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Precordial ST depression may be subendocardial ischemia or posterior STEMI. I have warned in the past that one must think of other etiologies of ischemia when there is tachycardia. Whether it is subendocardial ischemia or posterior STEMI, if you cannot get it to resolve, you must activate the cath lab. There is no ST elevation.
5] Back to the case The patient had serial ECGs over the next hour with no significant change: The first troponin came back at 1,400 ng/L (normal <26 in males and <16 in females), confirming MI – and the patient’s refractory ischemia indicated this was an Occlusion MI. Clin Cardiol 2022 4. Herman, Meyers, Smith et al.
Post by Smith and Meyers Sam Ghali ( [link] ) just asked me (Smith): "Steve, do left main coronary artery *occlusions* (actual ones with transmural ischemia) have ST Depression or ST Elevation in aVR?" That said, complete LM occlusion would be expected to have subepicardial ischemia (STE) in these myocardial territories: STE vector 1.
Computer read: "Non-specific ST abnormality, consider anterior subendocardial ischemia" There are very poor R-waves in V1-V4 suggesting old anterior MI. Firstly, subendocardial ischemia does not localize on 12-Lead ECG. But the real question at hand is: Are these precordial ST-depressions a result of subendocardial ischemia?
The patient continued to have ischemia after PCI, and in fact had an episode of polymorphic VT shortly after while in the ICU. Determinants and prognostic implications of persistent ST-segment elevation after primary angioplasty for acute myocardial infarction: importance of microvascular reperfusion injury on clinical outcome.
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