Wednesday, January 16, 2019

Inferolateral STEMI: is there right ventricular MI also?

A middle-aged patient called 911 for 1 hour of chest pain.

He was hemodynamically stable.

Here is the prehospital ECG:
Obvious inferior MI, but also with STE in V3-V6

Here is the first ED ECG:
Again, inferior and lateral STEMI.
Is there any right ventricular (RV) MI?

85% of inferior MI are due to RCA occlusion.  Even the majority of inferolateral MI are due to RCA occlusion. The RCA may have a large lateral branch.

RV MI is caused by RCA occlusion proximal to the RV marginal branch, especially when there are no collaterals from the LAD to the RV.

We showed that, if there is zero ST depression in lead V2, that lead V1 is 85% sensitive for RVMI.  When there is STD in V2, only 35% have any STE in V1.

In Inferior Myocardial Infarction, neither ST elevation in lead V1 nor ST depression in lead I are reliable findings for the diagnosis of right ventricular infarction.

We should have titled it: In Inferior Myocardial Infarction, for diagnosis of RV MI, ST elevation in lead V1 is only sensitive in the absence of ST depression in V2; lead I is not reliable.

We care about RV MI because it can cause RV failure, with shock and hypotension.

But only a minority of patients with RV MI have these adverse hemodynamics, and an even smaller number with proximal RCA occlusion have these hemodynamics because they may have blood supply from LAD collaterals.

Is it important to diagnose RV MI here?

Probably not so much.  He is hemodynamically stable.

Nevertheless, we took a look with a right sided ECG.  Here it is:
V1-V6 are really V1R (=V2) to V6R
There is STE in V3R to V6R.
This is diagnostic of RV MI.  This is one of the 15% of RVMI that have zero STD in V2 but no STE in V1.
Perhaps the absence of STE in V1 (=V2R) is a good prognostic sign?
Perhaps it means that the critical anterior wall of the RV is not ischemic, even if more right lateral portions are ischemic?  This is pure speculation.

The patient went to the cath lab and had a proximal RCA occlusion opened and stented.  He was never hypotensive.

Here is the post PCI ECG:

Acute Inferior ST elevation MI.
Culprit is 100% occlusion of the Proximal RCA .

LMCA: The LMCA has mild plaque.
LAD: No angiographic significant obstructive disease.
LCx: No angiographic significant obstructive disease.
RCA: RCA has Normal take off.  The Proximal segment of the RCA has 100% disease.
Lesion on Prox RCA:


The estimated left ventricular ejection fraction is 41 %.
Left ventricular hypertrophy concentric .
Regional wall motion abnormality-distal septum and apex.
Regional wall motion abnormality-distal inferior wall.
Regional wall motion abnormality-anterolateral.


Findings c/w ischemia/MI in vascular territory of LAD, proximal to a diagonal branch.
(However, concomitant MI/ischemia in distal PDA/watershed territory cannot be excluded)

Learning points:

1. Inferior STEMI is usually caused by RCA occlusion
2. RCA occlusion may be proximal to the RV marginal branch
3. Proximal occlusions may or may not result in ECG or hemodynamic evidence of RV MI
4. When there is no ST depression in lead V2 AND a proximal RCA occlusion, there is STE in V1 approximately 85% of the time.
5. STD in Lead I is not useful to diagnose RV MI except to differentiate RCA from circumflex occlusion.  (RVMI can only occur with RCA occlusion)
6. Diagnosis of RV MI is important in the presence of hemodynamic instability


  1. Is the presence of STE Lead III>II helpful in this case? Or do you find that it is sensitive enough for RV MI to make a presumptive diagnosis in the absence of a true R sided ECG?

    1. No. Lead III > lead II is the same as STD in lead I and only indicates RCA occlusion, not necessarily PROXIMAL RCA occlusion.

  2. Good case! Initially I would be thinking wraparound due to the anteriorlateral involvement aswell, yet culprit was proximal RCA. Why is there STE precordials, yet LAD was fine? And else would you consider this pt to be left dominant since there is no posterior involvement?

    1. The RCA often has large branches that wrap to the inferolateral wall (V5, V6). In this case it also affected V3, V4. Inferior MI is 85% RCA and 15% circ, and even when there is STE in V5 and V6, the infarct artery is more commonly the RCA.

    2. Is the STE in anterior leads omitting the STD(posterior recipricol changes)? Or is the posterior wall most likely being fed via the LCx?

    3. Circumflex probably supplies posterior wall here, so no posterior MI


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