Cardiovascular diseases

Objective: To describe the outcome of valve surgery, for rheumatic heart disease (RHD) and non-RHD, in residents of Cape York Peninsula and the Torres Strait Islands referred to the Cairns Base Hospital specialist outreach service.Design and participants: Retrospective review of medical records on all patients residing in the outreach area who had surgery for valvular heart disease between 1 January 1992 and 31 December 2004.Main outcome measures: Operation type and perioperative characteristics; 5- and 10-year survival rates; reoperation rates; complications.Results: Forty-seven patients met the selection criteria; the median age was 40 years (range, 4–76 years); and 39 patients were Indigenous. RHD was the predominant cause of valve dysfunction (30/47 patients). Thirty-seven patients had valve replacements, six had valve repair and four had balloon valvotomy as the initial procedure. There were three bleeding complications, two episodes of operated valve endocarditis, and six embolic complications. There were nine valve-related deaths (six in the first 5 years). At 5 years, all seven patients who had had valve repair or balloon valvotomy were alive. Seven of the 47 patients required reoperation. Survival analysis showed freedom from valve-related deaths to be 83% (95% CI, 66%–92%) at 5 years and 61% (95% CI, 33%–80%) at 10 years. Freedom from reoperation at 5 years was 88% (95% CI, 71%–95%). Among the 30 patients with RHD, freedom from valve-related death was 80% (95% CI, 60%–92%) at 5 years and 52% (95% CI, 21%–75%) at 10 years. In patients with RHD, freedom from reoperation at 5 years was 87% (95% CI, 65%–96%).Conclusion: Valvular heart disease results in substantial morbidity and mortality, despite intervention. Efforts need to focus on prevention of rheumatic fever and closer follow-up.

Anna McLean MB BS · Michael Waters MB BS(Hons) · Emma Spencer MB BS · Clive Hadfield MB BS

To the Editor: We report an exceptional case of a woman who underwent emergency “finger fracture valvuloplasty” (FFV) in 1954 to treat rheumatic mitral stenosis and required no further surgical intervention for 51 years. The woman presented in 1954 with pulmonary oedema due to mitral stenosis during the first trimester of her second pregnancy. She underwent FFV at Lewisham Hospital in Sydney. She had a prolonged convalescent period, was discharged after 5 months, and delivered a healthy child. She was one of two pregnant patients reported in the Medical Journal of Australia by Hall and Windsor.1 She remained well and active until 2005, when she presented with New York Heart Association Class III symptoms of dyspnoea on exertion, and ultimately underwent mitral valve replacement that year. She made a good recovery postoperatively and remains well. In the 1920s, 10 patients with mitral valve stenosis were treated surgically.2 In 1923, Cutler and associates from Boston operated on seven patients using a cardiovalvulotome (through the left ventricle) and, in the same year, Duff and Evarts from Washington used a cardioscope (through the left atrium) on one patient. In 1925, Soutter from London and Pribram from Germany used a “finger fracture method” and a valvulotome, respectively, on one patient each. However, of the 10 patients, only two survived, one of Soutter’s and one of Cutler’s. The procedure was subsequently successfully revived in 1948 by Harken in Boston, Bailey in Philadelphia, Blalock in Baltimore, Brock in London, and others, who performed various procedures including valvuloplasty and commissurotomy. However, the so-called FFV (Harken) became the favoured procedure. It evolved from using the forefinger, to using the little finger, to eventually using a knife. Most surgeons had difficulty in using the mitral knife to divide the medial commissure and thus developed their own instrument.2 There are few successful case reports of FFV in pregnancy. In the United Kingdom, Brock reported three, Logan and Turner, six, and Marshall and Pantridge, 18.3 Hall and Windsor in Sydney performed FFV in two of seven pregnant women who were being considered for FFV, including our patient. One of the other five, who were managed conservatively, died.1 In 1963, Windsor said, “Eleven years’ experience in the surgery of the mitral valve has brought with it a great respect for the ability of the mitral commissures to resist finger, knife and dilator”. He reported follow-up of 90 patients who underwent FFV. No more than 40 patients (45%) obtained good results. Sixteen patients in this group have since been reoperated upon by the more effective transventricular route using a mechanical expanding dilator.4 It should be noted that mitral stenosis in young women is rarely accompanied by calcification, and this may allow a more complete and successful valvuloplasty. All the procedures mentioned above occurred before the development of cardiopulmonary bypass and open heart surgery in 1954. Early pioneers in surgery faced many challenges and disappointments, as well as condemnation, criticism and ridicule from colleagues. Some, like Soutter and Bailey (the latter nicknamed the “butcher of Hahnemann Hospital [Philadelphia]” after his first four FFV patients died) lost their practices.5 We would like to pay homage to all surgical pioneers and conclude with a comment from Harken: “He who would not learn from the past is condemned to relive it”. Finger fracture mitral valvuloplasty technique (Hall and Windsor1)

John S Murala · Hugh D Wolfenden · George S Youssef · Daniel Friedman

Prediabetes, the presence of impaired fasting glucose/glycaemia and/or impaired glucose tolerance, affects about 16.4% of Australian adults. People with prediabetes are at increased risk of developing diabetes, and cardiovascular and other macrovascular disease. Management includes reducing cardiovascular disease risk factors, specifically lipid and blood pressure abnormalities, and smoking-cessation counselling. To help prevent progression to diabetes, people with prediabetes who are overweight or obese require intensive lifestyle intervention. Medication to help prevent diabetes may also be used, but only after a minimum of 6 months of lifestyle intervention. In people with prediabetes, there is no role for routinely testing: capillary blood glucose; glycated haemoglobin (HbA1c) levels; serum insulin or pancreatic C-peptide levels; or testing for ischaemic heart disease or the microvascular complications of diabetes. Follow-up assessment of glycaemia in prediabetes requires a formal 75 g oral glucose tolerance test, initially performed annually, with subsequent individualised testing frequency.

Stephen M Twigg MB BS, FRACP, PhD · Maarten C Kamp FRACP, MHA · Timothy M Davis FRACP · Elizabeth K Neylon DAA, CDE · Jeffrey R Flack FRACP, MMed

Objective: To assess whether a diagnosis of the metabolic syndrome (MetS) improves the prediction of cardiovascular disease or total mortality beyond that already provided by conventional risk factors.Design and setting: A longitudinal cohort study conducted in Dubbo, New South Wales.Participants: 2805 men and women aged 60 years and older living in the community, first assessed in 1988–1989 and followed for 16 years.Main outcome measures: Coronary heart disease (CHD) events, ischaemic stroke events, and total mortality.Results: MetS was present in 31% of men and 34% of women. Crude CHD, ischaemic stroke, and total mortality rates were higher in the presence of MetS in men and women. In proportional hazards models that included conventional risk factors, but excluded variables used to define the presence of MetS, MetS was a significant predictor of CHD, stroke and total mortality. In men, the respective hazard ratios were 1.64 (95% CI, 1.37–1.96), 1.31 (95% CI, 0.97–1.77), and 1.53 (95% CI, 1.30–1.79). In women, the respective hazard ratios were 1.70 (95% CI, 1.43–2.02), 1.37 (95% CI, 1.04–1.82), and 1.35 (95% CI, 1.15–1.59). The use of MetS variables on an ordinal scale produced broadly similar conclusions.Conclusions: A diagnosis of MetS provides additional prediction of CHD events, stroke events, and total mortality beyond that provided by other conventional risk factors.

Leon A Simons MD, FRACP · Judith Simons MACS · Yechiel Friedlander PhD · John McCallum DPhil

Objective: To assess the prevalence of obesity in patients undergoing coronary artery bypass grafting, heart valve surgery, or both procedures, and its association with postoperative outcomes.Design and setting: Retrospective analysis of data, collected by the Australasian Society of Cardiac and Thoracic Surgeons Victorian Cardiac Surgery Database Project, on patients undergoing coronary artery bypass grafting, heart valve surgery, or both procedures, between 1 June 2001 and 31 January 2006.Participants: 11 736 patients divided into four groups: underweight (body mass index [BMI], < 20), normal weight (BMI, 20–30), obese (BMI, > 30 to < 40), and morbidly obese (BMI, ≥ 40).Main outcome measures: Prevalence of obesity (compared with the age- and sex-matched adult Australian population); associations between obesity and morbid obesity in cardiac patients and adverse postoperative outcomes.Results: 30.4% of patients had a BMI > 30 (28.6% obese, 1.8% morbidly obese) compared with an expected prevalence of 21.2%. Morbid obesity was associated with prolonged ventilation (adjusted odds ratio [OR], 2.4; 95% CI, 1.6–3.7), readmission to intensive care (adjusted OR, 2.2; 95% CI, 1.2–4.1), and length of stay > 14 days (adjusted OR, 2.1; 95% CI, 1.4–3.3). Both obesity and morbid obesity were associated with renal failure (adjusted ORs, 1.4 [95% CI, 1.1–1.7] and 2.9 [95% CI, 1.7–4.9], respectively) and deep sternal wound infection (adjusted ORs, 2.4 [95% CI, 1.5–3.8] and 7.2 [95% CI, 2.8–18.7], respectively).Conclusions: Obesity is 1.4 times more prevalent in patients having coronary artery bypass grafting or heart valve surgery in Victoria compared with the general adult Australian population. Both obesity and morbid obesity are associated with early morbidity, but not mortality, after operation.

Cheng-Hon Yap MB BS, MS · Morteza Mohajeri FRACS · Michael Yii FRACS, MS

A 55-year-old woman was admitted to hospital with a 1-year history of recurrent haemoptysis. A chest radiograph showed a well defined, rounded left hilar mass with surrounding air-space shadowing (Box, A). Contrast-enhanced computed tomography revealed a thrombosed aneurysm of the left main pulmonary artery that extended into its branches, with surrounding lung consolidation (Box, B). Echocardiography excluded any valvular lesions or shunt. Tests for tuberculosis and HIV were negative, and antinuclear antibody levels were not raised. The aneurysm was thought to be idiopathic. It was surgically resected, and the postoperative course was uneventful. A: Chest radiograph showing a left hilar mass. B: Contrast-enhanced computed tomography of the thorax showing an aneurysm of the left pulmonary artery extending distally into its branches with evidence of curvilinear thrombus (1), patent vessels (left pulmonary artery [2], right pulmonary artery [3], ascending aorta [4], superior vena cava [5] and descending aorta [6]), and consolidation of lung parenchyma adjoining the thrombus, with pleural thickening (7).

Zubair Ahmad MD, FCCP · Imrana Masood MB BS · Saurabh K Singh MB BS

There are two types of coronary stents: bare-metal stents (BMS) that cost about $800 each, and drug-eluting stents (DES) that cost about $3300 each. DES reduce the rate of restenosis but have a higher incidence of late stent thrombosis, particularly if dual antiplatelet therapy with aspirin and clopidogrel is interrupted. Stent thrombosis has a myocardial infarction rate of 70% and a mortality rate of 31%–45%. Randomised studies of BMS versus DES show no increase in myocardial infarction or death with DES in simple coronary lesions, but in clinical practice, DES are mainly used in complex coronary disease where the rate of stent thrombosis is higher. Registry data suggest an increased rate of death and myocardial infarction of 0.5%–1.0% per annum with DES. Clinicians need to be aware of the risks associated with prematurely ceasing dual antiplatelet therapy in patients with DES.

Richard W Harper MB BS, FRACP, FACC

The incidence and prevalence of atrial fibrillation are increasing because of both population ageing and an age-adjusted increase in incidence of atrial fibrillation. Deciding between a rate control or rhythm control approach depends on patient age and comorbidities, symptoms and haemodynamic consequences of the arrhythmia, but either approach is acceptable. Digoxin is no longer a first-line drug for rate control: β-blockers and verapamil and diltiazem control heart rate better during exercise. Anti-arrhythmic drugs have only a 40%–60% success rate of maintaining sinus rhythm at 1 year, and have significant side effects. The selection of optimal antithrombotic prophylaxis depends on the patient’s risk of ischaemic stroke and the benefits and risks of long-term warfarin versus aspirin, but is independent of rate or rhythm control strategy. Ischaemic stroke risk is best estimated with the CHADS2 score (Congestive heart failure, Hypertension, Age ≥ 75 years, Diabetes, 1 point each; prior Stroke or transient ischaemic attack, 2 points). For patients with valvular atrial fibrillation or a CHADS2 score ≥ 2, anticoagulation with warfarin is recommended (INR 2–3, higher for mechanical valves) unless contraindicated or annual major bleeding risk > 3%. Aspirin or warfarin may be used when the CHADS2 score = 1. Aspirin, 81–325 mg daily, is recommended in patients with a CHADS2 score of 0 or if warfarin is contraindicated. Stroke rate is similar for paroxysmal, persistent, and permanent atrial fibrillation, and probably for atrial flutter.

Caroline Medi BMed · Graeme J Hankey MD, FRCP, FRACP · Saul B Freedman FRACP, FACC, FESC

Over a 3-year period, seven patients who were taking HMG-CoA reductase inhibitors (statins) presented to our respiratory service with interstitial pneumonitis. Clinical course varied, with the condition responding to prednisolone treatment and cessation of statins in three patients, and progressing slowly despite this management in another three, while one patient died of associated cardiac disease. While a causative role cannot be confirmed, clinicians should be aware of the possible association. Two patients who presented with interstitial lung disease to our hospital’s respiratory service in 2000 prompted us to research a possible association between this disease and therapy with statins (hydroxymethylglutaryl-coenzyme A [HMG-CoA] reductase inhibitors). A literature review revealed several isolated cases of pneumonitis in the setting of statin therapy.1-3 Thereafter, we prospectively recorded patients referred to our unit who had interstitial lung disease and were undergoing statin therapy, where no other clear cause of the pneumonitis was evident. All cases have been reported to the Adverse Drug Reactions Advisory Committee. Clinical recordsBetween January 2000 and December 2003, our service saw 58 new presentations of interstitial lung disease, including the two patients discussed above. Data on these patients were retrieved from an ambulatory care database of newly presenting patients kept prospectively by our service. Their diagnoses are shown in Box 1. Eight cases were thought to be drug-associated: five of these were potentially linked to statin therapy, two to nitrofurantoin and one to amiodarone. Another two patients were referred to our service during hospital admissions in other specialties not included in our database. Details of these patients were retained from consultation records. Clinical details of the seven patients taking statin therapy are shown in Box 2. Most patients presented with dyspnoea and non-specific examination findings consistent with interstitial lung disease, such as bilateral crepitations on chest auscultation. None had clubbing. Some patients had a background of smoking and mild chronic obstructive airways disease, while others had no specific risk factors. Statins potentially implicated were atorva-statin (10–40 mg daily), pravastatin (40 mg daily) and simvastatin (10–40 mg daily). No patients were taking other medications known to be implicated in interstitial lung disease. Pneumonitis was diagnosed based on clinical assessment, along with demonstration of interstitial infiltrates on high-resolution computed tomography and reduced transfer factor for carbon monoxide diffusion on lung function testing (Box 3). Management comprised prednisolone or other immune-modifying treatment and/or withdrawal of the statin. In three patients treated with both prednisolone and statin withdrawal, pneumonitis decreased (Patients 3, 5 and 7). In another three, the condition progressed slowly: one of these (Patient 1) did not take prednisolone, and another (Patient 2) initially continued statin therapy and experienced respiratory failure necessitating home oxygen therapy before it was ceased. He died 18 months later of respiratory failure. The third (Patient 4) experienced slow progression despite statin withdrawal and treatment with prednisolone and azathioprine. The remaining patient (Patient 6) was treated with prednisolone but continued statin therapy, and died from coexisting cardiac disease, probably exacerbated by interstitial lung disease. DiscussionStatins are the most often prescribed class of medication for treating hypercholesterolaemia. They act primarily by inhibiting HMG-CoA reductase, thereby inhibiting cholesterol biosynthesis and improving lipid profiles. However, recent research has revealed multiple immunomodulatory, vascular endothelial, antioxidant and other effects of statins.4 These so-called “pleiotrophic” effects have led to statins being studied in a host of unrelated clinical settings, including osteoporosis, multiple sclerosis and Alzheimer’s disease. While research is ongoing, it appears that statins have profound multisystem effects that extend well beyond lipid metabolism. Statins are, on the whole, well tolerated, with the most commonly reported adverse effects being gastrointestinal upset, headache, rash and a dose-dependent elevation in serum levels of liver transaminases. The best characterised rare, but potentially serious, adverse effects are myopathy and polyneuropathy. These adverse effects are probably dose-related and may occur more often in patients taking medications known to inhibit statin metabolism.5 There are also a few reports of lupus-like syndromes, polymyositis/dermatomyositis with lung involvement, and hypersensitivity pneumonitis associated with statin therapy.1-3,6-9 The timing of onset appears unpredictable, with many patients having been taking statin therapy for many months or years before symptoms develop. Clinical features varied in severity from mild dry cough and rash through to severe and progressive respiratory failure. Low-titre antinuclear antibody (ANA) positivity and a raised erythrocyte sedimentation rate were also described in some patients. There are only four reports of open lung biopsy in these cases, two showing hypersensitivity pneumonitis with granuloma formation, one showing diffuse alveolar damage and the other showing non-specific interstitial pneumonitis. Most — but not all — patients responded to drug cessation and therapy with prednisolone or other potent immunosuppressive agents.2,8,9 Our patients shared many features with these patients. However, we did not observe rash of a dermatomyositic, lupoid or urticarial type, or lupus or polymyositis-like syndromes in our patients. Instead, all presented with respiratory symptoms — shortness of breath with or without dry cough — generally of insidious onset. Two out of six patients tested were positive for ANA with no other clinical features of connective tissue disease. The findings on transbronchial biopsy, when performed, were non-specific. Radiological appearances varied between alveolitis and fibrosis, but none showed the characteristic subpleural basal honeycombing that is common in usual interstitial pneumonia. The occurrence of alveolar eosinophilia in two out of the four patients who underwent bronchoalveolar lavage, which has previously been described in drug-hypersensitivity pneumonitis, and the response in several patients to drug cessation and/or corticosteroid therapy also point to a potential drug-induced pneumonitis. One previous case of pneumonitis has been reported in the setting of statin therapy, which was confirmed by open lung biopsy, and where the findings closely resembled those in amphiphilic drug toxicity, such as that reported with amiodarone. The authors hypothesised that a toxic mechanism, possibly mediated by statin effects on lipid metabolism, led to the observed intralysosomal lamellar inclusions in pneumocytes and interstitial cells.9 Thus, while not fully characterised, there is a putative mechanism through which statins may cause interstitial pneumonitis. Detecting rare side effects of commonly prescribed medications has always been a challenging task for the clinician. It is even more difficult when symptoms present insidiously, months or years after medication has been commenced, and the disease process has multiple potential aetiologies, which are not fully characterised. Similarly, interstitial lung disease remains a challenging diagnostic area even for experts in the field. Failure to recognise an under-lying cause of the pneumonitis often leads to the diagnosis of usual interstitial pneumonia being accepted. With continuation of the causative agent, the expected clinical pattern is progressive deterioration leading to respiratory failure and death, which also closely resembles the expected course of usual interstitial pneumonia. We hope that our description of our patients and review of the possible role of statins in interstitial lung disease will raise awareness of the potential association between statin therapy and this uncommon and often fatal condition. The effects of withdrawal of statin therapy on development of interstitial lung disease in patients taking this class of medication require further study. 1 New presentations of interstitial lung disease, 2000–2003 Diagnosis Number of patients Sarcoidosis 26 Usual interstitial pneumonitis 10 Non-specific interstitial pneumonitis 9 Drug-associated 8 Hypersensitivity pneumonitis 2 Asbestosis 2 Connective tissue disease-associated 1 2 Clinical details of seven patients with interstitial lung disease receiving statin (HMG-CoA reductase inhibitor) therapy Patient Sex, age Presentation Comorbidities Medications at presentation Investigations* Treatment Outcome 1 F, 78 Progressive dyspnoea, dry cough Hypertension, type 2 diabetes, hyperlipidaemia, non-smoker Atorvastatin (10 mg, 1 year), fosinopril, sertraline HRCT: extensive bilateral fibrosis TLCO: 46% No lavage or biopsy ANA-positive (1/40) Colchicine, atorvastatin withdrawn Slow progression: lung function deteriorated but clinical condition stable, little dyspnoea on 3-year follow-up 2 M, 78 Progressive dyspnoea (3 weeks), no cough or fever Chronic obstructive airways disease, IHD, atrial fibrillation, stroke, hyperlipidaemia, depression, ex-smoker Pravastatin (40 mg, 10 years), aspirin, frusemide, isosorbide mononitrate, perindopril, sertraline HRCT: extensive mid and upper zone emphysema, coarse bilateral basal fibrosis TLCO: 14%, mildly obstructed flow volume loop No lavage No biopsy (as poor respiratory reserve) ANA-positive (1/640) Prednisolone (50 mg), pravastatin withdrawn Progression, discharged with home oxygen, died 18 months later (respiratory failure) 3 F, 74 Cough and fever (3 days) (consistent with pneumonia) on background of worsening exertional dyspnoea Chronic obstructive airways disease, IHD, congestive cardiac failure, hyperlipidaemia, ex-smoker Simvastatin (10 mg for 2 years, then 20 mg for 1 year), aspirin, thyroxine, frusemide, diltiazem, nicorandil, long-acting nitrates HRCT: diffuse ground glass left upper lobe and bilateral lower zone No TLCO Lavage: 78% macrophages, 12% neutrophils, 9% lymphocytes Biopsy: non-specific interstitial pneumonitis No ANA test Prednisolone (50 mg), simvastatin withdrawn Gradual reduction in infiltrative change on imaging, lung function stable at 9-month follow-up 4 M, 83 Progressive dyspnoea (6 months) IHD, CABG and aortic valve replacement, atrial flutter, hyperlipidaemia, ex-smoker Pravastatin (40 mg, 1 year), aspirin, digoxin, frusemide, ramipril, ranitidine HRCT: scattered bilateral fibrosis TLCO: 33% Lavage: 68% neutrophils, 26% macrophages, 3% lymphocytes, 1% eosinophils Biopsy: non-diagnostic ANA-negative Prednisolone (40 mg), azathioprine, pravastatin withdrawn Slow progression 5 F, 67 Chronic mild dyspnoea (9 months), dry cough (6 months) Hyperlipidaemia, atypical chest pain, non-smoker Simvastatin (40 mg, 5 years), aspirin HRCT: patchy bilateral upper and lower zone ground glass TLCO: 22% No lavage or biopsy Negative for ANA, ANCA, normal ACE Prednisolone (25 mg, reduced to 10 mg after 3 months), simvastatin withdrawn Marked improvement (TLCO: 51% after 1 month, then 65% after 1 year) 6 M, 68 Progressive dyspnoea and hypoxia IHD, CABG and aortic valve replacement (10 years before), gastro-oesophageal reflux disease, hyperlipidaemia, ex-smoker Simvastatin (10 mg, 2 years), atenolol, candesartan, esomeprazole, frusemide, warfarin HRCT: bilateral fibrosis TLCO: 46%, mild restrictive defectLavage: 19% eosinophils, 19% neutrophils Biopsy: mixed inflammatory and fibrotic change ANA-negative Prednisolone (37.5 mg), azathioprine, simvastatin continued Progressive cardiac failure, died 9 months after presentation 7 M, 64 Progressive dyspnoea, dry cough IHD, CABG and aortic valve replacement (11 years before), peptic ulcer disease, hyperlipidaemia, ex-smoker Atorvastatin (20 mg for 3 years, then 40 mg for 2 years), fosinopril HRCT: bilateral ground glass infiltrates, fibrosis, some traction bronchiectasis TLCO: 44%, mildly obstructed flow volume loop Lavage: 38% eosinophils, 15% lymphocytes, 5% neutrophils Biopsy: thickened alveolar walls with interstitial fibrosis, minimal inflammation ANA-negative Prednisolone (initially 50 mg, then 10 mg maintenance), atorvastatin withdrawn Slight initial improvement (TLCO: 52% at 2-month follow-up), then stable disease HMG-CoA = hydroxymethylglutaryl-coenzyme A. IHD = ischaemic heart disease. CABG = coronary artery bypass graft surgery. HRCT = high-resolution computed tomography. TLCO = transfer factor for carbon monoxide diffusion. ANA = antinuclear antibody. ANCA = antineutrophil cytoplasmic antibody. ACE = angiotensin-converting enzyme. * All patients underwent HRCT and TLCO measurement, while most underwent bronchoscopy with broncho-alveolar lavage and transbronchial biopsy. 3 Investigations in two patients with interstitial lung disease High-resolution computed tomography in Patient 7 at presentation showed bilateral interstitial infiltrates with an area of honeycombing. Transbronchial biopsy specimen from Patient 7 showed a lymphocytic interstitial infiltrate and intra-alveolar macrophages (haematoxylin and eosin stain; original magnification, × 100). Transbronchial biopsy specimen from Patient 6 showed thickened alveolar walls with a low grade inflammatory infiltrate (haematoxylin and eosin stain; original magnification, × 400).

Tim Walker MB BS(Hons) · Joe McCaffery MB BS · Chris Steinfort FRACP

To the Editor: In a recent observational study, Krum et al concluded that the treatment of heart failure after myocardial infarction in Australian teaching hospitals is suboptimal because angiotensin-converting enzyme (ACE) inhibitors, β-blockers and aldosterone antagonists are underutilised.1 We believe that another explanation, mentioned by the study’s authors, is worth exploring further — for valid clinical reasons, it was not appropriate for certain patients to start or continue taking some of these medications. An understanding of the enrolment criteria of relevant clinical trials is informative. The large, long-term ACE inhibitor trials quoted by Krum et al — SAVE,2 TRACE and AIRE4 — between them screened 34 037 patients with myocardial infarction and left ventricular dysfunction. Only 5986 patients (18%) met the inclusion/exclusion criteria to be enrolled in one of the trials. Unfortunately, the CAPRICORN5 (β-blocker) and EPHESUS (aldosterone antagonist) trials did not publish the number of patients screened versus the number randomised, but a glance at their exclusion criteria explains why, for some patients, it may not have been appropriate to start these medications during their hospital stay. Some of the exclusion criteria for CAPRICORN were: unstable angina, ongoing therapy with antiarrhythmics (except amiodarone), secondary or tertiary heart block or sick sinus syndrome unless paced, uncontrolled hypertension (> 160/95 mmHg), bradycardia (heart rate, < 60 beats/min), hypotension (systolic blood pressure, < 80 mmHg), requirement for intravenous diuretics or inotropes, chronic obstructive pulmonary disease with ongoing inhaled β2-agonist or steroid therapy, and unstable insulin-dependent diabetes. Is there any harm in prescribing outside the inclusion/exclusion criteria for clinical trials? A population-based, time-series analysis linking prescription-claims data and hospital admission records of 1.3 million adults in Canada6 showed that hyperkalaemia-related deaths in hospital doubled after the RALES trial (spironolactone) was published in 1999. There was no reduction in re-hospitalisation for heart failure or all-cause mortality. The authors speculated that part of the reason for this was prescription of spironolactone to patients who would have been excluded from the RALES trial. While we would not advocate prescribing strictly within the boundaries of the inclusion/exclusion criteria of clinical trials, it is important to understand these criteria, so that prescribing in “real world” patients is done with care. We are reassured that Krum et al’s study suggests there is discretion in the prescribing of drug therapy. Presumably, during ongoing medical assessment, it will be appropriate for some patients to commence some of these medications (potential benefit outweighs potential harm), while others may need to have their medications reviewed because of adverse events.

Lauren J Bailey · Vasi Naganathan

In reply: We thank Bailey and Naganathan for their thoughtful viewpoint regarding prescribing according to clinical trial criteria. We agree that prescribing in the real world often involves complex decision making, taking into account age, comorbidities, concomitant medications and other factors, whereby guidance regarding individual patients cannot readily be extracted from clinical trial literature. This may certainly contribute to underutilisation of evidence-based drug treatment.1 Nevertheless, several analyses support the contention that physicians who more closely adhere to evidence-based guidelines (which in turn are derived from randomised clinical trials) produce better outcomes for their patients.2,3 Therefore, we would still advocate prescribing as closely as possible to guideline recommendations, while acknowledging that these recommendations may not always be readily applicable to every patient.

Henry Krum

To the Editor: The guidelines for managing acute coronary syndromes, published in a supplement to the Journal in 2006, provide a readily accessible tool for clinicians to enhance patient care.1 However, unfortunately the recommendations concerning adjunctive anticoagulation in patients with acute coronary syndromes (ACS) are suboptimal. The 2006 guidelines recommend that high-risk patients with non-ST-segment-elevation ACS should be treated with aggressive medical management, including unfractionated heparin or the low molecular weight heparin (LMWH) enoxaparin, based on evidence from randomised trials showing that these agents reduce the risk of non-fatal myocardial infarction (MI).1 However, neither unfractionated heparin nor enoxaparin have been shown to reduce mortality in patients with non-ST-segment-elevation ACS, even when compared against placebo, and enoxaparin increases the risk of bleeding when compared with unfractionated heparin.2-4 By contrast, the OASIS-5 study, presented at the European Society of Cardiology Meeting in September 2005 and published in early 2006, showed that fondaparinux (a pentasaccharide inhibitor of factor Xa) compared with enoxaparin reduced death and stroke rates, and reduced the risk of bleeding by one half.5 Updating the recommendation so that enoxaparin was replaced with fondaparinux for patients with non-ST-segment-elevation ACS would save six Australian lives at 30 days for every 1000 patients treated, and would cause 19 fewer bleeds. The recommendations of the 2006 ACS guidelines concerning the management of patients with ST-segment-elevation MI are similarly suboptimal. There are now convincing data from randomised trials that enoxaparin is more effective than unfractionated heparin for preventing recurrent MI in patients with ST-segment-elevation MI who have been treated with fibrinolytic therapy.4,6 However, as in the case with non-ST-segment-elevation ACS, enoxaparin has never been shown to reduce mortality in ST-segment-elevation MI. By contrast, both the LMWH reviparin, and fondaparinux, reduce mortality,7,8 and fondaparinux does so without increasing the risk of bleeding.8 We appreciate that rapid advances in the management of ACS make it increasingly difficult for evidence-based guidelines to reflect the best evidence from clinical trials. However, when new evidence becomes available that is clinically relevant at the individual and population level, we believe the guidelines working group and the Journal have a responsibility to update the readers.

John W Eikelboom · Graeme J Hankey · Paul E Langton

In reply: We thank Eikelboom et al for presenting new data on acute coronary syndrome (ACS) management. In this field of rapid advances, another recent study, ACUITY, has also been published, which examined bivalirudin in ACS.1 The Australian guidelines2 are based on peer reviewed published reports, and neither OASIS-53 nor ACUITY1 were released at the conclusion of the formulation of the guidelines. Also, fondaparinux is only available on the Pharmaceutical Benefits Scheme (PBS) in Australia for thromboembolic prophylaxis, and bivalirudin is currently only approved by the PBS for therapy during percutaneous coronary interventions. The Australian guidelines are consistent with international guidelines for both unfractionated heparin and low molecular weight heparin considered as Grade A recommendations for treating non-ST-segment-elevation ACS, based on Level 1 evidence (American College of Cardiology/American Heart Association guidelines). For example, the FRISC trial showed a significant reduction in mortality and myocardial infarction with dalteparin (compared with placebo; 1.8% v 4.8%; P = 0.001) at 6 days, which persisted at 40 days.4 The Australian ACS guidelines are a living document, and new evidence, such as the OASIS-5 (fondaparinux)3 and ACUITY (bivalirudin)1 findings, will be considered on their relative merits in future updates of the guidelines (available on the National Heart Foundation Australia website at http://www.heartfoundation.com.au).

Constantine N Aroney · Philip Aylward

Objective: To document the risk-factor profile and risk-factor knowledge of patients with an acute coronary syndrome (ACS) not attending standard cardiac rehabilitation.Design and setting: Cross-sectional comparison in a tertiary hospital.Participants: Patients admitted to hospital with an ACS, residing within 20 km of the hospital, and without severe comorbidity who did not access cardiac rehabilitation (NCR) were compared with a group about to commence standard cardiac rehabilitation (SCR).Main outcome measures: Risk-factor profile, knowledge of risk factors via face-to-face assessment, quality of life.Results: Of the 446 patients eligible for cardiac rehabilitation, 208 attended for assessment (NCR: n = 144; SCR: n = 64). The NCR group had higher mean (± SEM) low-density lipoprotein (LDL) cholesterol levels (2.6 ± 0.1 v 2.3 ± 0.1; P = 0.02), and were more likely than the SCR group to have a total cholesterol level of > 4.0 mmol/L (78% v 53%; P < 0.001) and an LDL cholesterol level > 2.5 mmol/L (47% v 25%; P = 0.01). They were more likely than the SCR group to be physically inactive (77% v 22%; P < 0.001); obese (46% v 33%; P = 0.04); depressed (21% v 5%; P < 0.001); or current smokers (21% v 1%; P < 0.001). Compared with the SCR group, the NCR group also had higher risk scores (LIPID risk score) (4.5 v 2.1; P < 0.001); lower quality of life (Medical Outcome Short Form [SF-36] Health Survey); and significantly poorer knowledge of risk factors. Among patients with at least two modifiable cardiac risk factors, the NCR group were less likely than the SCR group to be able to state at least one risk factor (24% v 38%; P < 0.001).Conclusions: Patients not participating in cardiac rehabilitation after an ACS have more adverse risk profiles and poorer knowledge of risk factors compared with those about to commence cardiac rehabilitation. Alternate models for secondary prevention are required to improve health outcomes in patients not attending cardiac rehabilitation.

Julie Redfern BAppSc, BSc · Elizabeth R Ellis MHealthLaw, MSc, PhD · Tom Briffa BPhysEd, MPhysEd, PhD · S Ben Freedman MB BS,PhD, FRACP

Chronic heart failure (CHF) is found in 1.5%–2.0% of Australians. Considered rare in people aged less than 45 years, its prevalence increases to over 10% in people aged ≥ 65 years. CHF is one of the most common reasons for hospital admission and general practitioner consultation in the elderly (≥ 70 years). Common causes of CHF are ischaemic heart disease (present in > 50% of new cases), hypertension (about two-thirds of cases) and idiopathic dilated cardiomyopathy (around 5%–10% of cases). Diagnosis is based on clinical features, chest x-ray and objective measurement of ventricular function (eg, echocardiography). Plasma levels of B-type natriuretic peptide (BNP) may have a role in diagnosis, primarily as a test for exclusion. Diagnosis may be strengthened by a beneficial clinical response to treatment(s) directed towards amelioration of symptoms. Management involves prevention, early detection, amelioration of disease progression, relief of symptoms, minimisation of exacerbations, and prolongation of survival.

on behalf of the CHF Guidelines Core Writers

To the Editor: The recommendation for managing acute ST-segment-elevation myocardial infarction with percutaneous coronary intervention (PCI) is that the door-to-balloon inflation time should be 90 minutes. However, it can be up to 120 minutes, depending on when patients present to the emergency department (ED) after the onset of their symptoms.1 In such cases, an alternative immediate reperfusion strategy — fibrinolysis — should be considered. At first glance, a door-to-balloon time of 90 minutes seems readily achievable, but what if the patient presents after hours, or presents to a hospital without PCI facilities? The time required to refer the patient for PCI, organise ambulance transport and call in cardiac catheterisation laboratory staff can be considerable. In the PRAGUE-2 trial from the Czech Republic, the average door-to-balloon time was 97 minutes.2 The DANAMI-2 study from Denmark had a cohort of 27 080 patients and had door-to-balloon times of about 114 minutes for those patients transferred to another facility.3 The National Registry of Myocardial Infarction 4 investigators reported a median door-to-balloon time of 185 minutes for American patients transferred to centres capable of PCI, and a door-to-balloon time of less than 90 minutes for only 3% of patients.4 Doctors working in EDs without onsite access to PCI need to know the door-to-balloon times of the institutions to which they refer patients for PCI. Centres performing PCI may not be forthcoming with this information, as they have a vested interest in keeping their numbers up for PCI. Alternatively, this information may not be known to the clinician accepting the patient for PCI. In addition, doctors in EDs who opt to transfer their patients have the burden of organising transport for potentially unstable patients who may develop lethal arrythmias. As door-to-needle time for thrombolysis has become a clinical indicator for EDs, perhaps door-to-balloon times can be a clinical indicator for cardiac catheterisation laboratories. Finally, it is important to note that in some patients requiring urgent coronary artery reperfusion, the first electrocardiogram (ECG) is not diagnostic, so a more pragmatic indicator would be diagnostic ECG-to-balloon time. This would require an enforcement of the current recommendations for an ECG to be performed and critically reviewed shortly after a patient presents with symptoms suggestive of an acute coronary syndrome.

Jayantha I Weeraratne

In reply: We agree with the points highlighted by Weeraratne, and these have been broadly addressed within the new National Heart Foundation of Australia and Cardiac Society of Australia and New Zealand Guidelines for the management of acute coronary syndromes 2006.1 The guidelines emphasise the need for appropriate systems of care which are regionally based, have formal links with specialist centres, include appropriate monitoring, feedback and quality improvement components, and are sensitive to the cultural and personal beliefs and wishes of individual patients. Clinicians do need to know the achievable door-to-balloon times for primary percutaneous coronary intervention within their local contexts, and if there is any doubt about the timely availability of this treatment for patients with ST-segment-elevation myocardial infarction, the guidelines recommend that fibrinolysis be given promptly.

Philip Aylward · Constantine N Aroney

Objective: We aimed to assess the pattern of use of drug-eluting stents (DESs) in patients undergoing percutaneous coronary interventions (PCIs) in Victorian public hospitals.Design, setting and patients: Prospective study comparing the use of one or more DESs versus bare-metal stents (BMSs) only, in consecutive patients undergoing 2428 PCIs with stent implantation from 1 April 2004 to 31 December 2005 at seven Victorian public hospitals.Main outcome measures: Adherence to current Victorian Department of Human Services guidelines which recommend DES use in patients with high-risk features for restenosis (diabetes, small vessels, long lesions, in-stent restenotic lesions, chronic total occlusions and bifurcation lesions).Results: Of the 2428 PCIs performed, at least one DES was implanted in 1101 (45.3%) and BMSs only were implanted in 1327 (54.7%). In 87.7% (966/1101) of PCI with DESs, there was at least one criterion for high risk of restenosis. DESs were more likely to be used in patients with diabetes (risk ratio [RR], 2.45; 95% CI, 2.02–2.97), small vessels (RR, 3.35; 95%CI, 2.35–4.76), long lesions (RR, 3.87; 95% CI, 3.23–4.65), in-stent restenotic lesions (RR, 3.98; 95%CI, 2.67–6.06), chronic total occlusions (RR, 1.30; 95% CI, 0.51–2.88) and bifurcation lesions (RR, 2.23; 95%CI, 1.57–3.17). However, 66.2% (1608/2428) of all PCIs were in patients eligible for DESs according to Victorian guidelines, and in 39.9% (642/1608) of these PCIs, a BMS was used.Conclusion: In Victorian public hospitals, DESs have been largely reserved for patients at high risk of restenosis in accordance with Department of Human Services guidelines. However, many patients with high-risk criteria for restenosis did not receive DESs. Greater use of DESs in these patients may improve outcomes by reducing the need for repeat revascularisation.

on behalf of the Melbourne Interventional Group (MIG) investigators

Objective: To review the management of glycaemia, blood pressure and serum lipids in a hospital outpatient diabetes clinic, the director of which co-authored the current national diabetes management guidelines.Design: Retrospective audit.Setting: Outpatient diabetes clinic in a tertiary referral teaching hospital, Sydney, NSW.Study population: 96 patients with type 1 diabetes (mean age, 44.4 [SD, 12.8] years) and 509 patients with type 2 diabetes (mean age, 64.4 [SD, 12.0] years) attending the clinic in 2003, who had undergone formal review of complications.Main outcome measures: Weight, height, control and treatment of glycaemia, blood pressure and serum lipids, and prevalence of diabetic microvascular complications.Results: Glycated haemoglobin (HbA1c) was < 7% in 13% of type 1 and 30% of type 2 diabetes patients, and > 8% in 47% and 34%, respectively. 35% of patients with type 1 diabetes and 71% of patients with type 2 diabetes were treated with antihypertensive agents. Of these patients, 29% and 24%, respectively, had blood pressure readings ≤ 130/80 mmHg. Among patients not treated with hypertensive agents, blood pressure readings were ≤ 130/80 mmHg in 60% of type 1 and 38% of type 2 diabetes patients. About 30% of patients with type 1 diabetes and 50% of those with type 2 diabetes were being treated with lipid-lowering agents; of these, about 60% had low-density lipoprotein (LDL) cholesterol levels < 2.6 mmol/L. Among patients not treated with lipid-lowering agents, about 40% had LDL cholesterol levels < 2.6 mmol/L. Retinopathy was documented in 52% and 18%, and nephropathy in 9% and 36% of type 1 and type 2 diabetes patients, respectively.Conclusions: Despite the demonstrated benefits of tight glucose, blood pressure and lipid control in reducing the risk of macrovascular and microvascular complications in type 1 and type 2 diabetes, our results suggest that treatment targets are not being met in a large proportion of patients attending a tertiary referral hospital. Responsible practice suggests that treatment targets and the current means to achieve them should both be examined.

Wendy Bryant,* RN, CDE, GradDipDiabetesEdManagement · Jerry R Greenfield,* PhD, FRACP · Donald J Chisholm FRACP · Lesley V Campbell FRCP, FRACP

A 58-year-old man presented with a 1-month history of persistent nausea, vomiting, diarrhoea and fevers. He also reported worsening shortness of breath, lower extremity swelling, and a 4.5 kg weight loss. He was febrile and hypotensive, with pedal oedema and a soft diastolic murmur over the mitral area. A white cell count and chest x-ray were normal. A transthoracic echocardiogram, performed to assess cardiac function, showed a large, highly mobile left atrial mass prolapsing into the left ventricle (Box, A [arrowed]). At urgent surgery, an 8 cm left atrial myxoma arising from the interatrial septum was resected (Box, B). Histopathological examination showed dense colonies of yeast. Histoplasma capsulatum was grown from blood cultures and cultures of the surgical specimen (Box, C). HIV testing was negative. The patient made a full recovery after completing antifungal therapy. Infected left atrial myxoma is rare. We know of only one other reported case in which Histoplasma was the infective agent.1 A: Transthoracic echocardiogram B: Surgical specimen C: Microscopic view of Histoplasma capsulatum (Gomori methenamine silver stain)

Ahmed Awab MD · Mehdi Hamadani MD · Bhanu Sud MD · Gene W Voskuhl MD

To the Editor: The discussion of fibrinolysis in the recently published guidelines for the management of acute coronary syndromes 20061 is interesting. The recommendations clearly indicate that second-generation agents should be preferred to streptokinase in all circumstances. The guidelines reference the GUSTO-I trial data2 as the primary support for those recommendations. These data are, at best, debatable in terms of showing any benefit of front-loaded tissue plasminogen activator over streptokinase, and then only in limited circumstances (ie, patients aged less than 75 years with anterior infarcts and within 4 hours of the onset of symptoms).3,4 To my knowledge, there have been no head-to-head trials of this size of the other fibrinolytic agents discussed against streptokinase. Thus there is no justification for the blanket superiority that is accredited to these agents, both by implication and explicitly, in the guidelines. It is a matter of some concern that guidelines from such respected groups should make statements that will be used broadly by clinicians, but that go beyond the evidence base to which they refer. On the balance of information available there is no compelling case to relegate streptokinase from the front line.

Andrew J Bezzina

In reply: As Bezzina states, the GUSTO-I trial is the main source of evidence for the superiority of front-loaded alteplase (rt-PA) over streptokinase, showing a 1% absolute and 15% relative benefit.1 Subgroup analysis suggested that only certain groups benefited, but this is an inappropriate use of subgroups, and the result should be applied overall. A clear mechanistic reason for the advantage of rt-PA — greater 90-minute full coronary patency — has also been demonstrated.2 Meta-analyses of the percutaneous coronary intervention (PCI) trials in acute myocardial infarction have all shown benefit over fibrinolysis. However, the benefit of PCI is greater compared with streptokinase than with plasminogen activators.3 Although not providing a head-to-head comparison, these data also support the superiority of plasminogen activators over streptokinase. The second generation plasminogen activator studies have all compared these with the “gold standard” front-loaded rt-PA. These agents have been shown to not be inferior in relation to mortality,4,5 and tenecteplase showed a decrease in systemic bleeding.5 Administration as a bolus without the adverse reactions commonly seen with streptokinase (such as hypotension) make them much more convenient and safe, particularly in smaller institutions. In addition, streptokinase is an inappropriate choice in Indigenous patients because many have high levels of anti-streptokinase IgG and streptokinase resistance.6

Philip Aylward · Constantine N Aroney · Ken Hossack · Andrew M Tonkin

Objective: To evaluate the use of cardiovascular medications in patients with and without heart failure after myocardial infarction (MI).Design and setting: Multicentre study of drug therapy for patients with MI in 16 major metropolitan teaching hospitals in Australia over a 1-month period at each hospital in the period November 2004 – March 2005.Participants: 479 patients admitted consecutively to the individual hospitals.Main outcome measures: Proportion of patients with and without heart failure who were prescribed key cardiovascular medications after MI.Results: 116 of the 479 patients admitted for MI (24.2%) had heart failure at some point during their hospitalisation. Patients with heart failure were older (68 v 63 years; P < 0.05), more likely to be women (34% v 24%; P < 0.05) and a higher proportion had diabetes (26% v 21%). There was significantly reduced prescribing of β-blockers, clopidogrel and statins for patients with heart failure compared with those without heart failure. Mineralocorticoid receptor antagonist use was low (< 10%) in the former group.Conclusions: We found reduced prescribing of some prognostically relevant medications for patients with heart failure. For β-blockers, this may be explained by the greater clinical instability in patients with heart failure. Given the absolute benefit of drug therapy in patients with heart failure after MI, our findings suggest suboptimal prescribing in Australian teaching hospital practice.

Henry Krum MB BS, PhD, FRACP · Adam Meehan · John Varigos BSc(Hons) · Philippa R Loane BBiomedSc · Baki Billah PhD

William Heath was born on 23 July 1925 in Casterton, western Victoria. The eldest of seven children, he was educated by the nuns at the Convent of Mercy School in Casterton. Bill’s father died when he was 14, so at the age of 15 he commenced work as a clerk with the AMP Society, a relationship which continued throughout his life and culminated in the position of Chief Medical Officer of the AMP Society. At the age of 18, Bill joined the Royal Australian Air Force and trained as a pilot. After the war, he returned to AMP for a year before commencing a medical degree at the University of Melbourne. After graduating with honours in 1953, he completed his training at St Vincent’s Hospital, Melbourne. Awarded a National Heart Foundation Travelling Scholarship in 1961, Bill took his young family to the United States to work as a cardiovascular research fellow at Georgetown University in Washington, DC, from 1962 to 1964. Bill then returned to Melbourne and quickly established an extensive private practice in Collins Street. He was much sought after as a clinician, teacher and source of expert medicolegal opinion. He held many board appointments, including Medical Director of the Mercy Hospital, Chief Medical Officer at Munich Reinsurance Company, and Treasurer and Secretary of the Medical Defence Association of Victoria. Bill was Honorary Physician to Pope John Paul II, Queen Elizabeth II, the Duke of Kent, the Prince and Princess of Wales, and the Queen of Denmark and Prince Consort, during their respective visits to Victoria. A deeply religious and compassionate man, Bill worked tirelessly caring for the less fortunate in our community, looking after alcoholics, drug addicts, homeless people and many others. A man of great good humour, Bill held very definite and firm opinions about most matters and had a very select list of dislikes (with parking attendants and Mexican waves being near the top of the list). Bill was a keen traveller, a lover of good food and wine, and an enthusiastic supporter of various clubs, including the Essendon Football Club, the Melbourne Cricket Club and the Kooyong Lawn Tennis Club. His last 2 years were blighted by a very aggressive lymphoma, involving recurrent visits to hospital and the traumas of chemotherapy and septicaemia. He died on 22 October 2005. Bill will be remembered as an eminent cardiologist, a very fine doctor and a true gentleman. He is survived by his wife Ann and children Jane, Simon, Susan, John, David and Sarah.

Bernard S Gilligan

Accessible and culturally appropriate services are needed The National Heart Foundation of Australia and the World Health Organization recommend that all patients with cardiovascular disease are routinely referred to an appropriate cardiac rehabilitation program.1,2 Their recommendations are based on firm evidence that three-phase rehabilitation programs — inpatient, outpatient and maintenance — provide a range of short-term and long-term benefits to health and wellbeing. Key points for success Ensure that cultural competency is integral to the core business of an organisation and supported at all levels within the organisation (eg, employ Indigenous staff across the organisation, support cultural awareness training for non-Indigenous staff, ensure availability of and support for interpreters and cultural mentors). Involve Aboriginal health workers and family members in the care of Aboriginal and Torres Strait Islander patients and develop flexible approaches to raising awareness of the importance of cardiac rehabilitation. Ensure community involvement in planning, implementing and evaluating health promotion, including the development of culturally appropriate materials. Incorporate elements of cardiac rehabilitation and secondary prevention into existing activities or set up activities that draw on existing networks within the community. Develop and sustain partnerships between organisations (eg, a hospital providing outreach cardiac rehabilitation services through the local Aboriginal Community Controlled Health Service). Take the specific needs of Aboriginal and Torres Strait Islander patients into consideration in planning and delivering mainstream cardiac services and develop policies and procedures to address these needs (eg, identifying Aboriginal or Torres Strait Islander status, providing culturally appropriate information on hospital discharge). Develop a specialist education base for continuing training and support of all health professionals working in cardiac care, including Aboriginal health workers. Although the benefits of cardiac rehabilitation are clear, only a small proportion of the people in the general population who have experienced cardiac events attend programs.3 Aboriginal and Torres Strait Islander people are even less likely to participate in cardiac rehabilitation programs than non-Indigenous Australians,3-5 despite being twice as likely to die from cardiovascular disease.6 As there is little published literature specific to cardiac rehabilitation among Aboriginal and Torres Strait Islander peoples, the National Health and Medical Research Council convened a committee to investigate barriers to effective practice and develop guidance for health professionals working in the area. In November and December 2004, the committee conducted workshops, hosted by Aboriginal Community Controlled Health Services in Darwin, Townsville and Mt Druitt (Sydney). Indigenous health professionals and consumers were asked to share their stories and make suggestions about how cardiac rehabilitation services could be made more accessible. This information contributed to the development of a practical guide for health professionals — Strengthening cardiac rehabilitation and secondary prevention for Aboriginal and Torres Strait Islander peoples: a guide for health professionals.7 The guide was tested for suitability by potential users of the manual at a workshop held in Adelaide in June 2005 and was published in September 2005. Through the workshops, the following barriers to uptake of cardiac rehabilitation among Aboriginal and Torres Strait Islander people were identified. “Not enough black faces”: Aboriginal and Torres Strait Islander people are not sufficiently involved in planning, delivering and evaluating relevant health care services. Contributing to this is a lack of training, education and support for Aboriginal health workers. Communication and understanding: Cultural factors that are often not understood and therefore not taken into account in mainstream services include the diversity of Aboriginal and Torres Strait Islander peoples and culture; the complexity of Aboriginal law; the importance of family and community involvement; and a holistic view of health that includes the body, the land and spirituality. Continuity of care: The process of cardiac care usually involves many different settings and people. Lack of continuity and linkages between services, in particular between mainstream and Aboriginal and Torres Strait Islander services, mean that people can miss out on important aspects of care. This is made worse when people live in remote communities and have to travel long distances to access services. Taking the message back home: It can be difficult to maintain a healthy lifestyle back in the community, where adopting healthy behaviours may be less of a priority than meeting basic needs such as food and housing, expectations of health may be low, and there may be strong counteracting social pressures. Self-determination and control: Health intervention programs may be implemented without appropriate consultation and community involvement from the outset. Programs are unlikely to succeed unless they build on the leadership provided by the community and on real partnership with the local community. Addressing these barriers presents considerable challenges. No single solution can be applied, due to the diversity within the population, as well as the need to find approaches that are suitable to remote, rural and urban areas and that take into account cultural issues and staff availability. Multidisciplinary methods are therefore required2 that can be adapted to make use of the skills available in each setting while taking a standardised approach to supporting system change. The Indigenous health sector and Indigenous health professionals are best placed to provide cardiac rehabilitation to Aboriginal and Torres Strait Islander people and should be supported to do this. However, cardiac rehabilitation is more likely to comprise a combination of both Indigenous and mainstream services (ideally a team including an Aboriginal health worker and general practitioner, with other health professionals as required). Establishing and maintaining links between individuals and organisations involved in cardiac rehabilitation is therefore fundamental to improving outcomes. Such linkages support continuity and quality of care, broaden the capacity of the health organisation, increase access to resources and help to integrate mainstream and Indigenous health services, so that it is easier for patients to move between the two systems. At the centre of care are the patients themselves. Showing cultural respect, as well as learning from patients and their families, carers and the community, will increase understanding of how culturally competent health care can best be provided.8 For example, addressing chronic diseases together in an holistic way is more consistent with Aboriginal and Torres Strait Islander concepts of health and illness than considering single diseases or body parts. This approach can also better take into account the importance of spirituality to health and wellbeing, depression and other psychosocial factors increasing the risk of cardiovascular disease,9 and the cultural, environmental and historical risk conditions that place Aboriginal and Torres Strait Islander people at greater risk of the onset and complications of chronic diseases. There is considerable activity under way across Australia to improve the cardiovascular health of Aboriginal and Torres Strait Islander peoples. Systems are in place to assist health services to improve preventive and coordinated care for these patients10 and there is a growing knowledge base to support improved practice. However, continuing efforts are needed across all health care settings, at both individual and organisational levels, to implement sustainable changes that will ensure that appropriate cardiac rehabilitation services are available for Aboriginal and Torres Strait Islander Australians.

Noel E Hayman MB BS, MPH, FAFPHM · Mark Wenitong MB BS · Jenny A Zangger BA, DipApplSci · Elizabeth M Hall BSc