Stent thrombosis is an infrequent but severe complication after coronary stent implantation. Dual antiplatelet therapy has markedly reduced the occurrence of this potentially catastrophic event. The optimal duration of clopidogrel therapy in patients with drug-eluting stents is unknown. We describe a case of stent thrombosis 9 days after discontinuation of clopidogrel therapy, more than 3 years after placement of drug-eluting stents. (MJA 2008; 189: 229-230) Clinical record A 60-year-old man presented to his local community hospital with chest pain. He had had a percutaneous coronary intervention more than 3 years previously, when drug-eluting TAXUS stents (Boston Scientific Corporation, Natick, Mass, USA) were implanted in his left anterior descending coronary artery (LAD) and right coronary artery (RCA). Overlapping stents were placed in the LAD, measuring 2.5 × 16 mm and 2.5 × 8 mm, inflated to 1620.8 kPa. He had been taking aspirin and clopidogrel as dual antiplatelet therapy since that time. His past medical history included well controlled hypertension. At the time of presentation, he was haemodynamically stable, with normal resting electrocardiograms and normal troponin levels. As intermittent chest pain persisted despite medical management, he was transferred to an interventional centre for further investigations. Coronary angiography showed mild irregularities of his LAD with widely patent stents in both the LAD (Figure, A) and RCA, with normal left ventricular function. There was no evidence of in-stent restenosis or disease adjacent to the stents. The next day, the patient developed abdominal pain associated with liver function test abnormalities indicative of cholestasis. Ultrasound of his abdomen showed multiple gall stones. It was thought likely that his chest pain was the result of his subdiaphragmatic disease. His clopidogrel therapy was stopped in anticipation of surgery, and he underwent a successful laparoscopic cholecystectomy. Five days later, he was discharged and clopidogrel therapy was not reinitiated. The patient re-presented to his local hospital 4 days after discharge, with central chest pain. His electrocardiogram showed ST-segment elevation in the anterior leads, and reciprocal ST-segment depression in the inferior leads. In view of his recent surgery, he was not deemed a candidate for thrombolytic therapy, and was urgently transferred to our hospital. An angiogram showed thrombus within the stent in his LAD (1190 days after it was implanted), with slow antegrade filling of the distal vessel (thrombolysis in myocardial infarction [TIMI] grade 1 flow; Figure, B). His right coronary and circumflex arteries were normal, and a left ventriculogram showed severe hypokinesis of his apical wall. The clot was partially removed using a 6-French Export Aspiration Catheter (Medtronic Inc, Minneapolis, Minn, USA), and the artery was further dilated within the stent. No further stents were implanted. A small residual filling defect was noted after balloon angioplasty (Figure, C). Intravenous therapy with the glycoprotein IIb/IIIa inhibitor abciximab was initiated, and a loading dose of clopidogrel given. The period after percutaneous transluminal coronary angioplasty was uneventful, and the patient was subsequently discharged in a stable condition. A: Arrow indicates patent stents in the left anterior descending coronary artery. B: Arrow indicates thrombus within the stent in the left anterior descending coronary artery. C: Arrow points to a small residual filling defect after balloon angioplasty. DiscussionDrug-eluting stents (DES) have been shown to be more effective than bare-metal stents (BMS) in reducing angiographic restenosis, by limiting intimal hyperplasia. This reduces the need for subsequent revascularisation procedures.1-3 However, there is growing concern that delayed endothelisation and incomplete neointimal healing might lead to adverse cardiac outcomes and death as a result of late or very late stent thrombosis.4,5 Mortality rates have ranged from 16% in a recent published registry from Spain documenting definite angiographic thrombus6 to as high as 45% in another series including both definite and probable thrombosis.7 Stent thrombosis is an uncommon but life-threatening complication of stent implantation.7,8 Stent thrombosis may be classified according to the time since implantation:9 acute stent thrombosis occurs within 24 hours of the procedure; subacute stent thrombosis between 1 and 30 days after implantation; late stent thrombosis between 1 month and 1 year after implantation; and very late stent thrombosis more than 1 year after the procedure. The cumulative incidence of stent thrombosis with DES at 9–12 months has ranged from 0.5% to 1.5%, which is comparable to stent thrombosis with BMS,10,11 with an incidence as high as 0.6% per year thereafter.12 Recent clinical trials and registries have raised concern over increased rates of very late stent thrombosis with DES.10,13,14 The cessation of dual antiplatelet therapy has been implicated as a pathophysiological factor in late and very late stent thrombosis.7,11,15 Incomplete endothelisation of the metal struts because of the antiproliferative properties of the drug has also been implicated.7,12,15 Mechanical factors involved in stent thrombosis have included malapposition of the stent to the vessel wall when originally implanted, and late malapposition because of retraction of the vessel wall during vessel remodelling.11,12 Whether this is related to the drug, polymer, or stent platform itself is unknown.12 The optimal duration of dual antiplatelet therapy after DES placement is still unknown. Current guidelines recommend clopidogrel therapy for at least a month and ideally up to a year with BMS, and for at least a year for patients treated with DES after hospitalisation for an acute coronary syndrome.16 However, reports of very late cardiac events among patients with DES, particularly in relation to stent thrombosis and cessation of clopidogrel therapy, have cast doubt on these recommendations.10,17,18 A recent observational study comparing DES with BMS suggested that clinical events related to late stent thrombosis in patients with DES after the discontinuation of clopidogrel therapy might limit the benefit of DES.10 Though there have been similar case reports,17,18 ours is a unique example of an angiographically proven very late stent thrombosis, 3 years after placement of DES. During angiography 9 days prior to the event, no abnormality was noted within the previously implanted DES, nor at the stent edges before the cessation of clopidogrel therapy. Nine days after stopping therapy with this drug, filling defects were seen (Figure, B). This case highlights the concerns about the duration of clopidogrel therapy following implantation of DES. It also raises the question of whether life-long clopidogrel therapy may be warranted in some patients.

Rohit Barthwal MB BS, FRACP · Brian A Herman MD, PhD, FACC

VTE prophylaxis is effective and safe, but grossly underused in Australian hospitals In this issue of the Journal, Ho and colleagues report their findings from a Perth community-based study of venous thromboembolism (VTE).1 They found an incidence of VTE, which includes deep vein thrombosis and pulmonary embolism, of 0.83 (95% CI, 0.69–0.97) per 1000 population per year. This figure is consistent with hospital discharge data from the Australian Institute of Health and Welfare, which predict an estimated 14 716 VTE cases in 20082 or an incidence of 0.74 per 1000. This incidence comes with high costs to Australian society in terms of deaths, morbidity and health care expenditure. VTE is a major cause of hospital deaths — Australian Institute of Health and Welfare data indicate that 7% of all deaths in Australian hospitals are due to VTE,2 and autopsy studies suggest the percentage may be as high as 10%.3 Thus, VTE causes more deaths than any common cancer (breast, lung, prostate or bowel) and is 40 times more deadly than HIV/AIDS in Australia. VTE also causes significant long-term morbidity from post-thrombotic syndrome (chronic leg swelling, pain and skin ulcers) and pulmonary hypertension. A report by Access Economics estimated that the cost to Australia of treating VTE is currently $1.72 billion annually (0.15% of gross domestic product).2 This estimate includes costs attributable to direct health system expenditure ($148 million), productivity loss ($1.38 billion) and efficiency loss ($162 million). If costs relating to premature mortality are included, then VTE represents the most costly disease burden among the 16 diseases (including cancer, dementia, osteoporosis, cardiovascular disease and schizophrenia) that have been studied and ranked by Access Economics in recent years. The key to saving lives, improving patient outcomes and reducing the huge financial cost to individuals and the nation lies in prevention of this disease. Evidence-based findings from well designed studies have clearly shown that prevention is possible.4,5 With a modest outlay, VTE incidence can be significantly reduced, effectively and safely, using anticoagulants such as unfractionated or low-molecular-weight heparins, or, particularly if a risk of bleeding exists, by mechanical means (compression stockings and intermittent calf compression). However, current data suggest that VTE prophylaxis is grossly underused in hospitals in Australia and overseas.6 The ENDORSE study (which enrolled over 68 000 medical and surgical patients in 32 countries, including Australia) showed that 51.8% of hospital inpatients were at risk of VTE, but only 58.5% of at-risk surgical patients and 39.5% of at-risk medical patients received VTE prophylaxis.6 This is consistent with the findings of a prospective audit carried out by the National Health and Medical Research Council (NHMRC) National Institute of Clinical Studies in Australian hospitals in 2005–2006 (Dr Sue Phillips, Director, Research Implementation Program, National Institute of Clinical Studies, NHMRC, Melbourne, personal communication). These studies show that many at-risk hospital patients in Australia and overseas, especially medical inpatients, are left unprotected against VTE. Adoption of clinical guidelines by hospitals can lead to increased levels of appropriate prescribing of VTE prophylaxis.7 However, the risk of thromboembolic events continues after hospital discharge, and far less research has been conducted into the use of VTE prophylaxis in the community. There is an increasing trend for at-risk medical patients (eg, patients with chronic lung disease or cardiac failure) to be managed in the community, especially through hospital-in-the-home and early discharge programs.8 With increasingly short hospital stays for both surgical and medical patients, it is important that community-based doctors are aware of the importance of VTE risk assessment and the continuation or commencement of VTE prophylaxis for their patients. The Australia & New Zealand Working Party on the Management and Prevention of Venous Thromboembolism has been convened to formulate a national strategy to promote the optimal use of VTE prophylaxis. Initiatives of the Working Party will include: Developing simple, user-friendly VTE prevention guidelines that will assist doctors to identify and treat at-risk patients. The fourth edition of the Working Party’s VTE prevention guidelines — based on the recommendations of the American College of Chest Physicians4 and the International Union of Angiology,5 but adapted to local conditions (see http://stgcs.med.unsw.edu.au/stgcsweb.nsf/page/TBD) — has recently been published.9 Promoting hospital and community education programs to create awareness of the VTE prevention guidelines and enhance understanding of VTE risk assessment. Researching and developing recommendations for reminder systems, including computer alerts10 or interventions by a VTE nurse or pharmacist, with the intention of reminding doctors to prescribe appropriate VTE prophylaxis. Establishing VTE centres of excellence that will act to promote optimal VTE patient care. Lobbying federal and state governments to initiate health policies that will lead to increased use of VTE prophylaxis in Australian hospitals, including designating VTE prophylaxis rate as a hospital performance indicator. This is particularly relevant now, while the federal government is working with state governments to reduce surgical waiting lists. If patients undergoing surgery do not receive appropriate VTE prophylaxis, this could lead to increases in adverse outcomes of VTE and fatal pulmonary embolism. Hosting a national VTE summit to generate new ideas for improving VTE prevention. VTE is a significant health issue internationally and in Australia. It is a common cause of hospital deaths and a considerable financial burden on governments and individuals. Doctors, nurses, health administrators and governments should work together to ensure all surgical and medically ill patients in hospital have their VTE and bleeding risk assessed, and to maximise appropriate use of VTE prophylaxis. Achieving this will improve patient outcomes, save lives and reduce health costs.

Beng H Chong MB BS, FRACP, PhD · Jeffrey Braithwaite MBA, PhD, FCHSE · Mark F Harris MB BS, FRACGP · John P Fletcher MD, MS, FRACS

To the Editor: We report significant sinus bradycardia in a patient presenting with an acute coronary syndrome shortly after beginning bupropion therapy to assist with smoking cessation. A 53-year-old man was attended by paramedics for typical ischaemic chest pain. He had sinus bradycardia (45 beats/min) and hypotension (blood pressure, 85/60 mmHg), and was found to have a serum troponin I concentration of 1.2 μg/L, but no diagnostic electrocardiographic changes. He was admitted to our hospital with an acute coronary syndrome. He reported his medications at the time of admission as including metoprolol 50 mg twice daily (for hypertension) and paroxetine 20 mg daily (for depression). The patient was given multiple doses of intravenous atropine (total, 1.2 mg) and adrenalin (total, 2 mg). After an adrenalin infusion was begun, he developed ventricular tachycardia (170 beats/min), but his cardiac rhythm spontaneously returned to sinus bradycardia. Two days after admission, two coronary stents were successfully deployed in a critically stenosed right coronary artery. Bradycardia (45–50 beats/min) persisted. The following day, it was discovered that 3 weeks previously, the patient’s general practitioner had prescribed bupropion 150 mg twice daily to assist with smoking cessation, which he had been taking up until the day of admission. Bradycardia continued until hospital discharge. One month after discharge, he was in sinus rhythm (60 beats/min) and was clinically well. Bupropion is a selective noradrenalin, dopamine and serotonin reuptake inhibitor. The mechanism by which it enhances the ability of patients to abstain from smoking is unknown.1 Bupropion inhibits the activity of the cytochrome P450 2D6 isoenzyme, which metabolises metoprolol.2 Concurrent use of bupropion and metoprolol can increase serum metoprolol levels, and clinically significant bradycardia has been reported.3 Further, paroxetine, a selective serotonin reuptake inhibitor (SSRI), is a potent cytochrome P450 2D6 inhibitor, which would have further increased serum metoprolol levels. Bradycardia associated with metoprolol and paroxetine dual therapy has been described.5 Additionally, there is the potential for serotonin syndrome to develop in a patient administered multiple SSRIs. In our patient, the administration of bupropion and paroxetine could have potentially led to serotonin syndrome.6 Our patient’s pharmacological profile was complex, with potential adverse pharmacodynamic effects. The most likely precipitant of the patient’s bradycardia was his acute coronary syndrome, although bupropion may have contributed. The case highlights the potential for significant drug interactions when new drug therapies are initiated. Bupropion and metoprolol (and other drugs metabolised by the cytochrome P450 2D6 isoenzyme pathway) should be co-administered with caution. The importance of common pathways of drug metabolism should be recognised to avoid potential adverse events, particularly when multiple medications are used.

Jacqueline Landau · Andrew E Ajani

Objectives: To estimate prevalence of selected diagnosed chronic diseases among patients attending general practice, in the general practice patient population, and in the Australian population, and to compare population estimates with those of the National Health Survey (NHS).Design, setting and participants: In late 2005, 305 general practitioners each provided data for about 30 consecutive patients (total, 9156) as part of the BEACH (Bettering the Evaluation And Care of Health) program, a continuous national study of general practice activity. GPs used their knowledge of the patient, patient self-report, and medical records as sources.Main outcome measures: Crude prevalence of each listed condition currently under management among surveyed patients, and adjusted prevalence for the general practice patient population, and the national population.Results: 39.6% of respondents had none of the listed conditions diagnosed; 30.0% had a cardiovascular problem (uncomplicated hypertension, 17.6%; ischaemic heart disease, 9.5%); 24.8% had a psychological problem (depression, 14.2%; anxiety, 10.7%); 22.8% had arthritis, mostly osteoarthritis (20.0%); 10.7% had asthma; and 8.3% had diabetes, mostly type 2 (7.2%). Adjustment to the population attending general practice resulted in lower estimates for cardiovascular disease, arthritis and diabetes but had little effect on prevalence of asthma and psychological problems. After adjusting for non-attenders, about one in five people in the population had a cardiovascular problem, a similar proportion had a psychological problem, 14.8% had arthritis, and about 10% had asthma, hyperlipidaemia and gastro-oesophageal reflux disease. Estimates were similar to NHS results for any arthritis, asthma, and malignant neoplasms; higher for any cardiovascular problem; far higher for specific cardiovascular diseases, cerebrovascular disease and hyperlipidaemia; and almost twice the NHS estimate for psychological problems (particularly depression and anxiety). Estimates for type 1 diabetes aligned with NHS results, but were far higher for “all diabetes” and type 2 diabetes.Conclusions: This study offers an alternative, perhaps more accurate, approach to measurement of disease prevalence than the NHS approach, which relies on respondent self-report alone. It provides valid prevalence estimates with the help of GPs at a fraction of the cost of the NHS. This study could be repeated annually to augment other data sources and better define existing health needs in the population.

Stephanie A Knox BA(Hons), MPH, BSc · Christopher M Harrison BPsych(Hons), MSocHealth · Helena C Britt BA, PhD · Joan V Henderson BAppSc(HIM)(Hons), PhD

Objectives: To estimate the prevalence and patterns of multimorbidity in a sample of patients attending general practice, in the population who attended general practice in 2005, and in the Australian population.Design, setting and participants: Secondary analyses of data from a study of prevalence of selected conditions (a substudy of the BEACH [Bettering the Evaluation And Care of Health] program); data were provided by 305 general practitioners for 9156 patients seen in July–November 2005, based on knowledge of the patient, patient self-report, and medical records. Listed conditions were classified according to the Cumulative Illness Rating Scale morbidity domains.Main outcome measures: Prevalence of morbidity in each domain; prevalence of specific patterns of multimorbidity (defined as presence of morbidity in two or more domains).Results: Prevalence of multimorbidity was estimated as 37.1% of surveyed patients, 29.0% of people who attended a GP in 2005, and 25.5% of the Australian population. Prevalence and complexity (number of domains present) increased with age: 83.2% of surveyed patients aged 75 years or older had multimorbidity, 58.2% had morbidity in three or more domains, and 33.4% in four or more. Prevalence of multimorbidity did not differ between the sexes. The most common morbidity combinations were arthritis/chronic back pain + vascular disease (15.0% of sample), a psychological problem + vascular disease (10.6%) and arthritis/chronic back pain + a psychological problem (10.6%). We estimate that 10.6% of people attending a GP in 2005 and 9.3% of the population have arthritis/chronic back pain + vascular disease (± other morbidity types studied), and this group accounted for about 15.2 million Medicare-claimed general practice encounters in 2005.Conclusions: This study provides the first insight into prevalence and patterns of multimorbidity in Australia. Knowledge of the common combinations of multimorbidity may help in planning the health services needed in the future by an ageing population with an increasing burden of multimorbidity.

Helena C Britt BA, PhD · Christopher M Harrison BPsych(Hons), MSocHealth · Graeme C Miller PhD, FRACGP · Stephanie A Knox BA(Hons), MPH, BSc

To the Editor: We conducted a qualitative study to explore the perspectives of general practitioners and allied and other health professionals on their interactions in the care of patients with chronic disease, especially where Team Care Arrangements (TCAs) are involved. We interviewed 16 clinicians from urban and rural New South Wales who were involved in the care of patients with type 2 diabetes, ischaemic heart disease and hypertension — four GPs, two practice nurses, two medical specialists and eight allied health clinicians. Interviews took place from late 2006 to early 2007. While all those interviewed felt that a coordinated approach provided optimal management of chronic disease, this did not always seem to translate into smooth working relationships. Allied health clinicians and medical specialists described two types of attitudes of GPs to team care. They perceived some GPs as accepting of the involvement of others in patient care, leading to mutually respectful and highly satisfying working relationships. However, they felt other GPs did not value the opinions of allied health professionals and referred patients to them to fulfil a process (either for TCAs or at the patient’s request), or saw them as competitors. As one urban allied health clinician said, “I think they’ve got to realise that we’re not there to compete, we are there to assist”. TCAs provide financial incentives for GPs to coordinate care.1 We have previously reported that multidisciplinary care plans are associated with improved attendance at allied health services and improved metabolic control for patients with diabetes.2 However, in the present study some respondents felt that TCAs were little more than “paper shuffling” — predominantly a mechanism to attract reimbursement, rather than to facilitate two-way communication. Although TCAs provide an opportunity for communication between health care professionals, they have not overcome all the barriers to communication, especially in cases where an interprofessional relationship based on clear understanding of each other’s roles has not already been established. Our findings suggest that relationship-building and discussions about roles in shared care, including the power differentials between professionals, would improve the functioning of TCAs. Other recent studies have also reported on the lack of effective collaboration between GPs and other health professionals in managing chronic conditions.2,3 Respondents felt that it was uncommon for clinicians to discuss and agree on a plan of care. Optimal management of chronic disease requires a team approach and, consistent with other studies,4,5 we found that all the professional groups interviewed acknowledge the desirability of team care and its potential to improve patient outcomes. With increasing emphasis on team care, it is imperative that policies fund and facilitate a real team approach that is in the best interests of patients — one that places greater emphasis on two-way communication rather than paper shuffling or gatekeeping. This requires working with allied health professionals, medical specialists and GPs to improve communication and trust between clinicians. The Divisions of General Practice must surely be well placed to facilitate this process.

Sue E Kirby · Joyce L Chong · Maureen Frances · Gawaine Powell Davies · David A Perkins · Nicholas A Zwar · Mark F Harris

Objective: To examine the changes in cardiovascular disease (CVD) risk factors for a cohort of patients with type 2 diabetes in general practice.Design and setting: A 4-year retrospective cohort study using extracted data from an active Division of General Practice diabetes register in Australia.Participants: 628 patients (297 female; 331 male) with type 2 diabetes who participated in the diabetes program of the Southern Highlands Division of General Practice and for whom evaluation data were recorded each year from 2002 to 2005.Main outcome measures: Changes in the following CVD risk factors over time: body mass index (BMI), serum lipid levels (total cholesterol [TC], low-density lipoprotein cholesterol [LDL-C], high-density lipoprotein cholesterol [HDL-C], total triglycerides [TG]), systolic and diastolic blood pressure (BP), and glycated haemoglobin (HbA1c) level.Results: After adjusting for age, sex, duration and clustering, there was significant improvement in serum lipid levels (TC and LDL-C; P < 0.05) over time; and there was no significant change in BP, HbA1c level or BMI. Older patients had significantly worse systolic BP, but significantly better BMI and lipid levels than younger patients. Longer duration of diabetes was associated with worse systolic BP and HbA1c level, but better HDL-C level. People with higher BMI were likely to have worse systolic BP, and HDL-C and HbA1c levels, but better TC level than those with lower BMI.Conclusions: Improving BP, HbA1c level and BMI may be more difficult than improving lipid levels. There is a need for more intensive and comprehensive interventions to reduce the total risk of CVD.

Qing Wan MB BS, MPH, MMed · Jane Taggart BEd, DipPE, MPH · Mark F Harris FRACGP, MD · Upali W Jayasinghe MSc, PhD · Warwick Ruscoe MB BS, RACGP · Jill Snow RN · Gawaine Powell Davies BA, MHP

A cold never killed anyone ... did it? I went to work with a cold. My nasty sore throat woke me early, so I spent the time emailing our incoming clinical students: Get your influenza vaccinations before you start your clinical rotations — influenza kills people, vaccinating health care workers decreases mortality in nursing homes, and vaccination reduces other viral infections and days off work or school, and meets duty of care for oneself and others!1,2 Sincerely, your (vaccinated) Clinical Dean Sneezing and miserable, I considered staying home, abandoning the 20 complex, high-admission risk (general medicine) patients scheduled at the Aboriginal Health Centre and the hospital, many of whom had waited 2–3 months for an appointment. I thought of my mother — “Go to school, you’re not dying, you only have a cold!” Memories of my only previous sick day resurfaced: as an on-call intensive care unit senior registrar — feverish, achy, sneezing, nose running like a faucet, I had decided this wasn’t good for anyone. Caving at the prospect of working all night sick, I settled for guiltily calling in a fellow registrar. My “chief” had then rung — “How are you?” — Oh no, they think I’m skiving off! Peer pressure is strong stuff. So, this time, with patients waiting and my past lurking, I took some paracetamol, packed some tissues, and went to work. My first patient, recovering from a lung resection for bronchiectasis after last winter’s viruses almost killed him, is now surviving his first postoperative virus — not a drama. After warning him to stay far away and not shake my hand, I got through the rest of the day constantly apologising to my patients and colleagues, suppressing sneezes, washing my hands, and touching as few things as possible. After clinic, an email explained the coincidental absence of my medical students — “Sick with cough, unable to attend”. A colleague’s voice from the doorway wryly observed, “You’re sending the students mixed messages about getting vaccinated and duty of care while working with a cold yourself, potentially infecting everyone in sight”. I responded blithely, “I’m more dedicated to my work than the students are (different generation), and besides, a cold never killed anyone” ... but then, a moment of evidence-based-medicine horror hit me — That’s true, right? Although my work-despite-a-cold ethic hasn’t done me any harm (misery aside), I salved my skiving-off guilt with my greater desire to “do no harm”, collected kilos of paperwork and my laptop, and retreated home for a day in isolation. A hasty MEDLINE search for “common cold AND mortality” from 1997 to 2007 revealed 68 papers. Of these, the 13 highly relevant papers (gulp) fell into three categories: chronic obstructive pulmonary disease (COPD) or asthma complications (eight); childhood morbidity and deaths, largely related to cold medications (four); and HIV-related deaths (one). I quickly discovered that over 50% of COPD exacerbations are attributed to respiratory viruses — no big surprise.3 More concerningly, rhinoviruses are now well established culprits causing significant morbidity and even mortality.4-6 Indeed, only miniscule amounts of rhinovirus are needed to infect patients who then develop lung function changes typical of COPD exacerbations.7 If COPD causes 4% of all deaths per year in the United States (Australia should be similar)8 and viruses cause half of COPD exacerbations, then about 2% of mortality is potentially attributable to respiratory viruses. I began to worry about my patient with bronchiectasis. On the other hand, at least I hadn’t done any harm by prescribing over-the-counter cold medications with worrying potential for harm for any of my adult patients, let alone any children.9 Hmm ... non-steroidal anti-inflammatory medications seem to have evidence for relief (as long as I don’t have hypertension, stomach ulcer, heart failure, or kidney disease),6 so I think I’ll take some. What about vaccination? Reassuringly, at least for my reputation among my students and staff, several reviews supported influenza vaccination,10,11 especially since influenza viruses account for up to 10% of “common colds”.6 Distressingly, however, vaccination rates among health care workers are less than optimal — 82% of doctors and 40% of nurses had been vaccinated in one emergency department study (the best rates I could find).11 One dilemma remains. I, like 80% of doctors, worked with an illness for which I would have “sick-listed” my patients,12 but given that I care for under-served patients in a rural area with a shortage of doctors, is it worse to stay home and reschedule patients for appointments weeks to months later or to risk exposing them to my virus-laden self? Mortality rates for residents of rural and regional areas in Australia are 10% higher than for city-dwellers13 — largely due to health care access issues. My personal vaccination campaign should decrease the frequency of my own (and my students’ and staffs’) “colds” and, if I’m sick less often, this should increase access to me, thus decreasing my patients’ morbidity and mortality. Sadly, the evidence suggests that if I were working in an intensive care unit or a medical ward with high-risk COPD patients, I could justify staying home, but in my general medicine role and doctor-shortage situation, the mortality trade-offs suggest that I should probably go to work with a cold next time too (sigh). But as for you, dear health care providers: first, do what I say and what I do (get vaccinated against influenza); and second, do what I say and not what I did, and consider staying home with your own cold — because, you never know, it just might kill someone ...

Dawn E DeWitt MD, MSc, FRACP

Aim: To determine the feasibility of performing a large clinical trial of the use of aspirin for the primary prevention of cardiovascular disease in older participants — the ASPirin in Reducing Events in the Elderly (ASPREE) trial.Design and participants: A randomised double-blind placebo-controlled pilot trial of 100 mg of enteric-coated aspirin tablets daily, in men and women aged 70 years and over who did not have overt cardiovascular disease, and who were followed for 12 months. Participants were identified from the computer databases of general practitioners who were co-investigators in a previous trial.Setting: The Melbourne metropolitan area between March 2003 and June 2005.Main outcome measures: The level of response to participation by GPs; the level of response from potential trial participants; the screening-to-randomisation rate to ensure the recruitment target could be achieved; and the retention of participants in the trial after 12 months.Results: Forty-two GPs (23% of 180 mailed) expressed interest in participating in the pilot trial. Nineteen became co-investigators, of whom six were not required to meet recruitment targets. Letters were sent to 2614 patients, of whom 243 were screened and 209 (86%) were randomly allocated to receive aspirin or placebo. At 12 months,192 (92%) returned for follow-up, and 153 of these (80%) were still taking trial medication. There was a significant reduction in mean haemoglobin level in those taking aspirin.Conclusions: The recruitment strategy for ASPREE, based on methods developed for the conduct of a previous large-scale trial conducted in general practice, was successfully redeployed in this pilot study, with improved efficiency resulting from computerised database searching, telephone pre-screening, a simpler run-in phase and participant familiarity with the trial drug. We conclude that conducting ASPREE in Australian general practice with 18 000 participants is feasible.Trial registration: International Standard Randomised Controlled Trial Number Register ISRCTN83772183.

Mark R Nelson FRACGP, PhD, FAFPHM · Christopher M Reid BA, MSc, PhD · David Ames MD, FRCPsych, FRANZCP · Lawrence J Beilin MD, FRACP, FRCP · Geoffrey A Donnan MD, FRACP · Peter Gibbs MB BS, FRACP · Colin I Johnston MB BS, FRACP · Henry Krum FRACP, PhD · Elsdon Storey DPhil, FRACP · Andrew Tonkin MB BS, FRACP · Rory Wolfe BSc, PhD · Robyn Woods BSc(Hons), PhD · John J McNeil PhD, FRACP

Addiction medicine deals with problems arising from the use of psychoactive substances, and encompasses the disciplines of general practice and primary care, psychiatry, psychology, internal medicine, public health, pharmacology and sociology. Addiction is a chronic, relapsing illness that is difficult to cure. There are now effective, evidence-based interventions for the prevention and treatment of substance misuse disorders. Harm minimisation and treatment are more cost-effective than policing and supply-reduction methods of responding to substance misuse.

Brian R McAvoy MD, FAChAM, FRNZCGP