I saw “Chest pain” on the board and clicked to look at the ECG. Here it is:
|Much ST elevation in V2 (approx 5.5 mm at the J-point), but the QRS voltage is massive.
There is “inferior” STE, but it comes after very high voltage R-waves
The ST segment is about 11% of the preceding S-wave.
In a paper by Armstrong et al., they would have you believe that a ratio of 25% is the best cutoff for diagnosing STEMI in LVH (1). I believe this study was deeply flawed but do not have a derived cutoff.
I have estimated that any ST/S ratio > 15% in the setting of high S-wave voltage in V1-V3 is suspicious for new anterior STEMI: 15% of a 30-mm S wave is 4.5 mm, whereas a 25% rule would require 7.5 mm of STE.
I suspected that this STE was all due to LVH plus tachycardia.
There is so much overlap of S-waves that it is hard to measure the voltage, but the S-wave in V2 appears to me to be approximately 50 mm.
Remember that tachycardia is unusual in STEMI
unless there is either:
1. a second (possibly pre-existing) disorder or 2. cardiogenic shock
I looked to see if there was a previous ECG for comparison.
|This shows that, previously, there was less ST elevation but also a smaller S-wave.
The T-waves are much smaller.
Notice the ST/S ratio is approx 1.5/30 = 5%.
Now I was worried that there might indeed actually be STEMI superimposed on LVH.
I looked into the chart: it turns out the patient had DKA and slight hyperkalemia at 5.8 mEq/L, and the BP was elevated at systolic of 200.
After resuscitation, another ECG was recorded:
|Heart rate is slightly slower, K was a bit lower.
The STE is resolved and the S-wave is no longer so large.
The recording parameters were the same, this was not due to a change in mm per mV.
If there had been LAD occlusion that then reperfused, the ST elevation on that first ECG should have been associated with a smaller S-wave, not a larger one.
This phenomenon is not in the literature, but I have noticed it:
When there is LVH with STE and large S-waves in V1-V3, LAD occlusion usually causes:
1. The S-wave to diminish (very similar to terminal QRS distortion) and
2. The ST segments to elevate.
Because the S-wave usually diminishes, the ECG will rarely persistently show the high voltage of LVH: unless there is a previous ECG showing LVH, you won’t even recognize LVH without looking at that previous ECG.
This is why it is very difficult to find ECGs with precordial LVH and LAD occlusion: the LVH disappears with the LAD occlusion!
For this reason I doubted LAD occlusion as the etiology of these findings.
[I have attempted twice to study STE in LAD occlusion in LVH, and found it impossible because such ECGs are so rare.]
Therefore, in Armstrong’s study of STEMI in LVH (1), the example ECGs they published do not illustrate the problem. I conclude that these authors must also have been unable to find ECGs with BOTH LAD occlusion and large precordial S-waves.
Here are their examples of anterior STEMI in the setting of LVH:
|These anterior STEMI are not diagnostically difficult, are they?
They are not made more difficult by LVH, are they?
Yet Armstrong’s conclusions would make you think that a 25% rule is important in diagnosing the STEMI.
The troponin I rose and peaked at only 0.049 ng/mL (URL = 0.030 ng/mL).
An echo showed a new anterior wall motion abnormality.
Angiogram showed an LAD stenosis without apparent plaque rupture or thrombus. FFR (Fractional flow reserve) showed that the lesion was hemodynamically significant.
So this was apparently a Type 2 STEMI, superimposed on LVH, due to tachycardia and hypertension, with possibly some contribution to the ECG of hyperkalemia.
Here is a great case of proven anterior STEMI in the setting of LVH, with an extensive discussion of STEMI in LVH: