Here we go with another Cardiology Case at St. Emlyn’s. If you haven’t already, check out the other cases in this series:
Cardiology case 02: ST depression, no rush?
Cardiology case 03: Are you missing the STEMI?
Here is case 04:
A 50 year old man presents to the ED with ongoing central chest pain, which started 4 hours ago. He described it as dull in nature and the pain did not radiate. He felt short of breath, sweaty and nauseous with the pain. There was no objective evidence of dyspnoea but the patient looked clammy. There was no previous history and no risk factors for coronary heart disease except tobacco smoking.
Physical examination and baseline observations were unremarkable.
The initial ECG
So here is the ECG, recorded immediately on presentation to the ED:
Interpreting this ECG
There is ST depression in leads I, aVL, V5 and V6, which is really suspicious for ischaemia. For a start this means it’s an ECG we’re worried about. This is a high risk patient.
But is this a STEMI?
It definitely doesn’t fit any of the usual STEMI patterns. Looking at V1 we see unusually marked ST elevation, measuring at least 2mm. In V2 there’s approximately 1mm of concave upwards ST elevation. In aVR there’s also ST elevation, which does have a suspicious morphology for STEMI, although it measures just under 1mm.
Take a closer look:
There are no previous ECGs to compare to.
What should we do with this patient?
This patient has a history that’s certainly suspicious for an acute coronary syndrome. He has ongoing pain and his ECG shows highly suspicious ST elevation, although not in a distribution that we recognise.
Because it doesn’t fit the usual patterns, should we ignore it? Should we observe it with serial ECGs, echo, troponins? Or should we trust our judgement in interpreting ST segments as ST segments (regardless of the precise pattern) and activate the cath lab?
In practice the Cath Lab was activated. The patterns were sufficient for us to be reasonably confident that this was an atypical STEMI. The patient went directly to the Cath Lab from the ED and the duty interventional cardiologist proceeded to immediate angiography.
What was the outcome in this case?
At angiography the patient was found to have an occlusion to an anomalous large septal branch of the right coronary artery (see arrow).
The patient underwent successful revascularisation (below).
The troponin on arrival was 75ng/L (99th percentile 14ng/L), although that result hadn’t been available at the time of Cath Lab activation. It subsequently peaked at 550ng/L. The patient had an uneventful recovery from this STEMI
Learning points from this case
You might see this as a challenging ECG because the ST elevation was in a distribution that you don’t recognise as representing STEMI. For sure, in clinical practice this is an ECG that really caused people to stop and think. However, the right decision was made based on a few key factors:
- The patient history was convincing (symptoms that prompted suspicion of an acute coronary syndrome in association with ongoing pain and ‘looking the part’ for STEMIÂ – including objective diaphoresis)
- Forgetting its distribution, the pattern (or shape) of ST elevation in individual leads (particularly V1) and its magnitude in relation to the size of the QRS complex looked highly suspicious
- There was no obvious alternative cause for these symptoms
Putting that all together, the treating clinicians had reasonable confidence in the diagnosis of STEMI even though the ECG was unusual. They made the decision to activate the Cath Lab early with the agreement of the interventional cardiologist, which proved to be a good call.
There is some relevant evidence to this case. In 1998 Ben Gal et al noted that patients with their first anterior STEMI were more likely to have ST elevation in V1 if the RCA had a small conal branch that didn’t reach the intraventricular septum. That makes perfect sense as, in this case, we have that situation in reverse. Acute occlusion of a large septal branch of the RCA (in this case an anomalous coronary anatomy) leads to ST elevation predominantly in V1.
If, like me, you’d welcome the opportunity to revise the anatomy of the coronary arteries, their territories and common anomalies, there’s an excellent article on coronary artery anomalies at Medscape – check it out.
Rick
At St. Emlyn’s we know how important it is for clinicians to learn from cases. However, we also know how important it is that we are strict about patient confidentiality and we adhere to GMC guidance. When we present cases they do not necessarily relate to a single case but are based on our general experiences. All of the information presented is of course devoid of anything potentially identifiable, and we take a number of specific measures to ensure that no patients are identifiable, which may include creating entirely fictional cases to illustrate certain educational points. Check out our disclaimer for more info.
If you liked this post, you may also like these posts:
The MACS rule: Immediate rule in and rule out for suspected cardiac chest pain
Why hypertroponinaemia does not always equal acute myocardial infarction
Cullen on high sensitivity troponin
Deciding who to investigate for ACS: The problem of coronary bridge
Nice case! I see a lot of folks over-calling “old septal MI,” but acute septal MI doesn’t get much play (because it’s pretty unusual). Earlier this year I shared a case of my own except the culprit was the 1st septal off the LAD instead of the RCA: https://plus.google.com/u/0/+VinceDiGiulio/posts/V8M2GfUn3iz
Thanks a lot Vince. Thanks for linking to that case – it’s another great ECG to learn from!
Rick
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