Septal STEMI with ST elevation in V1 and V4R, and reciprocal ST depression in V5, V6

This was sent to me by a reader named Aaron.

A 36 yo male smoker presented to the ED with chest pain.  It had started the night before as "indigestion" and had progressed to 8/10 substernal chest pressure radiating to the right shoulder/jaw associated with diaphoresis, nausea, and SOB.

Here is a 15 lead ECG:

Sinus rhythm.  There is ST elevation in V1 (of 3.0 mm at the J-point), V2, aVR (1 mm, no matter how it's measured), and V4R (1.5 mm at J-point, 2.5 at 60 ms after the J-point), and very subtly in lead III.  There is reciprocal ST depression in I, II, aVL and V4-V6, as well as some very subtle STD in posterior leads V8 and V9 (which also have very low QRS voltage)

Here is his initial ECG, which the tech recorded as a 15-lead ECG (the doctors were not sure why).


Thus, there is a rightward, anterior, and slightly superior ST axis.

Here is a map of leads V1, V2, and V4R.  This is traced off a an actual MRI.

I did not label V8 and V9, but they would be on your left behind the lung.  You can see how V1, V2, aVR, and V4R would have ST elevation in either a right ventricular STEMI or with a septal STEMI, and how lateral leads, and even posterior leads, would have reciprocal ST depression.

The combination of precordial ST elevation and ST depression, simultaneously, should alert you to LAD occlusion.  This is frequently seen when there is LV septal involvement.  STE in V4R is confirmatory evidence.   In my early repolarization/anterior STEMI study, I excluded any ECG with any precordial ST depression, considering this to be diagnostic of STEMI because normal variant precordial ST elevation does not coexist with simultaneous precordial ST depression.

We now call this "Swirl
  
In this case, the emergency physicians were somewhat puzzled, and the interventionalist was highly skeptical, but took the patient to the cath lab and found an occluded LAD.   It is possible that there was also RV involvement - see explanation below.     


Here is another similar case.


In a 1999 study by Engelen et al. of patients with anterior STEMI, ST elevation of greater than or equal to 3.0 mm in lead V1 was 100% specific (but only 12% sensitive) for septal STEMI.  Smaller degrees of STE in V1 were not nearly as specific.  See more on STE in aVR in anterior STEMI, below.


STE in V4R
Interestingly, here is a paper (published as a letter) describing the results of recordings of V4R in 117 consecutive LAD occlusions and showed that this was associated with septal involvement and also higher risk.

In this study, 39 (33%) had STE of at least 1 mm (at 80 ms after the J-point) in V4R.There were no significant differences between the groups regarding indexes of infarct size.  None of the patients with STE in lead V₄R had echocardiographic evidence of right ventricular dysfunction or dilated right ventricles.  Only the middle anteroseptal segmental wall motion abnormality was significantly and independently associated with STE in lead V₄R. The odds ratio for akinesis (or more severe motion abnormality) was 6.1 (p = 0.036) and for hypokinesis (or more severe motion abnormality) was 12.0 (p = 0.033).  Patients with STE in V4R were more likely to experience the combined end point of primary VF, acute HF, or death (54% vs. 18%) and were also more likely to experience primary VF (21% vs. 2.5%)  and acute HF (39% vs. 17%). In multivariate analysis, STE in lead V₄R on admission electrocardiography remained a strong independent variable associated with acute HF and the combined end point of primary VF, acute HF, or death during hospitalization. 

What does ST depression in V5 and V6 signify? 
This paper addresses this for inferior STEMI, but is relevant here also, I think because it shows how V5, and V6 are reciprocal to V4R, and ST elevation on one side will lead to ST depression on the other:
http://www.cinc.org/Proceedings/2005/pdf/0651.pdf.   In this study of RV MI associated with inferior STEMI, ST depression in V5, V6 had 46% sensitivity and 96% specificity for proximal RCA occlusion.  Sensitivity increased to 58% with a small drop in specificity if STE in V4R was added.   Why are V4R and V5, V6 so insensitive for proximal RCA occlusion?  Would this not always cause RV infarction?  In fact, no.  This is because, in many patients, the RV is supplied by both the LAD and the RCA.  Therefore, the RV is often protected from RCA occlusion by the LAD.  Conversely, LAD occlusion could possibly lead to RV infarct if it is not adequately supplied by the RCA.  Autopsy studies in the '80s by HR Andersen showed this: JACC 1987l10:1223-32 and Br Heart J 1989;61:514-20.  This study used MRI to show the LAD supply to the RV.


How about STE in aVR?
Below is from a quote from part of a piece on aVR which I wrote for Current Emergency and Hospital Medical Reports: "Updates on the electrocardiogram in Acute Coronary Syndromes." DOI 10.1007/s40138-012-0003-1, published online Dec. 23, 2012.

STE in aVR in STEMI 
Not NonSTEMI: STE in aVR during left main ACS is usually NonSTEMI (no occlusion). 

"Approximately 10% of patients with anterior STEMI have STE of at least 1 mm in aVR (as measured at 60 ms after the J-point),(Wong, 2012) and 25% have at least 0.5 mm STE in aVR (as measured at 60 ms after the J-point, relative to the TP segment).(Aygul, 2008)  STE or STD of 1 mm or more in anterior STEMI portended a worse prognosis (compared to no STE or STD), even after correcting for STE or STD elsewhere on the ECG, but only ST depression in aVR (“reciprocal to injury in the area of lead V7”) remains significant when corrected for all other ECG and clinical factors.(Wong, 2012)  STE in aVR of at least 0.5 mm in anterior STEMI predicts septal AMI (occlusion of the LAD proximal to the first septal perforator) with a PPV and NPV of 70% and 80%(Aygul, 2008) better than STE in V1, which at a cutoff of greater than or equal to 2.5 mm had 12% sensitivity and 100% specificity, with PPV and NPV of 100% and 39%.(Engelen, 1999)   Kotoku et al. (2009) similarly found that STE in aVR correlated with proximal (vs. distal) LAD occlusion and was negatively correlated with a long (vs. short), or wraparound, LAD that affected the inferior wall.  This is intuitive, as a proximal occlusion would lead to basal wall STEMI (see below), and distal occlusion of a wraparound (long, “type III”) LAD would lead to inferior STE which would reciprocally attenuate the STE in aVR, or lead to STD in aVR.  To be complete, Wong also found that STE in aVR in inferior STEMI conferred worse outcomes.(Wong, 2012)"

1.            Wong CK, Gao W, Stewart RA, French JK, Aylward PE, White HD. The prognostic meaning of the full spectrum of aVR ST-segment changes in acute myocardial infarction. Eur Heart J 2012;33(3):384-92.

2.            Aygul N, Ozdemir K, Tokac M, et al. Value of lead aVR in predicting acute occlusion of proximal left anterior descending coronary artery and in-hospital outcome in ST-elevation myocardial infarction: an electrocardiographic predictor of poor prognosis. J Electrocardiol 2008;41(4):335-41.

3.            Engelen DJ, Gorgels AP, Cheriex EC, et al. Value of the electrocardiogram in localizing the occlusion site in the left anterior descending coronary artery in acute myocardial infarction. J Am Coll Cardiol 1999;34(2):389-95.

4.            Kotoku M, Tamura A, Abe Y, Kadota J. Determinants of ST-segment level in lead aVR in anterior wall acute myocardial infarction with ST-segment elevation. J Electrocardiol 2009;42(2):112-7.