I can’t believe how time flies. It’s over a month since Cardiology Case 01 and it’s gone by in the blinking of an eye. This month’s case is inspired by a discussion we had at a recent Virchester County Cardiac Meeting where the fine emergency physicians of Virchester meet with our cardiology chums to talk through the latest issues and discuss the evidence for potential changes in practice.
As usual, the case is actually an amalgam of cases from my practice. It’s based on genuine experiences but is essentially hypothetical, so any relation to real cases is entiely coincidental and unintentional. A 40 year old man with no previous history and no cardiac risk factors presents to the ED with chest pain, which started while walking his dog. He has walked his dog every morning for years but this morning he developed a dull ache in his central chest. The pain didn’t radiate and eased after 2-3 minutes. It didn’t stop him walking but recurred several times during his 45 minute stroll. Finally, after it recurred (transiently) at rest soon after getting home, he decided to seek attention at a Walk In Centre, and an ambulance was called.
The patient arrived in the ED pain-free and had an ECG recorded, as shown.
What does the ECG show?
The first ECG demonstrates downsloping ST depression in the lateral leads, V5 and V6. There is also some ST depression in lead I and, although the baseline is wandering in lead II, there is a distinct impression of a downsloping ST segment. The ST segment in V4 is subtly depressed and marginally downsloping. There is also some minimal ST elevation in lead aVR.
What is the significance of these findings?
This ECG had been signed without its significance being truly appreciated. Indeed, even the Cardiology team, when consulted, had been unimpressed by the changes. The changes do appear subtle, and we very commonly see ECGs with ST depression in the ED. Our patient is pain-free with normal vital signs and is otherwise fit and well. So do we really need to worry about this ECG?
I would be worried by this ECG in practice, even without seeing the patient. This patient’s pain may not seem typical for myocardial ischaemia, but it is certainly compatible with that diagnosis. There is no reason why a previously healthy 40 year old man should have an ECG like this as his baseline. Lead V6 is perhaps the most convincing for acute ischaemia. The ST depression is downsloping, which is more concerning for ischaemia than upsloping ST depression. What’s more, although you may expect downsloping ST depression in the context of LVH, the size of the QRS complex in V6 in relation to the extent of ST depression is extremely concerning for myocardial ischaemia. We should be really worried about ST depression in ED patients with chest pain as we know that, even though they have less myocardial necrosis than patients with ST elevation, their prognosis is roughly the same. In the era of high sensitivity troponin assays that can detect smaller infarctions than ever before, in this clinical context (and in the absence of evidence that the changes are old) this ECG is almost diagnostic of an NSTEMI.
Clearly, a full history and examination with consideration of possible alternative causes is imperative. We should never forget the importance of a good history. We need to know whether the clinical context fits with an NSTEMI and, if it doesn’t, we’ll re-consider that diagnosis. What’s more, even if we confirm the diagnosis of NSTEMI, we want to know whether this is likely to be a type 1 myocardial infarction (caused by plaque rupture or erosion, and likely to respond to the evidence-based therapies for ACS that we know and love) or a type 2 myocardial infarction (which is caused by a supply-demand imbalance, where the priority is to address that imbalance in order to treat the ischaemia).
If we suspect a type 1 AMI, we’ll no doubt be commencing some treatment at this stage. Aspirin 300mg is a standard of care. We probably also want to proceed to additional antiplatelet therapies including clopidogrel, or perhaps even ticagrelor as it’s highly likely that this patient will go on to be managed with an early invasive strategy. If you’re in doubt about this, you may choose to wait for more clinical information before committing to ticagrelor. Ticagrelor appears to be more efficacious than clopidogrel (NNT ~52 for vascular death, MI or stroke at 12 months) but has a higher rate of haemorrhagic complications, and the risk-benefit ratio may be more favourable in patients undergoing an invasive approach.
Now, how about another ECG? Here’s the repeat…
Here you can see that the ST changes are clearly dynamic. There is still downsloping ST depression in V6 but it appears to be much better. The ST depression in leads I and II has almost resolved. Clearly we have dynamic ST depression. Resolution of the ST depression may seem like a good sign, suggesting resolution of the ischaemia. However, the dynamic nature of the ECG changes has really helped us to nail this diagnosis. We can now be even more confident that this patient has NSTEMI or, if the troponin does turn out to be negative (which is actually unlikely in this context if you use a high sensitivity assay), unstable angina. If the clinicians were unimpressed earlier, they really ought to be convinced by now!
Shall we admit for late troponin testing then?
Of course, this patient should undergo serial troponin testing, just like every patient with suspected ACS. But we’re clearly not going to wait 6-12 hours to test for troponin. We want to be able to ‘rule in’ this diagnosis as soon as possible and, as troponin is essential for the diagnosis of NSTEMI, we want to know the zero-hour troponin level. In our patient, the first troponin comes back at 20ng/L (99th percentile 14ng/L). This is a very modest elevation and failed to impress the clinicians. Of course, we see so many false positives with high sensitivity troponin that it’s easy to get complacent about minor elevations. Indeed, if we were to treat every patient with a troponin elevation of this magnitude aggressively, we would undoubtedly do more harm than good.
What makes this case different is the clinical context. This patient gives us no reason to believe that he should have a troponin elevation of that magnitude during health. He is young, has no cardiovascular risk factors and no co-morbidities. The zero-hour troponin above the 99th percentile is another concerning feature. But what can we do in practice to convince the clinicians involved that things are pretty serious?
The value of early serial troponins
So let’s say we repeat the troponin after 1 hour and it comes back at 250ng/L. By this stage, we had clearly nailed the diagnosis. This is an NSTEMI. In fact, this 1-hour serial troponin testing is backed up in the literature. You may have seen this really interesting analysis from the APACE cohort – ‘1 hour rule in and rule out of acute myocardial infarction using high sensitivity troponin T’. Of course, this algorithm hasn’t yet been externally validated so we shouldn’t be using it to ‘rule out’ AMI. However, the evidence supports the idea that we can ‘rule in’ AMI within 1 hour in the majority of patients who will ultimately be diagnosed with NSTEMI. In this case, ‘rule in’ was important to get buy in from other clinicians – and having a 1-hour delta troponin successfully achieved that.
This patient is clearly a candidate for an early invasive strategy. If you work at an interventional centre, your cardiologists ought to know about the patient and the patient certainly ought to be under their care in an ideal world. If you work at a non-interventional centre, you ought to be asking about early transfer to an interventional centre.
There’s plenty of evidence to back an interventional approach in these patients, but what about timing? In STEMI, time is muscle. We rush these patients to the Cath Lab for revascularisation as soon as possible, and minutes matter. Is NSTEMI different? Herein lies an important and very topical question. On the one hand, you would intuitively think that the earlier the revascularisation, the less the opportunity for ongoing necrosis and the better the outcome of the patient is likely to be. On the other hand, patients may benefit from a longer period on antiplatelet therapy prior to revascularisation and clinical outcome may be better when the procedure is planned rather than emergent.
Fortunately we have some good recent evidence to answer the question. First, a meta-analysis of 7 trials involving 13,762 patients suggested that early (<24h) rather than late (>24h) coronary intervention does not lead to a lower rate of death or AMI within 30 days and is associated with a higher rate of repeat revascularisation within 30 days, although the rate of bleeding was lower for patients undergoing early revascularisation.
Then we had the LIPSIA-NSTEMI trial, which randomised approximately 600 patients with NSTEMI to receive either immediate (<2h) intervention, early invasive therapy on the next day (10-48h after presentation) or a selective invasive strategy (initial medical treatment with angiography when clinically necessary; median time to angiography 67.2h in those who underwent the procedure). An immediate invasive strategy did not lead to significant differences in the infarct size (measured by final CK-MB level) or in clinical outcomes (death, AMI, refractory ischaemia, rehospitalisation).
So, the evidence suggests that there is no rush to get to the Cath Lab for these patients. Primary PCI is probably not beneficial. That does not mean, however, that we should relax. These patients do benefit from coronary intervention so should be loaded with antiplatelets and brought to the attention of the interventional cardiologists. ST depression is frequently underestimated, which accounts for its relatively poor prognosis. Remember to take it seriously, repeat the ECG frequently to identify dynamic changes and, if ‘ruling in’ NSTEMI is really important, consider early serial troponins if it’s going to affect the clinical care of your patient.
Until next time!
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Case studies on St.Emlyn’s
We do present hypothetical cases on St.Emlyn’s. These are based on the experience of our team as educationally active emergency physicians. For centuries doctors and nurses have used stories to teach and learn from each other. However, we are careful not to break any patient confidentiality rules.
As a result if we present a case then it will always be fictional and not relating to any specific case or patient. For example if we present an (anonymised) X-ray or ECG we will create a clinical history that is compatible with the radiological/ECG findings but which does not relate to a specific time, location, patient or circumstance. Whilst it may be argued tha this detracts from the clinical learning we believe that patient confidentiality is more important in these matters.
We will create time, date, age, sex, details of the patient and their circumstances etc. Our cases are therefore an amalgam of different cases and experiences. Any resemblance to patients treated by us now, in the past or the future is entirely unintentional and accidental. Our cases are presented to help us all reflect and learn, in that way we might become better clinicians for our patients.
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