This 53 year old man presented with increasingly frequent episodes of chest pain, the longest lasting for 10 minutes. He was from Africa and had never seen a U.S. physician, but his doctor in Africa had told him something about blockages in his heart. His last pain was 3 days prior.
Note that there is terminal T wave inversion in V2 and V3, suggesting Wellens' syndrome. However, in this case there is no R-wave remaining. Wellens' syndrome should have a well developed R-wave. Wellens' syndrome is dangerous because there is a large amount of anterior wall myocardium that is viable but at risk. Here, the absence of any R-wave makes it highly likely that this man has already lost his anterior wall; thus, there is little more at risk. When I saw him, I suspected that this represented old MI, not acute MI. It could also represent subacute or evolving MI that is so far along that the anterior wall is nearly completely infarcted. So this could be an infarct that is12 hours old or 12 years, but is highly unlikely to represent acute MI; more accurately, it is unlikely to represent acute "injury."
FYI: "Infarction" is a misnomer for ST elevation MI because infarction implies irreversible death. The ST elevation implies myocardium at risk of infarction but still alive. Therefore, "injury" is the most appropriate term. The height of the T-wave in acute MI is the best predictor of whether the injured or "at risk" myocardium is salvagable: the larger and higher the T-wave, the more myocardium is salvageable.
A single troponin was negative. We did an ED emergency physician performed bedside ECHO that showed an apical wall motion abnormality. We then set him up for an outpatient stress sestamibi. He went today and it showed a large fixed infarct with apical dyskinesis, or LV aneurysm. He did not have any inducible ischemia. He will follow up in Cardiology clinic.
Below is an example of true Wellens'. Wellens' occurs when an area of STEMI (which goes unrecorded by an EKG) gets reperfused. You're seeing the after effects of an occlusion which is now reperfused. The T inversions are also called "reperfusion T waves" because they happen after therapeutic Reperfusion therapy for STEMI. In the case of Wellens', there was no EKG recorded at the time of occlusion. The first EKG was only recorded after the perfusion restored itself spontaneously and the pain resolved. That is why EVERY PATIENT in the Wellens' studies was pain free at the time of the EKG AND had either an open artery or collateral flow. Additionally, Wellens' has preserved R-waves because only a small amount of myocardium is infarcted.
This is Wellens' Type A (terminal T wave inversion). Type A will evolve into Type B (deep symmetric T wave inversion) over hours. If it does not evolve or resolve, it is not Wellens'.