Coolest ECG paper this month
August 31, 2016
Short Attention Span Summary
Coolest paper this month!
With posterior MI, once the affected area of myocardium is reperfused, the T-waves in V2 get bigger – statistically significantly bigger than in non-posterior MI. Why? Think of it like Wellen’s warning on the back of the heart. Compared with the baseline ECG, the T-waves increased in size in leads V2 and V3 after reperfusion from posterior MI. Want to see examples and get details on why? Go to Dr. Smith’s ECG blog. I wish we were related so I would have hereditary ECG prowess.
Will I see reperfusion in the ED?
Yes, you may. Imagine a patient with stuttering chest pain who presents asymptomatic. But the ECG now shows bigger T-waves in V2 and V3 compared to a prior ECG. This may represent reperfused posterior MI. The artery is going to close again…right after you discharge them. Don’t get caught.
A pic is worth 1000 words. See some examples.
Abstract
Emerg Med J. 2016 Jul 29. pii: emermed-2016-205852. doi: 10.1136/emermed-2016-205852. [Epub ahead of print]
Posterior reperfusion T-waves: Wellens’ syndrome of the posterior wall.
Driver BE1, Shroff GR2, Smith SW1.
Author information:
1Department of Emergency Medicine, Hennepin County Medical Center, Minneapolis, Minnesota, USA.
2Division of Cardiology, Department of Medicine, Hennepin County Medical Center, Minneapolis, Minnesota, USA.
Abstract
BACKGROUND:
Reperfusion after coronary occlusion (myocardial infarction, MI), as in Wellens’ syndrome, is often represented on ECG as T-wave inversion in the leads overlying the affected myocardial wall(s). As an extension of this logic, reperfusion of the posterior wall should manifest on right precordial leads (which are opposite the posterior wall) as enlarged T-waves.
OBJECTIVE:
We sought to determine whether T-wave amplitude (TWa) in leads V2 and V3 after reperfusion in posterior MI (PMI) is greater than in patients without PMI.
METHODS:
Review of ECGs from patients with ST elevation MI of the left circumflex or right coronary artery with post-procedure thrombolysis in MI (TIMI) flow >0 between 2007 and 2009. Blinded experts reviewed admission ECGs to determine the presence of PMI and measure TWa before and after reperfusion. Maximum TWa in V2 and V3 and the difference between maximum and admission V2 and V3 TWa were compared between those with and without PMI.
RESULTS:
Of 72 patients, 48 had PMI. Values expressed are medians and IQRs. Maximum TWa after reperfusion was greater in PMI than in non-PMI in V2 (5.00 mm (3.5 to 8.25) vs 3.9 mm (2.75 to 5.5), p=0.04), but not in V3 (4.0 mm (2 to 5.5) vs 3.0 mm (1.75 to 4), p=0.09). The increase in TWa in V2 and V3 after reperfusion was greater in PMI compared with non-PMI: (V2, 3.4 mm (2 to 5.25) vs 1.25 mm (-0.25 to 2), p=0.0005; V3, 2 mm (-0.5 to 3.25) vs 0.25 mm (-1 to 1.75), p=0.03).
CONCLUSIONS:
Reperfusion of the posterior wall results in higher right precordial TWa, and an even greater increase in TWa, as measured in leads V2 and V3. This observation has important implications for emergency physicians to accurately identify recent posterior infarction in patients who may be symptom free on presentation but at risk of reocclusion.
Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://www.bmj.com/company/products-services/rights-and-licensing/
PMID: 27473406 [PubMed – as supplied by publisher]