A 45 yo woman with several coronary risks but no history of coronary disease developed 10/10 "gnawing" retrosternal chest pressure at rest at 7:30 PM. She thought it was reflux, but antacids did not relieve it. She did not arrive in the ED after pain all night (not certain if it was constant or intermittent) until the next AM when this ECG was recorded:
|Here the ST elevation in leads III and aVL is more clear, with reciprocal ST depression in aVL are more apparent|
This is very suspicious for inferior MI of unknown age. It could be old MI with persistent ST elevation, or it could be subacute MI with new Q-wave, but is unlikely to be very acute (with a Q-wave and without large T-waves). If it is a subacute MI, there should be a positive troponin.
The first troponin I returned at 0.74 ng/ml, diagnostic of MI. Is this STEMI or NonSTEMI? That is an arbitrary definition, based on millimeters of ST elevation. Every physician should know that biologicial systems do not follow millimeter rules, so many "NonSTEMIs" are due to coronary occlusion.
The important thing is whether the patient has ongoing ischemia after almost 12 hours of chest pain, and as long as the ST segments are elevated or depressed, or the patient has chest pain, one must assume there is ongoing ischemia and do something about it. She did receive antithrombotic and antiplatelet therapy, and nitroglycerine, but her pain did not subside until she received hydromorphone. Then it was not until a second troponin returned at 4.40 ng/ml 4 hours later, that she was taken to the cath lab.
Cath revealed a 100% occlusion of the mid- first obtuse marginal (OM-1). Troponin I peaked at 49 ng/ml. Echo showed an inferolateral wall motion abnormality and concentric hypertrophy.
Here is her post cath ECG for comparison:
|ST segments are back to baseline|
1. Any ST depression in aVL is abnormal. Tikkanen et al. studied inferior early repolarization (baseline ECG with ST elevation). By personal communication, they have told me that only 1 of their 71 cases had reciprocal ST depression in lead aVL, and that this patient also had WPW. We are going to combine our data for inferior STEMI (159 of 160 had some ST depression in aVL) and our data on pericarditis (none of 39 had any ST depression) with their data on early repol to show that any ST depression in aVL is highly sensitive and specific for inferior MI.
2. "NonSTEMIs" may be large and due to complete persistent coronary occlusion that needs emergent reperfusion. Millimeters do not measure occlusion. Large MI may be very subtle on the ECG. This was not a small MI, with peak troponin of 49. I do not know what the convalescent ejection fraction or wall motion abnormalities were, but they might be significant here. (The initial echo shows stunned myocardium that may recover with time.)
3. Inferior MI does not always mean Acute MI. This patients initial ECG could represent old MI with persistent ST elevation, subacute MI, or old MI with superimposed acute MI. When the patient has such typical pain, and especially when you have a positive troponin, assume it is acute or subacute.
4. Opiates will obscure the diagnosis of MI. Morphine has been associated with higher mortality in ACS and I believe this is because the relief of pain is confused by physicians as relief of ischemia.
5. If in doubt, get an immediate echocardiogram. In this case, it would have confirmed MI and allowed for earlier cath lab activation. It may not differentiate old MI from acute MI, and I think the Q-wave here is diagnostic of old MI, so in this case echo is not so helpful.
6. Positive troponins alone are not grounds for cath lab activation. There must also be ongoing ischemia as evidenced by the ECG or ongoing pain, as in this case.