Anterior T wave inversions and PE.

Last week, I described the case of a middle-aged male with a vague history of heart failure who had been having progressive shortness of breath for 4-5 days. On the day he called 911, he had been walking a short distance when he syncoped. EMS obtained an ECG:

Inverted T waves are seen in III and aVF, as well as V1-V3

Inverted T waves are seen in III and aVF, as well as V1-V4.

Compared with the prior ECG, the anterior T wave inversions appeared new.

Subtle S1Q3T3, but no ATWI

Subtle S1Q3T3, but no ATWI

What can cause anterior T wave inversion (ATWI)?

There are some rare entities that show up with ATWI; e.g. ARVC. Young women can also have a benign variant, the so-called persistent juvenile T wave pattern.

But in this clinical context, we should consider two main categories: 1) myocardial ischemia, and 2) right ventricular strain.

ATWI and myocardial ischemia

Posterior STEMIs can initially appear as inverted T waves in the right-sided leads, but there is usually a degree (or more!) of ST depression in those same leads.



On the other hand, so-call “anterior ischemia” can cause ATWI too. But this usually is more prominent in the lateral leads, with a “strain” pattern of ST depression as well.



You can also see Wellen’s syndrome in the anterior leads, but these T waves are notable for being deep and/or biphasic.



Clinically, the patient describes days of symptoms, and it seems unlikely that the ECG would appear so benign after days of ischemia that was severe enough to provoke syncope.  Also, the echo, while not of the best quality, shows a markedly dilated RV, suggesting that RV strain is more probable than ischemia.

ATWI and right ventricular strain.

Conditions that cause RV enlargement or pressure overload can produce ATWI, as well as S1Q3T3. Clearly, PE is a huge possibility here, but it’s worth remembering that severe COPD can generate this pattern as well, by producing pulmonary hypertension through hypoxic vasoconstriction in the pulmonary arteries. Idiopathic pulmonary hypertension also can produce ATWI and S1Q3T3.

The clear lung sounds do not suggest COPD, and the very recent development of the ATWI means that he likely does not have chronic pulmonary hypertension.

Clinical course

The patient decompensated abruptly during evaluation by the ED physician. Based on the ECG, echo, as well as clinical exam (one leg was significantly swollen), tPA was administered during CPR, but this was unsuccessful. An autopsy confirmed massive bilateral pulmonary emboli.

The ECG can be useful in suspecting PE.

For diagnosing a PE, you basically need an imaging study: CT scan or a V/Q study. The ECG has been derided as being non-specific, missing many cases of PE, or only showing sinus tach.

But the ECG can be quite instrumental is suggesting the diagnosis of a large PE, but you can’t use just S1Q3T3. Inversion of the T waves in the right anterior leads has been shown to be quite helpful in suggesting the presence of a hemodynamically-significant PE, and the additional finding of T wave inversions in III and aVF is very helpful in distinguishing cardiac ischemia from PE.

Note the inverted Ts in III, F, and V1-V3. From

Note the inverted Ts in III, F, and V1-V3.

 Take-away point

In an ECG that looks “non-specific,” pay attention to the anterior T waves! You might just pick up a PE.


1 Comment

  • Stuart says:

    Studies (can’t remember them off the top of my head) have shown that TWI in V1-4 + III is 85% likely to be RV strain, 15% ischemia.

    If I see anterior TWI, the very next lead I look to is III

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