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I figured there were essentially three options for this patient (with a few minor variations possible) given that it was midnight and the “cardiology” registrar was a covering respiratory registrar:

1) Activate cath lab
2) Treat like a non-STEMI and consider a cath in the morning
3) Get an Echo looking for regional wall motion abnormalities and use that to guide decision re. primary cath urgently or not

Frankly, I think these are all reasonable options, with only logistical differences. He is a young man, and with his story is going to score a cath at some point anyway – only the timing of it remains to be decided. I thought he had myopericarditis, but that his more severe pain from two days prior sounded suspicious for ischaemic pain, so I wasn’t prepared to ignore that. I toyed with the idea of a late night Echo-tech call-in, but elected to treat him as a non-STEMI-plus, in that he got aspirin, clopidogrel, heparin and in consultation with the very sleepy on-call interventional cardiologist (who I think liked my plan because he got to stay in bed, rather than beacuse of innate superiority to other approaches), a tirofiban infusion. An Echo was organised for the morning and he went to CCU.

Echo report (paraphrased summary):

• Mildly impaired LV function with two regional wall motion defects (inferoposterior basal and mid segment hypokinesis) with an EF of 50%.
• There was a tiny posterior effusion.
• Valves and other chambers NAD other than mild TR.

He not suprisingly went for a cath that morning too:

• LAD: 70% stenosis, diffuse disease
• LCx: 100% stenosis
• Proximal 1st obtuse marginal: 70% stenosis
• RCA: 60-70% stenosis
• Conclusion – triple vessel disease, culprit lesion in LCx, akinetic inferior wall

The serial troponins went from 16 to 9 to 6 over the next 24 hours. The patient was discharged and referred for a CABG. The discharge summary prepared by the cardiology resident didn’t mention myopericarditis, but in discussion with the cardiologist himself, it was clear that his opinion was that the patient indeed had myopericarditis secondary to his infarct, which almost certainly occured 2 days prior and correlated with his more severe and typical sounding episode of pain.

This ECG from just before his cath and Echo is much more consistent with myopericarditis, with widespread saddle-morphology ST elevation, PR depression, and PR elevation in aVR:

So there you have it – a late-presenting MI (perhaps STEMI?) AND myopericarditis. This syndrome of early post-MI pericarditis may be rarer in the post-thrombolysis/PCI era, and is also known as PIP or PAMISP. It’s a bit too early for the autoimmune mediated Dressler’s syndrome (which is definitely rare in the post-interventional era), as suggested by some commenters, which tends to kick in from around 2 weeks post-MI. From emedicine on the topic:

“The incidence of early pericarditis after MI is approximately 10%, and this complication usually develops within 24-96. Pericarditis is caused by inflammation of pericardial tissue overlying infarcted myocardium. The clinical presentation may include severe chest pain, usually pleuritic, and pericardial friction rub.

The key ECG change is diffuse ST-segment elevation in all or nearly all of leads. Echocardiography may reveal a small pericardial effusion. The mainstay of therapy usually includes aspirin and nonsteroidal anti-inflammatory drugs (NSAIDs). Colchicine may be beneficial in patients with recurrent pericarditis.”

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Reblogged from the underneaths of EM:

This 53 year old man is an ex-smoker, with HTN well controlled by a single agent. He presented to the ED under duress from his wife and GP with intermittent atypical pain which is sometimes worse with exertion, has a slight pleuritic variation, and radiates to shoulders. He mentions a more severe pain 2 days ago lasting a couple of hours with onset at rest.

Read more… 27 more words

The full analytic and the transcript of the Twitter conversation can be accessed at the symplur website here, and customised as required.

What are your thoughts?