This is the discussion for 57 year old female CC: Shortness of breath and chest pressure.
Let's take another look at the 12-lead ECGs.
I posed the following questions for this case:
- What do you think of these 12-lead ECGs?
- What is the most likely cause of the ST-depression and T-wave inversion.
A strain pattern often presents with significant ST-elevation in the right precordial leads (V1 – V3) which is the main reason that it can mimic acute anterior STEMI. Often the ST-elevation can be quite dramatic.
Also consider this ECG from the 12 Lead EKG blog (with permission).
Here the ST-elevation in the right precordial leads (V1-V3) is impressive. However, the S-waves are very deep! This is the big tip-off that we're dealing with a STEMI mimic.
In this case the patient was cathed because he experienced a VF arrest while on the treadmill at cardiac rehab. You can't blame anyone for sending a patient like that to the cardiac cath lab!
What they found was extensive coronary artery disease and chronically occluded vein grafts but no acute thrombosis in the LAD.
Interestingly, Stephen Smith, M.D. from Dr. Smith's ECG Blog has stated that he has only seen one or two LAD occlusions in his entire career that met the conventional LVH criteria in the right precordial leads! Why should this be?
He theorizes that perhaps acute STEMI attenuates the S-wave voltage in the right precordial leads in the setting of pre-existing LVH.
Consider this ECG from the previous case of the 55 year old male with (possible) chest pain.
In this case the patient was cathed and ended up having a 100% chronic occlusion of the LAD. However, the T-waves do appear to be hyperacute in this ECG and there was a modest rise and fall of cardiac biomarkers.
We were unable to obtain an "old" ECG for comparison, but based on the appearance of lead V1 it certainly looks as if this ECG met the LVH criteria in the precordial leads prior to the development of pathological Q-waves in leads V2 and V3.
A "strain pattern" (evidenced by ST-depression and T-wave inversion) is still present in the high lateral leads (I and aVL).
Now let's get back to the case of the 57 year old female with shortness of breath and chest pressure.
Does it meet the voltage criteria for left ventricular hypertrophy?
The S-wave depth measures 23 mm in lead V1 and 29 mm in lead V2! The R-wave amplitude measures 12 mm in lead V5 and 13 mm in lead V6. So, if we add the S-wave depth in lead V2 and the R-wave height in lead V6 we get 44 mm (cut-off is 35 mm) so this meets the most commonly used voltage criteria for LVH.
Here's how I'm measuring the S-waves (see comments).
Here's a close-up of the right precordials from another ECG that was submitted with the case study that I didn't publish earlier due to poor data quality in the limb leads. Here you can see the separation a little bit better.
Based on this I would expect a significant ST/T wave abnormality in the opposite direction! To me the most striking thing about this case is the absence of significant ST-elevation in leads V1 and V2.
Having said that, the ST-depression and T-wave inversion in leads with an upright QRS complex are almost certainly due to left ventricular hypertrophy.