Cardiovascular diseases

To the Editor: A 71-year-old man presented with a firm erythematous painful swelling over the sternoclavicular region. He had undergone coronary artery bypass grafting (CABG) 18 months earlier. A chest x-ray showed the presence of sternal wires and mediastinal clips from the surgery, and pleural thickening in the right costophrenic angle. There were no focal abnormalities seen on the x-ray when compared with pre-CABG radiographs. A computed tomography scan of the chest showed a destructive lesion of the manubrium, with an associated soft tissue mass extending into the pectoralis muscle and anterior mediastinum. A sternal suture was noted within the lesion, and a separate surgical clip was identified in the suprasternal notch region (Box, A). Surgical exploration of the sternotomy wound revealed tumour in the muscle around the proximal sternum, with bone destruction. Histopathological examination of the tumour confirmed the presence of an osteosarcoma (Box, B). (A section of normal trabecular bone [Box, C] is shown for comparison.) There have been few reported cases of primary sternal tumours. To our knowledge, primary osteosarcoma arising contiguous to a surgical suture has never been reported. It is unknown why the osteosarcoma originated in the part of the sternum that contained the sternal suture rather than originating de novo in another part of the bony skeleton. Chronic localised sternal inflammation or mechanical irritation of the proximal sternum by the suture may have been contributory factors in triggering carcinogenesis in this uncharacteristic site.1 However, the effect of trauma and mechanical stimulation on development of primary cancers and their metastases has never been proven. Patients who present with bony tumours frequently have a history of previous trauma to the area where the tumour develops. While there have been numerous reports suggesting some relationship between trauma/chronic inflammation and oncogenesis,1-5 there is no evidence that a single incident of trauma can cause cancer. The combination of trauma, in-situ metal and malignancy after CABG is rare, and there are currently no grounds for suspecting a direct relationship between them. A: Computed tomography scan of the chest showing a destructive lesion in the cortex of the manubrium. A sternal suture, surgical clip and soft tissue mass are visible within the tumour (A = anterior, R = right). B: Histopathological section of osteosarcoma of the sternum. Pleomorphic and hyperchromatic cells are present in a disorganised immature bone matrix (osteoid) (haematoxylin and eosin stain; original magnification, × 20). C: Histopathological section showing normal trabecular bone of the sternum (haematoxylin and eosin stain; original magnification, × 2.5).

Laurence Weinberg · Joseph Mathew

To the Editor: I read with interest the article by Medi and colleagues,1 but note that the authors do not mention the effect of supraventricular tachycardia on atrial natriuretic peptide — a hormone that causes vasodilation and renal excretion of sodium and water. Plasma levels of atrial natriuretic peptide increase markedly during supraventricular tachycardia.2 Pacing studies reveal that release of atrial natriuretic peptide occurs when the heart rate is greater than 120 beats/min.3 The resultant diuresis would lead to an urge to urinate and, in a prolonged episode of tachycardia, to polyuria.4,5

Weekitt Kittisupamongkol

Objective: To determine the incidence of coronary heart disease (CHD) events in an urban Aboriginal population.Design, setting and participants: Cohort study of 906 Aboriginal people without CHD from 998 who had undergone risk-factor assessment in the Perth Aboriginal Atherosclerosis Risk Study (PAARS) in 1998–1999. PAARS cohort data were electronically linked to a range of databases that included Western Australian hospital morbidity data and death registry data. We analysed data from January 1980 to December 2006 to identify previous admissions for CHD from 1980 to baseline (1998–1999) and new events from baseline to 2006.Main outcome measure: First CHD event (hospital admission or death).Results: There were 891 linked records for the 906 participants without previous CHD. The event rate was 12.6/1000 person-years (95% CI, 10.2–15.6/1000 person-years). Annual CHD event rates ranged from 8 to 18/1000 person-years. After adjustment for age (sex was not associated with the risk factors assessed), factors associated with risk of a CHD event in the PAARS cohort were a history of diabetes, overweight or obesity (indicated by body mass index), smoking, and hypertension, but not waist circumference. People with these risk factors were 1.9–2.7 times more likely to experience a CHD event. Compared with previously published information from a remote Aboriginal community in the Northern Territory, the incidence of CHD events among urban-dwelling Aboriginal people was not significantly different (P > 0.05 overall and for subgroups defined by age and sex).Conclusions: City-dwelling Aboriginal Australians have an incidence of CHD events comparable to that of Aboriginal people living in remote northern Australia.

Pamela J Bradshaw PhD · Helman S Alfonso MSc, PhD · Judith C Finn RN, MEdStud, PhD · Julie Owen DipT, MPHC, PhD · Peter L Thompson MD, FRACP, MBA

Objective: To describe baseline characteristics, operative events and late mortality among Indigenous Australians undergoing cardiac surgery.Design, setting and participants: Prospective study of consecutive patients undergoing cardiac surgery at Flinders Medical Centre in Adelaide between January 2000 and December 2005.Main outcome measures: Operative (30-day) mortality and late mortality after cardiac surgery.Results: Of 2635 patients undergoing cardiac surgery, 283 (10.7%) were Indigenous. Indigenous patients were substantially younger than non-Indigenous patients (mean, 47 [SD, 14] years v 65 [SD, 12] years; P = 0.001) and were more likely to have diabetes (39.6% v 27.3%; P = 0.001), renal dysfunction (3.2% v 1.2%; P = 0.009), and valvular surgery (53.0% v 23.1%; P < 0.001). There was a non-significant trend toward excess operative mortality in Indigenous patients (Indigenous 2.5% v non-Indigenous 1.3%; hazard ratio [HR], 1.67 [95% CI, 0.74–3.75]). But in the under-55-years age cohort, the difference between the two groups was highly significant (Indigenous 3.3% v non-Indigenous 0.4%; HR, 7.99 [95% CI, 1.66–38.50]), even after adjustment for euroSCORE (the European System for Cardiac Operative Risk Evaluation). Survival at 1 and 5 years was 94.0% and 80.6%, respectively, for Indigenous patients compared with 96.7% and 87.7%, respectively, for non-Indigenous patients. There was an excess in euroSCORE-adjusted mortality in the Indigenous cohort overall (HR, 1.46 [95% CI, 1.03–2.07]) that strengthened when restricted to the under-55-years cohort (HR, 6.9 [95% CI, 1.42–33.5]).Conclusion: Indigenous Australians present for cardiac surgery nearly 20 years earlier than non-Indigenous Australians and experience excess age-stratified operative and late mortality.

Sam J Lehman MB BS, FRACP · Robert A Baker PhD · Philip E Aylward MB BS, FRACP, PhD · John L Knight MB BS, FRACS · Derek P Chew MB BS, MPH, FRACP

Do you have patients who could benefit from therapeutic pacing and defibrillator devices? In recent years, management of chronic heart failure has advanced considerably, especially the optimisation of key pharmacological strategies (angiotensin-converting enzyme inhibitors, β-blockers) and multimodal management. In parallel, there has been a quieter revolution: the use of therapeutic pacing and defibrillator devices in patients with heart failure has moved from experimental and clinical research to everyday clinical practice. Milestones include landmark trials establishing the definitive mortality benefit of implantable defibrillators in ischaemic cardiomyopathy,1 the clinical utility of electronically synchronising contraction of both ventricles,2 and mortality benefits of cardiac resynchronisation therapy (CRT).3 Nonetheless, therapeutic pacing and defibrillator devices appear to be underutilised,4 perhaps due to lack of awareness of their clinical benefits and concerns regarding cost. What are the established modalities? Sudden cardiac death is a significant risk in patients with impaired left ventricular function. The use of implantable cardioverter defibrillators (ICDs) is established in primary and secondary prevention of sudden cardiac death in chronic heart failure — large randomised controlled studies have demonstrated a significant mortality benefit.1,5 American6 and Australian7 guidelines for heart failure management state that an ICD may be used after cardiac arrest, ventricular tachycardia or ventricular fibrillation; ≥ 40 days after myocardial infarction in patients with New York Heart Association (NYHA) class I, II or III symptoms and left ventricular ejection fraction (LVEF) ≤ 30%; and in patients with ischaemic or non-ischaemic cardiomyopathy, NYHA class II or III symptoms and LVEF ≤ 35%. Newer “risk stratifiers” are being explored to better identify patients likely to benefit from ICD therapy.8 The implantation procedure for an ICD is identical, in principle, to that of a pacemaker, with some exceptions: the lead is larger (thus stiffer), so care is required during its manipulation within the heart; the battery is larger, so it requires careful positioning to avoid skin erosion; and testing of the device involves inducing ventricular fibrillation to ensure adequate sensing of arrhythmia and an adequate safety margin in terms of the threshold of defibrillation. Also, the sophisticated programming of ICD therapy requires a cardiac electrophysiologist. ICDs can be programmed to treat ventricular arrhythmias with either antitachycardia pacing (which is painless) or shock therapy. After the patient experiences their initial therapy, which unfortunately may involve a potentially distressing shock while the patient is conscious, individualised adjustments may be needed. Despite the survival benefit associated with ICDs, their impact on quality of life is uncertain. In contrast to other heart failure therapies, ICDs do not improve cardiac function. They would not be expected to improve a patient’s exercise capacity or ability to perform activities of daily living. Also, implantation can be associated with various immediate and late complications, including device infection, failure and inappropriate discharge.9 The failing heart is frequently characterised by abnormalities of mechanical synchrony, often reflected by abnormalities of electrical conduction. Based on adverse consequences of ventricular dyssynchrony in heart failure, researchers have sought to resynchronise the failing myocardium. One approach, CRT, involves pacing both ventricles in a coordinated manner to restore the normal physiological chronology of left- and right-sided contraction. Ventricular dyssynchrony can be crudely detected on an electrocardiogram by QRS prolongation.10 Epidemiologically, QRS prolongation has been associated with worsening of clinical outcomes in patients with heart failure. Echocardiography has been proposed as a better tool for evaluating mechanical dyssynchrony.11 The implantation of a CRT device extends the standard pacemaker or ICD implantation procedure by placement of a left ventricular pacing lead. This requires specialised sheaths to access the coronary sinus, angiographic identification of an appropriate lateral branch, and careful positioning of the lead. Several factors determine the ideal position for the lead, including proximity to the lateral wall at a position furthest from the right ventricular lead, stability of lead placement, presence of viable myocardium that can be captured by pacing at the site, and avoidance of diaphragmatic pacing. The procedure requires an experienced operator and a service that can optimise programming. CRT has undergone considerable evaluation and, according to American and Australian guidelines, it is indicated in patients with NYHA class III or IV symptoms, LVEF ≤ 35% and QRS duration on electrocardiogram > 120 ms.6,7 More than 4000 patients have been evaluated in randomised single- or double-blind controlled trials of CRT in heart failure and, in systolic heart failure, CRT has consistently been associated with improved patient wellbeing and ventricular systolic function, and reduced recurrent hospitalisation for heart failure. Meta-analyses and a stand-alone study have shown reduced all-cause mortality with CRT.3,12 These benefits add to those of standard drug therapies for systolic heart failure, and may be further enhanced by use of a defibrillator. Indeed, most CRT devices used in Australia include a defibrillator function. Ideally, patients should be in sinus rhythm for maximum benefits from this therapy. Some evidence suggests that CRT is also beneficial in patients with atrial fibrillation, and that this cohort may be better optimised with atrioventricular node ablation.13 However, current Australian Government Department of Health and Ageing guidelines do not support the use of these devices in patients with atrial fibrillation.14 In addition, not all patients who meet the criteria for CRT benefit from the therapy. There is a 20%–30% “non-response rate”, in that patients do not feel better or ventricular function does not improve.14 The reason for this is elusive, but improved evaluation of dyssynchrony, using measures more sophisticated than QRS duration (eg, echocardiography, magnetic resonance imaging), may reduce the non-response rate, and CRT trials that base entry criteria on results of imaging alone are underway. Nonetheless, CRT has gained popularity in recent years, particularly for patients who remain severely symptomatic despite drug therapy. What other modalities are being evaluated? Cardiac contractility modulation (a new form of electrical therapy) is currently being evaluated in patients with heart failure. A recent clinical study demonstrated improved exercise tolerance and quality of life,15 but these data need to be confirmed in large, randomised controlled studies. Ventricular pacing alone has also been trialled, but can result in deleterious mechanical effects. In patients with impaired left ventricular function, right ventricular pacing can cause further deterioration.16 Adverse effects may be minimised by pacing the right ventricular outflow tract or high septum rather than the apex.17 Perhaps more importantly, atrioventricular synchrony can be maintained, and many pacemakers allow minimisation of ventricular pacing by various programmable algorithms. What is needed now? Over the past decade, many pacing therapies have been rigorously evaluated in patients with chronic heart failure, and there are now proven indications for their application in clinical practice. The clinical outcomes, potential problems and costs of CRT, ICD and right-sided pacing are summarised in the Box. Doctors should be aware of these therapies and consider referring individual patients who meet the criteria for their use. Comparison of some features of pacing modalities for chronic heart failure and comorbid arrhythmias Cardiac resynchronisation therapy Implantable cardioverter defibrillator Right-sided pacing Clinical outcomes Decreased mortality, morbidity and hospitalisation Improved exercise tolerance, quality of life, NYHA class Decreased mortality Decreased incidence of sudden cardiac death No proven benefit in chronic heart failure Potential problems Relatively high non-response rate Procedural complications (early and late) Uncertain quality-of-life benefits Inappropriate discharge Procedural complications (early and late) Worsening left ventricular function in systolic chronic heart failure in certain modalities Cost14 High: public hospitals, $21 075; private hospitals, $59 100* High: public hospitals, $14 975; private hospitals, $45 100† Relatively low NYHA = New York Heart Association. RA = right atrial. RV = right ventricular. LV = left ventricular. * Costs for cardiac resynchronisation therapy include: (public hospitals) generator, $17 000; RA lead, $475; RV lead, $1500; LV lead, $2100; and (private hospitals) generator, $44 500; RA lead, $1350; RV lead, $8750; LV lead, $4500. † Costs for implantable cardioverter defibrillator include: (public hospitals) generator, $13 000; RA lead, $475; RV lead, $1500; and (private hospitals) generator, $35 000; RA lead, $1350; RV lead, $8750.

Henry Krum MB BS, PhD, FRACP · Prashanthan Sanders MB BS(Hons), PhD

Objective: To evaluate current evidence in support of therapies for preventing and treating cardiogenic shock (CS) after acute myocardial infarction that can be initiated in hospitals without invasive cardiac facilities.Study design: Systematic review.Data sources: MEDLINE and PubMed were searched from January 1985 to May 2008 using the MeSH terms “myocardial infarction”, “thrombolytic therapy”, “shock, cardiogenic”, “angioplasty, transluminal, percutaneous coronary”, “intra-aortic balloon pumping” and “platelet aggregation inhibitors”. Additional keyword and reference list searches were performed. Articles in English relating to adults were included.Study selection: Meta-analyses and comparative studies were included if they reported mortality or prevention of CS as an endpoint. In total, 35 articles were analysed (four meta-analyses, eight randomised controlled trials and 23 cohort studies).Data extraction: Studies were summarised by the first author and the level of evidence graded. Each study was checked by the second author and consensus was reached about inclusion and levels of evidence.Data synthesis: In the management and prevention of CS, the following are supported by high-level evidence: prehospital thrombolysis, transfer for emergency revascularisation (patients aged < 75 years) and thrombolysis for older patients (patients aged ≥ 75 years). In established CS, evidence supporting inhospital thrombolysis and intra-aortic balloon pump use in patients aged < 75 years and emergency revascularisation in older patients is limited to subgroup analyses and observational studies.Conclusions: In regional centres, prevention of CS is achieved with early fibrinolysis, preferably before hospital arrival. Patients of all ages should be considered for thrombolysis, early transfer for coronary revascularisation, and intra-aortic balloon pump insertion unless contraindicated. Glycoprotein inhibitors have no role in the management of CS in non-tertiary hospitals.

Enda O’Connor MRCPI, FJFICM · John F Fraser FRCA, FFARCSI, FJFICM

Clinical record A 68-year-old man presented to our general district hospital in December 2006 with the chief complaint of sore throat, which had started abruptly 2 hours earlier. The pain was described as intense with a stabbing character. He reported minimal improvement after being given 10 mg of morphine subcutaneously. The patient did not report experiencing any cardiac or pulmonary discomfort, and he had no pertinent past medical history. His family history included one sister who had died of a ruptured aortic aneurysm. The patient was a non-smoker and denied any recent medication use. Physical examination showed that the patient’s vital signs were stable, with a normal level of consciousness, a regular pulse of 61 beats/min, and a blood pressure equal at both arms of around 115/70 mmHg. He was slightly tachypnoeic and diaphoretic. An ear, nose and throat examination did not provide any diagnostic clues as to the cause of the pharyngeal pain. Findings of a cardiovascular examination were normal apart from an audible right carotid artery bruit. No other physical abnormalities were detected. Results of laboratory tests were unremarkable, except for a markedly elevated d-dimer level (8.41 mg/L; upper limit of normal, 0.50 mg/L). Routine chest radiography was suggestive of mediastinal widening (Figure A). On the basis of these findings, a thoracic computed tomography scan was performed, which showed a 5.4 cm dissecting ascending aortic aneurysm (Figure B). The dissection involved the aortic root, ascending part of the aorta and aortic arch, and propagated into the right brachiocephalic trunk and left common carotid artery (Figure C). Transthoracic echocardiography additionally showed the presence of a bicuspid aortic valve with moderate grade 2/4 aortic insufficiency. Thoracic aortic dissection was diagnosed, classified as a Stanford type A dissection, given the involvement of the ascending aorta. A congenital bicuspid aortic valve and an ascending aortic aneurysm were predisposing factors for aortic dissection. The patient successfully underwent emergency surgery with graft replacement of the aortic valve and the dissected aortic segment. A: Chest x-ray showing mediastinal widening. The upper normal mediastinal width is defined as a mediastinum to chest-width ratio of over 0.25, measured at the level of the aortic arch (illustrated by the length of the solid line); this is noticeably exceeded in our patient (dashed line). B: Computed tomography scan showing an aneurysmatic dilatation of the ascending aorta with a classical dissection flap (black arrowhead) separating a true and false lumen. C: Propagation of the dissection process into the supra-aortic vessels (white arrows). The clinical presentation in our case was rather trivial, but the combined results from two basic investigations — an elevated d-dimer level and an abnormal chest x-ray — heightened our clinical suspicion for aortic dissection and led us to perform aortic imaging. Thoracic aortic dissection generally results from a laceration of the intimal lining of the aorta. This allows blood leakage into the aortic wall resulting in a propagating separation of the aortic media, thereby creating a false blood-filled lumen.1 Hence, the major criterion for definitive diagnosis of aortic dissection includes visualisation of a so-called intimomedial flap that divides the aorta into a true and a false lumen. Several aortic imaging techniques can be used for this purpose, of which contrast-enhanced computed tomography (CT) and transoesophageal echocardiography (TOE) are the most feasible to perform in an emergency department setting.1,2 Moreover, these investigations help to localise the dissection, thereby allowing appropriate classification. Currently, the Stanford classification of aortic dissection is the most widely adopted system.1,2 This system has the virtue of merely dividing aortic dissection into two subtypes, depending on whether the ascending aorta is involved (type A) or not (type B).1,2 While the definitive diagnosis of aortic dissection is usually straightforward, making the initial clinical diagnosis can be extremely challenging. Aortic dissection is associated with a dramatic rate of misdiagnosis and delayed recognition.3 This is no doubt partially explained by the highly variable clinical presentation of the condition. Our case is a striking illustration of why acute aortic dissection is colourfully called a “clinical chameleon”.1 Although most patients with aortic dissection present with severe chest or back pain (Box 1), the pain can be variably localised to the neck, jaw or throat.4 Throat pain occurs most often in cases of a dissection of the aortic arch, particularly when the supra-aortic vessels are involved. Our patient complained only of a sore throat, and denied having thoracic pain. Only two similar cases have been previously reported.5,6 Moreover, findings on physical examination can be very subtle.1 Classical signs consistent with the diagnosis of thoracic aortic dissection, such as an aortic insufficiency murmur or decreased femoral arterial pulsation, were not present in our patient. According to the International Registry of Acute Aortic Dissection,7 these so-called typical findings are infrequently detected during physical examination (Box 1). In our case, the only notable features of the physical examination were diaphoresis and a right carotid artery murmur. The latter was presumably the result of propagation of the dissection into the right brachiocephalic trunk. Because symptoms and signs of aortic dissection can be diverse and sometimes treacherously trivial, the initial diagnostic suspicion might rely on abnormalities observed during the basal diagnostic work-up. This routinely consists of laboratory testing with d-dimer analysis and chest radiography. d-dimer analysis has only recently come to the fore, with several studies focusing on the stringent association between the d-dimer level and aortic dissection.3,8,9 The pathophysiological mechanism for this relationship is well explained by the release of tissue factor from the dissected aortic wall. This sets off a cascade of events — activation of the extrinsic coagulation system, generation of fibrin, and secondary fibrinolysis with d-dimer formation.8 The d-dimer assay is reported to have an excellent sensitivity and negative predictive value for aortic dissection (Box 1). The quoted sensitivity is equal for both types of dissection, although absolute d-dimer values tend to be higher in type A aortic dissections as they are usually more extended.10 Given its high sensitivity and negative predictive value, d-dimer testing is an attractive tool for the diagnostic work-up of aortic dissection, particularly in the setting of a low pretest probability for aortic dissection. In such cases, a normal d-dimer result can reliably exclude the presence of aortic dissection, hence obviating the need for further investigations.9,10 Besides elevation of the d-dimer level, the clinical suspicion for aortic dissection should also be heightened if the chest radiograph is abnormal (Box 1). Mediastinal widening (relative mediastinum to chest-width ratio > 0.25;11 Figure A) is the most common radiographic finding in aortic dissection.7 Of note, absolute estimations of the mediastinal width are practically inaccurate, as these measurements are influenced by the distance between the roentgenographic source and the thorax.12 It is worth mentioning that one in three patients with aortic dissection has a normal chest x-ray.11 Thus, relying on chest radiography alone as the initial diagnostic modality is inefficient as it clearly carries a high risk of misdiagnosis. When readily available, contrast-enhanced CT and TOE are the preferred imaging modalities in an acute care setting. Both investigations have a comparable diagnostic accuracy and allow a definitive diagnosis of aortic dissection to be established.1,2 However, the diagnosis must first be suspected before it can be confirmed — this case serves as a reminder of this life-threatening condition’s wide variability in clinical presentation, and the need to maintain continuing vigilance. 1 Clinical and basic diagnostic features of thoracic aortic dissection, and percentages of patients presenting with these features who are subsequently diagnosed with Stanford type A or B aortic dissection1,2 Stanford classification Features Type A* Type B† Clinical symptoms and signs7 Presence of any pain 94% > 95% Retrosternal pain 71% 44% Interscapular pain 33% 41% Back pain 47% 64% Abdominal pain 22% 43% Blood pressure Hypotension or shock/tamponade < 25% < 5% Hypertension 35% 70% Aortic insufficiency murmur < 45% < 15% Decreased or absent peripheral pulsations < 20% < 10% Laboratory analysis8,9 d-dimer sensitivity (cutoff, 0.50 mg/L) > 95% > 95% d-dimer negative predictive value (cutoff, 0.10 mg/L) 100% Not reported Chest radiography7 Mediastinal widening 63% 56% Abnormal or blurred aortic contour 47% 53% Other radiographic features‡ < 25% < 25% * Dissection with involvement of the ascending aorta. † Dissection of the descending aorta without involvement of the ascending aorta. ‡ Such as displaced aorta, aortic calcification, tracheal displacement, pleural effusion. Lessons from practice Thoracic aortic dissection is characterised by a highly variable clinical picture, which has led to the condition being called a “clinical chameleon”. d-dimer testing can be of value in excluding aortic dissection. A normal chest x-ray does not rule out the possibility of aortic dissection. Advanced aortic imaging should be performed early in patients who have symptoms suggestive of aortic dissection in order to prevent misdiagnosis.

Sébastien Anguille MD · Aurélie M Derweduwen MD · Jeroen Lenz MD · Luc Vanuytsel MD, PhD · Frank J Cools MD

Clinical records Over the past 3 years, we have identified five cases of coronary syndromes attributable to a left subclavian stenosis proximal to a left internal mammary artery (LIMA) graft for coronary artery disease. All occurred in men aged between 56 and 73 years, presenting a median of 52 months (range, 26–138 months) after coronary artery bypass grafting. One patient presented with stable angina, three had unstable angina, and one had a non-ST elevation myocardial infarction. Arm claudication was present in one patient. Three of the five patients had an exercise or pharmacological stress test — all with anterior wall ischaemia. At cardiac catheterisation, the diagnosis was recognised by careful comparison of the pressure tracings in the subclavian artery and aorta. All patients had a significant pressure gradient across the subclavian stenosis (median, 35 mmHg; range, 20–85 mmHg), measured by a 5F or 6F diagnostic catheter, and a significant angiographic stenosis (median, 70%; range, 50%–80%). Non-invasive left arm blood pressure measured at the time of cardiac catheterisation was substantially lower than aortic pressure (> 20 mmHg difference in all patients). Retrograde flow up the LIMA graft during native left coronary angiography, a characteristic of subclavian steal, occurred in one of the five patients (Figure 1). All patients were treated with percutaneous stenting, using 9–10 mm balloon expandable stents, with successful abolition of the pressure gradient in the proximal subclavian artery (Figure 2). The difference in non-invasive blood pressures between the arms after stenting was less than 5 mmHg in all patients. All patients had relief of their angina symptoms over a median follow-up of 20 months (range, 5–29 months). 1 A: Subtracted angiogram showing the subclavian stenosis prior to the left internal mammary artery (LIMA) origin. B: Selective left coronary angiogram showing flow down the left anterior descending artery (LAD) (1) then retrograde up the LIMA (2 and 3). C: Diagram showing the relationship of the stenosis to the left vertebral and LIMA origins. 2: Angiograms of the left subclavian stenosis before (A) and after (B) stenting, showing the improvement in antegrade LIMA flow. The intra-arterial subclavian pressure tracings are shown below the angiograms. Before stenting (left) the pressure tracing is blunted, while after stenting (right), there is an improvement in blood pressure and normalisation of the arterial waveform. A potentially clinically significant stenosis in the subclavian or brachiocephalic arteries will produce a difference in systolic blood pressure between the right and left brachial arteries of 15–20 mmHg or more.1 Therefore, bilateral arm blood pressure measurements should be taken in symptomatic patients after coronary artery bypass using internal mammary artery grafts. Unfortunately, this simple non-invasive assessment is often overlooked, as it was in the patients reported here. A haphazard approach to catheterisation of the left internal mammary artery (LIMA) graft can also cause the diagnosis to be missed, as the catheter can often cross a significant subclavian stenosis. Meticulous comparison of the subclavian and aortic pressure tracings will identify the gradient and enable diagnosis. The difference in pressure between the arms may be reduced or absent in patients with significant bilateral subclavian and/or brachiocephalic disease, a scenario more likely in patients with extensive atherosclerotic peripheral vascular disease elsewhere.2 Coronary subclavian steal syndrome describes angina related to a subclavian stenosis with retrograde flow up the LIMA graft. This reverse LIMA flow results from lower vascular resistance and blood pressure in the arm compared with the myocardial territory supplied by the LIMA. However, steal with reverse LIMA flow is not an absolute requirement for angina. In our patients, none had angina precipitated by left arm activity that would uncover a latent steal syndrome. In many cases, subclavian stenosis behaves physiologically more like a very proximal LIMA stenosis. In this case, “LIMA-inflow syndrome” may be a more accurate term. Regardless of the semantics, this is a rare phenomenon that is reported in 0.1%–5.0% of patients after coronary artery bypass grafting.2-4 The differential diagnosis includes other diseases obstructing large arteries such as Takayasu’s arteritis (especially in young women), post-radiation arteritis, and giant cell arteritis (especially in older patients). The management of subclavian and brachiocephalic stenoses depends on the clinical presentation. All patients require medical therapy with intensive atherosclerosis risk factor reduction, as the 10-year total and cardiovascular mortality approaches 40%–50%.1 Asymptomatic individuals do not need intervention, so non-invasive imaging is unnecessary. In symptomatic patients, non-invasive imaging with contrast computed tomography or magnetic resonance or conventional angiography can confirm the diagnosis when an intervention is anticipated. Traditionally, symptomatic patients were treated with carotid-subclavian bypass. However, percutaneous angioplasty and stenting are increasingly used because of their lower morbidity and similar long-term results.2,5-8 The risk of stroke from stenting is low, and no higher than for surgical bypass.2,5-8 Post-procedural management includes treatment with aspirin for life and clopidogrel for at least 1 month. Clinical follow-up includes surveillance for recurrent symptoms with a difference in brachial blood pressures. Although the LIMA-inflow syndrome from subclavian stenosis is a rare cause of angina, it is easily identified non-invasively by comparing the brachial blood pressures in both arms. Advances in percutaneous stenting permit a relatively easy and durable treatment in a cardiac catheterisation laboratory. Lessons from practice Systolic blood pressure should be measured in both arms with a standard sphygmomanometer in all patients with past coronary artery bypass grafting and progressive angina or acute coronary syndromes. A difference in systolic blood pressure of greater than 15–20 mmHg between the right and left arms is strongly suggestive of subclavian stenosis. Asymptomatic subclavian stenosis does not require imaging or revascularisation, but does denote high cardiovascular risk warranting intensive risk factor reduction. Symptomatic subclavian stenosis can be successfully treated with percutaneous stenting.

Daniel Tsyvine MD · Maryanne Hartzell MD · Marc P Bonaca MD · Gerard Connors MB BS, FRACP · Scott Kinlay MB BS, PhD, FRACP

Supraventricular tachycardia (SVT) is a common cardiac rhythm disturbance; it usually presents with recurrent episodes of tachycardia, which often increase in frequency and severity with time. Although SVT is usually not life-threatening, many patients suffer recurrent symptoms that have a major impact on their quality of life. The uncertain and sporadic nature of episodes of tachycardia can cause considerable anxiety — many patients curtail their lifestyle as a result, and many prefer curative treatment. SVT often terminates before presentation, and episodes may be erroneously attributed to anxiety. Sudden-onset, rapid, regular palpitations characterise SVT and, in most patients, a diagnosis can be made with a high degree of certainty from patient history alone. Repeated attempts at electrocardiographic documentation of the arrhythmia may be unnecessary. Treatment of SVT may not be necessary when the episodes are infrequent and self-terminating, and produce minimal symptoms. When episodes of tachycardia occur frequently, are prolonged or are associated with symptoms that affect quality of life, catheter ablation is the first choice of treatment; it is a low-risk procedure with a high success rate. Long-term preventive pharmacotherapy is an alternative approach in some patients.

Caroline Medi BMed, FRACP · Jonathan M Kalman MB BS, PhD, FRACP · Saul B Freedman MB BS, PhD, FRACP

To the Editor: The author of “High levels of confusion for cholesterol awareness campaigns”1 identifies my comment as the source of her perplexity. My remark, which Hall quotes in relation to the “Test the Nation” campaign, was actually given in response to a question about the Pfizer-sponsored “National Cholesterol Awareness Campaign”, which ran simultaneously. It seemed too inconsequential to request correction of the relevant newspaper article,2 because public health guidelines differ in regard to the target population for lipid testing. My comment reflected conservative Australian guidelines.3 It is well known that other sources recommend more widespread testing of adults.4 Hall’s confusion was a rhetorical device to justify her discussion of “condition branding” and to “explore the motivations” of the campaigns. Hall’s article attacks two programs that promote diet and lifestyle management of cardiovascular risk. It also criticises pharmacological treatment, thus eliminating all available options to address this important problem. The article undermines the tenuous availability in Australia of plant sterol-containing products, such as yoghurt, but provides no alternative strategies. It fails to take responsibility for its potential negative impact on the implementation of nutritional and other life-saving interventions. It is disconcerting that such a negative article has emanated from a so-called Centre for Health Initiatives. The cholesterol awareness campaigns are likened to “an unnecessary focus on an unimportant health problem” and disparagingly compared with a program devoted to public awareness of fungal nail infections. Understandably, the latter led to professional irritation and frustration. By contrast, the formal involvement of the Royal Australian College of General Practitioners in the Test the Nation–National Cholesterol Education Program of Australia (NCEPA) represents an effort to ensure that the initiative was justified, that the content was relevant, and that the logistics were attuned to primary care practice. The participation of professional organisations reinforced the quality, relevance and independence of the information provided. The dietary advice that was distributed by the NCEPA was widely acclaimed. Dyslipidaemia accounts for 49% of the attributable risk of coronary heart disease.4 Full implementation of risk factor guidelines could massively reduce cardiovascular disease,5 but public and professional adherence to guidelines is suboptimal.6 Chen and colleagues report that, in addition to those with diabetes or coronary heart disease, over 700 000 Australians are at high risk,7 but most Australians are unaware of the consequences. It seems extraordinary that anyone with a professed interest in public health could be so opposed to public education about risk factor management. Consequently, Hall’s article itself generates further confusion. The health sector is in the process of responding to calls for greater independence from commercial interests. Both cholesterol programs illustrate the implementation of many of the suggested changes. Unfortunately, Hall’s article suggests an open-ended list of demands that will be impossible to satisfy. Calls for further change need to be more constructive and clearly enunciate realistic proposals, supported by evidence that the net impact on Australian health care has been (or will be) beneficial. The article implies restrictions that would be impractical in other sectors. Standards for the interaction between industry and the health sector should be an example to emulate, rather than a soft target that loses step with normal practice.

David R Sullivan

In reply: My article1 was submitted for debate when two separate, industry-sponsored cholesterol awareness campaigns were simultaneously targeting the Australian public. There is potential for public confusion following exposure to concurrent campaigns with differing sponsors, creative techniques, and messages such as “Test the Nation”. My article did not diminish the importance of cholesterol screening (nor of the prevention of or treatment for hyperlipidaemia), and indeed it reiterated the National Heart Foundation guidelines. Its intent was to raise debate about industry-sponsored disease awareness campaigns, as there is growing concern in Australia about “disease mongering”2 and the evidence that this is occurring in the cholesterol market in the United States.3 I agree with Sullivan that the Australian public needs education about asymptomatic risk factors, including hypertension and hyperlipidaemia. Ideally, this would include clear information and non-emotive marketing techniques to convey who is most at risk, as well as transparent disclosure of sponsor interests.4 Contrary to Sullivan’s charge, I believe there are many opportunities for quality health education and behaviour change programs, several of which the Centre for Health Initiatives is currently undertaking.5 The intent of my article was to generate critical analysis of industry-sponsored campaigns in order to improve their public health benefit.

Danika V Hall

Objective: To assess the performance of the Framingham and United Kingdom Prospective Diabetes Study (UKPDS) cardiovascular risk equations in Australian patients with type 2 diabetes who were initially free of cardiovascular disease (CVD).Design and setting: The Fremantle Diabetes Study (FDS), a community-based longitudinal observational study; data for the period 1993–2006 were used.Patients: Of the 815 FDS participants with type 2 diabetes who were initially CVD-free, 791 (97%) were eligible for assessment using the UKPDS equations, and 697 (86%) using the Framingham equation.Main outcome measures: CVD endpoints during 5 years of follow-up. For the UKPDS equations, these were fatal myocardial infarction (MI) or sudden death (fatal coronary heart disease [CHD]); hospitalisation for/with or death from MI or sudden death (all CHD); fatal stroke; and all stroke. For the Framingham equation, they were all MI, sudden death or angina pectoris (CHD).Results: During follow-up to first CVD event, death or 5 years, there were 38 MIs (11 fatal) and 23 strokes (13 fatal) in the UKPDS-assessable cohort of FDS participants. The UKPDS risk equations for all CHD, fatal CHD, and all stroke overestimated the number of events by 6.5, 2.8 and 1.8 times, respectively. The risk equation for fatal stroke underestimated the number of events by 38%. The UKPDS CHD risk equations showed modest discrimination and poor calibration, while the stroke risk equations showed good discrimination and calibration. The Framingham equation predicted 28% fewer CHD events than occurred (93 v 130), and discrimination and calibration were poor.Conclusions: While the UKPDS stroke risk equations performed relatively well, the UKPDS and Framingham CHD risk equations are not suitable for predicting risk in Australians with type 2 diabetes.

Wendy A Davis MPH, PhD · Stephen Colagiuri FRACP · Timothy M E Davis DPhil, FRACP

Clozapine is a valuable drug for patients with treatment-resistant schizophrenia. Myocarditis is the most publicised cardiac complication of clozapine treatment, but cardiomyopathy and pericarditis have also been reported. Myocarditis has heterogeneous and non-specific presenting features, making it difficult to identify patients with clozapine-related myocarditis clinically. A high index of suspicion is required. The gold standard for diagnosis of myocarditis is an endomyocardial biopsy, but this is not a practical initial approach. Transthoracic echocardiography is a valuable, reproducible and widely available tool to assist in diagnosis of clozapine-induced cardiotoxicity. The level of B-type natriuretic peptide, a hormone secreted in response to ventricular wall stress, may be useful for evaluating patients with clozapine-induced cardiac dysfunction and may in the future be useful for screening asymptomatic patients. The mainstay of treatment of clozapine-induced cardiotoxicity is cessation of clozapine and provision of supportive care.

Jamie J Layland MB ChB, MRCP(UK) · Danny Liew MB BS(Hons), FRACP, PhD · David L Prior MB BS, FRACP, PhD

Patients with schizophrenia have a wide range of risk factors for cardiometabolic disease, at rates 1.5–5 times greater than the general population. Despite the provision of many sets of guidelines and protocols for screening and monitoring of cardiometabolic risks, morbidity and mortality rates for those with psychotic illnesses remain excessive and premature. Surveys of mental health practitioners reveal a clear acknowledgement of the importance of managing cardiometabolic risks and subsequent comorbidity. However, inadequate screening rates of patients with antipsychotic-treated mental illnesses suggest “knowing is not doing”. Surmountable barriers (at service, patient and illness levels) to adequate integrated health care are not being adequately challenged for this population. Recommendations to improve the situation include service reorganisation, communication enhancement, improved training and education, better incentives, accreditation rigour, and government leadership.

Tim J R Lambert MB BS, PhD, FRANZCP · John W Newcomer MD

To the Editor: A 56-year-old woman was recently admitted with recurrent large-volume haemoptysis associated with left-sided tearing thoracic pain. Growing up on a sheep farm in rural New South Wales, she had been diagnosed at age 8 years with pulmonary hydatidosis, which remained dormant on periodic clinical assessments. However, 2 years before presentation she started to cough up gelatinous material containing scolices of Echinococcus granulosus. Surgery was declined at that time due to the anticipated complexity of the operation and associated high perioperative risk. Long-term anthelmintic therapy was commenced. On admission, a computed tomography (CT) scan showed a contained aortic pseudoaneurysm (Box), consistent with rupture of the aorta into the hydatid cyst. Other images showed the cyst containing gas, indicating communication with the airway. After stabilisation, the patient was transferred to a cardiothoracic centre. A left upper lobectomy with dissection and removal of the mediastinal cyst was undertaken through a median sternotomy, and the aortic fistula was successfully repaired using bovine pericardial strips. Intraoperatively, there was no evidence of pericardial involvement. Histopathological examination showed a disrupted and degenerate hydatid cyst without a germinal layer and no protoscolices. The patient received albendazole for 6 months after surgery and her recovery was uneventful. Hydatid disease is caused by the intestinal parasitic tapeworm E. granulosus which, in Australia, is most prevalent in the eastern half of NSW at higher altitudes.1 Symptomatic intramural aortic-wall hydatidosis causing aortic-wall rupture and pseudoaneurysm formation has been described in fewer than a dozen cases.2 Hypotheses for arterial-wall invasion include dissemination during cardiac surgery; entry through vasa vasorum or pre-existing small intimal tears or aneurysms; or partial incorporation of the aortic wall into the hydatid pericyst.2,3 We identified four case reports in adults describing fistula formation between a pulmonary hydatid cyst and the aorta, including three European cases3-5 and one South African case (published twice).6,7 All patients were middle-aged men: two presented with chest pain and large-volume haemoptysis, one with anaphylactic shock and bilateral ischaemic lower limbs from aortic-wall hydatid cyst emboli, and one with a cyst eroding the abdominal aorta (found incidentally during surgery for a coeliac trunk aneurysm). One patient died during removal and another patient after removal of the primary cyst. Haemoptysis in pulmonary hydatid disease is a common presenting symptom. Mechanisms include pressure erosion of a bronchus, obstructive infection, cyst rupture or — very rarely, and emphasised in our case — erosion of a major vascular structure. Aortobronchial fistula resulting from pulmonary hydatidosis A: Contrast-enhanced thoracic computed tomography scan showing consolidation and cavitation within the left upper lobe. A multiloculated 4 cm diameter peripherally calcified hydatid cyst was present in the medial aspect of the left upper lobe (white arrows), penetrating under the aortopulmonary window. Contrast medium extended posteriorly into the base of the lesion, suggestive of an aortic leak (black arrow). B: Coronal reconstruction of the aortic arch demonstrated a round collection of contrast medium with a 1.4 cm base (black arrow), consistent with a contained saccular aortic pseudoaneurysm.

Stefan Buchholz · David Sowden · Troy Stapleton · Peter Pohlner · Craig Wright

Australia needs to develop its own guidelines based on local data New guidelines for testing and treating lipid abnormalities in children have recently been published by the American Academy of Pediatrics and the American Heart Association (Box).1,2 These recommendations, made partly in response to the high prevalence of obesity in children in the United States, provoke consideration of whether they should also be adopted in Australia. The previous US recommendations,3 which targeted cholesterol testing to children with a family history of premature cardiovascular disease or high cholesterol levels, had focused on a population-based approach to treatment through a fat- and cholesterol-restricted diet. Drug therapy was reserved for children with more persistent and extreme elevations in cholesterol level. In contrast, the recent guidelines recommend that testing be broadened to include all overweight or obese children, with the first cholesterol assessment to be done between the ages of 2 and 10 years. The new guidelines further recommend that initiation of drug therapy be considered at a younger age (from 8 years) and with a lower low-density lipoprotein cholesterol (LDL-C) level target for children with multiple cardiovascular risk factors. Indirect evidence suggests that childhood lipid abnormalities are important in the development of cardiovascular disease in adults. For example, autopsy studies indicate that atherosclerosis begins in the young and that the extent of lesions correlates with traditional cardiovascular risk factors, including lipid levels.4 However, advanced atherosclerosis rarely occurs in children and adolescents. Arterial wall thickness in adults, as assessed by carotid artery ultrasonography, is associated with childhood lipid levels, and children with lipid abnormalities display altered arterial structure and function.5,6 However, direct evidence for an association between childhood lipid levels and adult cardiovascular outcomes, such as myocardial infarction and stroke, is not available. Why, then, test children and adolescents at all? Would it be equally effective to test young adults? One important potential rationale for cholesterol testing in children is that lipoprotein levels tend to track from childhood into adult life.7,8 Detection of lipid abnormalities in young children could prompt changes in diet and physical activity that would be required through the whole of life. It is important to note, however, that both universal and targeted lipid testing in children result in a high false-positive rate for adult dyslipidaemia.8,9 Moreover, the predictive value of childhood lipid levels depends on the threshold values used to define dyslipidaemia. Threshold values derived from populations of US children may not be sensitive to trends in childhood lipid levels and overweight and obesity in Australia. The prevalence of childhood overweight and obesity is high and increasing in both Australia and the US.10,11 Moreover, in both countries, lipid abnormalities are common in overweight and obese children,12,13 with low high-density lipoprotein cholesterol (HDL-C) and high triglyceride levels particularly prevalent. Importantly, targeting overweight and obese children for LDL-C testing does not improve the specificity for detecting elevated LDL-C levels in adults.8 Although most overweight and obese children with low HDL-C levels become adults with low HDL-C levels, targeting overweight and obese children for HDL-C testing will not identify the majority of adults with low HDL-C levels.8 Overweight and obese children, whether or not they have high triglyceride and low HDL-C levels, require weight management through changes in diet and physical activity levels. But it is uncertain, particularly in the case of young children, whether knowledge of their lipid status will lead to greater motivation to implement such changes. Improved diet and increased physical activity are both safe and effective ways of reducing cardiovascular risk factors in children, and should be promoted across the whole paediatric population.14-17 Most overweight and obese children could be encouraged to adopt these lifestyle changes without testing their lipid status. Testing for lipid abnormalities could be reserved for older, obese children (> 10 years of age) in the context of an overall assessment of their risk for future cardiovascular disease. Screening based on family history may be hampered by inaccurate or incomplete information and the need for adult family members to have their cholesterol levels measured. However, obtaining an accurate family history, combined with testing of adults to detect those with significant elevation in LDL-C levels, may help identify children with inherited dyslipidaemias (eg, familial hypercholesterolaemia). Such children have the highest risk of premature cardiovascular disease and may benefit most from drug therapy at a young age. The new US recommendations also raise questions about which children should be considered for drug therapy for lipid abnormalities. A number of randomised clinical trials have demonstrated the short-term safety and efficacy of HMG-CoA reductase inhibitors (statins) in children.18 Statins are currently the first-line drug treatment for elevated cholesterol levels in children. However, there is a lack of evidence for their long-term safety, and animal studies have shown they may be toxic to the developing fetus.19 Although there have been no controlled epidemiological studies relating gestational exposure to statins with adverse human pregnancy outcomes, case reports of structural anomalies and the biological plausibility of a teratogenic effect mean that statins are contraindicated in pregnancy.20 Thus, a case can be made for reserving statin therapy for older children at high risk of future cardiovascular disease. In girls, it may be appropriate to delay statin therapy until an age when discussions about reproduction and contraception can occur. A strong family history of premature cardiovascular disease or a rapid progression in surrogate measures of atherosclerosis (eg, carotid arterial wall thickness, measured by ultrasound) may lower the age threshold for statin therapy. In Australia, we should be taking action to address the increasing prevalence of childhood cardiovascular risk factors. However, guidelines from the US may not be appropriate for Australian children, and it is imperative that we formulate new local recommendations based on recent local data. Guidelines for lipid assessment and management in Australia should also propose strategies for reducing cardiovascular risk factors in childhood more generally. This will require discussion and collaboration between clinicians, researchers, and governmental and non-governmental organisations, such as Diabetes Australia, the National Heart Foundation, the Paediatric Cardiac Council of the Cardiac Society of Australia and New Zealand, and the Royal Australasian College of Physicians. In the interim, a careful assessment of the risk of future cardiovascular disease is required for all paediatric patients. This will be based on ascertainment of an accurate family history of premature cardiovascular disease, information on diet and physical activity, anthropometric and blood pressure measurements made at routine paediatric health checks, and the targeted assessment of blood lipid levels in older children with a family history of premature cardiovascular disease or hyperlipidaemia and/or multiple other cardiovascular risk factors, including obesity. Summary of recent changes to recommendations in the United States for cholesterol testing and treatment in children1,2 Stronger recommendations for cholesterol testing in children who have cardiovascular risk factors other than lipid abnormalities — particularly overweight and obesity, but also hypertension, cigarette smoking or diabetes. A stronger recommendation on the timing of initial cholesterol testing: between the ages of 2 and 10 years. A recommendation to consider commencing drug therapy in children aged over 8 years (rather than 10 years), with a target low-density lipoprotein cholesterol level of < 3.3 mmol/L (rather than < 4.1 mmol/L).

Julian G Ayer BSc(Med), MB BS, FRACP · David R Sullivan MB BS, FRACP, FRCPA · Gary F Sholler MB BS, FRACP

Objectives: To determine the incidence and clinical features of acute rheumatic fever (ARF) in Fiji, and the clinical features of patients presenting to hospital in Fiji with rheumatic heart disease (RHD).Design and setting: A prospective surveillance study at the Colonial War Memorial Hospital in Suva over a 23-month period from December 2005 to November 2007.Main outcome measures: Incidence of ARF; clinical features of ARF and RHD.Results: The average annualised incidence of definite cases of ARF in children aged 5–15 years was 15.2 per 100 000 (95% CI, 9.0–22.6). The clinical features of ARF were similar to those in classic descriptions. Carditis was very common, occurring in 79% of cases. There were 103 admissions for RHD in which detailed information was collected, with the most common reason for admission being cardiac failure (51%). The median age at admission with RHD was 26.8 years, and there were 10 deaths of patients with RHD (case fatality rate, 9.7%).Conclusions: Although apparently declining in incidence since the middle of the 20th century, ARF remains a significant health problem in Fiji. RHD affects young people, leading to premature morbidity and mortality. There is an urgent need for effective control of ARF and RHD in Fiji.

Andrew C Steer MB BS, BMedSci, FRACP · Joseph Kado MB BS · Adam W J Jenney MB BS, PhD, FRACP · Michael Batzloff BSc, PhD · Lepani Waqatakirewa MB BS · E Kim Mulholland MB BS, FRACP, MD · Jonathan R Carapetis MB BS, FRACP, PhD

To the Editor: Cardiac rehabilitation (CR) is an underutilised evidence-based treatment.1 Between 1 March 1998 and 28 February 1999, we surveyed 1933 patients aged 20 to 85 years discharged from public hospitals in the Hunter region with principal discharge diagnoses of acute myocardial infarction, unstable angina pectoris, congestive heart failure, and ischaemic heart disease. Patients undergoing coronary artery bypass graft surgery and percutaneous coronary intervention were also included. Among the 1202 respondents (62%), 493 (41%) reported being referred to CR, 309 (26%) reported attending at least one session, and 233 (19%) reported completing all or all but one session.2 The factors associated with referral were younger age, previous participation in CR, admission to a hospital providing CR, a discharge diagnosis of acute myocardial infarction, and coronary artery bypass surgery.3 We provide the following data, pertaining to non-referred patients, within the context of recent government initiatives to improve access to evidence-based treatments. Fifty-seven per cent of respondents (688) had not been referred to CR (2% did not answer this question), 645 of whom had not attended previously. The median age of these 645 people was 70 years. Most were male (64%), married (62%), had not completed high school (54%), were not in full-time employment (81%), had not been admitted to a hospital that offers CR (55%), did not have a discharge diagnosis of acute myocardial infarction (78%), and had not undergone revascularisation (92%). These 645 patients were asked if they thought they would have benefited from attendance at an outpatient CR program. Of the 380 patients who did not think they would have benefited, 41% (157) reported having at least three coronary risk factors, 39% (150) were interested in further services, and 26% (100) reported participating in at least one risk-factor-specific secondary-prevention program (Box 1). In conclusion, many patients who are not referred for CR reported having multiple coronary risk factors, yet few felt they would have benefited from attending CR or had participated in any alternative risk-factor-specific programs. We agree that system factors resulting in failure to refer should be investigated and rectified,1 but our data suggest that many non-referred patients would not attend if invited. This highlights the importance of research testing the efficacy of alternative models of CR in the Australian setting,4,5 and the need for research assessing the effectiveness of these programs in routine health services delivery. 1 Coronary risk factors, and opinions on the need for and participation in risk-factor-specific secondary-prevention programs Felt cardiac rehabilitation would have been beneficial* Total Yes No Number of patients 645 143 (22%) 380 (59%) Number of self-reported coronary risk factors None 60 (9%) 8 (6%) 37 (10%) One 137 (21%) 32 (22%) 73 (19%) Two 180 (28%) 45 (31%) 108 (28%) Three or more 254 (39%) 55 (38%) 157 (41%) Felt the need for further services 321 (50%) 119 (83%) 150 (39%) Chose one or more of the following options: Information on how to prevent or manage further heart trouble 280 (43%) 112 (78%) 124 (33%) Help with how to cope with emotional issues arising from heart problems 169 (26%) 82 (57%) 61 (16%) Exercise classes 130 (20%) 76 (53%) 34 (9%) Nutrition classes 124 (19%) 71 (50%) 34 (9%) Quit-smoking programs 51 (8%) 21 (15%) 21 (6%) Help with stress management 142 (22%) 69 (48%) 51 (13%) Help with getting back to work 35 (5%) 25 (17%) 10 (3%) Undertook risk-factor-specific secondary prevention 187 (29%) 50 (35%) 100 (26%) Participated in the following programs: Home exercise plan provided by hospital 62 (10%) 15 (10%) 34 (9%) Other home-based exercise program 55 (9%) 10 (7%) 31 (8%) Fitness-centre program 7 (1%) 2 (1%) 2 (0.5%) Diet/nutrition program provided by hospital 85 (13%) 27 (19%) 46 (12%) Other diet/nutrition program 57 (9%) 14 (10%) 27 (7%) Quit-smoking program 25 (4%) 7 (5%) 15 (4%) * 19% of non-referred respondents (122/645) did not answer this question.

Natalie A Johnson · Kerry J Inder · Amanda L Nagle · John H Wiggers

To the Editor: The work presented by Chew and colleagues in setting up and using the Acute Coronary Syndrome Prospective Audit (ACACIA) is an important and influential initiative.1 It has the potential to provide a strong evidence base for the design and delivery of cardiac services in Australia. Their article and the accompanying editorial by Scott2 highlighted the difficulty in determining treatment benefit from uncontrolled observational studies. Among the unreported and possibly significant confounders underpinning the association between acute invasive care and the 47% improved 12-month survival in patients treated for acute coronary syndrome is participation in post-event secondary-prevention cardiac rehabilitation. A contemporary systematic review of randomised controlled trials of cardiac rehabilitation reported a significant relative risk reduction in all-cause mortality of 20% (95% CI, 7%–32%) over a median follow-up of 12 months.3 Despite this evidence and the long-term policy of the World Health Organization that cardiac rehabilitation should be available to all patients with cardiovascular disease,4 this secondary-prevention intervention is largely underused, and those who do attend are generally at lower risk of recurrent coronary events than those who do not.5 Further, secondary-prevention cardiac-rehabilitation programs are cost-effective relative to other coronary interventions6 and, along with proven cardioprotective pharmacotherapy and acute invasive care, should be given priority as part of an optimal treatment and management strategy for secondary prevention. The completion of cardiac rehabilitation or other forms of secondary prevention by ACACIA patients may have favourably impacted upon the marked improvement in 12-month survival seen in the ACACIA cohort. Chew and colleagues identified the fact that patients who underwent invasive therapies were also more likely to be treated according to best-practice guidelines.1 It may be that this same group were also more likely to be referred to cardiac-rehabilitation and secondary-prevention programs. It would be of great interest to know if attendance in cardiac-rehabilitation and secondary-prevention programs was recorded in the ACACIA registry and, if so, why those results were not incorporated.

Leigh D Kinsman · Julie Redfern · Tom G Briffa

In reply: It is often hoped that clinical studies can be “all things to all people”. Yet, in reality, clinical registries are optimally designed to answer a limited number of questions such as use of therapies, current treatment, and reassurance (but not proof) of treatment effectiveness. We decided not to collect data on referral to cardiac rehabilitation in our registry.1 In arriving at this decision, we were cognisant of the fact that, important to exploring the benefits or confounding effects of therapies is the ability to define the intervention accurately, and then adjust for the baseline differences between patients receiving and not receiving such treatment. This is problematic when considering “referral to cardiac rehabilitation”. How should cardiac rehabilitation (inhospital, outpatient, single-day, multi-day programs) be defined? Should one assess referral or attendance (partial or complete)? While the value of rehabilitation is well appreciated, it was not the focus of our study. We are designing future observational studies in this area with more focus on the later phase of patients’ admissions and their posthospital management, including rehabilitation. As we cautioned, the magnitude of benefit associated with invasive management in our study should not be overinterpreted. At best, these studies contribute to the totality of evidence, and offer insights into those patients not currently receiving the benefits of our rich evidence base.

Derek P Chew · John V Amerena · Steve G Coverdale · Jamie M Rankin · Carolyn M Astley · Ashish Soman · David B Brieger

To the Editor: Scott was correct in his recent article to emphasise the need for an Australian registry for percutaneous coronary interventions (PCIs).1 To that end, we report an initiative developed by a voluntary collaborative group of interventional cardiologists in Victoria — the Melbourne Interventional Group (MIG) — which has provided a significant volume of contemporary data on the efficacy and safety of PCI.2 Since July 2004, data on over 9500 coronary interventional procedures in over 7500 patients have been collected into this registry, using data elements and methods based on those of the United States National Cardiac Disease Registry and the Victorian Cardiothoracic Surgical Database.3,4 Methods for data collection and analysis, and the format of data forms have been published.5 The data elements, developed by an MIG working group, have been peer reviewed and are currently under review for publication. MIG has a formal governance structure with a constitution, steering committee and subcommittees that govern data quality, database development, research, publication and funding. Approval for the conduct of the registry has been obtained from the ethics committees of all participating hospitals; all patients enrolled provide informed consent for initial and long-term data collection in a manner similar to that used for the Victorian Cardiothoracic Surgical Database.3 Results from MIG to date show that PCI practice differs between Australia and the US, and that use of drug-eluting stents (DES) is safe and effective in reducing restenosis in patients with appropriate indications, leading to a DES usage rate of 30% in public hospitals.2 The MIG registry may provide an appropriate framework for a national PCI data registry. It satisfies most of Scott’s criteria, and many colleagues in other states have expressed interest in collecting similar data or collaborating in a joint registry. The limiting factor, as always, is funding. We join Scott in supporting the call for appropriate funding to be provided by government and professional societies to allow a national PCI registry to be established.

Christopher M Reid · Andrew E Ajani · David Eccleston

To the Editor: We read with great interest the case report by Barthwal and Herman,1 and agree with many of the points they raise. In-stent thrombosis after cessation of clopidogrel therapy in patients with drug-eluting stents (DES) is a significant problem in Australian medical practice, particularly in the perioperative period,2-4 as the case report by Barthwal and Herman confirms.1 It is often decided to cease clopidogrel therapy during the perioperative period to reduce the risk of bleeding. While clopidogrel given before cardiac surgery has been documented to increase transfusion rates and returns to the operating theatre,5 bleeding risk associated with clopidogrel and non-cardiac surgery remains poorly defined. Greater understanding of the risk of in-stent thrombosis after clopidogrel therapy withdrawal, and the risk of excessive bleeding if it is continued, in individual patients will provide rational perioperative planning and, hopefully, improved outcomes for our patients. Currently, the Cardiac Society of Australia and New Zealand has formed a multidisciplinary committee to create guidelines for the perioperative management of patients with coronary stents. In some instances, clopidogrel therapy may need to be replaced with alternative antithrombotic strategies to prevent in-stent thrombosis. We have proposed such a strategy, with excellent results so far.3,4 The complication of in-stent thrombosis was originally associated with a 50% mortality rate in the first series of cases reported.2 However, we have since reported three patients from Australia with in-stent thrombosis during the perioperative period, all of whom survived.4 We have set up a website (http://www. DESReporting.com) to enable clinicians worldwide to report perioperative management strategies and outcomes for patients with DES in their coronary arteries, and who undergo surgery.3,4 In view of the developing importance of perioperative late stent thrombosis, we strongly encourage reporting through this website. This will enable rapid accumulation of outcomes and associated antithrombotic strategies, with a view to dissemination and publication of the analysed data.

Myles M Conroy · Stephen N C Bolsin

To the Editor: The recent article by Barthwal and Herman highlights the problem of late stent thrombosis in a patient with a drug-eluting stent (DES) undergoing non-cardiac surgery (NCS).1 While the authors stated that clopidogrel therapy was ceased preoperatively and not restarted postoperatively, they did not say whether or not aspirin therapy was continued. In addition, emphasis was not placed on the role the surgical procedure played in this adverse cardiac outcome. Perioperative stent thrombosis as a result of discontinuation of dual antiplatelet therapy has been well described, to such an extent that the American Heart Association, American College of Cardiology, Society for Cardiovascular Angiography and Interventions, American College of Surgeons, and American Dental Association issued a joint advisory regarding the risk of premature cessation of dual antiplatelet therapy perioperatively.2 A prothrombotic state is well described in the perioperative period, as is a rebound hypercoagulable period following cessation of therapy with antiplatelet agents.3 Preoperative cessation of antiplatelet therapy by interventional teams is common in both routine and emergency procedures; this is sometimes unnecessary and not based on any evidence. Practitioners involved in ceasing antiplatelet therapy for procedures should be aware of the increased risk of major adverse cardiac events in patients with cardiac stents whose antiplatelet therapy is ceased prematurely.2 Duration of antiplatelet therapy following DES implantation is still a contentious issue, but the prothrombotic effect of NCS in addition to the baseline risk of late stent thrombosis in these patients is becoming less easy to ignore.4 Evidence-based guidelines for the perioperative management of patients with cardiac stents undergoing NCS are still to be established. Careful consideration should be given before perioperative cessation of therapy with antiplatelet agents in patients with coronary stents. Undertaking non-emergency surgery within 12 months of DES implantation should be avoided if possible.4,5

Simon J Pattullo · Rohan Jayasinghe

Objective: To determine the prevalence of elevated troponin levels after a marathon, and test for an association with reduced renal clearance.Design, setting and participants: Prospective observational study of entrants running the full (42 km) 2007 Perth Marathon, Western Australia.Main outcome measures: Elevated troponin levels (≥ 0.1 μg/L) after the race; pre- and post-race survey data, and biochemical parameters.Results: 27% of runners (92/346) enrolled in the study, of whom 88 (96%) completed it. Most were men (71%; 65/92); mean age was 43.1 years (SD, 9.8 years; range, 25–64 years) and mean body mass index (BMI) was 24.1 kg/m2. Raised troponin levels were seen in 32% of participants (28/88), the highest being 1.4 μg/L. The strongest predictor for developing elevated troponin levels was a decrease in weight (odds ratio [OR], 2.15; 95% CI, 1.27–3.65). Creatinine increase was also associated with elevated troponin levels (OR, 1.03; 95% CI, 1.01–1.06), but pre-race estimated glomerular filtration rate, age, sex, BMI, training factors, marathon experience and race time were not. Most runners (99%; 87/88) had elevated levels of ischaemia-modified albumin after the race.Conclusions: Troponin level increases were common among marathon finishers. The strongest predictors were weight loss and an increase in creatinine levels, suggesting that reduced renal clearance is an associated factor. Further study is needed to determine the clinical significance of these findings, and to understand the mechanism.

Kelley M Hubble MB BS · Daniel M Fatovich MB BS, FACEM · Jonathon M Grasko MB BCh · Samuel D Vasikaran MD, FRCPA

To the Editor: A 77-year-old woman with a history of idiopathic long-QT syndrome (presumed genetic) presented to hospital with a storm of defibrillator shocks from her implantable cardioverter defibrillator (ICD). She had a single-chamber Guidant Ventak Prizm VR, model 1850, and a Guidant ventricular lead, model 0148 (Guidant Corporation, Indianapolis, Ind, USA) implanted 12 months earlier after an episode of syncope. The lead had been implanted by left subclavian venous access. The patient’s postoperative course and responses to routine questioning indicated that the device was functioning normally. After presenting with device discharges, a 12-lead electrocardiogram showed oversensing suggestive of lead dysfunction. Stored electrograms from the defibrillator showed artifactual signals that were typical of lead disruption. These signals had triggered inappropriate detection of ventricular arrhythmia and subsequent device shocks (Box 1). The pacing threshold and lead impedance were normal. On close examination of the patient’s chest x-ray, a line of radiolucency was detected within the lead between the first rib and clavicle. At reoperation, the lead was extracted with minimum difficulty and the site of the insulation break was detected (Box 2). A new lead was implanted and the patient was discharged home well. Subsequent follow-up was uneventful. Lead failure can occur any time after implantation of an ICD, and should be suspected when patients present with inappropriate ICD discharges.1 This case illustrates oversensing as a result of the lead’s insulation being disrupted by crush compression between the first rib and clavicle. Alternative implantation techniques, such as cephalic vein cut-down or extrathoracic axillary vein puncture, have been suggested for venous access to avoid this complication.2 1 Stored electrograms from the patient’s implantable cardioverter defibrillator showed artifactual signals had triggered inappropriate detection of ventricular arrhythmia and subsequent device shocks (arrow) 2 Implantable cardioverter defibrillator lead after extraction showing the break in the insulation (arrow)

Chin V Hiew · James W Leitch