Anterior T wave inversion due to Pulmonary Embolism

A 32 year old male presented with a 4 day history of dyspnea, cough, palpitations, and chest pain. He had an ECG done immediately (shown above). This showed anterior T wave inversions, a QTc of 431, and also T inversion in lead III. There is sinus tachycardia and an S1Q3T3. This is all highly suspicous for pulmonary embolism.

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Oxygen saturation was 95%, there were some end expiratory wheezes. D dimer was 3000. A CT pulmonary angio confirmed large central PE.

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Kosuge et al. (Am J Cardiol 2007;99:817-821) compared patients with ACS and PE who had precordial T wave inversions in V1-V4. They found that in this select population, negative T waves in lead III were observed in only 15% of patient with ACS, compared with 88% of patients with Acute PE.

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It is tempting to diagnose Wellens' syndrome with anterior T wave inversions, but Wellens' T waves simply look different, should have a longer QTc, generally don't extend out to V6, and, most importantly, don't have T inversion in lead III.

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Of course the clinical scenario is most important.

This morphology can be seen in any acute right heart strain, including asthma, see here:

http://hqmeded-ecg.blogspot.com/2011/04/is-it-pulmonary-embolism.html

Very Subtle Inferior STE elevation seen only on 2nd ECG done 42 minutes later; Non STEMI with RCA occlusion

I'm having difficulty with the blogger software. It won't let me place the ECG where I want it, so just know that the top ECG is "ECG #1" and the next is "ECG #2"

A 45 year old male presented after several hours of stuttering chest pain (a "big chest pressure right in the middle of my chest"), now with constant pain that started approximately 100 minutes prior to presentation. He has a history of GERD with "heartburn", no history of cardiac disease, but does have hypertension and hypercholesterolemia. He has a 21 year pack year smoking history but quit 5 years ago. He also has a h/o HIV/AIDS.

See ECG #1 on presentation:

There is a significant Q wave in lead III, consistent with old inferior MI. There is a trace of ST elevation in inferior leads, but this was not different from a previous ECG. Appropriately, no action was taken.

The pain continued, and 42 minutes later ECG #2 was recorded:

There is now very subtle (less than 1 mm) ST elevation in leads III and aVF, with minimal reciprocal depression in aVL. This amount of ST elevation does not meet the definition of STEMI, but there is definite ACS with dynamic ST segments, and refractory chest pain. Thus it is appropriate to activate the cath lab.

There was a total occlusion of the RCA, thrombus was suctioned and the lesion was stented. The peak troponin was 38 ng/ml. The door to balloon time (DBT) is measured from the first diagnostic ECG, and so was 58 minutes. Technically, the record of this DBT need not be kept because without 1 mm of STE in 2 consecutive leads, this does not meet the definition of STEMI.

It is clear, however, that this definition is arbitrary: what is important is that there is an occluded artery and a significant amount of myocardium at imminent risk of infarction.

New Left Bundle Branch Block is a poor indicator of coronary occlusion

For a couple other very interesting posts on LBBB and STEMI, click here, and here and here for the most recent post.

Case 1:

A 55 yo male with a history of hypertension but no MI or CHF presented with 5 days of progressive dyspnea without chest pain. Here is his ECG:



There is sinus tachycardia with left bundle branch block (LBBB). A previous ECG from one year prior was normal without LBBB. According to the ACC and AHA, new LBBB in the presence of ischemic symptoms is an indication for reperfusion therapy. Cardiologists widely realize that, in reality, this is not a specific indication. Physicians do not follow this indication because, in their experience, most patients with new LBBB do not have coronary occlusion unless they also have some specific indicators of occlusion, known as the Sgarbossa criteria, or the Sgarbossa criteria as modified by Smith (data to be published). These criteria are dependent on the fact that, in LBBB, the ST segment and T wave (repolarization) are in the opposite direction from the major deflection of the QRS.

Sgarbossa criteria are 1) concordant ST elevation on at least 1 mm in at least 1 lead (5 points) 2) concordant ST depression in V1-V3 (leads that always have a negative QRS in LBBB)(3 points) and 3) 5 mm of discordant ST elevation in leads with a negative QRS (excessive discordance) (2 points because it was "only" 89% specific). I have modified only the last criterion by making it proportional to the QRS. Using angiographic data, I have adjusted the excessive discordance criteria number 3 so that the discordant ST elevation is only significant if it is out of proportion to the QRS. Specifically, I have found that if the ST segment as measured at the J point and relative to the PR segment is > 0.20 the depth of the preceding S-wave, in just one lead of V1-V4, that it is likely to be coronary occlusion.

This new LBBB shown above in case 1 has no concordance (all ST segments and T waves are in the opposite direction from the QRS; this is the normal configuration for LBBB). However, according to the Sgarbossa criteria, there is excessive discordance as defined by ST elevation of 5 mm in lead V2 (although this did not satisfy Sgarbossa's point system criterion, which gives only 2 of the necessary 3 points for excessive discordance). By the new criterion, the discordant ST elevation is not excessive (5/35 = 0.14 which is less than 0.20). Thus, by the new criterion this is a true negative, but by Sgarbossa's criterion, it would get 2 points and be highly suspicious for acute STEMI. The reason that Sgarbossa's criterion was not specific enough is that many patients have high QRS voltage and resulting high discordant ST elevation, at baseline.

The BNP was 1200; an echo revealed global LV dysfunction with EF of 20% and no evidence of wall motion abnormality. The troponins were negative. The use of a 5 mm absolute criterion would have resulted in a false positive cath lab activation.

Case 2:

This 89 yo m presented after syncope during exertion, with no chest pain. He had a loud systolic murmur at the left sternal border that radiated to the carotids, consistent with severe aortic stenosis.
Here is the initial ECG:


The first troponin returned positive at 0.20 ng/ml (LoD .04 ng/ml, 99% reference less than 0.1 ng/ml) and a second ECG was recorded. At no time did the patient have chest pain.


This is also new LBBB, this time without any specific criteria positive. The patient did have release of troponin but never had chest pain. The clinicians discussed activating the cath lab based on new LBBB, but this patient had neither CP nor dyspnea and thus is not a candidate even under ACC AHA guidelines. His only symptom was syncope, which was explained by aortic stenosis.

Furthermore, the troponin elevation can be explained exertion in the presence of aortic stenosis, due to demand ischemia (or "type II" MI, not caused by acute coronary syndrome and thus not requiring intensive antiplatelet or antithrombotic therapy).

A great majority of patients with ischemic symptoms and new LBBB do not have acute coronary occlusion and do not need immediate reperfusion therapy. Some do have "NSTEMI," but the vast majority who have coronary occlusion will meet the modified Sgarbossa criteria.

How this should affect global guidelines such as ACC AHA is unclear. But what is clear is that clinicians find new LBBB akin to crying wolf, and no longer follow the guidelines.