A near 60 year old male called 911 for increasingly severe fever and SOB. A prehospital ECG was recorded (not shown and not seen by me) which was worrisome for STEMI.
He presented very tachycardic with a very high fever.
Here was his initial ED ECG:
|There is sinus tachycardia at a rate of about 140
There is profound ST Elevation across all precordial leads, as well as I and aVL.
QTc was 374, and the formula value was quite high, consistent with LAD occlusion.
A previous ECG from 4 years prior was normal:
This looks like an anterior STEMI, but it is complicated by tachycardia (which can greatly elevate ST segments) and by the presentation which is of fever and sepsis.
If a patient presents with chest pain and a normal heart rate, or with shockable cardiac arrest, then ischemic appearing ST elevation is STEMI until proven otherwise.
But when the clinical presentation is sepsis, one must entertain the possibility that the ST elevation is due to demand ischemia, or some other process, and exacerbated by tachycardia.
It is prudent to treat the other conditions, get the heart rate controlled, and repeat the ECG.
A bedside echo was done:
Although the quality is suboptimal, it appears to me to show a hyperdynamic heart and possibly and apical wall motion abnormality.
The patient was treated for sepsis and had another ECG 35 minutes later:
|Heart rate is still fast at 120
The QTc = 410 ms
There is still scary STE
The formula is still positive
The patient continued to improve and had another ECG at 65 minutes:
|QTc = 419
It looks a lot better, though the formula is still marginally positive:
STE at 60 ms after J-point in V3 (STE60V3) = 3.5
R-wave amplitude in V4 (RAV4) = 10
Total QRS amplitude in V2 = 26
Formula value = 18.9
Any value greater than 18.2 should be assumed to be LAD occlusion until proven otherwise.
Cardiology was consulted and they did not think there was an indication for emergent cath lab activation.
He was admitted and serial troponins were measured:
Because of elevated troponins, a next day echo was done:
The estimated left ventricular ejection fraction is 50%.
The estimated pulmonary artery systolic pressure is 37 mmHg + RA pressure.
Normal estimated left ventricular ejection fraction lower limits of normal.
Regional wall motion abnormality-distal septum anterior and apex akinetic
Here is a repeat ECG:
|Looks like a reperfused LAD lesion (Wellens’ morphology)
The resident asked me what I thought about this case after the fact but before the angiogram.
I said I think there is a fixed stenosis in the LAD and the tachycardia and stress caused a type 2 STEMI.
In this abstract from 2011, we found that 4%(4 of 99) type 2 MI and 38% of type 1 MI had ST Elevation.
An angiogram was done:
It showed no culprit and no coronary disease, but did show a myocardial bridge in the mid LAD.
An excellent review of myocardial bridging, with full text:
Myocardial bridging is when the coronary artery, usually the LAD, dives into the myocardium.
Here is an excerpt from the article:
“Normally, only 15% of coronary blood flow occurs during systole, and because myocardial bridging is a systolic event on angiography, its clinical significance and relevance have been questioned. The presence of tachycardia could unmask the ischaemic effect of a myocardial bridge by shortening the diastolic period and increasing the importance of systolic blood flow. Also, tachycardia may worsen ischaemia because of a decrease in diastolic filling time and in coronary flow reserve (a measure of the ability to augment coronary blood flow under stress). According to one hypothesis, systolic kinking of the blood vessel may cause trauma to the intima and damage to the endothelium, especially at high heart rates. This, in turn, could produce platelet aggregation and vasospasm and result in an acute coronary syndrome.”
Summary of the pathophysiology of this case and the ECGs:
This was a type 2 LAD STEMI. In other words, there was transmural ischemia during the tachycardia due to both demand (high heart rate) and to the effect of myocardial bridging, which would mimic near occlusion. Then when the heart rate comes down, demand is decreased and full perfusion is restored, just like it is in Wellens’ syndrome. So the ECG findings are the same as if the patient had an anterior STEMI with reperfusion. Thus, there is a wall motion abnormality in the distribution of the LAD (not global apical dyskinesis, as in takostubo). This wall motion abnormality will almost certainly resolved with time (myocardial stunning).
Takotsubo stress cardiomyopathy is also a possibility, but the echo did not have the typical global apical hypokinesis, and the ECG, especially the reperfusion ECG, is more consistent with LAD ischemia.