I saw "Chest pain" on the board and clicked to look at the ECG. Here it is:
I looked to see if there was a previous ECG for comparison.
There was:
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.
Why?
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:
Case continued:
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:
 |
| Much ST elevation in V2 (approx 5.5 mm at the J-point), but the QRS voltage is massive. There is "inferior" STD, 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.
There was:
 |
| 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.
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. |
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.
Why?
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. |
Case continued:
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:
LVH with anterior ST Elevation. When is it anterior STEMI?
Reference
1. Armstrong EJ et al. Electrocardiographic criteria for ST-elevation myocardial infarction in patients with left ventricular hypertrophy. American Journal of Cardiology 110(7):977-983; October 2012.
Great challenging case. One suggestion is to do isolated V2 chest lead ECG (remove the other chest leads) to see the voltage clearly.
ReplyDeleteAlso, i would resolve to the echo findings if there is an ECG anomaly/confounder that reduces the specificity and sensitivity of the ECG.
A therapeutic intervention of lowering the BP and heart rate with Nitrates + beta blocker might bee helpful in LV strain cases.
There are a number of things that I LOVE about this case: i) It is impossible to be certain from the initial tracing alone ( = ECG #1) — IF the dramatically tall and peaked T waves in leads V1 and V2 are appropriate OR excessive, given the degree of anterior S wave amplitude increase in the setting of the tachycardia seen here. ii) This is a great tracing for emphasizing both the principle of “relativity” (regarding wave deflection in a given lead) — AND for illustrating how to estimate R and S wave amplitude when there is difficult-to-discern R & S wave overlap. You have to look VERY close to do this — which reveals the S in V1 to be >45mm, and >55mm in V2. (It clearly would have been easier if this tracing had been repeated at 1/2 standardization … — though careful scrutiny in our counting obviates the need for this). iii) Given anterior S waves as deep as any that you’ll ever see — AND, given the asymmetric shape of the T waves in leads V1 and V2 (in context with the limb inferior lead appearance that suggests LVH more than ischemia) — one should suspect (as Dr. Smith did), that despite their worrisome appearance, these anterior T waves might very well NOT reflect an acute STEMI (or, as per Dr. Smith’s last blog post — this might not reflect an “OMI” = occlusive myocardial infarction …). iv) Clinical correlation is ESSENTIAL to clinical ECG interpretation. Finding a prior tracing (for comparison), and learning that this patient was in DKA with hyperkalemia are KEYs to understanding this case. v) Sometimes you just won’t know the true meaning ( = exact interpretation) of the initial ECG at the time you need to begin treatment. Nevertheless, “Treating the Primary Problem” (which in this case was a critically ill patient with DKA) takes precedence — and will often, with follow-up tracings, provide a plausible explanation that in retrospect elucidates all that we initially saw. vi) The astute “detective-like problem-solving approach” that is impeccably illustrated here by Dr. Smith, is the way one truly attains MASTERY of ECG interpretation. It takes more than just reading numerous ECGs over a period of many years. One has to “LIVE the cases” with meticulous clinical correlation EACH-step-of-the-way — if one realistically aspires to attain true clinical expertise. THANK YOU to Dr. Smith!
ReplyDeleteThanks, Ken!
DeleteDr. Smith: what do u mean by “inferior” STE? STE at inferior leads? Or u meant STD?
ReplyDeleteDr Ken Grauer: what features in the inferior leads suggests LVH?
Ken,
DeleteThanks for catching my mistake! Fixed.
I'll answer for Ken: high R-wave voltage with "hockey stick" STD and T-wave inversion.
Steve
Agree with Steve re use of inferior leads to diagnose LVH on ECG. The voltage criterion that I use is R wave ≥20 mm in any one of the inferior leads. On occasion (especially in patients with a relatively vertical axis (ie, anything >70-80 degrees in the frontal plane) — this inferior lead voltage criterion may be the only one you see that satisfies LVH criteria.
Delete