Acute Chest pain which then resolves spontaneously

A 50-something woman presented with sudden onset of left sided chest pain while driving, radiating down left arm, in addition to feeling diaphoretic, dizzy, and lightheaded. 

She presented immediately to the ED and had this ECG recorded:

QTc was 432 ms

What do you think? 

One of our fellows and a resident were worried about the ST Elevation in V3-V5, and but they were uncertain if it was possibly normal variant STE.

They calculated the formula at 21.05, which very strongly suggests acute LAD occlusion.  18.2 is the most accurate cutoff value, but at 19.0 it is very very specific.  21.05 is nearly always an acute LAD occlusion.

See here for everything about the formula and how to use it:

12 Example Cases of Use of 3- and 4-variable formulas to differentiate normal STE from subtle LAD occlusion

The pain resolved after approximately 30 minutes total, and they did not activate the cath lab.

The first troponin I (Abbott, high sens) returned at 28 ng/L (Upper limit for women = 16 ng/L).  

The 2nd returned at 1332 ng/L, and another ECG was recorded 2.5 hours after the first: 

What do you think?

There is new T-wave inversion in V3-V6, biphasic.  This is Wellens' syndrome (Pattern A), which is indicative of reperfusion, though most Wellens' of the LAD is V2-V4. 

(The only difference from Wellens,' as described by Wellens, is that we were able to record an ECG during pain, and it showed what the true precursor to Wellens' waves is: ST Elevation of acute occlusion.  Wellens did not know at the time that his T-wave pattern was a sign of reperfused but unrecorded STEMI.  This was inferred after studies by Wehrens and also by Doevendans revealed identical T-waves after thrombolytic reperfusion)  

Moreover, this 2nd ECG confirms that the first ECG, recorded with pain, was indeed due to LAD occlusion and that when the pain resolved on its own, that resolution was due to spontaneous reperfusion of the LAD.

She was taken for angiogram shortly thereafter:

Angiogram:

60% diffuse Moderate CAD in the distal LAD at an a segment where the vessel appear to have an intra-myocardial course. This could represent atherosclerosis with or without a ruptured plaque but also raises the possibility of spontaneous coronary artery dissection (SCAD).

The LAD is a large caliber vessel.

The LAD has moderate, indeterminate disease in the distal segment of the vessel. 60% diffuse Moderate CAD in the distal LAD at an a segment where the vessel appear to have an intra-myocardial course.

So it is unclear to me whether this is SCAD or myocardial bridging, or both.  There was nothing to be intervened upon (no stent).

See below for posts on these 2 entities (Bridging and SCAD).

Echocardiogram

Decreased left ventricular systolic performance-mild. The estimated left ventricular ejection fraction is 45-50%.  Regional wall motion abnormality-distal septum anterior and apex.

Third troponin: 1263 ng/L.  Unfortunately, it was not measured to peak. Peak troponin has a rough correlation with infarct size.  Echocardiogram correlates with myocardium at risk, but not with infarct size because myocardium that is "stunned" by ischemia, but not infarcted, may have persistent wall motion abnormalities (WMA) that are not permanent.  In other words, WMA only tell you that the myocardium was ischemic, not whether it is permanently infarcted.

Clinical Course:

The patient was initiated on beta blockers and dual antiplatelet therapy, carvedilol, and lisinopril.  The patient's contraception was discontinued, as hormones are associated with SCAD.  

Cardiac MRI was pursued with patient but she was unable to tolerate this due to anxiety.  Underwent cardiac rehab during course of stay and was cleared for discharge by cardiology with plans for outpatient follow-up and follow-up TTE. 

Learning Points

1. The LAD Occlusion/Normal Variant ST Elevation formula can help you to assess whether ST Elevation is due to ischemia or due to normal variant.

2. ST Elevation in V2-V5 during pain, with subsequent terminal T-wave inversion after pain resolves, is Wellens' syndrome.  An identical pattern can be seen in inferior leads and also in lateral leads after reperfusion. An analogous finding can be seen after reperfusion of the posterior wall.

3. LAD Occlusion can be caused by SCAD, which usually (but not always) does not require stenting.

4. Myocardial Bridging can also result in transient occlusion.

Myocardial Bridging: Tachycardia, fever to 105, and ischemic ST Elevation -- a Bridge too Far

3 posts on Spontaneous Coronary Dissection (SCAD):