the case.
a 32 year old male presents to ED with a 4 hour history of retrosternal chest pain. He has had the pain since midnight and it “just isn’t going away”.
This is his ECG…
- Rate.
- ~ 48-60 (variable)
- Rhythm
- Irregular.
- P:QRS = 1:1
- Axis.
- Normal. [+ 6*]
- Intervals.
- PR ~ 140msec
- QRS normal.
- QTc ~ 381msec
- Segments.
- ST elevation: 1mm in lead III, 1/2mm II & aVF
- associated T-wave invesion
- ST depression: 1/2mm in leads I & aVL, plus subtly in V5-6.
- ST elevation: 1mm in lead III, 1/2mm II & aVF
- Others.
- Inferior Q-waves
Interpretation – Sinus arrhythmia with evidence of inferior ischaemia (old = Q-waves, new = ST elevations) and reciprocal changes in high-lateral leads.
He tells you, “It feels just like my heart attack I had in April !!”
Here is his ECG upon discharge following an inferior STEMI and subsequent placement of a RCA bare-metal stent…
It also turns out he has since stopped all his medications (including antiplatelet agents)…
The patient receives aspirin and clopidogrel loading followed by a dose of IV morphine. At this point his pain settles, but I keep printing ECGs…
- The cardiology team review the ECGs (via MMS) and agree to take him to the Cath-Lab.
- HS-Troponin returns at 278 ng/L (normal <5).
- At angiography.
- Instent thrombosis with distal RCA occlusion.
- Aspiration thrombectomy results in successful reperfusion.
- Repeat HS-Troponin = 1466 ng/L.
Inferior Myocardial Infarction – can we predict the culprit lesion ?
The occluded vessel may be either the right coronary artery (~80%) or the left circumflex artery. How can we tell the difference?
Right Coronary Artery.
- ST elevation III > II
- ST depression >1mm in leads I & aVL.
- Proximal disease is suggested by the addition of;
- isoelectric or elevated ST segment in V1
- significant ST depression in I & aVL (summation of STD > 5.5mm)
The STE in lead III is greater than that of II due to the ST-vector being directed toward the right.
Left Circumflex Artery.
- ST elevation in II & III. (Typically, II > III).
- Isoelectric or STE in lead aVL.
The STE in lead II is greater than that of III due to the ST-vector now being directed toward the left.
How about V1 & V2 ??
- ST depression in these leads (with inferior ST elevation) suggests involvement of the posterior wall of the left ventricle.
- This can happen in both a left circumflex lesion and a proximal right coronary lesion.
** Adapted from N Engl J Med 2003;348:933-40. **
Is this clinically relevant ??
Perhaps not !!
One study that I briefly reviewed suggested proximal RCA lesions did no better or no worse than those with distal RCA disease.
References.
- Chan TC, Brady WJ, Harrigan RA, Ornato JP, Rosen P. ECG in Emergency Medicine and Acute Care. Elsevier Mosby 2005.
- Zimetbaum, PJ & Josephson, ME. Use of the Electrocardiogram in Acute Myocardial Infarction. N Engl J Med 2003;348:933-40.
- Fiol, M et al. New criteria based on ST changes in 12-lead surface ECG to detect proximal versus distal right coronary artery occlusion in a case of acute inferoposterior myocardial infarction. Ann Noninvasive Electrocardiol. 2004 Oct;9(4):383-8.
- Kaushik, M et al. Comparison of outcomes of patients presenting with inferior STEMI with proximal and distal right coronary artery obstruction. J Am Coll Cardiol. 2013;61(10):E89.
Dr Smith discusses a similar scenario over at his blog. It is certainly worth a read….
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