Cardiovascular diseases

Michael McDonnell General Practitioner, and owner (with his wife) of Daisy and Cashew, 1/4 Mylne Street, Toowoomba, QLD 4350. To the Editor: Having read the article by Parslow and Jorm,1 I dashed to my surgery — praise the Lord, my diastolic blood pressure was 70 mmHg. So, I raced home again and reassured our labradors that they would not have to be shot. Let’s leave elderly pet owners and their blood pressures alone. Pet ownership is all about companionship, friendship, trust, care for your friend — the really important things in life — not your diastolic blood pressure!

Michael McDonnell

Johan H A Janssen,* David Henshaw† * Cardiologist, † General Physician, Kalgoorlie Regional Hospital, PO Box 8035, Hannans, Kalgoorlie, WA 6433. Johan. JanssenAThealth.wa.gov.au To the Editor: We read with interest the article by Hung on aspirin for cardiovascular disease prevention,1 and would like to alert readers to the fact that, from the same studies Hung discussed, it is clear aspirin fails to prevent 80% of recurrent serious vascular events, and that one in eight high-risk patients will suffer from another “event” in the next 2 years while taking aspirin.2 Recent studies have triggered discussion about the concept of aspirin resistance and competitive binding issues as possible causes for the observed failure of aspirin, or indeed the increased risk of all-cause mortality when aspirin is used in combination with ibuprofen.3,4 Although it may still be premature to recommend routine testing for aspirin resistance, the possibility that testing might lead to improved strategies for reducing the risk of thrombotic complications means that it should be considered. Another point for consideration is whether primary prophylaxis with aspirin might induce aspirin resistance, thereby nullifying the effect of taking it in the first place. We agree with Hung that the current main alternative to aspirin is clopidogrel, and that this agent could be used in cases in which there is any doubt about the efficacy of aspirin.

Johan H A Janssen · David Henshaw

Joseph Hung Associate Professor, School of Medicine and Pharmacology, University of Western Australia, and Head of Department, Cardiovascular Medicine, Sir Charles Gairdner Hospital, Verdun Street, Nedlands, WA 6009. jhungATcyllene.uwa.edu.au In reply: Janssen and Henshaw are correct to point out that aspirin fails to prevent 80% of recurrent serious vascular events among high-risk patients. However, to put this into perspective, simple treatment with aspirin produces about the same relative risk reduction as treatment with a statin or the angiotensin-converting enzyme inhibitor, ramipril, among patients at high risk of vascular events.1-3 Janssen and Henshaw raise the concept of aspirin resistance and the role of a screening test. However, aspirin resistance is a poorly defined term, and could mean the clinical inability of aspirin to protect individuals from arterial thrombotic events, or laboratory measures indicating the failure of aspirin to inhibit platelet activity. There is currently no specific, accurate, and reproducible measure of the antiplatelet effects of aspirin, nor are there methods that can reliably predict the clinical efficacy of aspirin.4 For now, with high-risk patients, doctors should: ensure that patients comply with aspirin therapy along with other proven preventive treatments; avoid regular concomitant use of non-steroidal anti-inflammatory drugs with aspirin because of the potential for competitive inhibition;5 and consider the addition of clopidogrel to therapy with aspirin, so as to block other pathways of platelet activation not blocked by aspirin, particularly in patients who experience thrombotic complications during aspirin therapy.1

Joseph Hung

Re: Lowering blood pressure in 2003, a Clinical Update article by Chalmers JP and Arnolda LF in the 15 September 2003 issue of the Journal (Med J Aust 2003; 179: 306-312). On page 308, second column, under the heading ANBP2, an error in the editorial process led to an incorrect statement: “ANBP2 was an open-labelled randomised study with blinded endpoints, a design in which study doctors knew whether the patient was on active treatment or placebo . . . ” ANBP2 is clearly a comparative study, not a placebo controlled study, as is made plain in the other sections of the article. The html and pdf versions of the article published online were corrected on 14 November 2003.

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

A 60-year-old woman presented with a gangrenous right index finger. She had a 44-pack-year history of smoking and no significant past medical history. On examination, brachial and radial arterial pulses were normal, minimal signs of atherosclerosis were apparent on fundoscopy, and no neurological abnormalities were present. Results of a full blood count, blood chemistry (including high-density lipoprotein and low-density lipoprotein cholesterol) and coagulation tests were normal. The erythrocyte sedimentation rate was 20 mm/h (normal range, < 20 mm/h). Potential indicators of hypercoagulability, including levels of protein C, protein S, antithrombin III, factor V, antinuclear antibody and lupus anticoagulant were normal, but the level of homocysteine was raised (16 μmol/L; normal range, 5–15 μmol/L). A transoesophageal echogram showed normal cardiac and valve function, with no obvious thrombi. However, there were diffuse atherosclerotic changes in the aortic arch, with a grade-IV protruding atheroma (7 mm) proximal to the innominate artery (Box). An arterial Doppler study of both upper extremities showed a lack of flow in the right ulnar artery. Angiography was not performed, in view of the risk of causing another embolus. The gangrenous right finger was amputated. Histopathological examination confirmed gangrene of the finger, with no evidence of vasculitis or cholesterol emboli. The protruding aortic atheroma was the likely source of emboli. Warfarin, simvastatin and folic acid were started. A month after a therapeutic warfarin level (target INR, 2.5–3.5) had been achieved, the patient presented with pain in the left third finger. The finger was oedematous, erythematous and tender, and INR was 1.7. Another episode of embolisation was suspected, although repeated arterial Doppler study showed no evidence of arterial insufficiency in the left arm. The warfarin dose was adjusted, and symptoms improved spontaneously. No embolic events were apparent in other organs during the course of treatment. The patient, who has continued to take simvastatin, folic acid and warfarin, has been symptom-free to date. Transoesophageal echogram showing a protruding atheroma proximal to the innominate artery, as marked by crosses.

Yasuhiro Oki MD · Farooq A Chaudhry MD, FACC

Objectives: To study the relationship of blood pressure to birthweight and current body mass index in a population with high rates of low birthweight (< 2.5 kg).Design: A cross-sectional population screening program conducted between 1992 and 1998, with retrospective retrieval of birthweights.Setting: A remote coastal Australian Aboriginal community with a high prevalence of diabetes, cardiovascular and renal disease.Participants: Eighty-two per cent of the community members (1473/1805) were screened. Birthweights were available for 767 (71%) of the screened participants aged 7–43 years.Main outcome measures: The association between birthweight and current blood pressure, accounting for current body mass index.Results: Mean birthweights were low, and 18% of children and 35% of adults had been low-birthweight babies. In children (7–17 years), blood pressure was not correlated with birthweight, but in adults there was an inverse correlation — a 1 kg increase in birthweight was associated with a 2.9 mmHg (95% CI, 0.3–5.5 mmHg) decrease in systolic blood pressure, after adjusting for age, sex and current weight. Overweight adults with low birthweight had the highest blood pressures.Conclusions: Low birthweight is significantly associated with higher blood pressure in adult life, and the effect is amplified by higher current weight. Given the high rates of low birthweight in Aboriginal people in remote areas, and the detrimental effect of higher blood pressures on chronic diseases (currently present in epidemic proportions), interventions should focus on improving birthweights and on weight control in adolescents and adults. Special attention should be paid to children with low birthweight to avoid their becoming overweight in adult life.

Gurmeet R Singh MB BS, MD, MPH · Wendy E Hoy MB BS, BScMed, FRACP

Zhiqiang Wang,* Wendy E Hoy† * Senior Research Fellow, † Professor, Centre for Chronic Disease, School of Medicine, University of Queensland, Herston, QLD. zwangATccs.uq.edu.au To the Editor: In a recent article, Thompson and colleagues provided useful information on the prevalence of cardiovascular risk factors in urban Aboriginal people.1 Using the Sheffield table of absolute risk,2 the authors estimated that “15% men and 6% women had an absolute risk > 15% of a cardiovascular event within 10 years”. The Sheffield risk table was developed for assessing the risk of coronary deaths rather than the risk of cardiovascular events.2 Moreover, the validity of applying the Sheffield table and other risk assessment tools based on the Framingham risk functions to Aboriginal people is yet to be assessed. The lower risk estimate in women reported by Thompson and colleagues may simply reflect the higher cholesterol concentration cut-offs for women in the Sheffield table. The true risk difference between sexes in Aboriginal people may not be as dramatic as Thompson and colleagues suggest. Firstly, data in Box 1 of their article show that there was little difference between men and women as regards past history of cardiovascular disease. Secondly, Aboriginal women experience a higher prevalence than men of some cardiovascular risk factors such as diabetes,1,3 abnormal HDL cholesterol level and overweight.3 Thirdly, our own research suggests that there may be a substantial difference between estimated and observed risks. Using data from a cross-sectional study of 681 Australian Aboriginal people in a remote community,3 we performed a similar analysis to that of Thompson et al. Based on the Framingham functions,4 we estimated that 10-year risks of coronary heart disease for women were much lower than those for men in all age groups (a finding similar to that of Thompson and colleagues). However, in a related study of the same Aboriginal community (as yet unpublished), when we analysed cohort data from 838 participants with 13 years of follow-up, the observed coronary disease rates for women were as high as those for men (Box). The discrepancy we found between estimated and observed risks is a warning that researchers and clinicians need to be cautious when applying existing risk assessment tools to Aboriginal people. Incidence rates per 1000 person-years of coronary heart disease (95% CI), by age and sex (based on a cohort study of 838 Aboriginal people in a remote community) Age (years) Women Men 20–34 4.1 (1.8–9.1) 3.2 (1.4–7.0) 35–44 15.6 (9.4–25.9) 8.6 (4.5–16.5) 45–54 19.3 (10.9–33.9) 26.5 (15.0–46.7) ≥ 55 50.2 (32.4–77.9) 31.9 (16.6–61.2)

Zhiqiang Wang · Wendy E Hoy

Peter L Thompson,* Pamela J Bradshaw,† Margherita Veroni,‡ Edward T Wilkes§ * Cardiologist, † Clinical Research Coordinator, ‡ Epidemiologist, Western Australian Heart Research Institute, Sir Charles Gairdner Hospital, Nedlands, WA 6009; § Senior Research Fellow, Centre for Developmental Health, Telethon Institute for Child Health Research, Subiaco, WA. peter.thompsonAThealth.wa.gov.au In reply: We appreciate the commentary by Wang and Hoy on the problems of the use of risk scores for assessing cardiovascular risk in Aboriginal people. In general, we agree that caution is essential in using tables that predict absolute risk of cardiovascular events. However, despite their limitations, absolute risk estimates are being encouraged by Australian, European, New Zealand and US authorities as a practical aid to targeting coronary disease preventive measures.1 An estimated risk of > 15% of a fatal cardiovascular event within 10 years, based on the Sheffield or Framingham scores, is now recommended as an indication for active treatment. Our prime purpose in providing an estimate of absolute risk in the Perth urban Aboriginal population was to demonstrate that a program of cardiovascular risk assessment with strong Aboriginal community support is capable of detecting high-risk people who will benefit from intensive risk-lowering strategies. Wang and Hoy’s caution about applying absolute risk estimates based on the Framingham population to unrelated populations is of particular importance in the case of Australian Indigenous people, in whom diabetes and the related metabolic syndrome may be the predominant risk factors. We have recently completed an analysis of the determinants of carotid atherosclerosis in the same population described in our earlier study.2 Our results confirm that, while the Framingham estimates (based on sex, age, LDL cholesterol and blood pressure) are indeed predictors of carotid atherosclerosis, their predictive value is significantly enhanced by the addition of markers of diabetes status and obesity. The 13-year follow-up study of the Aboriginal cohort referred to by Wang and Hoy will provide unique data to help identify reliable risk predictors specific to Aboriginal people, and we look forward to its publication.

Peter L Thompson · Pamela J Bradshaw · Margherita Veroni · Edward T Wilkes

Paul M Bailey Emergency Physician, Joondalup Health Campus, Shenton Avenue, Joondalup, WA 6027. pbaileyATiinet.net.au To the Editor: In the article by Davey1 no evidence other than deviation from a protocol published months before the study is produced to document the implied inappropriateness of single troponin assays. Emergency physicians are experienced in assessing undifferentiated chest pain. Acute coronary syndromes are but one cause of presentation to emergency departments (EDs) of patients with chest pain, and indeed are but one cause of elevated serum troponin levels. Many reasons may justify the “appropriate” ordering of single troponin assays. Some patients present to EDs many hours after their episode of chest pain. A single troponin test may be a very useful and sensitive test for a patient whose chest pain occurred yesterday. How many patients in the study group had their single troponin test done more than 12 hours after their episode of pain? How many patients discharged themselves against medical advice as they were unwilling to wait 6–8 hours for a second blood test to triage their risk for an acute coronary syndrome? How many patients died or were transferred to another hospital? How many patients had their single troponin test ordered in the investigation of a primarily non-cardiac illness, such as sepsis or pulmonary embolism? I have no doubt that many troponin assays ordered in the study population were inappropriate. But, by failing to conduct an explicit medical record review of those patients whose tests were deemed inappropriate, the author has failed to answer his stated aim of determining if the troponin assay is used appropriately when chest pain is encountered. We are left with no knowledge of whether this problem is small or large. Finally, does it matter? Are two consecutive negative troponin assays required to triage patients with chest pain? Recently, the Journal published a clinical outcome study that examined the implementation of a chest pain assessment protocol at a metropolitan university teaching hospital in Bankstown, Sydney.2 Patients presenting to the ED with “possibly cardiac” non-traumatic chest pain who were deemed to be low risk did not receive a second, late troponin assay, and yet this approach appeared to be safe. Those of us who have an interest in the rational use of diagnostic testing for patients with acute coronary syndromes eagerly await the publication of further evidence on this important matter.

Paul M Bailey

Richard X Davey Chemical Pathologist, Melbourne Health Shared Pathology Service, Western Hospital, Footscray, VIC 3011. Richard. DaveyATwh.org.au In reply: In acute myocardial infarction (AMI) diagnosis, the sensitivity and specificity of troponin rise with time after symptom onset. The sensitivity of troponin-I testing was shown to increase from 35% at 0–4 hours to 97% at 12–24 hours after an infarct.1 Similarly, a meta-analysis found that “multiple testing of individual biomarkers over time substantially improves sensitivity, while retaining high specificity” for AMI diagnosis.2 This position is taken by the National Academy of Clinical Biochemistry3 and European and American cardiologists.4 Furthermore, the diagnostic clock starts from a patient’s emergency department presentation if there is any unreliability suspected in the patient’s assessment of pain onset. Pain onset may have been stuttering, indeterminate, simply forgotten, some combination of these, or even absent. Bailey describes several situations such as these, thought to justify, or to explain, singlicate troponin testing, and suggests that, as I did not audit records, I was not able to quantify the true extent of inappropriate ordering. I acknowledged this shortcoming, but believe it does not detract from the endpoint found. The Bankstown low-risk patients5 are only a confounder here. In our protocol they probably would not have been thought to have cardiac pain, and all the remaining Bankstown patients had serial biomarker testing. In my audit,6 93% of singlicate troponin test orders did not diagnose an AMI, and if AMI were still considered, then the tests contravened the protocols.3,4 This is why they were called “inappropriate” — no arbitrary whim. I assumed, moreover, that no clinician ordered a troponin test unless seeking a cause for chest pain. Our protocol begins with chest pain, recognises uncertainty, and leads through to treating an AMI or reconsidering the diagnosis. Obliquely invoking Ockham’s principle is also dangerous here. Illnesses such as sepsis may “provoke” an AMI, but this must then be investigated independently, and according to its own rules of engagement, which do not alter solely because of the primary (co-)morbidity. In short, we did know what is appropriate troponin use, and surveyed it. Like Bailey, we look forward to seeing further evidence.

Richard X Davey

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