![]() Regional wall motion abnormality-apical septal, mid anteroseptal, mid to apical anterior, and apical lateral hypokinesis. Moderate to severe decrease in left ventricular systolic function with an estimated EF of 30%. Therefore the ECG abnormalities were definitely a result of the ischemia. The ST elevation is resolved (and the reciprocal ST depression) Flow eventually restored after multiple passes with thrombectomy aspiration catheter. So this OM does indeed supply the inferior wall. LCx large codominant, normal appearing until point of occlusion in mid-vessel The ST segments will resolve, or there will be T-wave inversion, or both. But the proof would be in the subsequent ECGs: did they evolve? If the EKG abnormalities are a result of the ischemia, the ECG will always evolve. In this case, due to the EKG abnormalities, it is likely. In a left dominant system, an OM could supply the inferior wall, but that would be unlikely. "Could the EKG abnormalities be baseline and he really had an occlusion that did not manifest on the EKG?" "Could an OM occlusion cause an inferior MI?" The resident wrote that the cath showed only an OM occlusion. Case Continued: The initial troponin I was 0.012 ng/mL (URL = 0.030 ng/mL)Ī 2nd troponin returned at 0.047 ng/mL (elevated) Here is the case we describe in the report: Ultrasound Before ECG for Chest pain? Whoever gets there first. Diagnosis of acute coronary occlusion in patients with Non–STEMI by point-of-care echocardiography with speckle tracking. Here is an article we wrote on the topic: Here are more cases with Speckle Tracking So if the inferior wall is not accurately marked, it will identify the wrong wall. ![]() The location depends on the operator who tells the machine what wall is what by placing dot markers on the endocardium. You might wonder why the inferior wall looks so medial. The lavender sector contracts less than 10 on the scale, so there is indeed an inferior wall motion abnormality.
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