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One very useful adjunct is ultrasound: Echo of his heart can distinguish aneurysm from acute MI by presence of diastolic dyskinesis, but it cannot distinguish demand ischemia from ACS. These must raise suspicion of old MI with persistent ST elevation. An angiogram showed no acute coronary lesions.
The old ECG has a Q-wave with persistent ST elevation in lead III, and some reciprocal ST depression (typical for aneurysm morphology). This is "Persistent ST elevation after previous MI" or "LV aneurysm morphology". LV aneurysm is very different for inferior vs. anterior MI. This is not pericarditis because: a.
The EKG is diagnostic of acute inferior, posterior, and lateral OMI superimposed on “LV aneurysm” morphology. Whether these EKGs show myocarditis, a normal variant, or something else, they are overall not typical of transmural ischemia of the anterior or high lateral walls. Patient 2 , EKG 1: What do you think?
Prior ECG available on file from 2 months before: We do not know the clinical events happening during this ECG, but there is borderline tachycardia, PVCs, and likely some evidence of subendocardial ischemia with small STDs maximal in V5-6/II, slight reciprocal STE in aVR. QS waves from V2-V5 consistent with LV aneurysm morphology.
No prior echocardiogram was available for comparison. However, the ST segments in patients with LVH may show significant variation over time in the absence of ischemia. 3 Some have also suggested that the typically asymmetric T wave inversion (TWI) of LVH might be distinguished from the typically symmetric TWI of cardiac ischemia.
You might think it is "Old MI with persistent ST Elevation" (otherwise known as "LV aneurysm" morphology.") That is a reasonable thought, but we have shown that if there is one lead of V1-V4 with a T/QRS ratio greater than 0.36, then it is STEMI, not LV aneurysm. Pain will resolve with completed infarct or with resolution of ischemia.
Next day echocardiogram showed inferolateral hypokinesia with an EF of %45-50. On echocardiogram you will not see a "posterior" hypokinesia (will see "inferolateral") and, as in this case, LCx may not give the blood supply of basal inferior segment (formerly called "posterior"). The patient recovered well. J Am Heart Assoc. 121.022866.
Look for Vascular Etiology -- think of these while doing H and P: --Bleeding: ruptured AAA, GI bleed, ruptured ectopic pregnancy, other spontaneous bleed such as mesenteric aneurysms. Evidence of acute ischemia (may be subtle) vii. ST segment and T wave abnormalities consistent with or possibly related to myocardial ischemia.
There are no Q-waves to suggest old inferior MI, or inferior aneurysm as the etiology of the ST Elevation. The patient was started on heparin for possible NSTEMI vs demand ischemia. increasing stenosis, ischemia, volume changes, increased blood pressure, atrial fibrillation, etc.) What "initiates" the aortic stenosis cascade?
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