A 60-something with h/o Coronary Bypass called 911 for acute chest pain.Here is the first prehospital ECG:What do you think?There is minimal ST Elevation in inferior leads which could easily be normal. However, aVL has minimal STD supportive of the diagnosis of OMI. More importantly, the ST depression in V2-4 is diagnostic of posterior OMI. There is a hyperacute T-wave in V6, which is the lateral part of the posterior wall and a common supportive finding in posterior OMI.The Zoll algorithm impressively stated: ***STEMI***A paramedic student had the PMCardio AI Queen of Hearts on his phone and this is what it reported:New PMcardio for Individuals App 3.0 now includes the latest Queen of Hearts model and AI explainability (blue heatmaps)! Download now for iOS or Android. (Dr. Smith is a shareholder in Powerful Medical.)On arrival, an ED ECG was recorded:Still diagnosticWhen a patient has severe chronic coronary disease, findings which appear to be acute can sometimes be chronic, so in this patient with h/o CABG (coronary bypass), it is wise to find a previous ECG if possible. Here it is:This confirms that all findings are new.The cath lab was activatedThe interventionalist disagreed with the assessment, but agreed to do the angiogram. Angiogram results are complicated because of the CABG:Severe three-vessel obstructive coronary artery disease, with chronic total occlusion of the mid LAD, total occlusion of the mid RCA, and severe subtotal occlusion and severe disease in the left circumflex coronary artery mid segment and proximal segment, as well as severe disease in the OM itself. Noteworthy that the LAD and the left circumflex coronary artery share 2 separate ostia with very close proximity to the origin of both vessels and severedisease in both vessels.Saphenous vein graft to the RCA is a large in diameter with significant conduit 2 vessel mismatch but there was no severe disease in the vein graft and the anastomosis to the distal RCA appeared to be okay.Patent LIMA to the LAD the LIMA is anastomosed to the mid LAD after the large LAD D1 and LAD D2.Saphenous vein graft to the obtuse marginal is small in diameter with severe ostial disease and total occlusion in the proximal body of the graft. This is most likely the infarct-related artery.Unfortunately, for technical reasons, it could not be stented.Should thrombolytics be given?I would say that, if there are no contraindications, yes. I have never seen a case in which the artery was unable to be opened for technical reasons and so therefore thrombolytics were given instead. Peak Troponin I was 22,000 ng/L (Typical of a moderate STEMI)Formal EchocardiogramNormal left ventricular cavity size, mildly increased wall thickness and mildly reduced systolic function; estimated left ventricular ejection fraction 45-50%.Regional wall motion abnormality: mid anterolateral and inferolateral hypokinesis. This is the term that is used for a posterior wall motion abnormality -- this confirms posterior OMI.The EF just 9 months prior was 64%, so there was significant myocardial loss.Learning Points: 1. If you cannot open the artery for technical reasons, consider thrombolytics.2. In the setting of acute chest pain, ANY ST depression maximal in V1-V4 is acute OMI until proven otherwise. We have proven this.ExceptionsOne should be circumspect (careful, that is, and not jumping to conclusions because the STD maximal in V1-V4 may NOT be due to OMI), when there is atrial fibrillation or abnormal vital signs:1. Atrial fibrillationGreat example: 60-something: chest tightness, palpitations, and ST depression V1-V3Other Examples:Cardiac arrest, defibrillated, diffuse ST depression and ST Elevation in aVR. Why?Chest Pain and Cardiogenic Shock with Profound ST Depression & STE in aVR. Activate the Cath Lab?Atrial Fibrillation w Rapid Ventricular Response and ST Depression Maximal V1-V4: Not always subendocardial.Does this ST Depression Maximal in V3 Represent Posterior OMI?Atrial Fibrillation with RVR and Inferoposterior ST elevation (Injury Pattern)2. Shock/Hypotension:Hypotension, chest pain, and precordial ST depression maximal in V3. Is this OMI?3. TachycardiaRegular, steady, and fast at 170 (wide or narrow?), hypoxic, crackles in lungs, B-lines, unconscious===================================MY Comment, by KEN GRAUER, MD (6/8/2025):===================================Today's case is of a 60-something man with known coronary disease — who called EMS for new-onset CP (Chest Pain).For clarity in Figure-1 — I've reproduced the first 2 ECGs in this case.=================================QUESTION: — How quickly can you make today's diagnosis?Beyond-the-Core: Has there been a change in the repeat ECG?Figure-1: Comparison of today's initial EMS ECG — with the repeat ECG on arrival in the ED.ANSWERS:The purpose of my comment in today's case is to highlight how quickly the diagnosis of acute posterior OMI should be made from ECG #1.Knowing this patient's age and his history of known coronary disease — immediately places him in a higher-risk group for an acute coronary event.Given this history — it should take no more than seconds to definitively diagnose acute posterior OMI because: i) There is maximal ST depression in leads V2,V3,V4 (RED arrows); and, ii) The shape of this ST depression in these 3 leads looks acute (straightened, "shelf-like" ST segments with terminal T wave positivity). There is a positive "Mirror Test" (See My Comment in the September 21, 2022 post, among many others for more on the "Mirror" Test).As per Dr. Smith — There is a hint in ECG #1 of ST elevation in the inferior leads, with abnormal ST segment flattening in lead aVL. That said, by itself — this would not be diagnostic because of how subtle these inferior lead findings are — and because the essentially flat ST segment in lead aVL is nonspecific, and not convincing of a reciprocal change.There is also ST depression in lead I of ECG #1. Most of the time with acute inferior infarction — the amount of reciprocal ST depression is usually greater in lead aVL than in lead I. Retrospectively (ie, knowing the cath findings) — this ST depression in lead I more likely reflects this patient's severe multivessel disease.What about the Repeat ECG?As stated — the diagnosis of acute posterior OMI (and the need for prompt cath with PCI) — should be immediately made on learning the history and seeing ECG #1. That said — I'd add 2 important points related to ECG #2:Point #1: There has been improvement in the ECG findings that were seen in the initial EMS tracing. Specifically: i) Although ST depression is still present and maximal in leads V2,V3,V4 — the amount of depression, and its acute appearance is less in ECG #2 (less of a "shelf-like" appearance to ST segments — with decreased height and less peaked terminal T wave positivity in these leads); ii) There is no longer ST depression in lead V5; and, iii) ST depression is less in lead I.Point #2: There is no mention of whether this patient's CP was less at the time ECG #2 was recorded. This is relevant — because IF this patient's CP had decreased at the same time that acute ECG findings were improving, this would provide further support of an acute cardiac event, as well as suggesting some degree of spontaneous reperfusion.