To march or not to march?

When I’ve marched in the past it has been to protest or celebrate.  The call for a March for Science, due to take place in New Zealand on the 22nd of April, has me confused as to its purpose.

When I first heard the suggestion of a March for Science in New Zealand I admit I was immediately sceptical (occupational hazard).  The suggestion had come in response to the policies of the Trump administration in the USA.  I am appalled by many of them and by the apparent ignoring of the scientific consensus – but then given the flip-flop on so much that was said in the campaign, it would take a brave person to predict there won’t be a similar flip-flop with respect to climate change policies and the like.  That aside, is the March in New Zealand intended to be a protest against Trump?

Nicola Gaston in a persuasive blog post  writes that with her Bachelor of Arts in her back pocket she will be marching for science and the scientists. Paraphrasing Niemoller she writes “First they came for the scientists, but I was not a scientist, so I did not speak out”. She hit a nerve with me, it is a sentiment that has resonated strongly in me ever since I walked though Auschwitz concentration camp and spent several years living in a country soon after the communists had relinquished power. It is right and proper to speak out for the oppressed, whoever they are and whether we agree with them or not. However, the title of Nicola’s post “Why scientists need to go to the barricades against Trump – and for the humanities” and the first few paragraphs paint the call to march  as a political protest against Trumpian rhetoric and policy.  This, for me, is not an encouragement to march in NZ.  There are many many countries and issues around the world that I abhor and that I think reflect more closely Niemoller’s sentiments– “First they came for the migrants”, “First they came for the children (for the sex trade)”, “First they came for private property” – and I struggle with what I can do about any of them.  However, marching in New Zealand protesting policies in another country is not something I see as effective unless we are demanding action from our government against those countries.


Photo: Brandon Wu 20 Jan 2017 , Wikimedia Commons.


Since Nicola wrote that piece, the March organisers have written about the reasons for the March (here and here).  While what has happened in the US is still very much to the fore, the organisers’ attentions seems to have turned towards a protest against policies of the current government “our current government has and continues to be ineffective in defending our native species and environment” (Geni- Christchurch organiser), “The government believes they are improving freshwater, yet they aren’t utilizing NZ freshwater ecology research outputs or freshwater scientists for these decisions.” (Erin-Palmerston North), “you only have to look at the Land and Water forum to open the discussion about the government ignoring the advice of scientists in regards to water quality.” (Steph-Auckland), and on the March for Science websiteThe dismissal of scientific voices by politicians is perhaps best encapsulated by our former Prime Minister’s dismissal of concerns about the impact of our dairy industry on water quality



The organisers in the spirit of peer review invite critique.  My first thought is that if people want to protest the government’s actions with respect to water quality – then please do so.  But, please don’t dress it up as a “March for Science” as if NZ politicians are inherently anti-science.  It comes across as a belief that the NZ Government is tarred with the same brush as the Trump administration with respect to its treatment of science.  I don’t think that comparison is fair.

As an aside, I believe we must be careful with the generalisation “anti-science”, a phrase I’ve regularly heard from the voices and pens of scientists in the past few years.  The phrase has almost always been used to describe people who take stances in opposition to the scientific consensus on matters such as vaccinations, fluoridation, or climate change.  I don’t believe these people are anti-science per se – indeed, they often try (and fail) to use science to back their views. Furthermore, they may well embrace the findings of science in general.  Troy Campbell and Lauren Griffen’s recent post in Scientific America is a good panacea against the loose and pejorative use of the term “anti-science”.

Another aspects of the call to March that I find difficult is the statement “We acknowledge that in Aotearoa New Zealand the scientific community has yet to live up to the principles of Te Tiriti o Waitangi, and that there is an ongoing process of decolonization required to achieve greater inclusion of Māori in the scientific community.” I admit I’m not entirely sure what this means. However, as a member of the scientific community it sounds like I’m being slapped over the wrist.  Further, I feel it is accusing me of some form of racism.  I’m sure this was not the intention, but it is the impression I get and one I don’t like getting.

This is all a pity, as I’d hoped that the March for Science would be more of a celebration with the added value of standing in solidarity with scientists who have been silenced or disenfranchised.  To be fair, celebration is obviously on the mind of some of the organisers such as Cindy from Dunedin “together to celebrate the quest for knowledge and the use of knowledge to protect and enhance life… hope that the March for Science Global initiative will empower scientists and other knowledge-seekers to continue their important work and to share it widely.”  However, this does not seem to reflect the overall tone of the call.

One of the goals of the March is to highlight that “Good scientists can be political.”  I applaud this sentiment and it is something I have tried to be take on board in the past – twice I stood as a political candidate in the general election (2005 and 2008).  Beyond protest, I would encourage all scientists to spend a few minutes with their local MP explaining why and what they do.  The temptation is to bemoan the lack of funding, but I would suggest that funding follows understanding, and we need to engage with politicians and as we do so to recognise the complexity of the decision making with all the competing interests that they have to make.

I began with a question, to march or not to march?  As I’ve written this, I’ve come to the conclusion that, on balance, the call has not resonated with where I’m at, or with what I think of as effective dialogue with politicians, therefore I will not be marching.  I appreciate that others will disagree, nevertheless I wish them a very positive experience.


Aunty Cecily

This international women’s day I read a re-post of a wonderful article about Otago University women in science.  I thought I’d add another one, my Aunt Cecily, or to the rest of the world Dame Cecily Pickerill.

Aunty Cecily was clever, determined, and, yes, a tough woman.   It was those qualities that helped her to help many people.

She was born, Cecily Mary Aroha Wise Clarkson in Taihape in 1903 less than 18 months after her parents had arrived from England. Taihape in those days was forests, mud, a building boom and horses.  It appears to have also been a place she could get a good education.  At a young age, just 18, she made it all the way to Dunedin to attend Otago Medical School.  By then her family was in Auckland.  I don’t know what drew her to medicine. Perhaps it was through world war 1 or the flu epidemic that followed that influenced her. Her own Father had been at Gallipoli as a chaplain with the NZ armed forces during the war and invalided home in late 1915.  Just a year after Cecily started University her parents took her two younger sisters and left New Zealand permanently, ending up in Laguna Beach in California.  Her two, slightly older, brothers remained in New Zealand. She needed to be independent at a young age.

She first came across the art and science of plastic surgery while a house surgeon under the tutelage of Professor Henry Pickerill.  Pickerill was the first director of the Otago dental school. During world war I he became one of the pioneers in facial and reconstructive surgery while with the New Zealand Medical Corp.  Many of the men being treated were transferred to Dunedin at the end of the war.

Cecily spent a few years in California working and living with her family before joining Henry in Sydney in about 1933.  She married Henry at the end of 1934.  Later they moved back to Wellington and both worked as plastic surgeons in Wellington and at Middlemore.   In 1942 they set up Bassam hospital in Lower Hutt for plastic surgery on children – mainly repairing cleft palates and the like.

One of the remarkable features of their work in Bassam was the elimination of hospital cross-infection in children.  They wrote of this in the Lancet in 1954  (Pickerill, C. M., & Pickerill, H. P. (1954). Elimination of hospital cross-infection in children: nursing by the mother. Lancet, 266(6809), 425–429.)

In that article they wrote “what chance of success has a plastic operation on the plate or lip if the child contracts a mixed viral and bacterial infection of the field of operation …”  They noted the lavish use of chromium plating, enamel and wearing of masks… but still there was infection.  The Pickerill’s solution was both simple and innovative – they brought the mother in to nurse the child and gave mother and infant a room to themselves. “Not only do they live together in their own room, but nobody except the mother bathes, dresses, or feeds the patient or changes his nappies.”  This, and other measures, resulted in the remarkable result that after 11 year’s work they had “no single case of cross-infection.”

Aunt Cecily was intelligent, and caring, but also strict (ask my mother about the spider in the bathroom if you want a story about just how strict).  It was that strictness which meant Bassam could be a tight ship and produce such remarkable results.

She was also a woman who loved to travel and garden.  She brought rocks home from travels overseas which ended up as part of her fireplace in a house, Beechdale, designed by my grandfather, in Silverstream.  Her beautiful garden featured in magazines and TV shows.

I recall visiting her in the mid ‘80s at Beechdale when I was in my first job after graduating with a BSc(Hons).  I wasn’t particularly happy with the job at the time.  She was sitting in a comfortable chair in her lounge with a magnifying glass and an open scientific journal.  I realised then, that science and the love of science are for life.

Later when I was doing my PhD on the use of a copper vapour laser to remove birthmarks, I felt even closer to her when one of the patients we treated had had the birthmark partly removed by her surgically.  Many years later a little of it had regrown around the edges which we were able to treat with the laser.

My last memory of her was when she was in her last few weeks of life.  She was in a room in Bassam hospital which was had by then been turned into a hospice.  She had the radio going with some very modern music – which we joked about.  It was fitting that she spent her final days being cared for in the place that she had spent so many days caring for others.


Big data + Big science = Big health

Big data and big science are buzz phrases in health research at the moment.  It is not at all apparent what the exact definition of these are or should be and whether they will be short lived in our lexicon, but I think it reasonable to assume that where there is buzz there is honey.

I think of big data in health as information routinely collected by our interaction with health systems, both formal (eg GPs or hospitals) and informal (eg networked devices that continuously monitor our heart beat).  Through ever improving connectivity such data may become available (anonymously) for the health researcher and policy maker.  The statistical tools needed to analyse this volume of data without producing spurious correlations are still being developed and there are some genuine ethical concerns that must be addressed.  Within New Zealand we have a unique alpha-numeric identifier for anyone who has encountered our formal health system.  This is very unusual internationally and puts us in a good position to pull data together from multiple sources and to monitor change over time.  Recently I have used this system to assess the performance of new emergency department chest-pain pathways at multiple hospitals throughout the country.  These pathways had been developed in research programs in Christchurch and Brisbane. Following a Ministry of Health initiative for each emergency department to adopt such a pathway, and with the financial support of a Health Research Council grant (and my personal sponsors), we were able to establish efficacy and safety parameters of the change in practice.  If we had used a traditional model of employing research staff at each hospital the costs would have run into many millions and would simply not have been possible given how health research is financed in this country.  This model of monitoring changes made to how health care is delivered is both pragmatic and affordable.  It is also necessary if we are to be reassured that change is really improving practice. We expect to see more big data used in this way.

Big science is often thought of in terms of hundreds or thousands of researchers in facilities like CERN costing hundreds of millions of dollars. I think big science need not be so large or expensive.  Rather it is large international collaborations whereby sufficient good quality clinical research data is gathered to answer important clinical questions.  The key is “sufficient”.  Because of the prevalence of a disease or the size of a population base any one research group may not be able, in a reasonable time frame, to collect sufficient data to answer the important questions.   Over the past two years I have been involved in several international studies where we have pooled data, some of which our group has led, some of which are led by colleagues overseas.  We are now formalising a “consortium” to further ensure data is well and appropriately used and collected.  This move had been particularly important as even million dollar studies of a thousand patients do not have sufficient data to answer some of the key safety questions around the diagnosis of heart attacks (my current focus).  A criticism of much academic clinical research is that it is just not useful1.  This is in large part because the studies are too small to give results that would change practice.  They are also often not pragmatic enough (eg by excluding significant portions of patients likely to be assessed or treated by the intervention under study).  Recognition that it is through large collaborative studies that useful practical change can occur will lead to more such collaborations.  They require people to be involved with a slightly different skill set than those whose research is purely local – in particular the “people” skills required to form productive and lasting cross-cultural relationships.  They also require flexibility in funding which may lead to how rules for some grants change (eg by allowing some portion of funding to be spent offshore).

The era of Big data and Big science for Big health is both daunting and exciting.  While there will no doubt be blind alleys and false starts as with any research or new venture, there will also be practical and meaningful evidence based changes to health delivery. Something to look forward to.

  1. Ioannidis, J. P. A. (2016). Why Most Clinical Research Is Not Useful. Plos Medicine, 13(6), e1002049.

Heart attacks in NZ – are women getting a raw deal?

Yesterday the NZ Herald published an article saying doctors are failing to spot heart attacks in thousands of women.  This sounds alarming, could it be happening in NZ? Are women getting a raw deal?  Important questions.  This post looks at the study behind the media and then at how heart attacks are being diagnosed in New Zealand.

The Herald article is evidently based on press releases related to a study published to coincide with the European Society of Cardiologist’s conference currently underway in Rome and attended by some 30,000 cardiologists, other physicians, industry types, and the Pope (yep!). The study in question comes from the University of Leeds. Here’s the Leeds Uni press release.

The US red-dress logo which is their national symbol for women and heart disease

The US red-dress logo which is their national symbol for women and heart disease

The study

The study is based on an audit of UK data collected about patients between 2004 and 2013 whose final diagnosis was a heart attack (in clinical jargon a myocardial infarction, either STEMI or NSTEMI).  The full article is available here.

The subjects were patients who at discharge from hospital had a heart attack diagnosis.  The authors looked at the preliminary diagnosis of patients when they first entered the hospital and compared that diagnosis to the final diagnosis of a heart attack.  The preliminary diagnosis was for about a 30% of patients not explicitly a heart attack – ie often something like “chest pain of uncertain cause.”  In the press release and news reports this was reported as a “misdiagnosis.”

Point 1:  The term “misdiagnosis” is inappropriately applied here.  While some forms of heart-attacks can be diagnosed in the ED, most can not.  Indeed, the guidelines for diagnosis of a heart attack require some blood measurements at least 6 hours apart.  Nowadays, the later blood sample is not done in the ED, but in a cardiology or general medicine ward.  That is, the ED physicians often don’t have all the data to make a definitive diagnosis – hence only a preliminary diagnosis is made. Most of the time the job of the Emergency department physicians is to rule-out some possible diagnoses and to identify patients at significant risk of a heart attack.  These patients are referred on to the specialist teams within the hospital who make the final diagnosis.*  Yesterday I was speaking with a cardiologist who was explaining how often cardiologists themselves disagreed over a diagnosis.  It ain’t easy.

The press releases and media reports emphasise that a larger proportion of women than men were likely to have a change between the preliminary and final diagnosis.  The Leeds University press release states women were 59% for a final STEMI diagnosis and 41% for a final NSTEMI diagnosis more likely than men to have a change from the preliminary diagnosis.

Point 2:  These numbers are not reported in the published paper!  Nor is anything about the differences between men and women discussed in the paper.  In the results section it is simply stated that those who had an initial diagnosis that changed were more likely to be older, female, and have a co-morbidity. There are some numbers related to this in a table. In the table I note that patients older than 61 compared with younger patients had at least (more if they were even older) the same odds of having a diagnosis changed as did females compared with males (it’s a little awkward in the paper because the odds ratio is written the opposite way around – but this can be rectified simply by taking the reciprocal of the odds ratio and comparing that).  There were also other predictors of a change in diagnosis (eg higher heart rate).  The cynic in me thinks that it may be for publicity reasons that the emphasis has been placed on the sex differences in press releases.

Point 3: What is important about the study is that in those who had a change in diagnosis the one-year mortality rates were higher.  While the suggestion is made that this is because of delay in time to treatment (known from other studies to be important), there are other potential reasons because of the differences in demographics and co-morbidities between the groups.

New Zealand

The study began at a time when the blood biomarkers indicative of a heart attack that are used now (troponins) were not in common use.  There have been several generations of markers, the latest of which are “high-sensitivity troponins.”  The authors’ recommended that:

“…our results… call for the earlier use and wider adoption of high sensitivity troponins as well as a focus on the systematic application of accelerated diagnostic protocols using risk scores rather than subjective clinical assessment.”

The good news is that New Zealand is now the only country in the world** to have accelerated diagnostic protocols using risk scores in place in every ED.  Furthermore, most ED’s are using the latest high sensitivity troponins.

In the Christchurch ED, different sex-specific thresholds of the troponin used for risk stratifying and diagnosing heart attacks are used.  This is because in the general healthy population males have slightly higher values of these troponin measurements than females.  Therefore, to avoid underdiagnoses of females a lower diagnostic threshold is used.  Furthermore, in a study we were part of and lead by our Brisbane based colleagues, using sex-specific threshold helped improvs risk prediction for future adverse events in women.


In New Zealand it is less likely that women are getting a raw deal.


*perhaps the Pope a.k.a @Pontifix [literally the “bridge builder”] could help bridge the divide between ED physicians and cardiologists – generally ED physicians rule-out heart attacks, Cardiologists rule-in heart attacks.

** although Queensland also has this and they like to think of themselves as a country sometimes

Cheesecake Files: Embargoed until

Every now and again a Journal doesn’t want us to talk publically about our own paper until it they publish it.  This is simply so they can make more of a splash with it.  This was the case of an article I have been involved with published today in the Cardiology journal of the American Medical Association*. 

What’s it about?

Ruling out a heart attack in the emergency department is difficult.  Readers of this blog would have read about various other ways we’ve developed to be part of it (eg here).  They depend on many things including the type of blood measurement used and the timing of that.  These markers – called troponins – detect damage to the heart muscle.

In this study led by Ed Carlton of Southmead hospital in Bristol, UK, we evaluated whether a single measurement of very low levels of a comparatively new blood biomarker called “High-sensitivity troponin I” could alone rule out heart attacks within 30 days when someone presented to the emergency department with chest pain (Here Ed speak about the study here).

3155 patients at 5 hospitals in New Zealand (Christchurch), Australia and the UK participated of whom 291 had a heart attack (277 were having a heart attack on the day they presented to ED, the other 14 had one within 30 days).

We found that 594 (18.8%) of patients had such a high sensitivity troponin I concentration below the limit at which it could reliably be detected.  ie next to nothing. These we can say tested negative.  Three of them (0.5%) it turned out did have a heart attack.

Why the splash?

The editor got quite excited about this and another study and wrote an editorial to accompany the studies:

“To manage costs and the adverse effects of overcrowding in the ED, it is a high priority to rapidly and safely identify patients with a sufficiently low probability for acute coronary syndrome (<0.5%-1%) so that they can be discharged efficiently and avoid unnecessary testing.”

He was impressed that this study had been “tested in robustly sized, geographically diverse, clinically relevant populations.”

And concludes

“Taken together with prior studies the findings from the studies of Neumann et al and Carlton et al lend strong support to the notion that accelerated diagnostic protocols that incorporate [high sensitivity troponins] can facilitate earlier triage while maintaining an acceptable [rate of false negatives].

One of the features of interest to the readers of this US journal is that the high-sensitivity troponins are not yet available in the US, however they eventually will be and how they are used is of particular interest.

Part of a figure from the publication showing how choosing different troponin thresholds to rule-out patients affects how sensitive the test is.

Part of a figure from the publication showing how choosing different troponin thresholds to rule-out patients changes how sensitive the test is.

Why not perfection?

Of course we would love to never have a false negative (or false positive).  However, the reality of medicine is that this is not possible.  We could, of course, simply admit everyone, do more invasive tests,  or “wait and see” if they develop a heart attack. There are, though, risks as well as costs with admitting people to hospitals.  If I may speculate for a moment, the rise in superbugs resistant to antibiotics is only likely to increase those risks in the future – hence the importance of studies such as this. It is important that we get the balance of risk right.

What are the next steps?

All of New Zealand now has some kind of accelerated diagnostic pathway for chest pain patients that incorporates serial troponin measurements.  At some stage we will implement, monitor, and measure the addition of an even more accelerated rule-out for some patients with just one troponin.  Watch this space.


* Carlton, E., Greenslade, J., Cullen, L., Body, R., Than, M. P., Pickering, J. W., Aldous, S.A., Carley, S,. Hammett, C., Kendall, J., Kevill, B., Lord, S.J., Parsonage, W.A., Greaves, K. (2016). Low concentrations of high-sensitivity cardiac troponin I at presentation in the evaluation of emergency department patients with suspected acute coronary syndrome. JAMA Cardiology.

Cheesecake files: A little something for World Kidney Day

Today is World Kidney Day, so I shall let you in on a little secret. There is a new tool for predicting if a transplant is going to be problematic to get working properly.

Nephrologist call a transplant a “graft” and when the new kidney is not really filtering as well as hoped after a week they call it “Delayed Graft Function.”  Rather than waiting a week, the nephrologist would like to know in the first few hours after the transplant if the new kidney is going to be one of these “problematic” transplants or not.  A lot of money has been spent on developing some fancy new biomarkers (urinary) and they may well have their place.  At this stage none are terribly good at predicting delayed graft function.

A while ago I helped develop a new tool – simply the ratio of  a measurement of the rate at which a particular substance is being peed out of the body  to an estimate how much the body is is producing in the first place.  If the ratio is 1 then the kidney is in a steady state. If not, then either the kidneys are not performing well (ie not keeping up with the production), or they have improved enough after a problem and are getting rid of the “excess” of the substance from the body.  This ratio is simple and easy to calculate and doesn’t require extra expense or specialist equipment.

A few months ago, I persuaded a colleague in Australia to check if this ratio could be used soon after transplant to predict delayed graft function. As it turns out in the small study we ran that it can, and that it adds value to a risk prediction model based on the normal stuff nephrologists measure! I’m quite chuffed about this.  Sometimes, the simple works.  Maybe something will become of it and ultimately some transplants will work better and others will not fail.  Anyway, it’s nice to bring a measure of hope on World Kidney Day.

This was published a couple of weeks ago in the journal Nephron.


Cheesecake files: A world second for heart attacks

Going to the Emergency Department with chest pain no longer means an almost certain night in hospital.  Friday saw the publication online of our randomised controlled trial comparing two different strategies to rapidly rule-out heart attacks in people who present with chest pain to hospitals.  Here’s a précis:

What’s the problem?

  • Chest pain is common – 10% or so of presentations to ED are for chest pain.
  • Heart attacks are not so common – only ~10-15% in NZ (and less overseas*) actually have a heart attack.
  • It is devilishly difficult for most chest pain to rapidly rule out the possibility of a heart attack.
  • Consequently, most people get admitted to hospital (in 2007 93% of those presenting with chest pain).

But – led by Dr Martin Than in Christchurch and an international group including Dr Louise Cullen in Brisbane – a series of observational studies and one randomised control trial have resulted in a gradual increase in the proportion discharged.  The trial was the first of its kind, it compared standard practice at assessing chest pain to a purpose built accelerated diagnostic pathway (ADP), which we called ADAPT.   In that study 11% of patients in the standard practice (control) arm and 19.3% in the ADAPT ADP arm (experimental arm) were discharged home from ED within 6 hours.  A great improvement which led to that ADP being adopted in Christchurch hospital.

So why another study?

Two reasons: First, 19% still means that there are many patients being admitted who potentially don’t need to be in hospital.  Second, the ADP was based around a risk assessment tool designed to rule-in heart attacks rather than rule-out.  In the meantime, the team had constructed a purpose build risk assessment tool that in observational studies looked like it could rule out 40-50% of patients.

What is the study just published?

The world’s second randomised controlled trial of assessment of chest pain compared the ADAPT ADP in use (now the control arm) with a new ADP based on the new Emergency Department Assessment of Chest pain Score (EDACS)[the experimental arm].  The only difference between the two arms of the study was the risk assessment tool used. The tool gave a risk score. Patients with a low score, no unusual electrical activity in the heart, and no elevated heart muscle injury proteins in either of two blood samples measured 2 hours apart, were considered low risk.

An important aspect of the study was that it was pragmatic.  This means that the doctors didn’t have to follow the ADP and could decide to send a patient home, or not send them home, based on any factors they thought clinically relevant.  This makes it very tough to run a trial, but it makes the trial more “real life.”

What were the results?

558 patients were recruited.  They all volunteered and are marvellous people.  I love volunteers.

The primary outcome was the proportion of patients safely discharged home within 6 hours.  We assessed safety by looking at all medical events that happened to a patients over 30 days to check to see if any patients discharged home had a major cardiac event that could potentially have been picked up in the ED.

34% of the control arm and 32% of the experimental arm were discharged within 6 hours.  In other words, there was no difference in early discharge rates between the two arms.  The surprising feature of this is that between 2012/3 (when the first trial was run) and 2014/15 the proportion of patients the first ADP ruled out increased from 19% to 34%.  This was unexpected, but pleasing. There were no safety concerns with any patients.

The secondary outcome was simply the proportion each arm of the study classified as low risk (ie not considering whether this led to early discharge or not).  The control (ADAPT ADP) classified 31% and the experimental (EDACS ADP) 42%.  This was a real and meaningful difference which suggests that there is “room for improvement” in early discharge rates as the clinicians become more familiar with the EDACS ADP.

Since 2007 in Christchurch hospital over three times more patients who present with chest pain can be reassured from within the ED that they are not having a heart attack and discharged home (see the infographic).EDACS infographic v2

What was your role?

My role: I managed aspects of the data collection for the later 2/3rds of the patients recruited, did the statistical analysis and co-wrote the manuscript.  In reality, there were a lot of people involved, not least of whom were the wonderful research nurses and database manager who did a lot of the “grunt work”.

What now?

Over the last year all EDs in New Zealand have implemented or in the process of implementing an accelerated diagnostic pathway.  The majority have chosen to use the EDACS pathway.  I am part of a team nationwide helping implement these pathways and monitor their efficacy and safety.


This study was funded by the Health Research Committee of New Zealand. The work was carried out with the collaboration or the University of Otago Christchurch, Christchurch Heart Institute, and the Canterbury District Health Board Emergency Department, Cardiology Department, General Medicine, and Canterbury Health Laboratories. My salary is provided through a Senior Research Fellowship in Acute Care funded Canterbury Medical Research Foundation, Canterbury District Health Board and the Emergency Care Foundation.

*Not because we have more heart attacks, just an efficient and well funded primary care sector that keeps the very low risk patients out of the ED.

**Featured Image: Creative Commons Share-Alike 3.0