catching the culprit…

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…

[DDET Describe & interpret this 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.
• 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.

[/DDET]

[DDET This has happened before !!!]

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)…

[/DDET]

[DDET Forward progress…]

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…

      
** These are taken approximately 10mins apart **

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[DDET The outcome.]

• 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.

[/DDET]

[DDET What can we learn from this case ??]

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.

1. Chan TC, Brady WJ, Harrigan RA, Ornato JP, Rosen P. ECG in Emergency Medicine and Acute Care. Elsevier Mosby 2005.
2. Zimetbaum, PJ & Josephson, ME. Use of the Electrocardiogram in Acute Myocardial Infarction. N Engl J Med 2003;348:933-40.
3. 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.
4. 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.

[/DDET]

[DDET Click here for more on these ‘borderline’ infarcts…]

Dr Smith discusses a similar scenario over at his blog. It is certainly worth a read….

Dynamic inferior MI: STEMI or Non-STEMI? Does it matter?

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