It’s been a while since we shared a cardiology case but here’s a cracker for you. As usual, see our Caveats and Cautions. While these cases are based on our genuine experiences (often pooling several experiences), we always alter details to protect the confidentiality of patients.
A 65 year old woman arrives in the Emergency Department by ambulance. She had experienced one hour of central, crushing chest pain radiating to both shoulders and vomited once. The pain had eased spontaneously in the ambulance and she is now pain free. There is no past history but the lady does smoke 20 cigarettes per day and has a family history of premature coronary artery disease.
By the time you see her in the Emergency Department, she looks very well and is pain free. Here’s the ECG.
What will you do now?
This lady has a typical history for an acute coronary syndrome – it couldn’t be much more classical. If you’ve read my post on ‘getting your chest pain evaluation right‘, you’ll notice that typical symptoms don’t seem to help predict which patients really have ACS. This is because so many patients have atypical symptoms. But you’d ignore this history at your peril. There are some factors that increase the probability of ACS: pain radiating to both shoulders and vomiting once, for example. Although overall risk factor burden doesn’t really help us in the ED, the lady does smoke. We’ve previously found tobacco smoking to be a fairly strong predictor of ACS – so we’re probably feeling pretty suspicious that the diagnosis is ACS based on this presentation.
Having had a good look at this ECG, you’ve probably not noticed too much that worries you. We could feel a little bit suspicious about the shape of some of the ST segments (particularly V5), where the ST segment looks subtly saggier than you might expect – but there’s really nothing diagnostic here.
Of course, we want serial troponins for this lady. The first troponin is 30ng/L using the high sensitivity troponin T assay. The normal range is 2 to 14ng/L – so this is an elevated level. It’s only marginally raised. If we had been using the previous troponin T assay (which isn’t high sensitivity) then this is still likely to have been undetectable. We therefore would have thought the troponin is normal.
However, there’s no reason to believe that this lady should have an elevated troponin at baseline. She has normal renal function, no major comorbidities and she’s otherwise well at the moment. This does therefore appear to be an NSTEMI. We’ll know more when we get the second troponin concentration.
So what’s the catch?
So far, so obvious, right? This is the sort of case we see every day. We treat these patients without even thinking about it. The lady needs admission, she needs to see a cardiologist, she needs angiography, she should get aspirin, ticagrelor/prasugrel, some fondaparinux at some stage, coronary intervention, secondary prevention and so on. But there’s no massive urgency as the lady’s pain free, has a normal ECG, etc. Right?
What other information might we have missed?
The lady arrived by ambulance. The paramedics/EMS tend to record 12-lead ECGs. Have you made sure that you’ve reviewed the 12-lead from the EMS? No. Well, let’s do that…
So the plot thickens, right? This has just changed everything. The ambulance ECG is totally different to the ECG recorded on arrival in the ED. We can see ST elevation in aVR and v1, peaked T waves in V3 together with widespread, deep ST depression in V4-6, I, II, III and aVF.
On seeing this ECG, especially when you know how dynamic the changes are over time, you can be virtually certain of the diagnosis. The patient has a lesion in the proximal LAD or even the LMCA. It’s a classic ECG for that.
The patient did go to the Cath Lab. The lesion was to the proximal LAD – a critical stenosis, close to total occlusion. This was stented and the patient recovered well. The troponin peaked at 900ng/L.
What’s the lesson?
Always remember to look at the ambulance ECG. It can often be our best insight into what was happening when the patient was in pain and most likely to have an ischaemic myocardium. Failing to look at this ambulance ECG would mean that a critical, proximal lesion would go unnoticed. The patient could wait 72 hours before revascularisation – but most interventional cardiologists would appreciate that with dynamic changes like this, early angiography is really a priority.
If you haven’t already, remember to check out our other Cardiology Cases:
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