Cardiovascular diseases

To the Editor:I thank Kritharides and colleagues1 for their review Cardiovascular disease in patients with schizophrenia. I agree with them and support their work, which seeks to improve the physical health of patients living in the community with a chronic mental illness such as schizophrenia, through an innovative, coordinated and multidisciplinary model of care. Clozapine side effects, including risks of myocarditis and cardiomyopathy, hypercholesterolaemia and weight gain, reduce years of life and require medical attention. But the management is not always straightforward. One challenge is patient compliance with often demanding allied health therapies. How do we keep our patients motivated to continue with prescribed regular exercise most days of the week? How do we encourage compliance with a weight-reducing, low salt, low glycaemic index diet? Multidisciplinary primary care and specialist teams may consider a rehabilitation approach to complement the model of care. Two essential elements are goal setting and measurement of function.2 Some patients will be motivated by their personal goals (eg, getting back to weighing 80 kg or playing a game of table tennis) and other patients will appreciate their gain in terms of function (eg, walking up the stairs without a rest or shopping for groceries independently) more so than in terms of presented data (eg, cholesterol levels or absolute cardiovascular risk reduction). For motivating patients with schizophrenia and significant cardiovascular risk, a rehabilitation approach may be worth a try.

David Skalicky

To the Editor:With reference to Batterham and colleagues,1 we applaud the call to better align research funding to disease burden. We also address this shortfall in the leading killer: cardiovascular disease (CVD). The federal government deserves praise for establishing the Medical Research Future Fund (MRFF), doubling funding by 2023. This augurs well for the future, but right now, we face an interregnum while the MRFF builds and the National Health and Medical Research Council funding flatlines. Every year, CVD claims the lives of 45 093 Australians,1 accounting for more than one in three deaths. The direct cost of caring for people with CVD in 2008–09 was $7.7 billion per year (or 12% of the total health budget),2 making it the costliest disease group of all. With the current budget at over $120 billion per annum,3 and assuming that CVD continues to cost 10–12% of the health budget, it is likely that the current cost is well over $12 billion per annum.3 The most recent data show that CVD deaths increased for the first time in 4 decades in men aged 55–64 years,3 an increase associated with the rising rates of obesity and diabetes.3 This reflects the unanswered questions related to heart health, which are ripe for exploration. Meanwhile CVD research is funded substantially less than the equivalent disease burden of cancer, receiving about 13.5% — cumulative frequency of about 22% — of the National Health and Medical Research Council total funding between 2008 and 2014.4 A clear consequence is that CVD research suffers from brain drain, as emerging researchers seek sectors where funding is more available. This workforce crisis was highlighted by a recent Australian Cardiovascular Alliance survey, where 65% of CVD researchers say they would leave the sector if funding is not secured. Australian CVD research is of international standing, providing the highest returns of any disease group on research investment, an extraordinary $8 in health benefits for every $1 spent.4,5 The need for a committed workforce skilled in heart research is clear. Funds from the MRFF must be invested in research that reflects the health priorities and disease burden facing the nation, particularly where the market is failing. Such research is an investment not a cost. In 2017, the Heart Foundation will boost research investment by an additional $9.3 million. While substantial for the only major health charity supporting heart research, this is a drop in the ocean to what is needed. Proportionate investment will ensure that the great legacy of cardiovascular research in Australia is retained.

Garry LR Jennings · Jaye Chin-Dusting

To the Editor:In their article, Chen and Jepson1 discussed the advances in coronary artery stent technology. However, the review did not outline the indications for the newer and more expensive technologies mentioned, and did not indicate how stenting compares with the established practice of coronary artery bypass grafting (CABG) for patients with coronary artery disease. How does percutaneous coronary intervention (PCI) compare with CABG based on current evidence? The SYNTAX2 trial is a multinational trial investigating PCI versus CABG. At 5 years, the number of major adverse cardiovascular and cerebrovascular events in the CABG group was 26.9% compared with 37.3% in the PCI group. The 5-year myocardial infarction rate was 3.8% in the CABG group compared with 9.7% for PCI. Moreover, registry data showed that the cardiac death rate was 3.6% for CABG compared with 9.5% for PCI. Therefore, the group concluded that CABG should remain the standard of care for patients with multivessel coronary artery disease.2 A 2014 meta-analysis in JAMA3 comparing PCI with CABG indicated a reduction in mortality (relative risk [RR], 0.73; 95% confidence interval [CI], 0.62–0.86), myocardial infarction (RR, 0.58; 95% CI, 0.48–0.72) and revascularisation (RR, 0.29; 95% CI, 0.21–0.41), with CABG compared with PCI at a follow-up of 4.1 years. The subgroup analysis showed benefits in patients with and without diabetes. The BEST trial4 compares second generation everolimus-eluting stents with CABG. This trial enrolled 880 patients with more than 70% stenosis of two or more coronary arteries, and followed them up to 4.6 years. At 2 years, the primary endpoint of death, myocardial infarction or revascularisation occurred in 11% of patients in the PCI group and in only 7.9% of patients in the CABG group. During long term follow-up, it occurred in 15.3% of patients in the PCI group compared with 10.6% of patients in the CABG group.4 When reviewing the available evidence in the literature, several articles support CABG over PCI.5 The benefits of CABG persist, despite the development of second generation drug-eluting stents. CABG provides superior long term results in patients with multivessel coronary disease in regard to mortality, myocardial infarction and need for revascularisation. Therefore, CABG remains the gold standard of treatment for these patients.

Rohen Skiba · Chris Merry

In reply

Nigel Jepson · Daniel Chen

To the Editor:We commend Kahn and colleagues1 for publishing their data on the pre-hospital use of fibrinolysis and showing that the outcomes were similar to those treated by primary percutaneous coronary intervention (PCI). However, we noted that the median first medical contact to device time for those receiving primary PCI was 130 minutes, and indeed > 75% of patients had longer than the 90 minutes recommended in the recent National Heart Foundation of Australia and Cardiac Society of Australia and New Zealand guidelines.2 Although there is still some uncertainty about acceptable time delays to PCI, these data suggest that even more individuals should be receiving pre-hospital thrombolysis. As an alternative, perhaps patients should be randomised in clinical trials that address the relative usefulness of these two reperfusion strategies in circumstances of likely moderately prolonged times to primary PCI. Moreover, among those patients undergoing pharmaco-invasive PCI, the dose of the fibrinolytic drugs used requires definition.3

John K French · Derek P Chew · Richard W Harper · Philip EG Aylward

In reply

Arshad A Khan · Peter J Fletcher · Andrew J Boyle

To the Editor:I read with interest the Medical Education article by Elder and Nair1 and I was surprised that it suggested that the assessment of the jugular vein pulsation should be done “in whatever position the patient is in”. I am often shocked by the fact that medical students are taught to look for the jugular venous pulsation with the patient positioned at 45 degrees. In a person who is asymptomatic and lying flat, without any obvious distress and who has no fluid retention clinically, the pressures in the right atrium will be in the range of 2–8 mmHg and it would be impossible to see the top of the jugular venous pulsation if the patient was elevated. In most patients, the jugular venous pulsation should be assessed by examining the patient in the supine position. Elevation should only be undertaken if there is obvious fluid retention or dyspnoea when lying flat. If there is any question after examining the patient in the supine position, then the patient may be elevated to ensure that the correct peak of the jugular venous pulsation is seen. However, if students are taught to examine the jugular venous pulsation only when the patient is sitting up, then it will seldom be seen in a person who has normal right atrial pressure. I believe this concern should be brought to the attention of all clinical educators so that they clearly explain when the jugular venous pulsation should be examined in the supine position and when it is necessary to elevate the patient to the 45 degrees position.

Stanley Peter Woodhouse

In reply

Andrew Elder · Balakrishnan (Kichu) R Nair

To the Editor:The use of public access automated external defibrillators (AEDs) has rapidly increased from 2003 to 2013 — with an 11-fold growth in Victoria — and has shown improvement in survival rates for out-of-hospital cardiac arrest.1 Prompt deployment relies on lay people to recognise a cardiac arrest, operate the device and manage basic life support.2 Lay people’s use of these devices located in public locations, as opposed to specialised health care settings, is unparalleled among medical devices. However, lay people are not involved in the clinical handover of the patient with the AED and it often remains with the private owner, who may not appreciate the importance of retrieving critical AED data. Lack of handover postresuscitation of initial rhythm and AED data has been shown to underdiagnose ventricular fibrillation (VF), as well as miss other significant rhythms such as complete heart block.3,4 AEDs use arrhythmia algorithms to analyse heart rate and QRS duration from the triggered digital recording, and are designed to have a specificity of 99% and a sensitivity of > 90% for detection of VF and of > 75% for rapid ventricular tachycardia (VT), without a specific cut-off rate defined. Of four commercially available AEDs, one study indicated a large divergence in how they managed VT and supraventricular tachycardia (SVT), with some devices even delivering a shock for narrow complex SVT, therefore leading to difficulty for clinicians in interpreting the significance of an AED delivered shock.5 Specific equipment operated by trained personnel is required to download the rhythm data from the AED.2 Standardised data transmission software, either via smartphone or cellular networks, to a central server or at the hospital may fill this current critical data void. Systematic capture and documentation of the initial AED rhythm analysis may incorporate the AED as an essential diagnostic clinical tool and may reduce critical diagnostic errors and unnecessary use of implantable cardioverter defibrillators. Rhythm documentation of AED data has significant implications in determining underlying cardiac disease, dictating management and influencing preventive measures to reduce the risk of malignant arrhythmia recurrence. With the rapid expansion and increasing access of AEDs in the public domain, collaborative review of current protocols and coordination between health services, emergency management services and owners of public AEDs are required to avoid further loss of crucial data.

Andrew D Mulligan · Omar Al-Mukhtar · Michael Wong

n/a

Anthony Rodgers · Clara K Chow · Rodney T Jackson · Anushka Patel · Tim Usherwood

In reply

Genevieve M Gabb · Arduino A Mangoni · Leonard Arnolda