Cardiovascular diseases

In patients hospitalised with acute coronary syndromes (ACS) and congestive heart failure (CHF), evidence suggests opportunities for improving in-hospital and after-hospital care, patient self-care, and hospital–community integration. A multidisciplinary quality improvement program was designed and instigated in Brisbane in October 2000 involving 250 clinicians at three teaching hospitals, 1080 general practitioners (GPs) from five Divisions of General Practice, 1594 patients with ACS and 904 patients with CHF. Quality improvement interventions were implemented over 17 months after a 6-month baseline period and included: clinical decision support (clinical practice guidelines, reminders, checklists, clinical pathways); educational interventions (seminars, academic detailing); regular performance feedback; patient self-management strategies; and hospital–community integration (discharge referral summaries; community pharmacist liaison; patient prompts to attend GPs). Using a before–after study design to assess program impact, significantly more program patients compared with historical controls received: ACS: Angiotensin-converting enzyme (ACE) inhibitors and lipid-lowering agents at discharge, aspirin and β-blockers at 3 months after discharge, inpatient cardiac counselling, and referral to outpatient cardiac rehabilitation. CHF: Assessment for reversible precipitants, use of prophylaxis for deep-venous thrombosis, β-blockers at discharge, ACE inhibitors at 6 months after discharge, imaging of left ventricular function, and optimal management of blood pressure levels. Risk-adjusted mortality rates at 6 and 12 months decreased, respectively, from 9.8% to 7.4% (P = 0.06) and from 13.4% to 10.1% (P = 0.06) for patients with ACS and from 22.8% to 15.2% (P < 0.001) and from 32.8% to 22.4% (P = 0.005) for patients with CHF. Quality improvement programs that feature multifaceted interventions across the continuum of care can change clinical culture, optimise care and improve clinical outcomes.

Ian A Scott MHA, FRACP · Annabel C Hickey MMSc(Clin Epi), BAppSc(OT) · Daniela C J Sanders BPharm(Hons) · Mark A Jones BSc(Hons) · Charles P Denaro MD, FRACP · Cameron J Bennett MB BS, MBiomedE, FRACP · Alison M Mudge MB BS, FRACP · Justine M Thiele BPharm · Judy L Flores BA, MD, FRACP · Beres Wenck FRACGP · John W Bennett BMedSc, MB BS, BA(Hons), FRACGP

Towards a Safer Culture (TASC) aims to provide a safer culture in hospital departments by introducing clinical pathways for the management of patients with acute coronary syndromes or stroke. Specific clinical pathways have been implemented for patients with different levels of risk to guide the most appropriate evidence-based medical care for each patient. Pathways facilitate continuity of care across different clinical departments by identifying gaps in care, and clarifying tasks and responsibilities. A multidisciplinary and interdepartmental approach to managing patients is seen as an effective way of effecting change. A system for “point-of-care” data acquisition, a centralised database and web-based reporting enable benchmarking for participating hospitals. A comprehensive range of educational/training strategies is used to facilitate multidisciplinary teamwork and promote clinical leadership. Phase 1 of TASC was successfully piloted at four hospitals in New South Wales, Victoria and Queensland. TASC is currently being rolled out to 29 hospitals in NSW and three hospitals in Western Australia.

Catherine T Ferry BN, GradDipPubHlth · M Andrew Fitzpatrick BSc(Med), MD, FRACP · Paul W Long GradDip(CommMgt) · Christopher R Levi BSc(Med), FRACP · Roderick O Bishop BSc(Med), MPH, FACEM

Objectives: To determine the incidence rate of coronary heart disease (CHD) in Australian Aboriginal people with type 2 diabetes, and to compare the impact of diabetes on CHD risk in Aboriginal women and men.Design: Cohort study.Setting: A remote Aboriginal community in the Northern Territory.Participants: 889 Aboriginal people aged 20–74 years followed up to 31 May 2003 after baseline examination in 1992–1995.Main outcome measures: Incidence rates of CHD (estimated for 123 participants with diabetes at baseline and 701 “non-diabetes” participants); rate ratios for diabetes risk (95% CI), with “non-diabetes” participants as the reference group.Results: Participants with diabetes at baseline had a higher rate of CHD (37.5 per 1000 person-years) than those without diabetes (7.3 per 1000 person-years). Adjustment for multiple CHD risk factors, such as age, smoking, alcohol consumption, systolic blood pressure, body mass index, high-density lipoprotein cholesterol and total cholesterol levels, resulted in a CHD rate ratio for women of 3.7 (95% CI, 1.6–8.9) (comparing women with diabetes with those without) and a CHD rate ratio for men of 1.4 (95% CI, 0.4–4.1) (comparing men with diabetes with those without).Conclusions: Aboriginal women with diabetes experienced a significantly higher risk of CHD than women without diabetes. Although the difference was not statistically significant, women with diabetes had a higher CHD risk than men with diabetes.

Zhiqiang Wang PhD · Wendy E Hoy MB BS, BScMed, FRACP

Atherosclerosis and heart disease. Andrew M Tonkin (editor). London: Martin Dunitz, 2003 (xi + 235 pp). ISBN 1 84184 123 4. The Internet is great for reviewing literature rapidly, but the more I use it, the more I realise that the classic “Review article” has a role. PubMed can be very efficient for accessing publications, but drawing accurate conclusions can be hard work and reliance on abstracts can stifle critical analysis. Independent critical comment is difficult to find electronically. Journals realise they have to hold back some full-text editorial material for their loyal subscribers, and websites may be “free” because they are heavily sponsored. Systematic Cochrane-type reviews are readily accessible on the Internet, and are great if one needs to quantify evidence, but they can be a dull read. Tonkin’s book very effectively uses the classic “Review article” format in an ambitious attempt to review current knowledge on atherosclerosis and heart disease. The book consists of 15 chapters, covering the pathophysiology of atherosclerosis, each of the major coronary risk factors, the scientific basis of management of the main clinical coronary syndromes and the complications of coronary heart disease, including cardiac failure and arrhythmia. Tonkin is Director of Health and Scientific Affairs at the National Heart Foundation of Australia and he has selected some of the world’s most respected and influential practitioners in cardiovascular research to present authoritative and balanced overviews. Each is a very useful summary of current knowledge. There is some inconsistency in the format, with some chapters omitting detailed referencing and recommending “further reading”, while others are completely referenced, but this does not detract from the information presented. Clinicians and clinical researchers who want rapid access to balanced and reliable information on the commonest cause of premature death in this country will appreciate this book. For a compact and highly readable review of all the current work in atherosclerotic heart disease between two covers, it achieves its aim. Peter L ThompsonCardiologist and Clinical Professor of Medicine and Population Health University of Western Australia Perth, WA

Peter L Thompson

John Coutsouvelis,* Carmela E Corallo† * Oncology Pharmacist, † Deputy Director of Pharmacy, Box Hill Hospital, Nelson Road, Box Hill, VIC 3128. John.coutsouvelisATboxhill.org.au To the Editor: Thalidomide has recently been approved for use in treating recurrence of erythema nodosum leprosum and multiple myeloma after failure of standard therapies. Common side effects of thalidomide treatment include drowsiness, sedation, rash and paraesthesiae.1 Dizziness, hypotension and bradycardia occur less commonly.1-3 Of 91 patients treated with thalidomide (80 with multiple myeloma), we have had one case of symptomatic bradycardia. We describe this patient, who was able to continue treatment on a reduced dose of thalidomide. A 71-year-old woman, with a history of breast cancer (treated with radiotherapy and tamoxifen), arthritis, crush fractures, and hip and knee replacement, was diagnosed with multiple myeloma. She was prescribed intravenous pamidronate 90 mg every month and oral therapy with melphalan, but she experienced haematological toxicity and the melphalan was stopped. After progression of the disease, 100 mg of thalidomide was commenced at night, with the aim of increasing the dose by 100 mg every fortnight until a response was achieved. Three weeks later, the patient presented to hospital for pamidronate infusion complaining of a 2-week history of shortness of breath, especially on exertion. There was no oedema present, and her blood pressure was 135/70 mmHg. Electrocardiography showed sinus bradycardia, with a heart rate of 46 beats/min. The dose of thalidomide had been titrated to 200 mg at night. Thalidomide was stopped, and the patient was referred to a cardiologist, who performed an echocardiogram, 24-hour Holter monitoring and a stress test. The results from these tests showed no underlying cardiac disease or abnormalities. Six weeks later, on review, the bradycardia had resolved (heart rate, 60 beats/min). Thalidomide was recommenced at 100 mg daily. However, after a further 6 weeks, her heart rate had decreased again to 45 beats/min, and the dose of thalidomide was reduced to 100 mg on alternate days. Thalidomide therapy has been continued in this patient at 100 mg on alternate days. Her heart rate has stabilised between 50 and 55 beats/min, and she has remained asymptomatic. The multiple myeloma is responding to treatment, as indicated by symptom control and serial measurements of IgG kappa. She continues to take hydroxychloroquine, rofecoxib and sertraline. Bradycardia is a rare side effect of thalidomide therapy, with an incidence of 0.12%.1,2 The mechanism is unknown, but could be related to thalidomide’s central sedative effect.1 There are isolated published case reports of thalidomide-induced bradycardia; in all cases the drug was stopped.2-5 Thalidomide is being used for various conditions for which no alternative therapy exists. As the drug is now commercially available in Australia, its use is likely to increase. In all patients taking thalidomide, we recommend measuring heart rate; and in those with underlying heart disease, or who are taking medications that can precipitate bradycardia, we recommend electrocardiographic monitoring. Our findings in this patient suggest that thalidomide-induced bradycardia can be successfully managed with dose reduction and regular monitoring.

John Coutsouvelis · Carmela E Corallo

RCT evidence for rehabilitation is strengthened by an observational cohort study The study by Sundararajan et al1 (page 268) is a novel data linkage study and is best described as a cohort study. The study showed 35% lower mortality in patients with cardiovascular disease who had undergone cardiac rehabilitation when compared with patients who had not undergone cardiac rehabilitation. However, even the best cohort studies can give only limited inference on treatment effects. For example, observational studies suggested that women who used hormone replacement therapy (HRT) had a lower incidence of cardiovascular events than did non-users.2 However, not only did prospective randomised controlled trials (RCTs) fail to confirm the protective effect of HRT,3 they suggested that such treatment might actually cause cardiovascular disease.4 The apparent impressive protection of HRT suggested by observational databases may have been accounted for by socioeconomic differences between the users and non-users of HRT. Thus, RCTs have assumed the strongest evidence in suggesting a relationship between treatment and outcome. So why does the database linkage study by Sundararajan et al1 appeal at all? Perhaps it is because the evidence base for cardiac rehabilitation programs fails to convince all medical practitioners, despite “level 1” evidence existing from other studies.5 Even the best RCTs have intrinsic limitations. The first is that most trials exclude older, sicker patients with multiple comorbidities and those who might not cooperate with the trial protocol. This often results in a clinical trial of low-risk patients, which may miss a beneficial effect of treatment. The second limitation of RCTs, more common in single-centre studies, is publication bias. It is hard work to prepare a study for publication — even harder for a negative study than for a positive one. As a result, investigators are less likely to submit negative studies and journal editors are less likely to accept them for publication. Publication bias is likely to exist in most, if not all, areas of published research. So, what are the limitations of the evidence specifically regarding cardiac rehabilitation? The Cochrane Library review of exercise-based rehabilitation for coronary heart disease reviewed 51 RCTs of 8440 patients.5 Total cardiac mortality was reduced by 31% (random effects model odds ratio [OR], 0.69; 95% CI, 0.51–0.94) and 26% (random effects model OR, 0.74; 95% CI, 0.57–0.96) in the exercise-only and comprehensive cardiac rehabilitation groups, respectively. Neither intervention had any effect on the occurrence of non-fatal myocardial infarction. In other words, exercise that did not affect cardiac risk factors was as effective in reducing cardiac mortality as a comprehensive program that included exercise and successfully reduced cardiac risk factors. The reasons for this are unclear given the level 1 evidence supporting the proven effects of lowering blood pressure6 or serum cholesterol7 in reducing cardiac mortality. Furthermore, one has to be currently active to experience the benefit of physical activity or fitness — loss of activity and fitness means loss of the protection of exercise. So, medical practitioners can have reasonable doubts about the protective effects of a 6- or 8-week cardiac rehabilitation program on cardiac mortality years after the event, despite the Cochrane evidence. And this is why the data linkage article by Sundararajan et al appeals.1 The clinical trial data in the Cochrane review were derived from selected patients who had undergone exercise training for periods varying from a few weeks to several years. Sundararajan et al show that Australian patients with coronary heart disease who had undergone cardiac rehabilitation for 6–8 weeks had a better survival rate than did patients not undergoing cardiac rehabilitation. Although the study may be fraught with problems similar to those described for the HRT studies, it is pleasing to note how similar is the magnitude of protection from death associated with cardiac rehabilitation in this Australian series compared with that described in the Cochrane review. This observational study lends strong support to the trial information. Patients surviving an acute coronary syndrome should be referred for cardiac rehabilitation, as the experience may save their life. There is another nugget in the article by Sundararajan et al.1 Patients with acute coronary syndromes not undergoing coronary artery bypass surgery are very much less likely to undergo cardiac rehabilitation than patients who have received surgery. Percutaneous cardiac intervention is now performed twice as often as cardiac surgery. Such patients are often younger and fitter and return to work and their usual life within days of their procedures. Alternative models of rehabilitation are required for these patients who have not been physically deconditioned. These were recently discussed in this journal by Scott et al.8 One such model is the COACH Program, which has been validated by two RCTs.9,10 The COACH Program is a training program for patients with coronary heart disease, in which a healthcare professional coach trains patients to aggressively pursue the target levels for their particular coronary risk factors while working in partnership with their own doctors. The COACH Program has been shown to have a favourable effect on many coronary risk factors, including total and low-density lipoprotein cholesterol, arterial blood pressure, dietary saturated fat intake, body weight, and the performance of regular walking.8,9 If patients do not attend cardiac rehabilitation, then alternative strategies for achieving secondary prevention are required. The COACH Program is one such effective method. In summary, the evidence supporting cardiac rehabilitation is less than convincing, particularly when the rehabilitation is confined to the period after an acute cardiac illness. The data linkage study by Sundararajan et al adds support to the Australian practice of convalescent-phase cardiac rehabilitation.

V Michael Jelinek MD, FRACP, FACC

Objective: To describe the patterns of use of cardiac rehabilitation in Victoria and to assess whether the survival benefits predicted in clinical trials have been realised in the community. Design: Cohort study based on data linkage. Participants: All patients admitted for acute myocardial infarction (AMI), coronary artery bypass grafting (CABG) or percutaneous transluminal coronary angioplasty (PTCA) in Victoria in 1998 (n = 12 821). Interventions: Attendance at one of 66 participating outpatient cardiac rehabilitation centres in Victoria. Main outcome measures: Rates of attendance at rehabilitation based on key factors such as diagnosis, age, sex, and comorbidity. Five-year survival for attendees compared with non-attendees. Results: Rates of participation in rehabilitation were 15% for AMI, 37% for CABG, and 14% for PTCA. Rehabilitation attendance rates dropped sharply after 70 years of age. Attendees had a 35% improvement in 5-year survival (hazard ratio for death associated with rehabilitation attendance, 0.65 [95% CI, 0.56–0.75]). Conclusions: Attendance rates at cardiac rehabilitation are suboptimal, even though attendance confers a clinically significant difference in 5-year survival. The elderly, women, and those with comorbid conditions may benefit measurably from increased rates of attendance.

Vijaya Sundararajan MD, MPH, FACP · Stephen Begg MPH · Ric Marshall PhD · Stephen J Bunker PhD · Helen McBurney PhD

QuestionWill implantation of defibrillators improve survival in patients with prior myocardial infarction and severely impaired left ventricular function? Trial detailsDesign: A prospective, randomised, non-blinded, multicentre, controlled trial of medical therapy versus implanted cardiac defibrillators (ICDs) in patients with severely impaired ventricular function resulting from prior myocardial infarction. Background: Patients with severely impaired left ventricular function are at high risk of sudden death from ventricular arrhythmias. The presence of spontaneous arrhythmias or arrhythmias induced at cardiac electrophysiological (EP) study identifies a high-risk group, but even in the absence of spontaneous or induced arrhythmias the risk of sudden death is considerable. The ICD is known to be effective in treating malignant ventricular arrhythmias. The MADIT-II trial was designed to evaluate the effect of an ICD on survival in patients with severe left ventricular dysfunction caused by previous infarction. Methods: 1232 patients from 76 sites were enrolled over 4 years. All had prior myocardial infarction and a left ventricular ejection fraction of 0.30 or less, and were randomly assigned in a 3:2 ratio to receive a defibrillator (742 patients) or conventional medical therapy (490 patients). Spontaneous ventricular arrhythmias or EP testing were not required for entry into the trial. The primary endpoint was death from any cause. Results: The two treatment groups were similar at baseline with respect to clinical characteristics and medication use at the last follow-up. During a mean follow-up of 20 months, the mortality rate was 19.8% in the conventional therapy group and 14.2% in the ICD group. The hazard ratio for the risk of death from any cause in the defibrillator group compared with the conventional therapy group was 0.69 (95% CI, 0.51–0.93; P = 0.016). Subgroup analysis showed that defibrillator therapy improved survival regardless of age, sex, ejection fraction, New York Heart Association class or QRS interval. Conclusion: In patients with a prior myocardial infarction and advanced left ventricular impairment, prophylactic implantation of a defibrillator improves survival. CommentaryRationale for the trialFor several years, it has been routine clinical practice to implant ICDs in survivors of cardiac arrest or malignant ventricular arrhythmia. The prophylactic use of ICDs in high-risk patients who have not yet had a ventricular arrhythmia is more controversial. Patients with impaired left ventricular function are at high risk of malignant ventricular arrhythmias, but the implantation of a defibrillator is relatively expensive. There are large numbers of patients with impaired ventricular function, and to implant ICDs in all would place a considerable burden on the health budget. A possible solution is to identify those at highest risk using cardiac EP testing. The MADIT1 and MUSTT2 trials reported that ICDs improved survival in patients with coronary artery disease, reduced left ventricular function, non-sustained ventricular tachycardia, and inducible ventricular tachycardia at EP testing. Recent research, however, suggests that the EP study may be a relatively insensitive method of identifying those at highest risk.3 Moreover, it appears that the lower the left ventricular ejection fraction, the less sensitive the EP study becomes. The MADIT-II study was designed to investigate the potential survival benefit of ICDs in those without spontaneous arrhythmias and without performing EP testing.4 Trial methodsThe trial methods were relatively sound. The sample size (1232 patients from 76 sites in the United States and Europe) was adequate. Random allocation of patients resulted in well-matched treatment groups with similar baseline characteristics and similar medical therapy at last follow-up. Treating physicians were encouraged to prescribe effective drug therapy for heart failure and to minimise the use of conventional antiarrhythmics. Similar proportions in both groups received angiotensin-converting enzyme inhibitors, β-blockers and statins. Attendance rates at follow-up were 94% in the conventional therapy group and 97% in the defibrillator group. The trial was open label because blinding was not practical, but the primary end-point was unequivocal — death from any cause. However, a criticism is that mean follow-up was only 20 months, and this may impair assessment of cost-effectiveness. Another criticism is that when the trial commenced in 1997, a selection criterion was that patients have frequent spontaneous or repetitive ventricular premature contractions. This requirement was removed 6 months later, but only 23 of the 1232 patients were enrolled in those first 6 months. New informationThe trial showed that ICDs improve survival in patients with severely impaired left ventricular function caused by previous myocardial infarction, even in the absence of spontaneous arrhythmias or inducible arrhythmias at EP testing. A disturbing finding was that new or worsening heart failure requiring hospitalisation was more frequent in the ICD group. The cause of this is uncertain. One possible explanation is that the patients in the ICD group lived longer and therefore had more time to develop cardiac failure. Another is that the cardiac failure was caused by asynchronous ventricular contraction caused by ventricular pacing. The results of the recent DAVID5 trial tend to support the latter hypothesis. If this is indeed the case, the cardiac failure can probably be reduced by judicious programming of the pacing function of the ICD. Implications for clinical practiceThe routine use of ICDs in patients with an ejection fraction of 0.30 would have profound implications for healthcare spending. Routine use of ICDs for this indication would potentially increase the number of implants by a factor of between 10 and 30 per annum. Currently, about 950–1000 ICDs are implanted annually in Australia and New Zealand, at a total cost for hardware alone of about A$30 million (my estimates based on information obtained from device manufacturers). A 15-fold increase in the implantation rate would result in an increase in the annual cost for the hardware alone of about A$420 million. This is about twice the annual budget of a large Australian teaching hospital. This figure does not take into account the increase in hospital and professional fees. Moreover, it is uncertain that there are enough trained cardiac electrophysiologists to implant defibrillators in and follow up such a large number of patients. By comparison, Australian national spending on the lipid-lowering “statin” drugs in the 2001–2002 financial year was about A$670 million.6 Australian cardiologists have not yet embraced the findings of MADIT-II. This is probably because of the cost implications, preferring to wait until the findings are confirmed in other large trials. However, preliminary reports of the COMPANION7 trial appear to confirm the MADIT-II findings (the study populations of these two trials are not strictly comparable). The findings of another large trial of prophylactic ICD use, the Sudden Cardiac Death in Heart Failure Trial (SCD-HeFT), will soon be reported, and might shed additional light on this question. The true cost of implementing the MADIT-II findings awaits a detailed cost–benefit analysis. The cost of ICD hardware has been falling for several years, but it is difficult to predict the magnitude of future cost reductions. It may be possible to identify a low-risk cohort which will not benefit from ICD implantation, but the preliminary results are not encouraging. Recently, in the United States, the Centers for Medicare and Medicaid Services approved the use of ICDs in Medicare patients meeting the MADIT-II inclusion criteria and having a QRS duration of more than 120 ms. This decision was based, in part, on a subsequent analysis of the MADIT-II data, which showed that the benefit was greatest in this group of patients.8 The MADIT-II trial is likely to provoke vigorous debate over the best use of healthcare spending for some time to come.

Bruce P Wilson FRACP · Mark A McGuire PhD, FRACP

Objective: To assess if there are any differences in statin prescribing across Australia by socioeconomic status or sex and to relate prescribing rates to coronary heart disease (CHD) mortality rates.Design: Cross-sectional study using data on statin prescribing by age, sex and patient postcode for the period May to December 2002.Setting and participants: The Australian population, stratified by sex and quintile of Index of Relative Socio-Economic Disadvantage (IRSD).Main outcome measures: Age-standardised rates of statin scripts per 1000 population per month for each sex and IRSD quintile.Results: 9.1 million prescriptions for statins were supplied between May and December 2002, for a total cost of $570 million. The age-standardised rates for statin prescribing in women varied from 56.9 (95% CI, 56.6–57.2) scripts per 1000 population per month in the most disadvantaged socioeconomic quintile through 53.4 (95% CI, 53.0–53.7), 50.3 (95% CI, 50.0–50.6), 48.4 (95% CI, 48.1–48.7) to 46.3 (95% CI, 46.0–46.6) in the least disadvantaged quintile. For men the figures were 52.6 (95% CI, 52.3–52.9), 50.9 (95% CI, 50.6–51.2), 48.8 (95% CI, 48.6–49.1), 47.7 (95% CI, 47.4–47.9), and 51.9 (95% CI, 51.6–52.2). There was a significant linear association between statin prescribing and CHD mortality by quintile of socioeconomic disadvantage in women (weighted least squares slope, 0.380; 95% CI, 0.366 to 0.395; P < 0.0001), but not in men (slope, − 0.002; 95% CI, − 0.010 to 0.006; P = 0.65).Conclusions: Our results suggest that in men there is either overprescribing of statins in the highest socioeconomic quintile or underprescribing in the lowest. Furthermore, contrary to expectation, women — relative to men — are prescribed statins at higher rates at lower levels of risk (using CHD deaths as a proxy measure of risk).

Nigel P Stocks MD · Heather McElroy DipStats · Philip Ryan MB BS · James Allan MB BS

Neil H Cradick General Practitioner, PO Box 1127, Buderim, QLD 4556. cradwhitAToptusnet.com.au To the Editor: On opening the MJA Focus document “Prevention of cardiovascular disease: an evidence-based clinical aid”,1 I expected to find useful and contemporary guidelines for general practice. However, I was surprised to read two of the recommendations — for the use of antihypertensive and antiplatelet drugs in “low risk” patients (those without risk-associated clinical conditions or end-organ damage). The document recommends drug treatment only if systolic blood pressure is > 180 mmHg or diastolic blood pressure is > 100 mmHg in people under 60 years, or systolic blood pressure is > 160 mmHg in people over 60 years. While Fulcher et al1 volunteered that this was at odds with clinical practice, they supported the recommendations by stating that they were in accordance with published guidelines. The data for these conservative hypertension parameters were published nearly 10 years ago,2 or derived from textbooks,3 and are at odds with the 1999 WHO/ISH guidelines,4 and even more at odds with the excellent Joint National Committee (JNC 7) report.5 The latter publication recommends, after lifestyle recommendations, drug treatment for a blood pressure of 140–159/90–99 mmHg for those without end-organ damage. Furthermore, the focus document recommends primary prevention with aspirin in those with a calculated annual cardiovascular event risk > 3%. Hayden et al6 suggest antiplatelet treatment should be offered to those with a 5-year cardiovascular event risk > 3%, which equates to a > 0.6% annual risk. The benefit to harm ratio needs to be explained to the individual, and therapy should only be initiated once blood pressure is controlled. As an interested general practitioner and user of evidence-based guidelines, I usually check the funding of publications, and, with the heavy emphasis on the use of ACE inhibitors (in particular ramipril) and statins (which are produced by Aventis Pharma), it is difficult to rely on the evidence as presented. I would hope that independent bodies such as the National Prescribing Service or Australian Prescriber could take the pharmaceutical lead and produce desktop references with a more unbiased opinion on the latest collection of evidence that is shaking us up in primary care medicine. I would again refer readers to the excellent hypertension guidelines mentioned above4,5 (in particular the JNC 7 reference card available on the Internet at www.nhlbi.nih.gov/guidelines/hypertension/jnc7card.htm), and caution them to remain wary of easy-reference desktop items funded by pharmaceutical companies.

Neil H Cradick

Gregory R Fulcher,* John V Amerena,† Greg W Conner‡ * Director, Department of Diabetes, Endocrinology and Metabolic Medicine, Level 3, Main Block, Royal North Shore Hospital, St Leonards, NSW 2065; † Cardiologist, Department of Clinical and BioMedical Sciences, University of Melbourne, Melbourne, VIC; ‡ Vascular Physician, Cardiovascular Diagnostic Services, Sydney, NSW. gfulcherATmed.usyd.edu.au In reply: We thank Cradick for his critical review of our publication.1 His interesting points illustrate some of the reasons we were keen to publish this work. Firstly, the average practitioner is confused about which guidelines (both national and international) to follow. Cradick refers to the JNC 7 report and WHO/ISH guidelines (the committee is familiar with these), but which to follow? The committee decided a priori that Australian national guidelines, if they existed, would be referenced in preference to overseas ones. We mentioned that current Australian hypertension guidelines should be revised, and that clinical practice was probably at odds with these recommendations. Secondly, guidelines quickly become dated. Cradick cites the recommendation of Hayden et al that aspirin should be introduced if the annual risk of a cardiovascular event is > 0.6%.2 The latest Australian guidelines3 recommending a > 1% annual risk as the treatment threshold were published just after we received Cradick’s letter. The Hayden article is thus (for some patients) at odds with current local recommendations. Consistent with our approach, we will include the Australian recommendations in the first update of our document (July 2004). Cradick’s comments imply bias in the presentation of the data; yet he fails to substantiate this. Neither the clinical trials quoted (nearly all of which are funded by the pharmaceutical industry) nor the conclusions or inferences drawn have been challenged. He refers to the “heavy” emphasis on the use of ACE inhibitors and statins, implying that this is inappropriate. We would argue that, given the strength of the evidence, this emphasis is appropriate, and reflects current specialist practice in tertiary centres. Careful reading of the National Prescribing Service publications will show that “heavy” reference is made to the 4S,4 LIPID,5 CARE,6 and WOSCOPS7 studies (for example, NPS News 20 February 20028), as well as to the prescribing information for Lipitor (Pfizer), Pravachol (Bristol-Myers Squibb) and Zocor (Merck Sharp & Dohme). We must caution against “throwing the baby out with the bathwater”. The HPS, CARE, LIPID, WOSCOPS, HOPE, PROGRESS, 4S, CURE, and CREDO studies represent substantial and widely acclaimed clinical trials that have had a positive impact on clinical care. They have all been funded by the pharmaceutical industry. Finally, about 130 GPs in clinical practice had some input in compiling and formatting this document. The document was tested before publication in over 30 000 patients, and was peer reviewed by several clinicians. It is a pity that Cradick was not a participant in any of these processes.

Gregory R Fulcher · John V Amerena · Greg W Conner

Objectives: To determine the causes of sudden cardiac death in people aged 35 years or younger.Design and setting: A review of all autopsies performed between 1 January 1994 and 31 December 2002 at a major Sydney forensic medicine department serving an area with over 2 million people.Main outcome measures: Incidence of various types of cardiac disease causing sudden death in those aged ≤ 35 years; proportion of deaths in which no cause was found at autopsy.Results: There were 10 199 autopsies performed during the study period. Of these, 2986 (29.2%) deaths occurred in people aged ≤ 35 years; 193 were classified as sudden cardiac deaths. The cause of sudden death in this group was not established in 60 (31%), and was presumed to be due to primary arrhythmogenic disorders. Coronary artery disease occurred in 46 (24%), hypertrophic cardiomyopathy/unexplained left ventricular hypertrophy in 29 (15%), and myocarditis in 23 (12%).Conclusions: Unexplained deaths, presumed to result from sudden primary arrhythmogenic causes, occur in young Australians with structurally normal hearts. That underlying disease-causing genetic defects may be involved has clinical implications for family members.

Alessandra Doolan BMedSc · Christopher Semsarian MB BS, PhD, FRACP · Neil Langlois MB BChir, MD, FRCPA

Matthew T Naughton,* Darren R Mansfield,* David M Kaye,† Peter Bergin,† Meroula Richardson† * Respiratory Physician, † Cardiologist, Alfred Hospital, PO Box 315, Prahran, VIC 3181. m.naughtonATalfred.org.au To the Editor: We were surprised that Campbell’s recent article on heart failure1 made no mention of sleep apnoea. This is despite the fact that about 50% of heart failure patients have sleep apnoea (either central or obstructive) and that quite a large body of literature now supports a causative relationship between obstructive sleep apnoea and congestive heart failure, supported by recent authoritative reviews. 2-4 Canine studies have shown that, in the absence of any other variable, obstructive sleep apnoea results in left ventricular systolic and diastolic dysfunction. Importantly, the impact of continuous positive airway pressure (CPAP) in acute cardiogenic pulmonary oedema and subacute pulmonary oedema (central sleep apnoea) and heart failure in the setting of obstructive sleep apnoea are not mentioned. Identification and treatment of sleep apnoea in people with heart failure is supported by a trial we have recently conducted in which significant improvements in quality of life and objective markers of cardiac function were seen in patients treated with nasal CPAP.5

Matthew T Naughton · Darren R Mansfield · David M Kaye · Peter Bergin · Meroula Richardson

Duncan J Campbell Senior Research Fellow, St Vincent's Institute of Medical Research, 41 Victoria Parade, Fitzroy, VIC 3065. J. CampbellATmedicine.unimelb.edu.au In reply: I am grateful to Naughton and colleagues for their contribution to the debate about how we might prevent the epidemic of heart failure. I agree that both obstructive and central sleep apnoea are frequently associated with heart failure and that treatment of sleep apnoea can improve cardiac function. However, as indicated by its title, my article focused on how we might prevent heart failure. Central sleep apnoea in heart failure is usually the consequence of the heart failure.1 Heart failure may contribute to obstructive sleep apnoea as well,2 and obstructive sleep apnoea may, in turn, be an important contributor to heart failure pathogenesis. Epidemiological evidence links obesity with hypertension and obstructive sleep apnoea.3 Significant sleep apnoea is present in about 40% of obese people, and about 70% of people with obstructive sleep apnoea are obese.3 Obesity and obstructive sleep apnoea may each contribute to one another, and both may contribute to hypertension. The need to prevent obstructive sleep apnoea is an argument for more effective prevention of obesity. In addition to reducing its metabolic consequences, preventing obesity is likely to reduce the incidence of hypertension and obstructive sleep apnoea, and to thereby decrease the incidence of heart failure. For people with obstructive sleep apnoea not caused by obesity, alternative strategies will be required to prevent and treat the sleep apnoea and thus prevent its consequences.

Duncan J Campbell

Balakrishnan R Nair,* Brendan Flynn† * Director, † Medical Registrar, Division of Geriatric Medicine, John Hunter Hospital, New Lambton, NSW 2291. knairATmail.newcastle.edu.au To the Editor: We refer to the recent article by Parslow and Jorm1 and the editorial by Headey2 on the link between pet ownership and health outcomes. There is no evidence that pet ownership per se confers cardiovascular benefits. Indeed, the findings of the study were that pet owners were more likely to smoke, had a higher diastolic blood pressure and a higher body mass index than the non-pet owners. The editorial points out that, based on sociological studies, it is likely that pet ownership does have a positive effect on health, but the medical data demonstrating how this is achieved are lacking.2 Might there be other negative effects of pet ownership on health outcomes? A patient under our care recently demonstrated the potential risks involved in pet companionship for elderly people. An 81-year-old woman who was living independently was admitted after a fall caused by tripping over her delightful Himalayan Persian cat. Her presenting symptom was severe back pain exacerbated by weight bearing. However, no bony abnormality was identified. She had difficulty mobilising initially, and the outcome of her fall was significant morbidity with some loss of her previous mobility, even on discharge. She stayed in hospital for 12 days. A follow-up phone call revealed that the patient was still experiencing difficulty mobilising some 2 weeks after discharge. This case raises the possibility that the risks may outweigh the benefits of pet ownership in elderly people who are already at risk of falls. A MEDLINE search, using the terms elderly, trauma, cat, pet and fall (and combinations of these), did not reveal any relevant literature. A recent case report highlighted other cardiovascular issues relating to cat ownership.3 It described a patient who had recurrent episodes of syncope whenever her cat slept on the right side of her neck. The underlying mechanism was carotid sinus hypersensitivity. She required a single-lead ventricular pacemaker and for the cat to lie on her left side. Anecdotal evidence from colleagues highlighted the danger of “dogs taking elderly patients for walks”, resulting in rotator cuff injuries. Additionally, older patients with peripheral vascular disease and fragile skin have presented with non-healing ulcers from dog scratches. Pet ownership for the purpose of modifying cardiovascular risk factors would seem to be unwise in this population. However, the benefits of companionship and the pleasure derived from pets may outweigh the risk of falls for many elderly patients. Should we be doing more “cat scans” or “pet scans” in older patients?

Balakrishnan R Nair · Brendan Flynn

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