Epigastric pain, Syncope, and Saddleback ST Elevation

A male in his 30's who is an elite athlete with no risk factors for coronary disease had brief epigastric pain followed by brief syncope.  He presented to the ED never having had any chest pain or SOB, and with mild epigastric pain.

Here is his prehospital ECG:

There is sinus rhythm with a large peaked P-wave in lead II, and there is some minimal right axis deviation with S > R is lead I.  ST Elevation is minimal in V2, and more pronounced in V3 and V4.   There is also some supsicious ST elevation in aVL and I, with large T-waves and reciprocal ST depression in lead III.  Application of the STEMI vs. Early Repol formula, with values for QTc (computer) = 408 ms, STE60V3= 4 mm, and R-wave Amplitude V4 = 14.5 mm gives a value of 24.13, which is greater than 23.4 and thus indicates anterior STEMI, but not by much.  The closer the number is to the cutpoint of 23.4, the more uncertain the result.

The ST segment in V2 has a saddleback morphology.  In my experience, a saddleback in V2 has always been a STEMI mimic, not STEMI.  So I approach these with great skepticism.

There is an rSR' in V1 and V2, possibly due to right ventricular hypertrophy (given the right axis deviation), but without right bundle branch block (QRS duration is only 102 ms).   There is right ventricular conduction delay.  The large P-wave in lead II supports right atrial enlargement and possible right ventricular hypertrophy, which may all be affecting the ST segments.

The absence of chest pain in a young healthy male should make you more skeptical of STEMI and suggest a false positive.  However, we all know that chest pain is far from universal in STEMI.  In a recent study, 14% of men under age 55 do not complain of chest pain with their ACS.

On arrival in the ED, he underwent another ECG:

The saddleback is even more pronounced.  But so is the ST elevation.  Admittedly, this looks scary.  And the formula here, given STE60V3 of 5mm, QTc of 414 ms, and R amplitude V4 of 18.5 mm, gives a value of 24.38, still high.

The cath lab was activated and the patient was taken for angiogram, which was normal.  There was a small first diagonal and the angiographer noted that "a ruptured plaque that may have caused a temporary D1 occlusion is not inconceivable." 

An echocardiogram the next day was completely normal.  Initial Troponin I was 0.058 (99% reference 0.025) and succeeding ones were 0.073, 0.044, and 0.069.  This rather random rise and fall suggests false positives, which we have had many of since changing to our new Abbott assay.

Here is his ECG at 24 hours:

Sinus bradycardia.  The ST elevation remains, there is a less pronounced T-wave in precordial leads, but this could be due to the slow heart rate.  There is little evidence that there was any infarct.  This confirms that all the findings on the initial ECGs were baseline.

Conclusion:

This is a tough case and the safe thing to do was done: an angiogram, in order to be certain this was not a STEMI. 

Because of some reasonable doubt, it would also have been reasonable, if it could be obtained quickly, to get a stat echocardiogram with high resolution (using contrast (Definity).  I think it would have shown normal wall motion all around and saved the patient an angiogram. 

Nevertheless, it is good to remember:

1. Saddleback in V2 should make you doubt the diagnosis of anterior STEMI
2. Absence of Chest pain or SOB in a young, healthy male should make you skeptical and lead you to think about seeking confirmation of your ECG diagnosis.
3. The early repolarization/anterior STEMI formula does have false positives and negatives.  Accuracy was about 90% (which was far better than ST elevation)