Episode 35: Acute Coronary Syndrome Part 1—Diagnosis

Episode 35: Acute Coronary Syndrome Part 1—Diagnosis
Date:
3 May 2018
Category:

Fellows of the RACP can claim CPD credits via MyCPD for listening and using resources related to this episode.

This is the first of two episodes on acute coronary syndrome (ACS). Part 1 deals with diagnosis of patients presenting with possible ACS, while Part 2 addresses secondary prevention and new findings about predictors for adherence to therapy.

Chest pain and other symptoms suggestive of ACS make up the majority of presentations to hospital. 11 to 17 per cent of patients presenting to ED with such symptoms end up having the diagnosis confirmed. But follow-up studies of discharged patients show that up to six per cent of diagnoses are missed, and inappropriately discharged patients have a twofold higher mortality rate than those who are admitted.

The 2016 guidelines of the Cardiac Society of Australia and New Zealand were developed to guide the rapid differentiation of patients presenting with suspected ACS. ACS takes in STEMI and non-STEMI heart attacks, and also unstable angina. This episode outlines the investigations used to distinguish these and other differential diagnoses associated with chest pain. First, electrocardiogram recordings are used to identify the occurrence of a myocardial infarction with ST segment elevation. If STEMI is discounted, the next most important step is to rule out other life-threatening causes of chest pain. Third in the diagnostic hierarchy is to establish whether there has been myocardial infarction without ST elevation, or unstable angina. This is where high sensitivity troponin markers become useful, and can feed into stratification protocols for assessing the risk of patients suffering future acute cardiac events.

Guest: Associate Professor Louise Cullen FACEM (Royal Brisbane and Women’s Hospital, University of Queensland).

Related RACP College Learning Series Lectures

Management of acute coronary syndromes [Lefkovits]
Update in coronary intervention [Brooks]

Principal Literature

National Heart Foundation of Australia and Cardiac Society of Australia and New Zealand: Australian Clinical Guidelines for the Management of Acute Coronary Syndromes 2016 [Heart and Lung Circulation]
Australian clinical guidelines for the management of acute coronary syndromes 2016: summary (MJA)
Acute Coronary Syndrome: New Zealand Management Guidelines 2013  [CSANZ]
Appropriate use of serum troponin testing in general practice: a narrative review [MJA]
High Sensitivity Troponin Testing [ALiEM]
Stress electrocardiography and stress echocardiography [AFP] 

Risk Stratification Protocols

2-Hour accelerated diagnostic protocol to assess patients with chest pain symptoms using contemporary troponins as the only biomarker [Cullen, JACC]
Association of high-sensitivity cardiac troponin I concentration with cardiac outcomes in patients with suspected acute coronary syndrome [Cullen, JAMA]
Performance of the high-sensitivity troponin assay in diagnosing acute myocardial infarction: systematic review and meta-analysis  [CMAJ Open]
The Manchester Acute Coronary Syndromes (MACS) decision rule for suspected cardiac chest pain [Heart]
Acute chest pain evaluation using coronary computed tomography angiography compared with standard of care: a meta-analysis of randomised clinical trials [Heart]
Outcomes of non-invasive diagnostic modalities for the detection of coronary artery disease [BMJ]

ECG Basics

Top 5 MI ECG Patterns You Must Know [Healio]
ECG Library [Life in the Fast Lane]
Using the ECG to localize myocardial infarction and determine the occluded coronary artery [Clinical ECG Interpretation]
A Noob’s Guide to ECG [Irfan Ziad, Slideshare]

Credits

Written and produced by Mic Cavazzini. Additional audio recording from Michelle Ransom-Hughes. Music courtesy of Jason Shaw (‘Minstrel, Pioneers’), Lee Rosevere (‘Become Death’), Sergey Cheremisinov (‘Pulsar’) and Loch Lomond (‘Listen, Lisbon’). Image courtesy of Science Photo Libary. Executive producer Anne Fredrickson.

Editorial feedback for this episode was provided by RACP members Paul Jauncey, Pavan Chandrala, Rebecca Grainger, Phillip Gaughwin, Rhiannon Mellor, Alan Ngo, and Mahesh Dhakal.

Transcript

MIC CAVAZZINI: Welcome to Pomegranate Health. I’m Mic Cavazzini.

This is the first of two podcast episodes on acute coronary syndrome. In mid-May we’ll talk about secondary prevention therapy, and some new findings about predictors adherence. But today we’re going to discuss the diagnosis of patients presenting with possible ACS.

Before getting into the show I want to highlight another great resource for members of the RACP. The College Learning Series is a catalogue of video lectures on every topic related to the basic training curriculum, with new lectures added every week. Once you’re done listening here, you can check out talks on the management of ACS and on coronary intervention at elearning.racp.edu.au.

The incidence of all acute coronary events in 2015 was around 406 per 100,000 Australians over the age of 25, according to estimates from the Australian Institute of Health and Welfare. In New Zealand, this would scale to over 610 people per 100,000, where the mortality due to ischaemic heart disease is worse than the average for OECD member countries.

Calculating mortality rate associated with ACS is complicated, but somewhere between 10 and 25 per cent of acute coronary events are fatal [see also]. These aren’t just STEMI heart attacks, but also non-STEMIs and cases of unstable angina pectoris. Distinguishing these and other differential diagnoses sometimes requires a range of investigations and the expertise of an emergency physician. But there will be generalists listening who make these workups while manning the fort in an understaffed or rural ED.
The 2016 guidelines of the Cardiac Society of Australia and New Zealand were developed to assist in the evaluation of patients presenting with symptoms suggestive of acute coronary syndrome. One the main authors was Associate Professor Louise Cullen.

LOUISE CULLEN: OK, my name is Louise Cullen. I’m an emergency physician at the Royal Brisbane and Women’s Hospital here in Queensland. I’ve been interested for a number of years in troponin and testing of patients who’ve got symptoms that may be an acute coronary syndrome. I’ve done over 10 years worth of research in this area and have been very fortunate to be involved with the Australian National Heart Foundation and the Cardiac Society of Australia and New Zealand Guidelines that came out in 2016, in terms of management of patients with possible acute coronary syndromes.

MIC CAVAZZINI: And that's why we’ve got you here to walk us through those guidelines, for those that haven’t read the full 60 pages.

LOUISE CULLEN: There’s a longer version!

MIC CAVAZZINI: It took me a couple of days, but I managed to get it down to three, so we’ll see…

LOUISE CULLEN: It took me a couple of years to write—seriously, it was a two-year process writing my section alone.

MIC CAVAZZINI: So of course, the key symptom that raises concern for an acute ischemic event is, of course, chest pain. And importantly, you say in the guidelines, it must’ve lasted for 20 minutes or more, but may have resolved by the time that the patient gets to hospital. Can you elaborate a bit more about how else the pain or the symptoms might be described by a patient, other less obvious symptoms?

LOUISE CULLEN: One of the most challenging things about patients with acute coronary syndromes is the way that they present. It’s very easy with the typical symptoms, the chest pain that you talk about, but we know that up to half of people that do have ACS don’t actually have those symptoms. They present things like shoulder pain, jaw pain. Sometimes it’s upper abdominal pain, but it may not be pain at all or discomfort at all. It might be things like shortness of breath or nausea or vomiting.

Fatigue is something that we see, particularly in our older female population, but they might also present with sweating or palpitations as well. So it can be quite varied, which is why it’s not an easy diagnosis to make, particularly not on history alone.

MIC CAVAZZINI: The guidelines tell you to keep an eye out for patient cohorts in whom atypical presentations are more frequently encountered; for example, people with diabetes, women, older patients, those with mental illness. It’s also mentioned that no historical features can rule out acute coronary syndrome in someone with chest pain, and that referral to ED should not depend on troponin results. As you’re getting the ECG on them, starting the workup, would you administer any anticoagulants or antiplatelet therapy as a precaution right away?

LOUISE CULLEN: So, in patients that we believe have got possible acute coronary syndrome, aspirin should be given unless there is any contraindications and we should give that as soon as possible for its antiplatelet properties. But other therapies that are talked about in the actual management of patients who have a proven ACS, things like beta blockers we don’t give unless there is confirmation of that diagnosis.

MIC CAVAZZINI: And what about any pain medication?

LOUISE CULLEN: There’s a number of options available to us at the moment. You’d find that probably the first option is always GTN, or nitroglycerine. Sublingual is usually what is the route of administration initially and that can be by a tablet or a spray. But, if after three doses, there’s no relief of pain we need to look for other alternatives. They include things like giving the GTN intravenously, but also giving IV narcotics.

 We tend to use fentanyl over morphine after some recent studies have shown that the onset of action to Tigagrelor can be slowed with morphine. We also don’t tend to give nonsteroidal anti-inflammatories because they actually increase the risk of cardiac events in patients who have got an acute coronary syndrome.

***

MIC CAVAZZINI: Chest pain and other symptoms suggestive of acute coronary syndrome might make up a quarter of all hospital admissions. In a study at the Royal Brisbane emergency department led by Louise Cullen, eleven per cent of suggestive presentations went on to have a diagnosis of ACS confirmed. A multi-centre U.S. study put this figure at 17 per cent.

But follow-up studies of discharged patients show that up to 6 per cent of diagnoses are missed, and these patients have a twofold higher mortality rate than those who are admitted. A 2000 paper in the New England Journal of Medicine reports that missed diagnoses were more likely in women under 55 years of age, patients who reported shortness of breath as their chief symptom, in those without an aberrant ECG and in non-white patients.

The Cardiac Society guidelines present a systematic way of differentiating ACS from other forms of chest pain in order of clinical urgency. First, you want to identify the occurrence of a myocardial infarction with ST segment elevation on electrocardiogram recordings.

If STEMI is discounted, the next most important step is to rule out other life-threatening causes of chest pain. Third in the diagnostic hierarchy is to establish whether there has been myocardial infarction without ST elevation, or unstable angina, but we’ll get to that later.

MIC CAVAZZINI: So, starting with STEMI, the diagnosis, of course, requires a 12-electrode ECG. And the Cardiac Society Guidelines recommend that these be read by an expert within 10 minutes of initial contact. How commonly does this happen?

LOUISE CULLEN: So, I think that it depends a little bit, of course, in your space and place that you’re at. There wouldn't be a clinical shift where I wouldn't see 10 or 20 ECGs to interpret. Outside of metropolitan areas you would find that there would be people that might be less familiar with the interpretation of these ECGs. A number of patients will be presenting to their primary care, to general practice as well. There is, though, with most ECG machines that are available, some inbuilt interpretive functions as well. They are often useful in the setting of your classic STEMI.

The computer-assisted interpretation is actually not too bad. If it says it’s an acute myocardial infarction you really need to find a reason why it’s not, if you’re going to go against it. The trouble with some of these interpretive functions is that they’re not sophisticated enough to pick up some of the subtle changes or some of the what we call STEMI equivalents. And depending on whereabouts you live, there are also different strategies which support our primary care physicians in rural practices, sending the pre-hospital ECGs through for interpretation. And even in this day and age, with iPhones and other things, taking a photo and sending it to your local cardiologist for support is, hopefully, readily available for everyone. 

MIC CAVAZZINI: So, we might just describe what this looks like for the physician that does end up reading these themselves. So the ST segment of the ECG is normally a small plateau representing a shift from depolarization to repolarisation of the ventricles. How dramatic is the elevation in a STEMI?

LOUISE CULLEN: It can be subtle, and believe it or not, there’s actually gender differences as well, and age differences. So it’s become more complex recently with some new guidelines that suggest that for men who are under 40, we’re talking about more than 2.5 millimetres of ST segment elevation. For men that are over 40, it’s 2 millimetres alone. In women, 1.5 millimetres. And in terms of left bundle branch block, for example, if there’s a new development of left frontal branch block, it’s more than 1 millimetre.

And there’s also other subtle things. What we see early in STEMIs is, really, a ramping rather than a plateau. This, although it doesn't meet the criteria for thrombolysis, it is a situation we want to do repeated ECGs to look for changes. And anyone with ongoing chest pain, you want to continually repeat those ECGs to see if you then meet the criteria for intervention.

MIC CAVAZZINI: Let’s just recap on some of the nomenclature perhaps: the ECG traces of V1 to 6 correspond directly to voltage recorded at those chest electrodes. Whereas the traces labelled in Roman numerals correspond to the subtractive differences or leads between two of the limb electrodes. Now depending which of the ECG traces show an ST elevation, an expert can localise the infarct to a specific wall of the left ventricle. But the Cardiac Society guidelines, as a first point, say to focus on chest electrodes V2 and V3. What’s the rationale for that recommendation?

LOUISE CULLEN: The rationale is very much that an anterior myocardial infarction is the ‘widow-maker.’ So, these anterior or septal leads, V1 to 2, and then the anterior V3 to 4, have high mortality. For that reason we’re wanting people not to miss those.

MIC CAVAZZINI: So it’s pointing to the most severe outcomes, not necessarily the majority of presentations.

LOUISE CULLEN: That's right. When we talk about ST segment elevation, we’re very much looking at particular leads. There are STEMI equivalents. For example, a posterior MI where you won’t have ST segment elevation at all. You’ll actually have ST segment depression, and yet, it’s pathognomonic of a STEMI that needs acute treatment. So it’s rather complex in its interpretation, unfortunately.

MIC CAVAZZINI: So ST elevation is a sensitive and specific marker of myocardial infarction. The guidelines say that this is enough on its own to require progression to immediate reperfusion of the patient. So how immediate, typically? Do you have to take serial recordings before you’re absolutely sure?

LOUISE CULLEN: Generally, not in the right clinical context. Any delays, for example, if you’re in a region which does not have access to PCI, you may be beginning to organize your thrombolytic agent while you do a second ECG for sometimes backup and reassurance. If you believe you’ve got that STEMI, time is of the essence to ensure the best outcome for this patient—and this is where you get the classic ‘time is muscle.’

MIC CAVAZZINI: You mention PCI—the guidelines suggest that percutaneous coronary intervention is preferred over fibrinolytic therapy as it saves two additional lives per hundred, and it may even be worth transferring patients from a non-PCI-capable centre. But that benefit is lost if there’s a delay greater than two hours?

LOUISE CULLEN: Yeah, look, absolutely. There are some caveats to that though. And for many of our places in regional and non-metropolitan centres, and even in some metropolitan centres without ready access to the cardiac catheter lab, the only option is fibrinolytic therapy. We know though that if you have given fibrinolytics and that there is ongoing chest pain and discomfort, or there is less than 50 per cent ST segment recovery at the one-hour mark, we should then be thinking about access for rescue angioplasty for these patients.

So, there’s a place for both of these because even though this ideas of transferring patients is a good one, you have to be able to ensure that the person’s going to be able to get that blood vessel open within a short period of time. And just the sheer means of inter-hospital transfers often means that it’s longer than two hours so we’ve got to be very careful about what we advise. But there are some contraindications. There’s patients who are high risk of bleeding, for example, where that is contraindicated.

MIC CAVAZZINI: And the guidelines also point to other conditions that may cause ST elevation on the ECG, pericarditis, Brugada syndrome, and Takotsubo cardiomyopathy, which may require angiography for their differentiation. But if you haven’t done that, would you still rather risk reperfusion someone with that condition rather than not reperfusing someone who’s suffered acute MI?

LOUISE CULLEN: So, the key part here is really in the context of what’s going on. The clinical picture with someone with pericarditis is very, very different, and the same also for Brugada. You often see those changes in someone that is pain free without suspicion of an ACS. There are some additional—apart from the ST segment changes, there’s other changes that you’ll see in an ECG in someone with Brugada that will let you know that it’s there.

There are difficulties, of course, in some conditions, such as the Takotsubo’s cardiomyopathy. But here we’re at a harm versus benefit situation. So the harm that is done by not reperfusing someone with a STEMI is significant. The most common serious condition that we see with ST segment elevation is a STEMI, and not some of these other ones that are mimickers of it. And equally, I think when you put it in the right context it’s not as difficult as what it probably sounds, if you just look at the ECG alone.

***

MIC CAVAZZINI: If there’s no elevation of the ST segment in the ECG, the next most important step on the diagnostic checklist is to rule out other life-threatening conditions that could cause chest pain. These are pulmonary embolism, aortic dissection and tension pneumothorax.

In younger patients, myocarditis and pericarditis might also be considered though they are quite rare. To detect tension pneumothorax, a chest x-ray is the way to go, but ruling out the other differential diagnoses requires a combination tools and clinical assessment.

A sensitive biomarker for myocardial necrosis is circulating troponin protein. In the context of acute chest pain with normal ECG, a positive cardiac troponin assay would suggest heart attack without ST elevation. But pulmonary embolism can also raise blood troponin, so as Louise Cullen explains, the profile and timing of signals is all important.

LOUISE CULLEN: Yeah, look, it tells us that there is myocardial injury or myocardial necrosis, but it doesn't tell us the cause of it. Unfortunately, troponin can be elevated in a pulmonary embolism as well. If we’re going to think down that way then we need to thing about our other investigative modalities, and equally, about their levels of risk. So lower risk patients, we would use D-dimers, but intermediate and high-risk patients need either VQ scanning, so nuclear med scanning, or CT pulmonary angiography to rule out or identify pulmonary embolism.

And as our troponin assays are getting more sensitive in terms of analytical sensitivity, we can detect troponin in a lot more conditions. So, people who have got renal impairment, for example, subarachnoid haemorrhages, sepsis, burns, that you can also see in the people who are ultra-fit marathon runners.

MIC CAVAZZINI: So, despite these other conditions that can also elevate troponin, if you do see it continually increasing, that’s a way to differentiate acute myocardial infarction from other causes.

LOUISE CULLEN: Absolutely, because, as you can imagine, if there’s acute infarction, you’d see an elevation and you’d see an increase over a period of hours if it’s acute. There are occasions though where you see patients that have presented late and they have sometimes had chest pain two or three days before, but it hasn’t gone away. So, you then might be at the tail end of their troponin release, and so you might be beginning to see a fall then. Your single value is not going to help us. You need to do serial tests to see if there a change, because you need to see a rise or fall of troponin values.

MIC CAVAZZINI: OK. Now, newer high sensitivity troponin assays can detect concentrations of blood troponin ten times lower than the previous ones and allow earlier detection of myocardial damage. How has this increased sensitivity and precision changed the dynamics of the diagnostic process?

LOUISE CULLEN: It’s important to remember that when we talk about the increased sensitivity for the detection of troponin, it’s not the same thing as sensitivity for myocardial infarction. Because, as you can see, we’re actually now picking up a number of different conditions. So, one of the benefits of the higher sensitivity troponin assays is that we can do serial testing over a shorter period of times. We also don’t need additional tests. You know, gone are the days when we used to do a number of different biomarkers to try and identify if people had had a myocardial infarction. It also means there’s been a little bit of a shifting around in terms of more patients are now diagnosed probably with non-STEMIs and fewer with unstable angina, which is your troponin-negative state, because we have got this ability to detect accurately very small, or very low elevations of troponin now with the high-sense assays.

MIC CAVAZZINI: One caveat of troponin assays is that the time range over which the patient might show an elevation can vary quite a bit. Can you elaborate on this, and whether it’s the tests or just patient biological variability?

LOUISE CULLEN: So, in terms of the timing and how long do you need to do blood tests to ensure that someone has a heart attack or doesn't have a heart attack, it very much does depend firstly on the test that you’re using and the analytical sensitivity of it. The second part, though, is the troponin getting into the circulation as well. The pathophysiology that’s going on, is there any circulation past that necrosed myocardium that actually then circulates that troponin back to allow us to detect it peripherally.

It gets really complex in this area in the sense that all of these different assays by different manufacturers perform slightly differently, So, for example, our point-of-care troponins, you may actually need to extent testing out to 10 to 12 hours. But in our high-sensitivity troponins, for most people you will be able to detect that change within three. And then the sensitive ones that are still commonly available, it might be a field of six hours. When it is elevated, it can remain elevated for two weeks.

So, we are in a situation now where we’re having to do research to ensure that we have got the right rules for the right assays. And what I mean by that is the right difference, numerical values that we should be applying, and that includes us being able to rule out people, but also identify people who have had myocardial infarction sooner as well. Because there is such a difference in the way these tests perform, you need to know what your local assay is. You need to know what its cut points are and how it performs, and you need to use that really well. When you’ve got patients that are presenting that have had blood tests done across two different assays you can’t just change around your decimal places, for example, or change the reference intervals and use those same values. You need to start again.

MIC CAVAZZINI: Now, in terms of managing non-ST elevation MI, the recommended management is angiography and revascularization by PCI, or in some cases bypass surgery. Except in the case of type II myocardial infarction, which makes up 14 per cent of cases. So, if we describe type I as your classic plaque rupture and thrombus, what causes the damage in type II myocardial infarction?

LOUISE CULLEN: Type II MI is a term that is given where you have a supply/demand imbalance of oxygen that's caused by something other than coronary artery disease. So you can have something like coronary artery spasm, for example, or sepsis, for example, with pneumonia, where patients have got increased demand but just may not be able to maintain the adequate coronary perfusion to therefore cause that myocardial necrosis. You can also have things like tachyarrhythmias that cause that same sort of condition. A lot of underlying seriously unwell people have got type II MIs if we looked for them all.

The issue at the moment is that we don’t have specific treatment targeted for the type II MI itself. The key thing that we need to focus on to optimize these patient’s outcome is by treating the underlying condition well; identifying the sepsis, treating that. Treating whatever is causing the tachyarrhythmia, for example, rather than having something that is specifically cardiologically directed at the myocardium themselves.

***

MIC CAVAZZINI: In patients with normal troponin and ECG, then myocardial infarction is ruled out. If their chest pain is brought with less and less stress on each attempt at exertion, then a diagnosis of unstable angina should be suspected. Patients in the high-risk category can be investigated with coronary angiography to localise obstructed arteries, which may lead to percutaneous coronary intervention or bypass surgery.

Risk stratification is important for reducing unnecessary investigation and therapy. With conventional troponin assays, serial testing over several hours could lead to overnight stays for many patients, increasing the burden to them and to the healthcare system. High-sensitivity troponin assays have enabled accurate assessment to take place within two hours of presentation. Accelerated Diagnostic Protocols take this measure into account along with scores for other risk factors such as family history, comorbid diabetes, and smoking. Louise Cullen explains other criteria which contribute to a high-risk classification.

LOUISE CULLEN: Probably the commonest thing that we see is people with ongoing symptoms of ischemia, so ongoing chest pain that is very difficult to manage. But there are other things, such as haemodynamic compromise, for example, if they develop arrhythmias or acute heart failure. If they’ve got ECG changes that are recurrent in terms of they get better as you improve things, and as I said, they’re symptomatically not improving, and so they get recurrent dynamic changes of their ST segments or also T-wave changes, they’re the sorts of conditions that would put a person into a high-risk category for UAP.

Then there’s a few criteria that we believe are a low risk population now. Young people under the age of 40 just generally don’t have acute coronary syndromes, but there’s caveats to that. There are populations that aren’t necessarily grouped in that same – People, for example, like indigenous populations and people with accelerate atherosclerosis.

MIC CAVAZZINI: And they really emphasise the importance of stratifying risk at discharge of having another major adverse cardiac event in the next 30 days. Are the protocols pretty good at differentiating those patients?

LOUISE CULLEN: There’s a term called the accelerated diagnostic protocols, or ADPs. So we’ve got a number of different protocols now that are confidently being used around the world. One of them is the ADAPT ADP, which embraces and incorporates the TIMI score. There’s also the Heart Protocol, which uses the heart score plus serial troponins that is used as well. And there are others, such as the MACS Score, which is a Manchester ACS score as well, that are reported and are used in different pockets.

So it is the best evidence that we’ve got and a lot better than what we used to do 10 years ago, I can tell you. It gives us some concrete guidance in the emergency setting, which is, ‘Which patients can I send home safely?’ What is the likelihood of events within the next 30 days?

MIC CAVAZZINI: And then finally if we rule out unstable angina, the next thing would be to determine the presence of stable angina. And so what’s the time window there of differentiating that?

LOUISE CULLEN: Depends a little bit on the system as to what you will do. So some places will observe these patient in an ED observation ward and do inpatient testing, definitive testing for these people at that point in time. Further testing, though, might also happen in an outpatient setting as well. So we’ve, in the guidelines, clarified now that objective testing for underlying coronary artery disease can be performed up to 14, but ideally, 7 days after presentation to the ED.

MIC CAVAZZINI: As part of the ADAPT study conducted in Brisbane and Christchurch, patients with possible cardiac symptoms excluding STEMI were stratified using an accelerated diagnostic protocol and observed prospectively. Twenty per cent of patients were classified as low-risk for a major adverse cardiac event within 30 days. Of these 392 patients, only one went on to re-present with acute cardiac symptoms, demonstrating this protocol’s effectiveness in identifying patients who can be safely discharged.

In low to intermediate-risk patients without contraindications for exercise, underlying ischaemia can be revealed a number non-invasive tests starting with stress echocardiography. If this is unavailable, exercise stress testing involving ECG is possible but has a higher rate of false positives and false negatives.

Improvements in computed tomography have meant that CT coronary angiography now matches nuclear imaging modalities for sensitivity and specificity. It is capable of accurately localising even sub-clinical atherosclerosis, at lower direct costs and with shorter associated hospital stays.

This has prompted the UK's health service to list CT coronary angiography as a first-line test for all patients with suspected ischaemic heart disease. But according to two meta-analyses published this year, use of this technique also leads to higher rates of referral for invasive angiography and revascularisation than other diagnostic strategies without long-term improvement in mortality. In fact, the studies in BMJ and Heart found that, for low-risk ACS patients or those with stable disease, the recurrence rate of acute coronary events was comparable regardless of which functional or anatomic modality was used to investigate. Time will tell how this field unfolds.

The Cardiac Society guidelines indicate that all patients given a diagnosis of ischaemic heart disease be discharged with a copy of their ECG and an angina symptom management plan. This would include guidance on the use of prescribed medications, how to recognise future symptoms and when to call an ambulance should they recur. We’ll get into this further in the next episode.

For now, many thanks to Professor Louise Cullen for contributing her expertise for this episode Pomegranate Health. I also want to thank the members who provided editorial feedback on early drafts of this story- they’ve got most specialties and localities covered. For every episode, these clinicians are credited by name at the web page racp.edu.au/pomcast.

You’ll find links to all the literature mentioned embedded in a complete transcript of the podcast. Please refer to the 2016 Australian clinical guidelines we’ve been talking about, or the summary published in the MJA. The New Zealand-specific guidelines, last updated in 2013, are also provided.

There are links to the College Learning Series lectures and other great resources. And you can claim CPD credits for listening, reading and watching by clicking through to MyCPD. 

I’m Mic Cavazzini, for the Royal Australasian College of Physicians.

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17 Oct 2018
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