This 55 year old woman presented with chest pain:
No, it is not acute MI. Notice that there is a prominent S-wave in lead I (right axis deviation) and a large R-wave in V1. This is diagnostic of right ventricular hypertrophy, which is an abnormality of depolarization (abnormal QRS) that results in secondary abnormal repolarziation (ST-T wave). These negative T-waves and abnormal ST segments are entirely due to RV hypertrophy.
The physician recognized the abnormal QRS and the appropriate ST-T changes and did not activate the cath lab or initiate anti-ischemic or antiplatelet therapy other than aspirin.
The patient ruled out for MI. Echocardiogram showed RV hypertrophy and pulmonary hyptertension.
EMS 12-lead has a great discussion of pulmonary pressures and ECG patterns, and they show another example of this.
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| There is sinus rhythm. There is ST depression and there are negative T-waves in V1-V4. There is also STE in aVL, with reciprocal ST depression in II, III, and aVF. Looks like acute posterolateral MI, no? See below. |
No, it is not acute MI. Notice that there is a prominent S-wave in lead I (right axis deviation) and a large R-wave in V1. This is diagnostic of right ventricular hypertrophy, which is an abnormality of depolarization (abnormal QRS) that results in secondary abnormal repolarziation (ST-T wave). These negative T-waves and abnormal ST segments are entirely due to RV hypertrophy.
The physician recognized the abnormal QRS and the appropriate ST-T changes and did not activate the cath lab or initiate anti-ischemic or antiplatelet therapy other than aspirin.
The patient ruled out for MI. Echocardiogram showed RV hypertrophy and pulmonary hyptertension.
EMS 12-lead has a great discussion of pulmonary pressures and ECG patterns, and they show another example of this.
This tracing brings to mind ECG #15 from this paper http://jaha.ahajournals.org/content/2/5/e000268.full.pdf+html, one of the few I got wrong.
ReplyDeleteWhat would be the give-away in that case that there was a culprit lesion? The upright terminal T-waves in the precordials? In spite of the CHB I called with RVH w/ no culprit and got it wrong. Thanks!
Yes. And also the hyperacute T waves in inferior leads.
DeleteThat's a great paper Vince !! Thanks ...
DeleteVery interesting case! The patient ruled out for MI (I assume by labs). How did the physician rule out ischaemia? At the end, what was the cause of chest pain? How was it treated? I think the patient would benefit from coronarography (maybe an elective one), especially if the chest pain was typical. I would appreciate your opinion about this!
ReplyDeleteShe did not get angiography, but had completely stable ECG, exactly the same, over 3 days. No evolution means no Acute MI.
Deletethanks!
Steve Smith
can we be worried about the tall Rwave in V1 V2 being suggestive of posterior ? or is it impossible because of the t wave inversion ( which means tall t wave in posterior leads ) ?
ReplyDeletethanks
It is probably possible for a posterolateral MI to look like this, but the key finding is the deep S-wave (right axis) in I, and the R-wave in V1 is so much larger than the S-wave that I don't think you would find posterior infarction that looks like this.
DeleteThought this looked 'wrong' for posterior changes but haven't seen any RVH ECGs with this pattern before (lots with T wave inversion alone). Is it the amplitude or the width of R waves that rule them out as posterior Q waves?
ReplyDeletecombination of the excessive R/S ratio in lead V1 and the prominent S-wave in lead I. Did you see the one at EMS 12-lead which I linked to?
ReplyDeleteYes saw the EMS one, very similar pattern but even more convincing with significant RAD. Pattern is now logged in the memory banks. Thanks again.
DeleteHi Dr. Smith,
ReplyDeleteShould this patient also be ruled out for PE based on this EKG?
Alex
There may be reasons you would evaluate this patient for PE, but the EKG would not be one of them. The tall R-wave in V1, along with the S-wave in I, is specific for chronic RV hypertrophy and is not seen in acute heart strain.
DeleteHere is a primer on the ECG in PE, from this post: http://hqmeded-ecg.blogspot.com/2012/04/cardiac-ultrasound-may-be-surprisingly.html
The ECG in PE:
The ECG is not sensitive for PE, but when there are findings such as S1Q3T3 or anterior T-wave inversions, or new RBBB, then they have a (+) likelihood ratio and the S1Q3T3, or even just the T3, may help to differentiate Wellens' from PE.
Stein et al. found normal angiograms in only 3 of 50 patients with massive PE, and 9 of 40 with submassive PE. Today, however, that number would be lower because we diagnose more of the submassive PEs that have minimal symptoms.
This is a paper worth reading: Marchik et al. studied ECG findings of PE in 6049 patients, 354 of whom had PE. They found that S1Q3T3 had a Positive Likelihood Ratio of 3.7, inverted T-waves in V1 and V2, 1.8; inverted T-waves in V1-V3, 2.6; inverted T-waves in V1-V4, 3.7; incomplete RBBB 1.7 and tachycardia, 1.8. Finally, they found that S1Q3T3, precordial T-wave inversions V1-V4, and tachycardia were independent predictors of PE.
What is an S1Q3T3? Very few studies define S1Q3T3. What is it? It was described way back in 1935 and both S1 and Q3 were defined as 1.5 mm (0.15 mV). In the Marchik article, (assuming they defined it the same way, and the methods do not specify this), S1Q3T3 was found in 8.5% of patients with PE and 3.3% of patients without PE.
Kosuge et al. showed that, when T-waves are inverted in precordial leads, if they are also inverted in lead III and V1, then pulmonary embolism is far more likely than ACS. In this study, (quote) "negative T waves in leads III and V1 were observed in only 1% of patients with ACS compared with 88% of patients with APE (p less than 0.001). The sensitivity, specificity, positive predictive value, and negative predictive value of this finding for the diagnosis of PE were 88%, 99%, 97%, and 95%, respectively. In conclusion, the presence of negative T waves in both leads III and V1 allows PE to be differentiated simply but accurately from ACS in patients with negative T waves in the precordial leads."
Witting et al. looked at consecutive patients with PE, ACS, or neither. They found that only 11% of PE had 1 mm T-wave inversions in both lead III and lead V1, vs. 4.6% of controls. This does not contradict the conclusions of Kosuge et al. that when there are T-wave inversions in the right precordial leads and in lead III, PE may indeed by more common. In my experience, this is true, but needs validation in a study of similar methodology. Supporting Kosuge, Ferrari found that anterior T-wave inversions were the most common ECG finding in massive PE.