Cardiovascular diseases

The burden of atherosclerosis has triggered intense interest in the study of “vulnerable” plaques at high risk of rupture. Optical coherence tomography (OCT) has recently contributed to the in-vivo visualisation of plaque, providing unique insights into the atherosclerotic process, previously only attainable through postmortem examination. This technique uses near infrared light and an optical imaging wire attached to a patient interface unit with a pullback speed of up to 3.0 mm/s. In this patient, a 62-year-old man with treatment-resistant dyslipidaemia and stable angina, coronary angiography revealed possible non-flow-limiting plaque in the proximal left anterior descending coronary artery (arrow; Figure, A). OCT images confirmed extensive non-flow-limiting plaque (Figure, B–D), consisting of lipid (L)-rich areas with characteristic low reflectivity and homogenous appearance (Figure, B and C), and a fibrous (F) plaque with a high reflective and homogenous appearance (Figure, B). The images revealed almost circumferential thin cap fibroatheroma (TCFA; Figure, D), a marker of plaque vulnerability, as well as the plaque’s necrotic core (NC; Figure D). This case demonstrates the potential of OCT to visualise plaque and detect TCFA. This is particularly useful in stable patients in whom aggressive management of risk factors might prevent future adverse events.

Peter Barlis · Giuseppe Ferrante · Francesca Del Furia · Carlo Di Mario

Hypertension. A companion to Braunwald’s Heart Disease. Henry R Black and William J Elliott. Philadelphia: Elsevier Saunders, 2007 (xxii + 615 pp). ISBN 978 1 4160 3053 9. At the clinical interface little seems to be new in the area of hypertension. Non-pharmacological strategies have been unchanged for decades and there have been no new drug therapies since the advent of the angiotensin receptor blocker class in the mid to late 1990s. However, much has changed in the past few years with regard to our understanding of the genetics of hypertension, the underlying pathophysiology of the condition and recognition of hypertension as the main risk factor driving cardiovascular morbidity globally. Furthermore, a number of new classes of agents are being developed and indeed (the renin inhibitor class) have been approved in a number of countries outside Australia. For all of these reasons a comprehensive update on new developments in hypertension, anchored by sections on the fundamentals of knowledge regarding this condition, is clearly warranted. Is Black and Elliott’s Hypertension: a companion to Braunwald’s Heart Disease the definitive textbook in this regard? It is certainly a handsome volume with an easy-on-the-eye layout accompanied by appropriate figures, tables and drawings. Its chapters fall along classical lines comprising epidemiology, pathophysiology, diagnosis, risk stratification, treatment, concomitant diseases and management in special populations. Thus, it appears to provide a comprehensive overview of this condition. To test whether this is in fact the case I consulted a similar publication, Hypertension: a companion to Brenner and Rector’s The Kidney by Oparil and Weber (interestingly, put out by the same publishers, Elsevier Saunders). I would have to say that the Black and Elliott text suffers by comparison. One is struck by the much more comprehensive approach by Oparil and Weber in outlining the pathophysiology of the condition. As well, there is much greater attention to diet and nutrition, with six separate chapters on non-pharmacological management of the condition. There are also extremely thorough assessments of individual drug trials contributing to the evidence base of hypertension management. Drilling down into my own area of interest (the interface between hypertension and heart failure), again the Black and Elliott book came across as somewhat superficial with little discussion on left ventricular hypertrophy (an important disease entity in its own right) and essentially a restating of management strategies for heart failure per se, rather than as it specifically pertains to hypertension patients. Despite these reservations, there are particular areas of strength in Black and Elliott’s text. There are extremely important and sorely needed chapters on hypertension in special populations and across Third World geographic areas, which underscores the global epidemic we face (expected to reach almost 50% of the adult population by 2025). Furthermore, chapters on the drug development process in hypertension and a focus on guidelines and their differences across regions also give the text a comprehensive feel. Clearly, with sections and chapters of this type, this textbook will not be for everyone. For the busy general practitioner requiring guidance as to how best to manage the individual hypertension patient, this is not the book. For others requiring an in-depth review of the fundamentals of hypertension, pathophysiology, diagnosis and management, Black and Elliott is a worthy addition to one’s library (or that of one’s institution). Oparil and Weber may, however, be an even worthier addition!

Henry Krum

When I first learned about the Dr Ross Ingram Memorial Essay Competition through the Healthy Vibe section of Deadly Vibe magazine, I realised it was an opportunity to publicly discuss an issue of significance to all Australians, Indigenous and non-Indigenous alike. Specifically, the issue is about cardiovascular health, rehabilitation and, more to the point, the levels of participation and non-compliance with treatment of people affected by cardiovascular disease. Like Ross Ingram, the Koori GP after whom the essay competition is named, I have been directly affected by heart disease. As I read about Dr Ingram and how heart disease cut short a dedicated young Indigenous leader’s life, I decided to do something to sound a warning and be a positive influence on others. I tell my story to raise awareness of cardiovascular disease, which is claiming the lives of our brothers, sisters, uncles, aunties and grandparents. I would also like to discuss what actions we can take to help our people, the Indigenous community and ourselves. First I will give some background information about myself. I am 41 years young, of Aboriginal and Australian South Sea Islander descent. At 39 years of age, I experienced an acute myocardial infarction (commonly referred to as a heart attack). I mistook the severe chest pain for heartburn or indigestion, and did not present to a GP until the following morning. On examination it was clear that I was experiencing acute coronary syndrome. Within less than an hour, I was an inpatient in a hospital coronary care unit receiving all the necessary acute care available. Eventually I was diagnosed with cardiovascular disease (ischaemic heart disease). I was told I had a 99% blockage of the left anterior descending coronary artery and that 10% of my heart was damaged irreparably. Surgery was ruled out, as the affected area was “dead” because I had not recognised the symptoms of a heart attack at the time. Had I sought medical assistance earlier, I might have received thrombolytic medication designed to dissolve the blockage. I did not know any of this information — knowledge is power. I was in total shock and denial when told by the attending GP what was happening inside my body. I thought, “This doesn’t happen to youngish people like me — only to older people in their 60s and 70s!” However, on reflection, all the signs were there: I smoked 30–40 cigarettes per day; I used and abused alcohol habitually and heavily; My diet included anything, any time I wanted, regardless of nutritional value; I had not exercised regularly for over 10 years; and Both my parents had experienced cardiovascular health conditions. On reflection, my behaviour seemed as if I was determined to self-destruct. After adjusting to the new reality that I had experienced a heart attack and survived, I realised it was time to make some deadly serious lifestyle improvements as soon as possible. The changes I made included decisions to attend and complete cardiac rehabilitation, to seriously consider therapeutic lifestyle changes and to comply with all prescribed medications and subsequent follow-up appointments. After I was discharged from hospital, I quit smoking immediately (and have not looked back); completed a hospital-based cardiac rehabilitation program; began to exercise regularly (resulting in gradual loss of 20 kg of excess weight); stopped all use of alcohol; and adopted a low-sugar, low-salt and low-fat diet, including avoidance of red meat and experimentation with low-fat, low-calorie, vegetarian alternatives. From my perspective, I have been given a second chance. I tell people (anyone who will listen) that surviving a cardiac event can present opportunities to make quality-of-life improvements. A heart attack need not be a death sentence. My health and fitness levels have improved dramatically. I have 10–15 kg more to lose, but I know it’s possible now. I have also experienced a spiritual awakening that, in turn, has led me to renew my faith and commit to a purpose-driven life. Despite all this, it took a surprising amount of time to regain my confidence and a healthy level of self-assurance. When this finally happened it was, I think, an outcome of participating in rehabilitation and self-management measures, like taking greater responsibility for my future health. A major factor in my recovery was support from family and friends. It was the existence of these interdependent relationships that was very important in helping me to find my equilibrium again. Cardiac rehabilitation and Indigenous health management in the broader context of cardiovascular health have become important matters for me since my recovery. Even though I have plenty of fight in me, I am always conscious of the need to not overcommit myself. All the while, there is a sense of impending urgency to give back to others in the Indigenous community who also need assistance. I think of others who don’t know or understand what is happening to their bodies. They may not know how to cope with surviving a cardiac event or heart surgery, and may not be aware of what they can do to reduce the risk of future cardiovascular damage. The journey from cardiac patient to cardiovascular health advocateThere were many uncomfortable changes after my heart attack. I was left without a job, as my previous employer decided I was an unacceptable risk as a fly-in-fly-out plant operator on Cape York Peninsula. My personal and social life disintegrated due to psychological aspects such as unanswered questions, post-traumatic stress, self-imposed social isolation, depression and anxiety. Eventually it was family and true friends that made the difference by being there when it really mattered. Prior to operating machinery for mining companies, I had been an Indigenous community development worker, so I decided it was time to do a refresher course at TAFE* to update skills I hadn’t used for over 10 years. With updated community services knowledge and abilities, I approached the Cardiac Rehabilitation Coordinator at Cairns Base Hospital and the Wuchopperen Health Service, offering to serve as a volunteer in some capacity. Their eager response was surprising and welcome. They were keen to try something different to improve Aboriginal and Torres Strait Islander (ATSI) cardiovascular health. We discussed employment in a mentoring/coordinating role in an Aboriginal Medical Service-based outpatient cardiac rehabilitation program. * A Technical and Further Education college. We had several discussions by phone and email about matters that concerned me. I noticed that many of the Indigenous people admitted to the coronary care ward did not go on to attend rehabilitation sessions. I noted the age differences between Indigenous and non-Indigenous people affected with cardiovascular disease, and thought about the reasons why I had not enjoyed the hospital-based cardiac rehabilitation sessions. I was very curious about what was happening to all those Murri and Islander people once they were released from hospital. Indigenous cardiovascular health began to affect me again personally only a few months later, with my older brother (aged 45) experiencing heart problems resulting in several unstable angina events, arrhythmias leading to unconsciousness, and several minor heart attacks. He required triple coronary artery bypass graft surgery and a permanent pacemaker, and has to take medication for the rest of his life. My brother refused to attend rehabilitation and is non-compliant with his medication. He stubbornly believes the heart surgery and the insertion of a permanent pacemaker were a cure-all for his heart problems. He is living on borrowed time as it is, yet he casually spouts that his days are numbered, like everyone else’s, surgery or not. This difficult reality has driven me to become more involved in Indigenous health. Today I am employed with Wuchopperen Health Service, based in Cairns, as a health worker in the chronic disease management program area. I work with the Continuous Improvement Program team as program coordinator for the Healthy Hearts Cardiac Rehabilitation Program. This is a community-based outpatient cardiac rehabilitation (OCR) program operating from an Aboriginal-controlled community health organisation (ACCHO), working in partnership with the Cairns Base Hospital’s Cardiac Rehabilitation Unit to provide a culturally appropriate and relevant program focused on ATSI people. The availability of this support through an Aboriginal health service, as opposed to a hospital, is a major positive point for ATSI people attending the Healthy Hearts program. To date, there have been over 30 people attending regular exercise sessions and education days held at Wuchopperen Health Service since the program began in August 2006. I have been able to assist the cardiac rehabilitation coordinator with a Cardiac Rehabilitation for Indigenous Communities project that is jointly funded by the Australian Government Department of Health and Ageing and Queensland Health. This project is about training staff like me at Wuchopperen and also at the pilot sites of Yarrabah, Coen and Thursday Island. The overall aim of the cardiac rehabilitation project is to enable the delivery of flexible OCR models to these Indigenous communities. I assist the project when and how I can as a cultural adviser, contributing to or participating in cardiac rehabilitation training. Our program provides an Indigenous OCR program role model for similar emerging programs. We have been contacted by over a dozen services seeking advice and information about setting up ATSI OCRs. I have since become the Indigenous representative for the Queensland Cardiac Rehabilitation Association (QCRA), allowing me to raise matters from an Indigenous perspective in a state forum, attend a Queensland Cardiac Rehabilitation Collaborative forum as a guest speaker and contribute Indigenous-related articles to the national newsletter of the Australian Cardiovascular Health and Rehabilitation Association. I enjoy my role and believe that my story also demonstrates the level of interest and support in northern Queensland for workable solutions to very difficult health issues. Recently, I have been seeking to promote the Wuchopperen Health Service Healthy Hearts program through interviews with media groups such as the Brisbane Indigenous Media Association, the local Bumma Bippera Media broadcast service and the national Indigenous newspaper Koori Mail. I think it’s really important to advertise positive things happening in the Indigenous community. In closingIn the past few months, two young men I knew (seemingly fit and healthy) have died from coronary arrest in their mid to late 30s. It is a very sad thing when young Indigenous men leave their wives, children and extended families at such an early age. I am certain that, throughout Australia, many Indigenous families can tell similar stories — but this does not have to continue. It serves as a reminder of why I got involved in this quite serious business, and why people like my two young friends and my non-compliant brother need help. Health crisisEvery article written on Indigenous cardiovascular health problems inevitably calls for an urgent long-term solution. As an inpatient and now as an allied health worker, I can understand both sides of the coin. I deal with people associated with a health system in which the following issues are a daily reality: Tyranny of distance issues; Chronic comorbidities that result in surgery being contraindicated for ATSI people; Non-compliance with medication and follow-up appointments; Mistrust of hospitals by Indigenous people; A high proportion of Indigenous people refusing to undergo cardiac investigations; An unacceptably high rate of people refusing cardiac surgery; Long waiting times for life-saving surgery; Low uptake and follow-through of lifestyle changes and behaviour modification; Unwillingness to attend traditional hospital-based and ACCHO-based cardiac rehabilitation; and Primary, secondary and tertiary prevention measures missing their mark. These are only some of the issues I have become aware of in my work as an Indigenous health worker. I am sure there are far more qualified, knowledgeable people in the health field who can discuss the issues and solutions in more detail than I can. These people need to stand up and speak out too. Regardless, the issues raised represent serious unmet needs that require an urgent solution. Without a concerted effort, I predict the consequences will be dire for the Indigenous community throughout Australia. Governments, health departments, ACCHOs and the Indigenous community must demonstrate they are absolutely serious about improving the future health of Indigenous Australians. All groups mentioned have a role, particularly governments and Indigenous people. What’s needed is strong leadership from both sides and a coordinated effort, including, for example, examining funded regionalised agreements between ACCHOs and government health service providers and non-government organisations as a possible way forward. These kinds of partnerships and other creative solutions ought to be given due consideration before being dismissed. The issue of Indigenous health has always been controversial, certainly in my lifetime, and no doubt will continue to be so until the powers that be, namely federal and state health departments, decide to stop the blame-shifting and buck-passing and work together for the greater interest to create policy-driven outcomes, accordingly matched by funding and providing the right people and the necessary resources. Any review of past and current data relating to Indigenous cardiovascular health makes it clear that it’s time for all of our leaders to show some heart and exercise the political will needed to engage cardiac service/support providers and consumers in a long-term, committed, national response.

Barry N Fewquandie

The medical community lost one of its most passionate, innovative and hardworking members with the recent death of Ralph Reader. He changed the way Australians thought about cardiovascular disease, raising awareness of risk factors and promoting policies to counter the disease. He also championed cardiovascular research, being one of the key drivers of National Health and Medical Research Council (NHMRC) policies and decisions during the 1960s and 1970s. Ralph was born in Brisbane in 1918, but grew up in Sydney, where he attended Fort Street Boys’ High School and the University of Sydney. After graduating in medicine in 1940, he became a Resident Medical Officer at Royal Prince Alfred Hospital (RPAH) before joining the navy and serving as a surgeon until the end of World War II. In 1941, he married Hazel Scanlon, to whom he remained married until her death in 1994. After the War, Ralph conducted research into renal disease at the University of Sydney. In 1948, the grant of a Nuffield Medical Fellowship took him to Oxford, UK, where he completed a PhD. On his return to Australia, he set up a private practice, worked as an Honorary Medical Officer at RPAH and lectured at the University of Sydney. His research led to kidney transplants at RPAH, where he established the first nephrology unit. In 1961, Ralph was appointed inaugural Medical Director of the National Heart Foundation (NHF), and was its Director and Chief Executive until 1980. It was during this period that he played a key role in the establishment of the triple-0 emergency telephone line. Over two decades, Ralph became the face of the NHF, devoting his time and energy to public education and professional practice, as well as developing the Foundation’s research program. He was also very active in the NHMRC. Between 1966 and 1975, he was a member of several of its committees and subcommittees, including the Medical Research Advisory Committee, the Standing Postgraduate Scholarship Committee and the Medical Statistics (Standing) Committee. In 1968, Ralph was the first to report a plateau then a fall in the number of deaths related to heart attacks, heart failure and stroke. Australia was the first country to reverse the upward trend. (At its peak, cardiovascular disease was the cause of two in three Australian deaths.) He also helped to develop policies for reducing cholesterol levels and oversaw the establishment of coronary care units in hospitals across Australia. He discovered the effectiveness of prescribing antihypertensive drugs for patients with mild hypertension and conducted the groundbreaking Australian National Blood Pressure Study. Ralph was made a Companion of the Order of St Michael and St George in 1976 and was awarded an honorary doctorate by the University of Sydney in 2006. Ralph died in Canberra on 13 January 2008. He is survived by his children Brian, Carolyn and Jeremy.

Warwick P Anderson · John S Horvath · Phil Mayne

A 25-year-old woman presented with progressively worsening shortness of breath, which was attributed to cardiac tamponade caused by pericardial effusion. Urgent pericardiocentesis revealed haemorrhagic fluid, which continued to accumulate after the procedure. A repeat echocardiogram after pericardiocentesis showed dilatation of the right ventricle and severe pulmonary hypertension. Subsequent computed tomography revealed a massive pulmonary embolism in the right lung (Figure) and multiple small emboli in the left lung, while cytological examination of pericardial and pleural fluid showed adenocarcinomatous cells from a primary lung cancer. Pericardial effusion and pulmonary embolism usually present in isolation. Their coexistence in this patient — presumably related to the underlying neoplasm — may paradoxically have saved her life, as the raised right ventricular pressure created by the pulmonary emboli delayed the onset of cardiac tamponade.1 Her condition improved initially with chemotherapy and anticoagulation, but she died a year later due to progression of the lung cancer. PE = pulmonary embolism. PCE = pericardial effusion. PLE = pleural effusion.

Namal Wijesinghe · Cherian Sebastian · Hugh McAlister

The benefits are greater efficacy and faster onset of action; the price is increased risk of bleeding . . . The mainstay of antiplatelet therapy for patients with acute coronary syndromes (ACS), including those undergoing early percutaneous coronary intervention (PCI), is the combination of aspirin and clopidogrel.1-3 Aspirin inhibits platelet thromboxane A2 production and platelet activation, and reduces the relative risk of recurrent ischaemic events in patients at high risk of vascular events by about 22% (absolute risk reduction [ARR], about 2%) at the expense of an increase in the odds of major bleeding events by about 60% (absolute risk increase [ARI], about 0.5%).1 Clopidogrel inhibits ADP-induced platelet activation by blocking the platelet P2Y12 receptor. When added to aspirin therapy in patients with ACS, it reduces the risk of recurrent ischaemic events by a further 20% (ARR, about 2.1%) at the expense of an increase in major bleeding events by approximately 38% (ARI, about 1%).2,3 Clopidogrel has several potential limitations, however. First, the onset of action is delayed, with a “therapeutic” level of 50% inhibition of ADP-induced platelet aggregation, as measured by light transmission aggregometry (LTA), not being reached until 4–6 hours after a 300 mg loading dose, and 2 hours after a 600 mg dose. Second, there is a “ceiling” effect — even a 900 mg dose achieves only around 60% inhibition of ADP-induced platelet aggregation. Third, laboratory testing suggests that “therapeutic” platelet inhibition is not achieved in a substantial proportion of patients because of individual variability in platelet inhibition by clopidogrel.4 Finally, there is uncertainty about the clinical benefit with higher loading doses of clopidogrel of 600 mg or 900 mg compared with 300 mg.5,6 Prasugrel is a novel thienopyridine prodrug whose rate, magnitude and consistency of platelet ADP inhibition is greater than for clopidogrel. It achieves more than 50% inhibition of platelet aggregation (measured by LTA) within 1 hour of a 60 mg loading dose.7,8 The safety and effectiveness of prasugrel have been compared with standard-dose clopidogrel in the Trial to Assess Improvement in Therapeutic Outcomes by Optimizing Platelet Inhibition with Prasugrel — Thrombolysis in Myocardial Infarction (TRITON–TIMI 38).9 A total of 13 608 patients with moderate-to-high-risk ACS scheduled for PCI were randomly assigned to receive prasugrel (60 mg loading and 10 mg daily maintenance dose) or clopidogrel (300 mg loading and 75 mg daily maintenance dose) for 6 to 15 months. Aspirin 75–162 mg daily was recommended for all patients. After a median duration of 14.5 months, the primary efficacy outcome of cardiovascular death, non-fatal myocardial infarction, or non-fatal stroke occurred in 12.1% of patients taking clopidogrel and 9.9% of those taking prasugrel (hazard ratio [HR], 0.81; 95% CI, 0.73–0.90). Stent thrombosis was also reduced (2.4% clopidogrel v 1.1% prasugrel; HR, 0.48; 95% CI, 0.36–0.64). However, the key safety endpoint of major bleeding not related to coronary artery bypass graft (CABG) was increased (1.8% clopidogrel v 2.4% prasugrel; HR, 1.32; 95% CI, 1.03–1.68). All major bleeding (including CABG-related) was increased (1.7% v 2.5%; HR, 1.31; 95% CI, 1.16–1.50), as was fatal bleeding (0.1% v 0.4%; HR, 4.19; 95% CI, 1.6–11.1). Overall mortality did not differ significantly between treatment groups. A post-hoc subgroup analysis identified less clinical efficacy and greater bleeding among patients with a history of stroke or transient ischaemic attack, older people (age > 75 years), and those with bodyweight less than 60 kg. It is likely that these results are externally valid. However, by design, the study drug was only given after the coronary anatomy had been defined by angiography. This does not reflect usual clinical practice where clopidogrel is given at the time of presentation with ACS. Because there is a delay in the onset of action of clopidogrel, the design was biased in favour of prasugrel. Also, the prescribed standard 300 mg loading dose of clopidogrel was lower than that now adopted by many clinicians following reports of an improved inhibition of platelet aggregation with higher loading doses of clopidogrel such as 600–900 mg in patients with PCI.6 These caveats aside, the data suggest that treating 1000 patients with ACS at moderate-to-high risk of vascular events with prasugrel (compared with clopidogrel at the standard approved dose) for a median duration of 14.5 months would prevent about 22 major vascular events and cause eight major haemorrhages, including three fatal bleeds. The implications for clinicians, should prasugrel gain regulatory approval, are that it may allow cardiologists to delay their decision to administer a P2Y12 inhibitor until after coronary angiography (thus avoiding the bleeding risk of clopidogrel in patients who need urgent CABG), and to use prasugrel instead of clopidogrel in the acute phase of ACS, possibly using clopidogrel for long-term maintenance therapy. The implications of these results for researchers are that it is important to determine whether the risk of long-term bleeding with prasugrel may be reduced, without compromising efficacy, by using lower doses and by avoiding its use in those with previous stroke or low bodyweight, and older people. A lower dose of prasugrel is presently being compared with clopidogrel in the TRILOGY study, involving 10 000 patients with ACS who are treated medically. Research is also needed to evaluate the potential for individualised antiplatelet therapy based on the results of point-of-care testing of platelet function and genetic polymorphisms. Meanwhile, large randomised trials are presently comparing: the efficacy and safety of a high loading dose and maintenance dose of clopidogrel (versus a low loading dose and maintenance dose); the oral reversible non-thienopyridine ADP receptor antagonist, AZD6140, with clopidogrel; and the parenteral reversible non-thienopyridine ADP receptor antagonist, cangrelor, with clopidogrel, all in patients with ACS treated with an early invasive strategy.

Graeme J Hankey MD, FRACP, FRCP · John W Eikelboom MB BS, FRACP, FRCPA · Paul E Langton MB BS, FRACP

A 14-year-old boy was admitted with a 2-week history of increasing breathlessness and fatigue. He had a pulse rate of 130 beats/min and blood pressure of 100/66 mmHg with 16 mm paradox. Jugular venous pressure was raised 10 cm above the sternal angle, and heart sounds were faint. He had been diagnosed with refractory iron-deficiency anaemia in early childhood, for which he had been receiving blood transfusions. He denied any history of epistaxis, haemoptysis, malaena, haematuria or overt bleeding from any other site. On examination, the patient had multiple, blue-black, papular and nodular, compressible, non-pulsatile, vascular skin lesions, ranging in size from a few millimetres to 1–2 cm, distributed over the trunk and limbs, including the soles of the feet, perineal region (Figure A) and lips. A chest x-ray showed an enlarged cardiac silhouette suggestive of pericardial effusion (Figure B). This was confirmed by transthoracic echocardiography. Therapeutic pericardiocentesis showed haemopericardium. Blue rubber bleb naevus syndrome (Bean syndrome) is diagnosed in the presence of distinctive venous malformations on the skin, in the gastrointestinal tract and, less often, in other organs, leading to occult or overt gastrointestinal bleeding and chronic anaemia.1-3

Pankaj Malhotra · Madhav C Menon · Subramaniyan S Anand · Arshjyot Narula · Subhash Varma

Heart failure and palliative care: a team approach. Miriam Johnson, Richard Lehman, editors. Oxford: Radcliffe Publishing, 2006 (x + 150 pp). ISBN 978 1 85775 643 2. At first glance, this appeared to be another of the “palliative care for another subspecialty” works that have been appearing over the past few years. The amount of new and truly specialty-specific material in these can be limited, and one can only suppose that they are sometimes driven as much by publisher catalogue agendas as by real need. This is not the case with this short and well written book from the United Kingdom. The editors are a palliative care physician and a general practitioner who have developed an interest in this subpopulation of patients, for whom palliative and supportive care needs have hitherto tended to be largely ignored. They are modest about their aims, and write clearly with what appears to be comprehensive referencing to the small but growing literature on caring for patients who have end-stage heart failure. The syndrome of advanced heart failure is explained, with very readable accounts of epidemiology, pathophysiology and treatment. There is much reference to the work of one of the contributors, Scott Murray, and his coworkers in primary care at the University of Edinburgh, who have published on comparative needs of patients with heart failure and lung cancer. They highlight the fact that decision making and prognostication are, in general, harder in heart failure, which tends to run a more protracted and unpredictable course than many cancers. Murray has proposed a simple but radical alternative to attempts at precise prognosis as a guide to care planning, by asking: “Would I be surprised if my patient were to die within the next 12 months?” If the answer is “no”, then it is time to start thinking about the deployment of supportive and palliative care.1 The work is certainly UK-centric, however, for Australian readers this is still a good summary of the issues and the literature, together with some useful experience of setting up services in selected UK centres. The heart content would be of no interest to a cardiologist, just as most of the palliative care content would not be news to specialists in that discipline, but each discipline can learn about the other, and generalists will probably find some benefit in both.

Michael A Ashby

Should we be devoting energy and resources to reversing obstructive sleep apnoea in patients without symptoms? Over the past four decades, obstructive sleep apnoea (OSA) has emerged as a prevalent, clinically important disorder. Snoring, which is often a hallmark of OSA, is seemingly ubiquitous in middle-aged men. Over 80% of Australian middle-aged men snore for more than 10% of the night.1 Snoring is also common in women. Although it is undoubtedly an important social nuisance, it remains unclear whether snoring alone (in the absence of sleep apnoea) carries with it any serious health risk. Twenty-five per cent of middle-aged men and 10% of women have OSA, defined as > 5 obstructed breathing events per hour of sleep.2 The prevalence in women rises sharply after menopause. Other risk factors are obesity, older age and a family history of OSA. Population-based studies in China and India indicate that its prevalence is at least as high as that reported in Western countries. A complex interplay between regulation of breathing during sleep, facial anatomy and obesity predicts the development of OSA.2 In contrast to the uncertainty of the effects of simple snoring, OSA clearly has significant health consequences. Many patients with OSA experience excessive daytime sleepiness and impaired cognitive function, increasing the potential for traffic crashes, work accidents and reduced productivity at work.3 Over 50% of Australian truck drivers have mild OSA or worse.4 Moreover, Access Economics has estimated that the cost of sleep disorders to the Australian community is over $7 billion, and much of this cost relates to OSA.5 Increasing awareness of OSA has been followed by an appropriate increase in clinical investigations of sleepy patients with suspected OSA. This is further driven by the availability of cost-effective treatments, notably continuous positive airway pressure (CPAP) and mandibular advancement splints. Recent studies have suggested that OSA is associated with an increased risk of cardiovascular disease.6 Publicity about this research has led to an increasing tendency for people who are not sleepy or who have minimal symptoms to be referred for assessment and treatment of OSA. However, in contrast to the sleepy patient, for whom CPAP usage is reinforced by reduction in sleepiness, asymptomatic patients have more variable compliance.7 Should we be devoting substantial clinical energy and resources to reversing OSA in such patients to prevent cardiovascular disease and death? Certainly, data from cross-sectional and prospective population studies and sleep clinic studies indicate that OSA is associated with a higher prevalence of cardiovascular and cerebrovascular disease and insulin resistance.6 Untreated male patients with severe OSA have significantly greater risks of fatal and non-fatal cardiovascular events than healthy controls (odds ratios, 2.87 and 3.17, respectively).8 However, cross-sectional and observational studies have unmeasured confounders, such as visceral obesity.6 In addition, observational studies can be affected by treatment bias. Patients who refuse to use CPAP and seemingly have higher cardiovascular risk than those who comply with CPAP treatment8 may be the same people who refuse to stop smoking or take lipid-lowering or blood pressure-lowering medication. In contrast, there is good evidence from randomised controlled trials that CPAP lowers blood pressure (mean decrease in systolic and diastolic blood pressure of 2.46 and 1.83 mmHg, respectively), but most studies are relatively short (less than 8 weeks), and treatment effects are hard to demonstrate in patients who are not sleepy.9 The remaining short-term CPAP trials that have focused on other intermediate markers of cardiovascular disease (lipids, glucose control, high-sensitivity C-reactive protein) have been inconclusive. For example, a recent short-term randomised trial failed to show any improvement in insulin sensitivity in patients with type 2 diabetes and OSA.10 No data are available from long-term, well powered, randomised controlled trials assessing the effect of CPAP on hard cardiovascular endpoints, such as myocardial infarction and stroke, in patients with OSA. Medical research is well populated by “positive” results from cross-sectional, observational or short-term intervention studies, but their results have not been reproduced in rigorous, long-term, large-scale clinical trials. To remedy this lack of information, several long-term trials of CPAP treatment in OSA are being planned or have commenced, including one initiated by Australian investigators (Sleep Apnea CardioVascular Endpoints Study [http://www.savetrial.org]). These trials will determine whether treatment of OSA decreases the incidence of new cardiovascular events. In the interim, how should we manage patients with a diagnosis of repetitive OSA who present with complaints of snoring but have minimal or no daytime sleepiness? First, it is important to establish whether such patients are genuinely asymptomatic or simply underreport symptoms that are obvious to their families or work colleagues.11 Second, the disorders of these patients typically are characterised by higher rates of central adiposity, glucose intolerance and other vascular risk factors.6 Given that middle-aged men often neglect to monitor such risk factors, referral for snoring may provide an excellent opportunity for a general health assessment and to institute an intervention, such as advice to exercise and lose weight. Moreover, it would be reasonable to prescribe a trial of CPAP for a patient with asymptomatic OSA and hypertension refractory to maximal medical therapy and to monitor the blood pressure response over 24 hours. Finally, it would be reasonable also to inform asymptomatic patients with severe OSA and coexisting cardiovascular disease of the possible association between OSA and a risk of future vascular events. However, it would be inappropriate to coerce these patients into accepting a treatment that might falsely make them feel secure about future risk and might result in neglect of proven risk factors. Future research, ideally, will enable clinicians to get to the “heart of the matter” when discussing cardiovascular risk management and sleep apnoea with these patients.

Ronald R Grunstein MD, PhD, FRACP · Craig L Phillips BSc

To the Editor: Abdulla and Ward’s excellent article on tako-tsubo cardiomyopathy (TTC)1 raises two important issues. The first issue is the diagnostic dilemma faced by emergency physicians and cardiologists in differentiating TTC from ST-elevation myocardial infarction (STEMI) in centres that lack coronary angiogram capabilities. In patients presenting with chest pain and ST elevation on electrocardiography, the diagnosis of TTC might be suspected on recognition of risk factors and the common psychological, physical and emotional stressors that precipitate TTC.1 Supporting evidence can be obtained by demonstration of basal hyperkinesis and apical or midventricular hypokinesis on transthoracic echocardiography. This modality is now available in many centres without coronary angiography. However, if the diagnosis is incorrectly made as STEMI rather than TTC, the patient runs the risk of unnecessary thrombolysis. Alternatively, after risk–benefit analysis, the clinicians may transfer the patient to a facility with coronary angiography to confirm TTC. The second issue is the therapeutic dilemma facing intensivists treating TTC-related shock with adrenergic inotropes. Although cardiogenic shock in TTC is uncommon, it can still occur (4.2%).2 As increased endogenous catecholamines are thought to be central to the pathophysiology of TTC,3 treating shock with inotropes puts the clinician in a quandary. Agents such as adrenaline, dobutamine, dopamine, milrinone and noradrenaline increase cyclic AMP within the myocardial cell, and are commonly used to restore blood pressure and cardiac output. However, in TTC, inotropes may theoretically delay resolution of the apical ballooning. A recent echocardiographic study showed no improvement in apical and midventricular akinesis with the use of low-dose dobutamine.4 Levosimendan is a calcium sensitiser that has been used successfully to stabilise shock secondary to TTC (with and without use of an intra-aortic balloon pump).5 Levosimendan is non-adrenergic and allows earlier introduction of β-blockers than would be possible with adrenergic inotropes. I agree that prospective trials are needed to guide management in this intriguing condition.

Laven Padayachee

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