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57 year old male patient with Chest Pain

by on February 6, 2014

Patient presented to ED via local EMS with intermittent CP over past several days, acutely worse 30 minutes prior to arrival.  ED EKG showed ST-elevation in leads V1 through V3 with reciprocal depression in II, III, aVF, V5, and V6.  STEMI alert was called and patient taken emergently to the Cardiac Catheterization Laboratory.  Cath revealed 95% tubular stenosis in the proximal left anterior descending artery (LAD).  The LAD was treated with balloon angioplasty and stent.  Patient was discharged home


Door-to-Balloon (D2B): 55 Minutes / First Medical Contact to Balloon (E2B):74 Minutes

From → Case File

  1. Jonathan H. Talin permalink

    Obviously there is ST-Elevation in leads V1, V2, and V3 with inverted T-Waves in lead aVL and maybe in lead I. There is ST-Depression in lead II, slightly in aVF, V6 and tough to tell maybe V5. These inverted T-Waves and ST-Depression are not reciprocal changes from the LAD occlusion.

    The ST-Depression in leads V5 (if there is any, I can’t zoom in on the ECG) and V6 are most likely caused by the myocardial tissue being ischemic from the LAD occlusion.

    Reciprocal changes are a 180 degree view of the myocardium. If a modified ECG were conducted V8 and V9 would most likely show reciprocal because they are 180 degrease from V1 and V2.

    Also the ECG shows a left anterior fascicular block meaning the tri-fascicular system is now a bi-fascicular system, along with poor R-Wave progression. Some causes of poor R-Wave progression: lead placement, COPD, LAFB, and MI are some.

    The coolest part of this ECG is the ST-Elevation in lead aVR the T-Wave is normally inverted, however, there is elevation indicating there is occlusion in the LAD.


    • While you can see true subendocardial ischemia along with acute STEMI in the setting of diffuse CAD plus a culprit lesion, that’s probably not the case here. With a proximal LAD occlusion the ST-elevation vector points not only anterior and superior, but also quite a bit to the right (which is why aVR is elevated). Because the injury vector is directed essentially towards V1 and 30 degrees or so cephalad, it is very correct to expect reciprocal ST-depression in leads located inferior and to the left, such as II, V5, and V6.

      So the ST-depression we’re seeing on here really is 180 degrees from the injury vector, we just have to recognize that the injury vector isn’t pointed directly anterior (like it would be with a classic mid-LAD occlusion).

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