.8% for rhythm control) in the corresponding subgroup analysis of the Dutch study. These two trials do not spell the end for electrical cardioversions and antiarrhythmic medications in the management of AF. They concentrated on older, high-risk patients, excluding or under-representing some subgroups of patients who experience AF, for example: patients considered unsuitable for one of the strategies (eg, those with hypertrophic cardiomyopathy, those too symptomatic in rate-controlled AF, or those at unacceptably high risk of bleeding with anticoagulation); and patients under 65 years of age and with no other risk factors for stroke or death. For many such patients, and for most patients' first episode of persistent AF, it remains appropriate to cardiovert once, with a level of anticoagulation appropriate to the patient's risk–benefit profile for some weeks or months, meanwhile treating any concomitant predisposing conditions (congestive heart failure, lung disease, etc), and then review. Many issues need to be considered when deciding and revising optimal treatment in an individual patient. In selected individuals, potentially curative non-pharmacological treatments (eg, pacing,7 catheter ablation,8,9 or maze operation10) may be appropriate. However, for patients represented in the AFFIRM and Dutch trials, a line in the sand has been redrawn. Rate control is safe and should not be considered inferior to rhythm control for minimally symptomatic patients in whom AF is considered likely to recur after cardioversion, particularly if they are older than 64, or have coronary artery disease or hypertension. Healthcare professionals should make assiduous efforts to help patients maintain their INR between 2.0 and 3.0 continuously, and to achieve adequate rate control (defined for the AFFIRM trial as resting rate ≤ 80 beats per minute, and either a 6-minute walk test with a rate ≤ 110, or a 24-hour Holter recording with average rate ≤ 100 and no individual rate more than 110% of the predicted maximum).11 Summary of the findings of two major studies examining rate control and rhythm control in atrial fibrillation AFFIRM3 Dutch study4 Number of participants 4060 522 Mean duration of follow-up 3.5 years 2.3 years Mean age at baseline 70 years 68 years Females 39% 36% Event Rate Rhythm Difference significant? (P ) Rate Rhythm Difference significant? Primary endpoint* 21.3% 23.8% No (0.08) 17.2% 22.6% No Congestive heart failure 2.1% 2.7% No (0.58) 3.5% 4.5% No Thromboembolism 5.5% 7.9% No Cerebral 5.5% 7.1% No (0.79) Other systemic 0.5% 0.4% No (0.62) Pulmonary 0.1% 0.5% No (0.16) Haemorrhage 4.7% 3.4% No Primary intracerebral 1.1% 1.3% No (0.73) Subdural or subarachnoid 0.8% 0.8% No (0.68) Non-central nervous system 7.7% 6.9% No (0.44) Severe adverse effects of drugs (other than anticoagulants) 0.8% 4.5% Yes Torsades des pointes 0.2% 0.8% Yes (0.007) Resuscitated cardiac arrest due to bradycardia or pulseless electrical activity < 0.1% 0.6% Yes (0.01) Pulmonary events† 1.7% 7.3% Yes (< 0.001) Gastrointestinal events† 2.1% 8.0% Yes (< 0.001) Bradycardia† 4.2% 6.0% Yes (0.001) Prolongation of corrected QT interval (> 520 ms)† 0.3% 1.9% Yes (< 0.001) Other adverse events† 14.0% 25.4% Yes (< 0.001) * All-cause mortality for the AFFIRM trial,3 and a composite primary endpoint which included heart failure, thromboembolism, bleeding, need for pacemaker implantation, death from cardiovascular causes, and other severe adverse effects of drugs for the Dutch trial.4 † Prompting discontinuation of a drug.

Michael J Kilborn FRACP, DPhil

Objective: To describe the levels of inflammation and vascular endothelial activation in an Aboriginal community, and the relationship of these factors to coronary heart disease (CHD) risk factors and markers of nutritional quality.Design and participants: A cross-sectional survey of 95 women and 76 men participating in a chronic-disease prevention program.Setting: A remote Aboriginal community in Western Australia in 1996.Main outcome measures: Concentrations of markers of inflammation (C-reactive protein [CRP]) and vascular endothelial activation (soluble E-selectin [sE-selectin]); presence of metabolic syndrome; concentrations of diet-derived antioxidants.Results: Participants exhibited very high plasma concentrations of CRP (mean, 5.4 mg/L; 95% CI, 4.6–6.3 mg/L) and sE-selectin (mean, 119 ng/mL; 95% CI, 111–128 ng/mL). Both CRP and sE-selectin concentrations were significantly higher in the presence of the metabolic syndrome. There were significant inverse linear relationships between concentrations of CRP and plasma concentrations of the antioxidants lycopene, β-carotene, cryptoxanthin and retinol. Even stronger inverse associations were evident between concentrations of sE-selectin and lycopene, β-carotene, cryptoxanthin and lutein.Conclusions: Vascular inflammation and endothelial activation may be important mediators of elevated CHD risk in Aboriginal people. Inadequate nutrition and physical inactivity may contribute to this process.

Kevin Rowley BAppSci PhD · Jacob Cohen BSc · Alicia J Jenkins FRACP FRCP · David O'Neal MB BS, MD, FRACP · James D Best FRACP FRCPath · Karen Z Walker PhD MND · Qing Su MSc PhD · Kerin O'Dea BSc PhD

Formal risk-based protocols and clinical audits of process indicators and outcomes are needed "Missed" myocardial infarction occurs when a patient with an unrecognised acute coronary syndrome is discharged from hospital prematurely. The correct diagnosis becomes apparent only when the patient has an infarct or cardiac arrest, or is later found to have biochemical evidence of myocardial injury. There has been a paradigm shift in management of patients with chest pain over the past decade, with the focus moving from establishing a diagnosis towards ensuring the safety of the management strategy. This change was heralded by the publication of Australian guidelines in 1996 that recommended: Initial risk stratification of patients using clinical variables; Admission of intermediate- and high-risk patients for 48 hours of clinical observation to identify those with recurrent ischaemia at rest or evidence of myocardial damage (raised levels of cardiac biomarkers or electrocardiogram [ECG] changes); and If these features are absent, stress testing to exclude exercise-induced ischaemia in all remaining patients before discharge.1 Studies in the United States showed that the period of observation can be shortened to eight hours without affecting patient outcomes.2,3 Management guidelines were updated accordingly.4 Missed myocardial infarction usually results from a breakdown in the system of care — the patient's risk has been underestimated or formal protocols have not been fully implemented. Two studies in this issue of the Journal provide excellent examples of hospital strategies to improve the safety of chest pain triage. Aroney and colleagues (page 370) demonstrate that implementation of a protocol adhering to current Australian guidelines4 minimises missed myocardial infarction.5 They provide a benchmark for other hospitals to compare their practice. Boufous and colleagues (page 375) show that local implementation strategies can reduce medical error which contributes to missed myocardial infarction.6 A new "gold standard" for care. Aroney et al describe an "accelerated chest pain assessment protocol" that minimised hospital stay without jeopardising patient safety.5 After identifying intermediate-risk patients, they implemented a rapid, two-step process to ultimately identify those who were low risk and suitable for early discharge. They shortened the period of observation to a minimum of six hours. The absence of a single infarct in the 409 patients classified as low risk is an excellent outcome, clearly confirming the safety of the protocol. Of interest, 11% of the study population had diabetes but were safely triaged by the protocol. Thus, the recent recommendation to classify all patients with diabetes as high risk may not be necessary. Validation of new markers of increased risk, such as C-reactive protein, may allow risk-stratification algorithms to be further refined.7,8 Aroney et al achieved their outcomes in a large teaching hospital where coronary care nurses and "on-call" cardiology registrars were used to implement weekend stress testing, the final step in risk stratification before discharge. As many Australian hospitals have fewer resources, it is worth identifying non-essential elements of the protocol. The study data allow limited assessment of the incremental value of each step in the protocol, excluding the 78 patients who were unable to perform an exercise test. Most of the remaining 142 at-risk patients were identified by clinical, ECG or cardiac biomarker findings. Continuous ST-segment monitoring detected less than 2% of at-risk patients. As this monitoring is expensive, its use is difficult to justify in smaller hospitals. On the other hand, 42 at-risk patients (30%) were identified by an exercise ECG. Thus, this test should not be omitted. Coronary angiography was recommended in high-risk patients, but was performed in only 41%, as many were frail or had significant comorbidities. It is interesting to speculate whether outcomes in this group could have been improved by attention to optimal medical therapy and routine stress imaging. Are patients selected appropriately? Aroney et al do not report the numbers and outcomes of patients who were classified as low risk at initial clinical assessment and who were therefore not included in the study. Some at-risk patients may have been misclassified and discharged prematurely, predisposing them to missed myocardial infarction. Boufous et al audited this phenomenon.6 Their method was imperfect, as the reviewing cardiologist had to rely on the original clinical records. Despite this reservation, it is reassuring that formal adoption and use of a risk-stratification algorithm by clinical staff halved the rate of inappropriate discharge from 20% to 10%. Nevertheless, some potentially at-risk patients were discharged against current guidelines. The study was too small to detect an impact on their outcomes, and, to my knowledge, there are no published data on outcome in this group. However, the value of such a study is illustrated by an eight-month audit of emergency chest pain triage performed at my institution five years ago. Using a risk-stratification algorithm, we identified 136 intermediate-risk patients who were discharged contrary to guidelines. In most cases, patients were observed for at least eight hours, and serial biomarkers were measured. The guideline violation was primarily a failure to perform exercise stress testing, either because it was not available or because there was no in-patient bed to hold the patient until the test could be performed. Outcome was determined in all patients at one month. One death (documented ventricular fibrillation after recurrent chest pain) and five myocardial infarctions occurred during this period: three of these events, including the death, occurred within 24 hours of discharge. While the outcome for this group of patients was not statistically different from the outcome in 116 patients managed appropriately and discharged within 24 hours (one missed myocardial infarction), the clinical significance of the data persuaded our hospital managers to fund exercise stress testing on weekends. Coupled with an education program and a protocol similar to that described by Aroney et al, we subsequently reduced our underadmission rate substantially. How can hospitals improve triage of chest pain? It is unlikely that there will ever be high-level evidence to guide chest pain triage. As outlined above, poor outcomes such as missed myocardial infarction arise through medical error or inadequate resources, and the changes required to conduct a randomised trial would reduce the likelihood of the former and, by ethical necessity, ensure the latter. In the absence of high level evidence, hospitals should adopt methods to improve clinical practice,9,10 such as strategies similar to those described by Aroney and Boufous. Risk stratification and standardised protocols can reduce medical error, as shown by Boufous et al.6 To optimise bed use, all hospitals should adopt accelerated chest pain assessment protocols similar to that described by Aroney et al.5 Lack of stress testing, particularly at weekends, is the major impediment to their widespread adoption. To inform local resource allocation, hospitals should audit indicators of process, such as appropriate risk stratification and underadmission of at-risk patients. They should also measure patient outcomes, and, if these outcomes do not match those of Aroney et al, then hospitals should revise their current management strategies.

M Andrew Fitzpatrick MD FRACP

Infarct angioplasty has the potential to increase the disparity in outcomes between rural and urban patients with myocardial infarction The need for rapid treatment of coronary syndromes has been recognised for many years. Despite recent emphasis on the benefits of rapid thrombolysis, the main advantage of early presentation remains resuscitation from ventricular fibrillation. Defibrillation has been estimated to save about six times as many lives as thrombolytic treatment,1 but patients must reach medical assistance in time for it to be effective. On average, patients delay more than an hour before seeking help for symptoms of acute myocardial infarction, and about another hour elapses before they arrive at hospital.2-4 Attempts to shorten patient delay by education campaigns have been generally ineffective5 and, in recent years, efforts have been mainly directed towards expediting transport and hospital treatment of patients with myocardial infarction.2,3,6 In Australia, these efforts include fast-track pathways and delivering thrombolysis in emergency departments, before cardiological review.2,7 Significant improvements in call-to-needle times have been achieved,6 but, as Kelly and colleagues document in this issue of the Journal (page 381),2 not all patients are treated as rapidly as is desirable. The study by Kelly et al is particularly useful because it includes many of the patients treated with thrombolysis in Victoria over their study period of 30 months, and includes patients from rural and urban regions. Their data show that patients from rural areas delay longer before seeking attention and are slower to receive treatment than patients from large urban areas. While the association between delay in treatment and increased mortality in this study is likely to be partly confounded by unmeasured variables, few would dispute that these delays increase infarct size and the likelihood of dying during and after hospitalisation. Delayed treatment of myocardial infarction is one more manifestation of the geographic gradient in healthcare and outcomes in Australia.8 Controlled trials have shown that prehospital thrombo-lysis reduces mortality by about 20%.9 Prehospital thrombolysis is particularly suitable for remote regions with long ambulance transport times, and has been successfully implemented overseas without the use of mobile intensive care units.10 Even in urban areas, significant reductions in treatment delay have been achieved (between 30 and 60 minutes9), perhaps partly because a diagnosis is established before patients arrive at hospital and the hospital assessment process is circumvented. Yet, in Australia, prehospital thrombolysis has not been implemented in a systematic way. Kelly et al identify many of the barriers to the use of prehospital thrombolysis, including lack of appropriate ambulance equipment and failure to train and empower paramedics and nurses to give thrombolysis.2 They argue for a "bottom up" approach where individual healthcare ser-vices develop and own their strategies. Unfortunately, by itself, this is unlikely to effect change because of the complex funding mix of healthcare services in Australia and the parlous financial state of many rural health services. While rural and regional centres struggle to treat patients expeditiously with limited resources, metropolitan hospitals with cardiac catheterisation laboratories are moving steadily towards infarct angioplasty instead of thrombolysis.11 Whether this proceeds on a 24-hour basis depends mainly on the ability of individual cardiology departments to corral the necessary resources from their hospitals and the willingness of their staff to work nights and weekends. There is a strong body of evidence showing that infarct angioplasty is a better treatment than thrombolysis,12 but it is certainly more expensive to institute upfront. Proponents argue that it is cost effective compared with thrombolysis as it reduces hospital stay, but experience has taught hospital administrators to be wary of these claims as they rarely result in real cost savings. However, there is little doubt that infarct angioplasty is here to stay and that it will improve outcomes from myocardial infarction in patients fortunate enough to have access to it. If current trends continue, it has the potential to further increase the disparity in outcomes between rural and urban patients with myocardial infarction. How then should we respond to the data provided by Kelly and colleagues? Time delays in administering thrombolysis need to be seen in the context of the emergence of widespread use of infarct angioplasty and the particular geographic difficulties imposed by the Australian setting. In areas with transport times of more than 20 minutes, systematic use of prehospital thrombolysis could substantially improve outcomes at a modest cost. In urban areas, rapid transit to a facility with the ability to perform percutaneous transluminal coronary angioplasty (PTCA) is likely to become the standard. A combination of the two strategies could also be trialed in patients from areas without rapid access to PTCA (so called facilitated infarct angioplasty). Finally, in the debate about how best to achieve early revascularisation, it should not be forgotten that most of the delay occurs before the patient contacts the ambulance service and that, in this period, death is usually the result of ventricular fibrillation. As no strategy has been identified that encourages patients to present earlier, research should be directed towards improving the treatment of cardiac arrest with interventions such as prehospital thrombolysis13 and public access defibrillators.14

James W Leitch MB BS, FRACP

Objective: To determine the feasibility, safety and effectiveness of a structured clinical pathway for stratification and management of patients presenting with chest pain and classified as having intermediate risk of adverse cardiac outcomes in the subsequent six months.Design: Prospective clinical audit.Participants and setting: 630 consecutive patients who presented to the emergency department of a metropolitan tertiary care hospital between January 2000 and June 2001 with chest pain and intermediate-risk features.Intervention: Use of the Accelerated Chest Pain Assessment Protocol (ACPAP), as advocated by the Management of unstable angina guidelines — 2000 from the National Heart Foundation and the Cardiac Society of Australia and New Zealand.Main outcome measure: Adverse cardiac events during six-month follow-up.Results: 409 patients (65%) were reclassified as low risk and discharged at a mean of 14 hours after assessment in the chest pain unit. None had missed myocardial infarctions, while three (1%) had cardiac events at six months (all elective revascularisation procedures, with no readmissions with acute coronary syndromes). Another 110 patients (17%) were reclassified as high risk, and 21 (19%) of these had cardiac events (mainly revascularisations) by six months. Patients who were unable to exercise or had non-diagnostic exercise stress test results (equivocal risk) had an intermediate cardiac event rate (8%).Conclusions: This study validates use of ACPAP. The protocol eliminated missed myocardial infarction; allowed early, safe discharge of low-risk patients; and led to early identification and management of high-risk patients.

Con N Aroney MD, FRACP · Heather L Dunlevie BHlthScN · JH Nicholas Bett FRACP

Objective: To evaluate the impact of a chest-pain guideline on clinical decision-making and medium-term outcomes of patients presenting to a hospital emergency department (ED) with non-traumatic chest pain.Design: Before-and-after guideline implementation study.Setting: Bankstown–Lidcombe Hospital, Sydney, NSW (454-bed metropolitan teaching hospital), in the six-month periods before and after guideline implementation in February 2001.Participants: Patients presenting to the ED with non-traumatic chest pain who had chest-pain assessment forms completed by ED doctors, comprising 422/768 (54.9%) of those presenting before and 461/691 (66.7%) after guideline implementation.Main outcome measures: Appropriateness of admission/discharge decisions compared with decision of senior cardiologist based on guideline; death, recurrent chest pain, ED re-presentation and hospital readmission in the ensuing three months.Results: After guideline implementation, appropriate admission/discharge decisions increased significantly from 180/265 (68%) to 261/324 (81%) (difference, 13%; 95% CI, 6%–20%). The largest increase was for patients at moderate risk of death or acute myocardial infarction within six months, from 39/96 (38%) to 57/103 (55%) (difference, 18%; 95% CI, 4%–31%). Increases were seen for both junior doctors (interns and resident medical officers) (18%; 95% CI, 7%–30%) and senior doctors (11%; 95% CI, 2%–19%). Logistic regression showed that implementation of the guideline, seniority of assessing doctor and patient history of coronary disease were independent predictors of appropriate decisions. There was a significant decline in re-presentations to ED with recurrent chest pain in patients previously presenting with cardiac or possibly cardiac pain, from 46/201 (23%) before implementation to 32/247 (13%) after (difference, 210%; 95% CI, 217% to 23%).Conclusions: The chest-pain guideline resulted in a significant improvement in clinical decision-making in the ED and reduced re-presentations with cardiac/possibly cardiac chest pain.

Soufiane Boufous MPH(Hons) · Bin B Jalaludin PhD, FAFPHM · Charles H Pain FAFHPM · Susan Ieraci FACEM · Anne-Louise Gray BAppSc, PGCertMgt · Susan E Harris B Phty, MPH · Craig P Juergens FRACP · Peter W Kelleher FRACP · Linda M Dann FANZCA, FACEM

Objective: To determine the proportion of patients in Victoria treated within the British Heart Foundation 90-minute call-to-needle (CTN) time benchmark for thrombolysis of ST-elevation myocardial infarction (STEMI), and to validate the British Heart Foundation 90-minute benchmark with respect to mortality.Design: Cohort study.Setting: 20 hospitals and two ambulance services in the State of Victoria, Australia.Participants: 1147 patients with STEMI transported to hospital by ambulance and eligible for thrombolysis.Main outcome measures: CTN time, and in-hospital mortality.Results: Median CTN time was 83 minutes (mean, 93.2 min; range, 29–894 min). Median door-to-needle (DTN) time was 37 minutes (mean, 46.5 min; range, 0–853 min). 61% of patients received thrombolysis within the 90-minute benchmark. Patients with CTN times > 90 minutes had an increased risk of dying (relative risk, 1.8; 95% CI, 1.3–2.7). Factors associated with CTN time < 90 minutes were lower DTN time, prior notification of the receiving hospital and transport time less than 20 minutes.Conclusion: The British Heart Foundation CTN time benchmark is being met for 61% of eligible STEMI patients in Victoria. Strategies to reduce CTN time should be region-specific, and should include attempts to reduce DTN and to enhance ambulance–hospital communication. Prehospital thrombolysis may be appropriate for some regions.

Anne-Maree Kelly MD, FACEM · Debra Kerr BN, MBL · Ian Patrick BParamedStud, MICAcert · Tony Walker BParamedStud, GDipEd

An Expert Working Group of the National Heart Foundation of Australia undertook a review of systematic reviews of the evidence relating to major psychosocial risk factors to assess whether there are independent associations between any of the factors and the development and progression of coronary heart disease (CHD), or the occurrence of acute cardiac events. The expert group concluded that (i) there is strong and consistent evidence of an independent causal association between depression, social isolation and lack of quality social support and the causes and prognosis of CHD; and (ii) there is no strong or consistent evidence for a causal association between chronic life events, work-related stressors (job control, demands and strain), Type A behaviour patterns, hostility, anxiety disorders or panic disorders and CHD. The increased risk contributed by these psychosocial factors is of similar order to the more conventional CHD risk factors such as smoking, dyslipidaemia and hypertension. The identified psychosocial risk factors should be taken into account during individual CHD risk assessment and management, and have implications for public health policy and research.

Stephen J Bunker PhD, RN · David M Colquhoun MB BS, FRACP · Murray D Esler PhD, FRACP · Ian B Hickie MD, FRANZCP · David Hunt FRACP, FACC · V Michael Jelinek FRACP, FACC · Brian F Oldenburg PhD, MPsychol · Hedley G Peach PhD, FFPHM · Denise Ruth FRACGP, FAFPHM · Christopher C Tennant MRCPsych, FRANZCP · Andrew M Tonkin MD, FRACP

To the Editor: The publication of the main results of the Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial (ALLHAT), and the accompanying editorial, triumph the role of thiazide diuretics as first-line management for hypertension.1,2 It brought to mind the lines from the nursery rhyme Old Mother Hubbard — "And when she went there, the cupboard was bare." Simple frequency analysis of diuretic antihypertensive medications listed in the Australian Medicines Handbook (1998 and 2003) revealed that the total number of thiazide diuretics available as monotherapy in 1998 was six (bendrofluazide chlorothiazide, chlorthalidone, hydrochlorothiazide, methyclothiazide and indapamide), and in 2003 three (bendrofluazide, chlorthalidone and indapamide).3,4

Mark R Nelson

To the Editor: Kuchar et al1 describe a patient who received an implantable defibrillator discharge after a single ingestion of loratadine. We are concerned that their conclusion — that this patient "probably" had drug-induced torsade de pointes — is incorrect. Review of the intracardiac electrograms from this patient (shown in Box 2 of their article) with known monomorphic ventricular tachycardia (VT; shown in their Box 1) shows a relatively fixed rate of the VT without the large variations in cycle length consistent with torsade de pointes. While there are no established guidelines for determining torsade de pointes based on intracardiac electrograms, it is clear that during monomorphic VT electrocardiograms can show variability in amplitude and orientation. Consistent with the early stages of monomorphic VT,2 the first three electrograms have a different orientation compared with the remaining electrograms, which are largely similar. Unfortunately, as the transition from supraventricular rhythm to tachycardia was not shown, it cannot be ascertained whether the tachycardia began with a pause-dependent mechanism, an important criterion to help diagnose torsade de pointes.3 Given that this patient's implantable defibrillator intracardiac electrograms do not show a continually changing electrogram pattern, that the cycle length is relatively constant, and that there is a lack of documented QT prolongation, there is no evidence of the patient's arrhythmia being torsade de pointes. Incidentally, it is unclear whether these electrograms were recorded before (as specified in the discussion) or after defibrillator discharge (title of Box 2). It is well documented that a defibrillator discharge can have significant effects on the recording of intraventricular electrograms. Most likely, this patient, with documented pre-existing monomorphic VT (their Box 1[b]), had an episode of VT (not torsade de pointes) appropriately treated by the implanted defibrillator, probably having no direct relationship with loratadine. Notably, their Box 3 shows torsade de pointes in another patient, not receiving loratadine. In summary, Kuchar et al1 correctly state that there have been no documented episodes of torsade de pointes after ingestion of loratadine. Similarly, their report does not appear to document an episode of torsade de pointes.

Philip T Sager · Enrico P Veltri