Cardiovascular diseases

In reply: I thank Padayachee for his interest in our review.1 We read Padayachee’s published case series of the use of levosimendan to help recovery of left ventricular dysfunction in tako-tsubo cardiomyopathy (TTC)2 after our review was published. I agree that levosimendan is the inotropic agent of choice in this situation, and this approach has been used successfully in my hospital on two occasions. This is, in fact, what we meant by “In our experience, β-blockade in conjunction with non-adrenergic inotropes can prevent this vicious cycle and allow the ventricle to recover (unpublished data)”. As Padayachee rightly points out, definitive evidence on this point would require a proper randomised trial, which would be very difficult to organise, given the low incidence of tako-tsubo cardiomyopathy and the small fraction of patients who develop cardiogenic shock requiring inotropic support. I think that it is probably better to simply state that levosimendan therapy works and makes scientific sense, so “just do it”. However, Padayachee also surmises that, if the patient has a typical wall-motion abnormality and a typical history, it might be possible to avoid unnecessary thrombolytic therapy in cases of TTC. Unfortunately, my understanding is that this is not the case. Occlusion of the left anterior descending artery (LAD) may result in the classic TTC wall-motion abnormality if the LAD extends far beyond the apex (usually with a non-dominant right coronary). As myocardial infarction can be precipitated by stressful events, and the evolution of electrocardiographic changes in TTC is similar to that seen with an anterior infarct after thrombolysis, there is still no clear way to discriminate between the two diagnoses apart from immediate coronary angiography. Whether computed tomography (CT) angiography can accurately discriminate remains to be seen — this might be useful in centres that have CT but not a cardiac catheterisation laboratory. Until then, I believe it is probably less harmful to give TTC patients thrombolysis than to withhold thrombolysis from patients with large anterior infarcts. Lastly, I invite Padayachee and other interested clinicians who frequently manage these patients to participate in an ongoing study of genetic predisposition to TTC for which we are currently enrolling participants.

Michael R Ward

Results from recently published clinical trials provide additional information to be considered in the choice of therapies in the management of acute coronary syndromes. This addendum summarises the important findings and their implications for recommended practice. This addendum supplements the recommendations outlined in the National Heart Foundation of Australia/Cardiac Society of Australia and New Zealand “Guidelines for the management of acute coronary syndromes 2006”.1 Results from recently published clinical trials provide additional information to be considered in the choice of therapies in the management of acute coronary syndromes. This new evidence provides additional information that strengthens the recommendations in the guidelines or provides alternatives to current recommended practice that should be considered based on the circumstances of the individual patient and setting. The specific implications of this new evidence on recommended practice are highlighted in the “Implications of the findings” sections of this addendum. Reperfusion and revascularisation for ST-segment-elevation myocardial infarctionImportant findingsThe REACT (Rescue Angioplasty versus Conservative Treatment or Repeat Thrombolysis) study,2 MERLIN (Middlesbrough Early Revascularisation to Limit Infarction) study and a recent meta-analysis3 have demonstrated a decrease in the composite endpoints of death, re-infarction, stroke and heart failure with rescue percutaneous coronary intervention (PCI). The OAT (Occluded Artery Trial)4 trial showed no reduction in death, re-infarction or heart failure during 4 years of follow-up in stable patients with occlusion of the infarct-related artery 3 to 28 days after myocardial infarction who underwent routine PCI. Implications of the findings (Guidelines page S19)Rescue PCIThe evidence for rescue PCI has strengthened since the development of the 2006 guidelines. Patients who receive fibrinolytic therapy and have not reperfused by 90 minutes should be considered for rescue PCI, which optimally should be performed within 12 hours. Transfer between facilities may be necessary to achieve this, and systems need to be in place to facilitate transfer of appropriate patients. If it is not possible for transfer within the 12-hour window, then transfer can be delayed if the patient is asymptomatic. RevascularisationPatients in whom the infarct-related artery is completely occluded do not benefit from re-opening the artery routinely if this occurs more than 24 hours after the initial event. If patients are symptomatic, revascularisation may be considered. Antiplatelet and antithrombin therapyRecent evidence, while providing additional information on outcomes for individual agents, does not provide conclusive evidence of the superiority of one agent over another, nor of one combination of therapies over another. The risks and benefits of these therapies and strategies should be evaluated individually in each patient. Important findingsThe EXTRACT (Enoxaparin and Thrombolysis Reperfusion for Acute Myocardial Infarction Treatment) trial5 demonstrated that, in patients receiving fibrinolysis for ST-segment-elevation myocardial infarction (STEMI), the use of enoxaparin (a low molecular weight heparin; 30 mg intravenous bolus followed by 1 mg/kg every 12 hours in patients younger than 75 years, omission of the bolus but 0.75 mg/kg every 12 hours in patients aged 75 years or older) results in less re-infarction than the use of unfractionated heparin, but is associated with an increase in episodes of major bleeding. The OASIS-6 (Sixth Organization for the Assessment of Strategies for Ischemic Syndromes) trial6 demonstrated that fondaparinux in comparison to no heparin or unfractionated heparin reduces mortality and produces less bleeding in patients with STEMI. Patients treated with fondaparinux who went on to PCI required additional heparin to reduce catheter thrombosis. The OASIS-5 (Fifth Organization to Assess Strategies in Acute Ischemic Syndromes) study7 and the ACUITY (Acute Catheterization and Urgent Intervention Triage Strategy) study8 on the treatment of non-ST-segment-elevation acute coronary syndromes (NSTEACS) demonstrated non-inferiority of two new agents, fondaparinux and bivalirudin, in the treatment of patients with NSTEACS when compared with “standard” antithrombin therapy, but with a significant reduction in major bleeding. The OASIS-5 study demonstrated non-inferiority of fondaparinux (2.5 mg daily) compared with enoxaparin (1 mg/kg twice daily) at the composite clinical endpoint, but reduced the rate of major bleeding at 9 days and reduced total mortality at 30 days and at 6 months. The ACUITY study demonstrated non-inferiority at a composite ischaemic endpoint, but a reduction in the rate of major bleeding and an improvement in the net clinical outcome endpoint when comparing bivalirudin with a glycoprotein IIb/IIIa (GP IIb/IIIa) inhibitor with standard treatment with unfractionated heparin or enoxaparin. The ISAR-REACT 2 (Second Intracoronary Stenting and Antithrombotic Regimen: Rapid Early Action for Coronary Treatment) study9 demonstrated that GP IIb/IIIa inhibition with abciximab administered among heparin-treated NSTEACS patients undergoing PCI and being pretreated with clopidogrel 600 mg, at least 2 hours before intervention, reduces rates of death, myocardial infarction or urgent target vessel revascularisation at 30 days, driven largely by the reduction in myocardial infarction. Following further analysis, it appeared that all of this benefit was evident among the troponin-positive patients. The ACUITY Timing trial10 demonstrated that “in-lab” initiation use of GP IIb/IIIa inhibitors (abciximab or eptifibatide) just before PCI compared with routine “upstream” use (for a median time of 4 hours before intervention with tirofiban or eptifibatide) in high-risk NSTEACS patients could be associated with a 25% increase in ischaemic events, but is associated with a reduced rate of major bleeding. Implications of the findingsAntithrombin therapy for acute STEMI (Guidelines page S14)Enoxaparin and fondaparinux are appropriate antithrombin agents and may be considered for use in patients with STEMI. Antithrombin therapy for NSTEACS (Guidelines page S22)Fondaparinux and bivalirudin, both currently not licensed for upstream therapy of NSTEACS, may be preferable alternatives to standard therapy with unfractionated heparin or low molecular weight heparin with a GP IIb/IIIa inhibitor for patients with high-risk NSTEACS, particularly where there is an increased risk of bleeding. The selection of the most appropriate upstream therapy may best be determined for any individual patient from their risk of ischaemia versus bleeding. Fondaparinux may be particularly useful in patients for whom invasive management is significantly delayed or those not suitable for invasive management. Bivalirudin has the advantage of monotherapy for both upstream and procedural administration at the time of PCI, and therefore may be particularly useful in patients planning to have an early invasive intervention. Antiplatelet therapy for NSTEACS (Guidelines pages S21–S22)GP IIb/IIIa inhibition with abciximab reduces adverse cardiac events in biomarker-positive NSTEACS patients undergoing PCI who have been pretreated with clopidogrel. Pretreatment with high-dose clopidogrel is not an adequate alternative to abciximab among biomarker-positive NSTEACS patients. A deferred in-lab initiation approach to the use of intravenous GP IIb/IIIa inhibitors (particularly with abciximab) may be preferable to short-term (median 4 hours) upstream administration in patients presenting with high-risk NSTEACS.

Constantine N Aroney MD, FRACP · Philip Aylward PhD, FRACP, FCSANZ · Derek P Chew MB BS, MPH, FRACP · Nancy Huang MB BS, DipRACOG, MPH · Anne-Maree Kelly MD BS, MClinED, FACEM · Harvey White DSc, FRACP, FCSANZ · Michelle Wilson BHSc

Objective: To examine trends in preoperative clinical characteristics, risk profiles and postoperative outcomes of patients undergoing isolated coronary artery bypass graft (CABG) surgery in Victoria.Design, setting and patients: A prospective analysis of 9372 patients undergoing isolated CABG surgery between 1 July 2001 and 30 June 2006 in six Victorian public hospitals, using the Australasian Society of Cardiac and Thoracic Surgeons database.Main outcome measures: Trends in patient baseline characteristics and risk factors, postoperative morbidity and 30-day mortality rate.Results: Over the 5 years, the mean age of patients undergoing isolated CABG surgery increased, from 65.4 years in 2001–02 to 66.0 years in 2005–06 (P < 0.001). There was also an increase in the proportion of patients with hypertension (70.2% to 75.8%; P < 0.001), respiratory disease (83.2% to 89.5%; P < 0.001) and left main coronary artery disease (22.1% to 26.1%; P = 0.03), while the number of patients undergoing repeat CABG surgery decreased (4.4% to 2.6%; P = 0.002). The overall 30-day mortality rate remained unchanged (2.2% to 1.8%; P = 0.983). Rates of other major postoperative complications showed no significant change over the study period.Conclusion: Rates of 30-day mortality and postoperative morbidity after CABG surgery have remained steady, despite the surgical population being older. Short-term outcomes after CABG surgery in Victoria remain among the most favourable reported in any population undergoing this surgery.

Diem T Dinh PhD · Geraldine A Lee BSc, RGN, PGDE · Baki Billah PhD, MAS · Julian A Smith FRACS · Gilbert C Shardey FRACS · Christopher M Reid DipEd, MSc, PhD

Objective: To evaluate the use of clinical practice guidelines for the management of acute coronary syndromes published by the National Heart Foundation (NHF) of Australia and the Cardiac Society of Australia and New Zealand (CSANZ) in patients presenting with chest pain.Design: Cross-sectional study of consecutive patients admitted with chest pain.Setting: Prospective case note review was undertaken in 2380 patients admitted to 27 hospitals across five states in Australia between January 2003 and August 2005. Patients were divided into two groups: those who presented to centres with angiography and percutaneous intervention facilities (n = 1260) and those treated at centres without these facilities (n = 1120).Main outcome measures: The proportion of patients whose care met quality of care standards for diagnostic and risk-stratification procedures and management according to NHF/CSANZ treatment guidelines.Results: Significant delays were identified in performing electrocardiography, administering thrombolysis, transferring high-risk patients to tertiary centres, and performing revascularisation. Medical therapy was underused, especially glycoprotein IIb/IIIa antagonists in patients with high-risk acute coronary syndromes. Patients treated at centres without interventional facilities were less likely to receive guidelines-based medical therapy and referral for coronary angiography (20.11%) than patients treated at centres with interventional facilities (66.43%; P < 0.001).Conclusion: There are deficits in the implementation and adherence to evidence-based guidelines for managing chest pain in hospitals across Australia, and significant differences between hospitals with and without interventional facilities.

Darren L Walters MB BS, MPhil, FRACP · Constantine N Aroney MD, FRACP · Derek P Chew MPH, FRACP · Linden Bungey BSc, MSc · Steven G Coverdale MB BS, FRACP · Roger Allan MB BS, FRACP · David Brieger MB BS, FRACP

Objective: To study persistence and adherence with the use of common antihypertensive (AHT) medications.Design, setting and participants: Longitudinal assessment of Pharmaceutical Benefit Scheme claim records covering the period January 2004 to December 2006. We analysed a 10% random sample of all Australian long-term health concession card holders who had been commenced on an angiotensin II receptor antagonist (A2RA), an angiotensin-converting enzyme inhibitor (ACEI) and/or a calcium channel blocker (CCB), but for whom no AHT medication had been dispensed in the previous 6 months.Main outcome measures: Proportion of patients failing to fill a second prescription; median persistence time with medication (ie, non-cessation of therapy); persistence with medication over 33 months; median medication possession ratio (MPR, defined as the proportion of prescribed medication actually consumed by patients persisting with treatment).Results: The database yielded information relating to 48 690 patients prescribed AHT medication. Nineteen per cent of patients failed to collect a second prescription. The median persistence time was 20 months. The data were little different from the population average with respect to A2RAs or ACEIs, but persistence was 57% poorer with respect to CCBs (log-rank P < 0.001) (28% of patients prescribed CCBs failed to collect a second prescription; median persistence time, 7 months). There were differences in persistence between individual drugs in the respective classes, the best outcomes being with candesartan and telmisartan (A2RAs; 10%–20% better), perindopril (ACEI; 25% better) and lercanidipine (CCB; 25% better). Median MPRs were generally around 100%, indicating that most patients who collected prescriptions also showed good adherence to treatment regimens.Conclusion: There is an ongoing problem of poor persistence with commonly used AHT medications. This may represent a diminished opportunity for cardiovascular disease prevention.

Leon A Simons MD, FRACP · Michael Ortiz BPharm, PhD · Gordon Calcino BA, GradDipMedStats

To the Editor: The editorial by Woollard and Newman1 discussing the best management of stable coronary artery disease is welcome and timely, but we believe their conclusions undervalue the benefits of optimal medical therapy. The authors correctly point out that the early trials comparing surgery with medical treatment did not include aspirin, β-blockers or lipid-lowering drugs in the medical treatment group. Clearly, the benefits of these treatments have been so dramatic as to make these original trials irrelevant to current practice. After reviewing trials comparing percutaneous coronary intervention (PCI) with coronary artery bypass graft (CABG) surgery and discussing their limitations, the authors conclude that: The best interpretation of currently available data is that, for patients with severe coronary artery disease, the more invasive procedure with a longer recovery time (CABG) has a better long-term clinical outcome and is more cost-effective than the less invasive fast-recovery procedure (PCI). We believe this conclusion is only appropriate for those patients in whom an adequate trial of medical therapy has failed to achieve sufficient relief of anginal symptoms. Based on current evidence, including that from the MASS II2 (comparing medical therapy with both CABG and PCI), COURAGE3 (comparing PCI with medical therapy) and AVERT4 (comparing intensive lipid-lowering therapy using atorvastatin with PCI) trials, we conclude the following about the management of stable coronary artery disease: Irrespective of whether patients under-go CABG or PCI (or neither), aggressive medical therapy combined with appropriate lifestyle measures is the means by which patients are protected from major adverse cardiovascular events. There is no evidence that either PCI or surgical treatment is superior to the current best medical treatment in preventing death or myocardial infarction. Patients with stable angina should be informed accordingly and be reassured that their symptoms are likely to abate or resolve with optimal medical treatment over a period of time. Intervention should be reserved for patients in whom an adequate trial of medical treatment has failed to relieve symptoms or in whom medication is poorly tolerated, and possibly for patients in whom satisfactory anti-atherosclerosis treatment targets cannot be achieved. Performing PCI and CABG in patients with stable angina consumes a significant portion of the Medicare budget. We believe many patients with absent or relatively minor symptoms consent to these procedures in the mistaken belief that their lives will be prolonged. Application of evidence-based guidelines would significantly reduce the number of interventions currently performed and make much needed resources available for prevention strategies and for selected patients with acute coronary syndromes in whom this expensive treatment has proven benefit. Lastly, we strongly support the implication by Woollard and Newman that patients should “undertake consultation with other providers” regarding treatment options — including medical therapy.

Richard W Harper · Esther M Briganti · Brett H R Forge

In reply: We agree with Harper and colleagues that for most patients with stable coronary artery disease, prevention of death or other cardiac events is best achieved with medical treatment. Many patients and even some doctors are so impressed by the restoration of coronary blood flow achieved with angioplasty that they incorrectly assume it will provide a prognostic benefit. However, we do not agree that intervention should be reserved for patients in whom medical treatment has failed. It is unlikely that a trial comparing current medical treatment with coronary artery bypass graft (CABG) surgery for severe left main coronary disease will ever be performed, and current evidence favours CABG at least in this group. In addition, many patients with angina prefer a mechanical intervention to long-term antianginal medications, and why should they be denied that choice?

Keith V Woollard · Mark A J Newman

To the Editor: Drug-eluting coronary stents (DES) were approved for use in Australia in 2002, after they were found to be effective in limiting the incidence of restenosis.1 However, their cost is three to four times that of traditional bare-metal stents, and most Australian states restricted their use in the public health system. In 2006, we reported in the Journal that DES were used in 45% of patients undergoing percutaneous coronary intervention (PCI) in Victorian public hospitals, and that they were largely reserved for patients with risk factors for restenosis, such as diabetes, small vessels, and complex lesions.2 However, in the private health system, DES can be claimed as prostheses from insurance funds, so their use is not limited by financial constraints. In early 2007, multiple reports from around the world noted a small but significant increase in late stent thrombosis occurring 1–4 years after implantation of DES.3,4 This caused concern, as stent thrombosis has a mortality rate approaching 50%. It is now recommended that all patients with DES maintain aspirin and clopidogrel therapy for at least a year, although the appropriate duration of this treatment remains unknown.5 Further, long-term dual antiplatelet therapy is associated with an increased risk of bleeding and is problematic for patients requiring surgery.4,5 We examined the use of DES from February 2006 to June 2007 in 674 patients undergoing PCI by 10 operators in a Victorian private hospital. Monthly use dropped dramatically, from a peak of 91% of patients in July 2006 to 34% in June 2007 (Box). In 118 PCIs performed between March and May 2007, DES were used more often in: diabetic than non-diabetic patients (67% v 47%; P = 0.05); small (≤ 2.5 mm) vessels compared with large vessels (74% v 53%; P = 0.04); and long lesions (> 20 mm stent length) compared with shorter lesions (62% v 52%; P = not significant). This mirrors the pattern previously seen only in patients treated in the public health system.2 Given the issue of late stent thrombosis and the need for prolonged dual antiplatelet therapy, reserving DES for patients who are at high risk of restenosis in both the public and private health systems seems very appropriate. Utilisation is likely to change again with a better understanding of the long-term safety of DES, but a cautious approach should be maintained. Drug-eluting stent (DES) use per month (February 2006 – June 2007) in patients in a Victorian private hospital

Suzanne M McLean · David J Clark

To the Editor: We report a case of successful resuscitation after cardiac arrest associated with obstruction of the airway by chewing gum. In December 2005, in Port Hedland, Western Australia, a 57-year-old electrician was found unconscious by workmates 5 minutes after he was seen working normally. He was not breathing and had no pulse. Bystander cardiopulmonary resuscitation (CPR) was commenced immediately and an ambulance arrived within 3 minutes. Cardiac monitoring showed the patient was in ventricular fibrillation. Direct-current defibrillation was performed three times, resulting in reversion to ventricular tachycardia, rapid atrial fibrillation and, within minutes, spontaneous reversion to sinus rhythm. The time from ambulance dispatch to arrival at Port Hedland Regional Hospital was less than 15 minutes. Rapid transport to hospital enabled prompt assessment of the patient, who was found to be maintaining sinus rhythm with left bundle branch block but no ST segment changes. Following the return of spontaneous circulation and consciousness, the patient’s Glasgow Coma Score and oxygen saturation unexpectedly deteriorated. On rapid sequence intubation, chewing gum was found lodged in the patient’s larynx; it was removed, and intubation completed. An urgent computed tomography scan found no intracranial cause for the deterioration in his condition. The patient was transferred to a tertiary centre by the Royal Flying Doctor Service. There was a rise in the patient’s troponin level after the cardiac event, but normal coronary arteries with globally depressed ventricular function were seen on angiography, and an ejection fraction of 30% on echocardiography, suggesting an underlying cardiomyopathy. An implantable cardiac defibrillator was inserted. The patient recovered, with a diagnosis of hypoxia associated with myopathic cardiac arrest complicated by laryngeal obstruction from chewing gum. He suffered a moderate hypoxic brain injury during the event and underwent a short period of inpatient rehabilitation, before returning to work within 6 months. He had no significant sequelae 18 months after the cardiac event. There have been previous reports of sudden death due to airway obstruction by chewing gum in children and one recent report of adult death, but no reports of successful resuscitation after cardiac arrest and hypoxia associated with chewing gum obstruction.1,2 There have also been reports of delayed problems with ventilation due to migration of previously aspirated chewing gum.3 While it is unlikely that the chewing gum airway obstruction was the primary event in this case, given the finding of cardiomyopathy, we believe that the laryngeal obstruction contributed to the patient’s secondary deterioration. This case demonstrates the importance of CPR training in the community, rapid paramedical and medical response, and the need to consider complicating causes in the event of cardiac arrest when return of spontaneous circulation does not result in clinical improvement as expected. It is made all the more remarkable by its occurrence in a remote regional centre of north-west WA.

Angus G Thompson · Shakeeb Razak · Rohan Jayasinghe

A 45-year-old man presented with frequent palpitations. Clinical examination and electrocardiogram were unremarkable. Transthoracic echocardiography suggested asymmetrical septal hypertrophy, although the acoustic windows were poor. Transoesophageal echocardiography revealed a broad false tendon within the left ventricle, extending from the basal septum to the apical lateral wall (Figure). Holter monitoring showed frequent premature ventricular complexes, indicating right bundle branch block morphology. The incidence of false tendons — fibromuscular intracavitary bands anatomically distinct from the valvular cusps — is 0.4% to 3.0%.1 They may be associated with malignant ventricular arrhythmias, which should be excluded before making a diagnosis of benign premature ventricular complexes in a healthy patient.1 Transoesophageal echocardiogram: the arrow shows the false tendon from the basal septum to the apical lateral wall of the left ventricle (LV).

Robin A P Weir · Henry J Dargie · Iain N Findlay

Clinical record A 34-year-old woman was diagnosed with grade III infiltrating ductal carcinoma of her left breast, and had a mastectomy. Reconstructive cosmetic surgery was subsequently performed, with placement of a fluid-filled silicone-encased breast implant in the left chest wall. She had previously been well with no known cardiac history. A nuclear medicine gated heart pool scan (GHPS) was performed before planned chemotherapy involving anthracycline. On the GHPS (Figure 1) a radiolucent pericardial halo was apparent, raising concerns for pericardial effusion. The rest of the study was unremarkable, with normal regional wall motion and quantitative ejection fraction of the cardiac ventricles. Comparison with a recent chest x-ray (Figure 2) revealed radiolucency external to the chest wall. Subsequent transthoracic echocardiography (Figure 3) ruled out the presence of pericardial effusion. 1: GHPS left anterior oblique 45° (1A) and anterior (1B) views. Pericardial halo suggestive of pericardial effusion (arrows). 2: Anterior–posterior chest x-ray showing the saline-filled breast implant as a radio-opaque shadow on the left anterior chest wall (arrows). 3: Two-dimensional echocardiogram. 3A: Subcostal views showing pericardial border anteriorly and posteriorly (arrows) without evidence of pericardial effusion. 3B: Subcostal view with the transducer directed anteriorly to image the saline-filled breast implant (arrow). 3C: Anterior chest wall imaging depicting the implant (arrows). Current national surveys estimate that up to 4 million women, or more than 3% of the adult female population in the United States, have breast implants.1 Of clinical importance, more than 35 000 women each year received breast implant surgery for reconstruction after a mastectomy,1 and most of these patients would have one or more gated heart pool scan (GHPS) studies for the assessment of cardiac function before chemotherapy. In Australia, the incidence of breast cancer has been steadily increasing since the early 1980s, and this is now the most common cancer among women. One in eight women will be diagnosed with breast cancer by the age of 85 years, with more than 13 000 new cases in 2006. In part because of improved and more aggressive treatment strategies, survival prospects following diagnosis continue to improve.2 The accompanying rise in the use of adjuvant chemotherapy, including the anthracyclines, has brought about a concomitant increase in the use of GHPS for monitoring drug-induced cardiac toxicity.3 Lessons from practice Gated heart pool scan (GHPS) studies are commonly used for monitoring drug-induced cardiac toxicity in cancer patients. Many female cancer patients will have breast implants, and these can mimic pericardial effusion on GHPS. Clinical input, chest x-ray and, if necessary, other imaging modalities such as two-dimensional echocardiography, computed tomography or magnetic resonance imaging, are prudent for confirmation of pericardial effusion on GHPS. GHPS was among the earliest imaging tools to be used for the diagnosis of pericardial effusion.2-7 In 1958, Rejali and colleagues,4 after observing the disparity in the size of the cardiac silhouette on radionuclide ventriculography and the chest x-rays, reported the clinical efficacy of radionuclide ventriculography in detecting pericardial effusion. Since the mid 1970s, because of its inherently higher spatial resolution, two-dimensional echocardiography has been the technique of choice for diagnosing pericardial disease in general and pericardial effusion in particular.8 Nevertheless, GHPS remains effective for diagnosing moderate to large pericardial effusion. A report in 1987 of 154 patients documented a high degree of sensitivity (100% for large and 55% for moderate to large effusions) and specificity (98%) by GHPS for diagnosing pericardial effusions.7 False-positive results may be due to benign and sinister aetiologies. Although some researchers have reported subepicardial fat as the most common cause of a false-positive finding of pericardial effusion by GHPS,9 others have documented mediastinal tumours, left ventricular hypertrophy or blood clot as some of the pathologies mimicking pericardial effusion on the GHPS.10,11 The high (98%) specificity previously reported used a set of criteria for moderate to large pericardial effusion,7 including the need for clear perceptibility of pericardial halo around all visible cardiac chambers in both the anterior and 45° left anterior oblique views of the GHPS. In the cancer population, however, the test specificity is anticipated to be lower because distortion and loculation of pericardial effusion is not uncommon.12 Test specificity is likely to be further degraded by the increasing number of women worldwide receiving breast implants for both cosmetic and postsurgical reconstruction purposes. Of clinical importance, extracardiac and intrathoracic pathologies, including pericardial effusion, found on GHPS by and large do not impede the interpretation of cardiac function (which is the principal indication for performing the test), and the incidental findings might even provide relevant diagnostic or prognostic information.13,14 Our case highlights, particularly among female cancer patients, the need for vigilance in assessment of GHPS with extracardiac findings suggestive of pericardial effusion, with breast implant posing as a differential diagnosis of potential false-positive findings. The use of clinical input, chest x-ray and, if necessary, other imaging modalities such as two-dimensional echocardiography, computed tomography or magnetic resonance imaging9 is prudent for confirmation of pericardial effusion on GHPS.

Kiran Swaraj MB BS, FRACP · Hosen Kiat MBBS, FRACP · Michael Lin MB BS, FRACP · Peter Lin MB BS, FRACP · Ivan Ho-Shon MB BS, FRACP · Sithoeun Sam BSc · John Chu MB BS, FRACP

To the Editor: Scott and colleagues have shown that Australia is no different to the rest of the world in applying evidence-based treatment predominantly to patients at lower risk.1 They suggest that therapy may be withheld from high-risk patients because of over-estimation of the risk of treatment, under-estimation of the actual absolute risk of non-treatment, and consideration of cost-effectiveness and social inequalities. I suggest that their data support the concept that the patient at highest risk who misses out on evidence-based treatment may in fact be being managed with kindness and wisdom. Such a patient is old, has comorbidities, can be frail, and may be taking 10 pills or more per day, so questions of optimal prognostic therapy must be balanced against quality-of-life factors. There is abundant evidence that patients at highest risk do not receive the maximum amount of therapy. I suspect the kindness and wisdom factor is underestimated in clinical decision making. What we need now is some good qualitative data — market research — to help explain this phenomenon before we intensify the evidence-based mantra.

V Michael Jelinek

In reply: Jelinek rightly draws attention to the need, when caring for patients with acute coronary syndromes, to distinguish disease-related risk from age-related risk arising from frailty, comorbidity, physical disability, cognitive impairment, depression, social isolation, age–treatment interactions, and quality of life. All these factors affect treatment goals in older patients and may, as we conceded, justify withholding certain treatments in individual cases. However, even after accounting for “wise compassion”, under-treatment is still likely because: our treatment eligibility criteria excluded patients with advanced comorbidity or who declined treatment; population-based studies of risk–benefit trade-offs argue for more intense treatment use in patients ≥ 75 years,1,2 in whom absolute risk reductions exceed those in younger patients by as much as 10%;3 and all four key treatments at discharge (aspirin, β-blocker, angiotensin-converting enzyme inhibitors or angiotensin II receptor blockers, and statins) can be administered as once-daily, single tablet formulations, which are usually well tolerated. Given that a third of patients presenting with acute coronary syndromes are aged 75 years or older, for whom 30-day risk of death or myocardial infarction exceeds 20% and who account for 60% of all deaths related to myocardial infarction,4 we recommend, similar to expert bodies,4,5 judicious (not mantra-driven) use of evidence-based treatments in all eligible older patients.

Ian A Scott

Tako-tsubo cardiomyopathy (TTC) is an important differential diagnosis of acute coronary occlusive myocardial infarction that should be understood by all clinicians. Although TTC is frequently clinically indistinguishable from acute left anterior descending coronary artery occlusion, it is readily differentiated with coronary angiography. The increasing frequency of acute angiography and revascularisation for patients with acute myocardial infarction has resulted in TTC being far more frequently diagnosed. Most common in postmenopausal women, TTC is frequently precipitated by physical or emotional stress, and after an acute phase during which the patient may be significantly haemodynamically compromised, there is rapid recovery and an excellent prognosis. After diagnosis the patient can be reassured and advised of the low rates of recurrence. Currently, no specific preventive therapy has been proven to be effective.

Irfan Abdulla BSc · Michael R Ward MB BS, FRACP, PhD

To the Editor: The Guidelines for the management of acute coronary syndromes 20061 state: “Enoxaparin may be used in conjunction with fibrin-specific fibrinolytic agents in patients under the age of 75 years, provided they do not have significant renal dysfunction. An intravenous bolus dose of 30 mg followed by a 1 mg/kg subcutaneous injection every 12 hours in combination with tenecteplase is the most comprehensively studied therapy.”1 In Australia, enoxaparin is not licensed for intravenous use (Tony Hall, Team Leader, High Risk Medications and Systems, and Christine Maclean, Associate Director, Safe Medication Practice Unit, Queensland Health, personal communication) and there is no recommendation for the intravenous use of enoxaparin in the drug product information.2 Are the authors recommending “off-label” use of intravenous enoxaparin, or do they wish to modify the guidelines to reflect what the management should be if clinicians are unable to use intravenous enoxaparin?

Mark Little · Chris Johnstone

In reply: The guidelines were published to provide clinicians with the most contemporary information on the management of acute coronary syndromes based on the international literature, and may include treatments which are not currently available, officially licensed or available through the Pharmaceutical Benefits Scheme in Australia. In the context of adjuvant therapy for patients with ST-segment-elevation myocardial infarction (STEMI), the guidelines recommend that antithrombin therapy should be used with fibrin-specific fibrinolytic agents.1 Based on the best evidence available at the time, the guidelines mention two antithrombins, unfractionated heparin and enoxaparin, to be considered for use in this setting. The recommendation for enoxaparin is based on comprehensive evidence of clinical benefit with the regimen of an initial intravenous (IV) bolus dose followed by subcutaneous injections every 12 hours. It is up to individual practitioners to determine whether the IV dose should be provided “off-label” or omitted, based on the evidence and the circumstances of the individual patient and setting. The issue of superiority of enoxaparin over unfractionated heparin as adjuvant therapy for patients with STEMI is currently being evaluated in light of recent evidence,2 and will be included in a future update of the guidelines.

Constantine N Aroney · Philip Aylward

In Australia, many deaths and significant cardiac disability result from delayed response to symptoms of heart attack. Although delays due to transport and initiation of reperfusion therapy in hospital may contribute to late treatment, the major component of delay is the time patients take in deciding to seek help. A critical examination of campaigns to shorten patient delay concludes that they were based on a factual, short-term, non-targeted approach that included education and mass media strategies. They achieved equivocal results. One randomised controlled trial has been conducted. Although this showed an improved understanding of heart attack symptoms, it did not shorten pre-hospital delays. The implications of these findings are that future campaigns to shorten patient delay are likely to be more effective if they address the psychosocial and behavioural blocks to action, are ongoing rather than short term, and focus on people at highest risk, including those with known or high risk of coronary heart disease, those in rural locations, and Indigenous Australians. The National Heart Foundation of Australia proposes a comprehensive strategy to incorporate this approach into its future campaigns to reduce patient delay for suspected heart attack.

on behalf of the National Heart Foundation of Australia Chest Pain Every Minute Counts Working Group

Postural syncope is a transient loss of consciousness secondary to a reduction in cerebral blood flow and is typically precipitated by standing. It is the commonest cause of recurrent transient loss of consciousness. Recurrent unexplained postural syncope is most often due to one of the five disorders of circulatory control: vasovagal syncope, postural tachycardia syndrome, chronic autonomic failure, initial orthostatic hypotension, or persistently low supine systolic blood pressure. Failure to identify the underlying cause of postural syncope can result in ongoing morbidity, impaired quality of life and high health care costs. With a detailed history, examination, blood pressure assessment and electrocardiography, most disorders of circulatory control can be diagnosed. In difficult cases, analysis of sympathetic nervous system and circulatory responses during head-up tilting can aid diagnosis. Treatment is challenging and compounded by a lack of evidence. Most patients can be managed in an outpatient setting, and hospital admission or emergency department assessment is rarely warranted.

Gautam Vaddadi MB BS, BMedSci, FRACP · Elisabeth Lambert BSc, PhD · Susan J Corcoran MB BS, FRACP · Murray D Esler MB BS, FRACP, PhD

To the Editor: Clark et al have claimed to map the distribution of services for people with chronic heart failure (CHF) against the distribution of these people.1 An examination will show that they have mapped the distribution of people likely to have CHF, using age and Aboriginality as surrogate markers. The stated mapping of the services shows the services probably available to these people. A map is drawn to show us what the cartographer wants us to see.2 The authors note that high prevalence in remote regions has been shown on the maps, but they have not considered different mapping methods to provide a better representation of their results.3 This has led to an anomaly so that, when calculating numbers of people with CHF, the maps show remote areas with giant households containing between 24 and 300 people. CHF programs were located by a snowball sampling technique, which by its nature will miss isolated examples. Isolation is a feature of rural and remote practice, so this method is biased to finding metropolitan examples. In my own rural practice in Griffith, I found a local program that had been operating in 2004 and a distance program run by a health fund, neither of which had been identified by Clark et al. On the medical front, the authors asserted that access to a CHF management program is a mark of equity in health services. This is based on a metro-centric model looking at admission with CHF to a major teaching hospital, and showing that rates of readmission and death were reduced where a nurse and a pharmacist made a single visit to someone with CHF in their home after hospital discharge. The relevance of this activity to a rural person with a single community pharmacist who may make a home visit, a single point of contact with medical services in their general practitioner, and the possible availability of a community nurse to visit them regularly is unproven. Perhaps the city folk were copying the principles of the services we already had?

Elizabeth A Dodd

In reply: We thank Dodd for her commentary on our article.1 We concur with many of the highlighted issues relating to our suboptimal response to the burden and management of chronic heart failure (CHF) in rural and remote Australia. These include the lack of rigorous epidemiological data and lack of specialist services “beyond city limits”. Unfortunately, we have limited space to respond fully. However, we re-emphasise that, although our previous estimates2 complement that of the Canberra Study,3 neither can replace an Australia-wide study of CHF that samples metropolitan, regional, rural and Indigenous communities. We also stand by (within the context of the stated limitations) the accuracy of our mapping of the CHF programs and the location of general practice services in Australia for the study period. Our geo-mapping approach and data have been well validated by the National Centre for Social Applications of Geographic Information Systems (GISCA).4 For example, Jenks’ (natural breaks) classification is used for all sociodemographic thematic mapping at GISCA. Overall, we identified only four CHF programs which were located in regional areas. Other rural programs were excluded as they did not meet our prespecified definition of a CHF program. In summary, we acknowledge the need for better data to describe the burden of CHF throughout Australia. We also explicitly acknowledge the need for a less “metro-centric” approach to CHF service: perhaps by using remote monitoring techniques.5

Robyn A Clark · Andrea Driscoll · Justin Nottage · Skye McLennan · David M Coombe · Errol J Bamford · David Wilkinson · Simon Stewart

To the Editor: Walker and colleagues recently reported a series of patients with interstitial pneumonitis following use of statin cholesterol-lowering drugs.1 They state that other investigators have previously reported biopsy findings resembling amiodarone-induced pulmonary toxicity in pneumonitis associated with statin therapy. We believe this observation is pivotal to understanding the authors’ findings. Amiodarone produces mitochondrial toxicity, which is recognised to be a potential initiating event in amiodarone-induced pulmonary toxicity.2 Statins also produce mitochondrial toxicity in vulnerable individuals. Adverse effects of statins on muscle have been linked to mitochondrial abnormalities,3 and other clinical manifestations of statin mitochondrial toxicity have been reported. Mitochondrial respiratory chain disease is famously protean in its manifestations, but most classically produces a mitochondrial encephalomyopathy — with muscle, brain, or both affected. Consistent with this, muscle and cognitive symptoms are the most widely reported adverse effects in our reporting database of statin adverse effects (comprising 2478 patients to date), and these symptoms frequently occur together, consistent with a common mechanism. Statin–amiodarone combinations have produced heightened toxicity relative to each agent alone. Interference with cytochrome P450 metabolism has been the presumed mechanism,4 but additive or synergistic mitochondrial toxicity may also be a factor. The occurrence of amiodarone-like interstitial pulmonary disease in statin users adds to concerns that a range of clinical presentations of mitochondrial toxicity may ultimately be reported with statins in susceptible individuals, with mitochondrial heteroplasmy and threshold effects determining the specific manifestations.5

Beatrice A Golomb · Marcella A Evans

CABG offers a cost-effective and better long-term clinical outcome for many patients Coronary artery disease is still the single largest cause of premature death in Australia, according to the Australian Institute of Health and Welfare.1 Also documented is the dramatic decline in age-related mortality from heart disease, which is largely attributed to reductions in smoking and better intervention for hyperlipidaemia and elevated blood pressure.2 As many as 85% of elective percutaneous coronary intervention (PCI) procedures are done in patients with stable coronary artery disease.3 However, the only data showing prognostic benefit of intervention in reducing death and infarction in such patients come from subgroup analyses in old surgical trials,4-6 which showed benefits for patients with left main, triple vessel or proximal left anterior descending stenoses, especially if there was additional left ventricular damage. These benefits lasted up to 11 years, but the surgery was compared with medical therapy that did not include aspirin, β-blockers or lipid-lowering therapy for most patients. The surgical group did not receive arterial conduits. Subsequently, 11 randomised trials comparing PCI with coronary artery bypass graft (CABG) surgery for patients with multivessel coronary artery disease showed that the frequency of death and myocardial infarction was similar in both arms.7 These results cannot be used to claim an outcome benefit for PCI, as the trials entered only about 5% of screened patients, and the patients were not equivalent in the severity of their coronary artery disease to those in the original CABG trials. Further, analysis of the comparative trials shows that the highest-risk group (those with diabetes) showed benefit with CABG over PCI.8 Outcomes after CABG now show that, despite this surgery being performed in increasingly sick and complex patients, the overall mortality is less than 2%.9 Average length of hospital stay is now 3–5 days and return to work is usual in less than 2 months. Improved techniques have reduced the problem of cognitive impairment, and comparative studies have shown no difference with PCI in this respect.10 Long-term outcomes of CABG have improved due to the increased use of arterial conduits. Repeat CABGs now make up only 3%–4% of total CABG surgery, although this low figure may reflect a preference for PCI in repeat procedures. PCI has flourished since its introduction 30 years ago, with its offer to patients of a sound and timely intervention for coronary artery disease — but it has not been without problems. Recoil restenosis with balloon angioplasty was largely solved by the introduction of bare-metal stents. Acute stent thrombosis is less of a problem with better anticlotting agents, and drug-eluting stents have significantly reduced the problem of late restenosis. Despite these improvements, no reported studies have shown convincing evidence that PCI reduces the finite end points of death or myocardial infarction for patients with stable coronary artery disease. Controversy has recently arisen over the finding that patients with drug-eluting stents have an ongoing excess risk of late stent thrombosis of around 0.5% a year, presumably due to failure of endothelialisation of the stent. These events are usually associated with acute myocardial infarction, which carries a 50% mortality rate. It is now recommended that patients with drug-eluting stents stay on combined treatment with clopidogrel and aspirin for at least 12 months after implantation, and possibly permanently.11 This adds to patients’ financial costs and places them at extra risk of bleeding. Two recent reports provoke additional comment. First, Griffin et al used a complicated analysis of previous data to assess the cost-effectiveness of PCI and CABG in patients with multivessel disease considered suitable for revascularisation. CABG reached the accepted level of cost-effectiveness (US$60 000 per quality-adjusted year of life gained) but PCI did not, mainly due to the ongoing need for repeat procedures in PCI patients.12 Second, Boden et al reported a randomised trial comparing PCI with medical therapy in patients with stable coronary artery disease, which found no difference in the rate of death or non-fatal myocardial infarction at a median follow-up of 4.6 years. The PCI group initially had a reduced rate of angina, but this difference had disappeared at 5 years, largely because the medical therapy group had improved.3 The best interpretation of currently available data is that, for patients with severe coronary artery disease, the more invasive procedure with a longer recovery time (CABG) has a better long-term clinical outcome and is more cost-effective than the less invasive fast-recovery procedure (PCI). Three ongoing randomised clinical trials (CARDia, SYNTAX and FREEDOM) should further clarify the roles of PCI and CABG in treating severe coronary artery disease. The question then arises of whether, in current practice, PCI is being used in patients with severe coronary artery disease who would be more appropriately treated with CABG. Surgeons and cardiologists have argued that patients are not being adequately advised of the surgical option.13 Indeed, use of CABG is in such decline that training programs for young surgeons are at risk.14 In practice, the patient decides between CABG and PCI following discussion with a cardiologist, often while still in the angiography suite. This arrangement bypasses one of the recommendations on self-referral issues: to undertake consultation with other providers.15 It has been suggested that the technical suitability of a lesion for angioplasty determines the advice given to patients, rather than the relative benefits of CABG, PCI or even medical treatment alone.16 Smoking cessation and treatment to lower lipids and blood pressure are remarkably effective in improving the outlook for patients with stable coronary artery disease. Both CABG and PCI will provide benefits if revascularisation is performed for relief of symptoms, and patients may be influenced in their choice by both the less invasive nature of PCI and by the fewer recurrent procedures offered by CABG. However, for patients with prognostically important stable coronary artery disease (ie, severe left main or triple vessel disease), current evidence indicates that CABG offers a better long-term outcome.

Keith V Woollard MRCP, FRACP · Mark A J Newman DS, FRACS

To the Editor: Awareness about atypical and malignant modes of presentation of a clinical condition can avoid catastrophic outcomes, assist in correct diagnosis in the appropriate clinical setting and, as typified by the following case, offer complete cure. A 39-year-old woman presented with a 5-year history of intermittent, recurrent brief syncopal episodes. During an episode at presentation, telemetry showed torsade de pointes with ventricular fibrillation (Box), and external defibrillation was required to restore sinus rhythm. Amiodarone infusion was initiated at a local hospital before the patient was referred to our institution for further investigation and management. On presentation, her heart rate was 50 beats/min and her blood pressure was 170/95 mmHg. No other abnormalities were detected on examination. A resting electrocardiogram (ECG) showed prominent U waves, with a long QT interval (QTc of 540 ms). As the patient had mild hypokalaemia (serum potassium level, 3.1 mmol/L), mild hypocalcaemia (serum calcium level, 2.10 mmol/L) and a prolonged QT interval, the amiodarone infusion was discontinued, and supplementation with potassium and calcium was initiated. In view of the hypertension and hypokalaemia, primary aldosteronism was suspected. Serum cortisol, 24-hour urinary cortisol and 24-hour urinary catecholamine levels were normal. The plasma aldosterone/renin ratio was markedly elevated (1920/1.2 = 1595; normal, < 99). Failure of aldosterone suppression after acute saline loading was also noted. Computed tomography of the abdomen showed a right adrenal ovoid mass (1.9 × 1.2 cm). Adrenal vein sampling confirmed right lateralisation (right to left ratio, 40 : 1; aldosterone level in the right vein was 224 000 pmol/L while that in the left vein was 5570 pmol/L). Despite initial potassium supplementation, the hypokalaemia persisted and only improved after initiating diuretic therapy with amiloride. Two weeks later, laparoscopic right adrenalectomy was performed, and adrenocortical adenoma was confirmed histologically. After surgery, plasma aldosterone and renin levels normalised to 106 pmol/L and 8.9 mU/L, respectively. Nine months later, the patient was normotensive (without treatment) and had a normal ECG with no further recurrence of arrhythmias. This was a case of primary aldosteronism presenting as aborted sudden cardiac death and malignant syncope secondary to hypokalaemia-induced torsade de pointes. Most patients with primary aldosteronism are either asymptomatic or have symptoms related to hypertension or hypokalaemia (eg, polyuria, cramps, paraesthesia or muscle weakness); the diagnosis is often missed because of the non-specific clinical features. Primary aldosteronism presenting with cardiovascular collapse caused by hypokalaemic torsade de pointes and recurrent ventricular fibrillation is extremely rare, as is presentation as sudden cardiac death secondary to ventricular fibrillation.1 A prolonged QT interval has been reported in cases of primary aldosteronism,2 with values normalising after adrenalectomy.3 Torsade de pointes noted on telemetry in a 39-year-old woman

Aditya Kapoor · Timothy A Wells · Daniel Wong · John P O’Shea

Objective: To assess the management of patients with type 2 diabetes mellitus in the primary care setting, with respect to risk factors associated with coronary heart disease.Design: Retrospective cross-sectional audit.Setting: Specialised diabetes assessment clinic in a tertiary referral teaching hospital.Participants: 328 patients with type 2 diabetes mellitus (mean age, 58.3 years [95% CI, 57.5–59.1]) and no existing coronary heart disease (CHD) referred to the clinic by general practitioners during 2004–2005.Main outcome measures: Comparison of glycated haemoglobin (HbA1c), systolic blood pressure and total cholesterol levels and smoking frequency with current RACGP (Royal Australian College of General Practitioners) targets (< 7.0%; < 130/80 mmHg; < 4 mmol/L; and smoking cessation, respectively). Estimation of patients’ 10-year absolute risk of CHD events using the United Kingdom Prospective Diabetes Study risk engine, and its relation to primary prevention of CHD.Results: 42%, 61% and 43% of patients were receiving medication to treat hyperglycaemia, hypertension and hypercholesterolaemia, respectively; 46%, 29% and 15% of patients, respectively, had achieved the recommended RACGP target values for HbA1c, blood pressure, and total cholesterol; and 22% of patients were current smokers. The mean 10-year absolute risk of CHD was 16.8% (95% CI, 15.7%–17.9%), and 48% of patients were classified as “high risk” (absolute risk, > 15%). Based on the 10-year absolute risk, there was no difference between high- and low-risk groups with respect to prescription of aspirin, statins or angiotensin-converting enzyme inhibitors. If all the recommended RACGP goals were achieved, the mean 10-year absolute risk would decrease to 12.6% (95% CI, 11.8%–13.4%).Conclusions: Recommended treatment targets are not being uniformly achieved. Medication for primary CHD prevention is not being preferentially directed at those patients at highest risk, based on the estimated 10-year absolute risk of CHD events. Our findings suggest new initiatives are required in the way target goals and primary CHD prevention measures are set for patients with type 2 diabetes mellitus.

Tuck Y Yong MB BS · George Phillipov BSc(Hons), MSc, PhD · Patrick J Phillips MB BS, MA, FRACP

“First responders” are people trained in advanced first aid who can respond at the same time as, and often more quickly than, ambulance services to suspected medical emergencies. Hatzolah is a volunteer First Responder group, based on halakhic (Jewish legal) principles, in a localised area of metropolitan Melbourne with the highest density of Holocaust survivors outside Israel. Low numbers of “call-outs” to Victoria’s Metropolitan Ambulance Service (MAS) from this community suggested that many were reluctant to make contact with a “uniformed” external agency. Hatzolah is an autonomous organisation operating under adapted MAS clinical practice guidelines and clinical governance processes. Hatzolah responders undergo an 18-month MAS training course comprising first aid, cardiopulmonary resuscitation, the use of semiautomated defibrillators, and oxygen therapy. We describe the first 11 years (1995–2005) of the Hatzolah service. The number of patients attended to annually has risen steadily, peaking at 867 in 2005. The most frequent reasons for call-outs were falls (19.4%), chest pain (9.7%), or respiratory distress (7.6%). Hatzolah’s median response times were 2 or 3 min for all cases. They attended 35 patients with cardiac arrest (median response time, 2 min), and arrived before the MAS to 29 call-outs (83%). Nineteen patients (54%) with cardiac arrest were resuscitated and transported from the scene alive. Among those transported, significantly more had a shockable cardiac rhythm (50% v 13%, P = 0.03). Five (14%) survived to hospital discharge. Hatzolah has evolved into an organisation providing a complementary service to the MAS. It serves as a model for the establishment of other metropolitan community First Responder groups.

Tony Chan MB BS · George Braitberg MB BS, FACEM · Danny Elbaum BBus(Accounting) · David McD Taylor MD, MPH, FACEM