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We present a case of a 22-month-old boy with a hypokinetic and thin-walled aneurysm of the left ventricle apex. Cardiac magnetic resonance imaging revealed an akinetic aneurysm of the LV apex with a full-wall ischemic scar. Determining the origin of the aneurysm is challenging.
06:44 - T-waves in V2 are smaller now - Overall resolution of prior findings (which qualifies as a dynamic change) The initial note by the cardiologist states that the presentation is more consistent with pericarditis. Remember, pericarditis is the thing you say and write down when youre actively trying to miss an OMI.
The old ECG has a Q-wave with persistent ST elevation in lead III, and some reciprocal ST depression (typical for aneurysm morphology). This rules out pericarditis, which essentially never has reciprocal ST depression. This is "Persistent ST elevation after previous MI" or "LV aneurysm morphology".
When there is MI extending all the way to the epicardium (transmural), that infarcted epicardium is often inflamed (postinfarction regional pericarditis, or PIRP). What complication is the patient with post-infarction regional pericarditis at risk for? 3) Oliva et al. (4) One should be on the alert for myocardial rupture.
This may be permanent and may be associated with echocardiographic dyskinesis (aneurysm). LV aneurysm is common in completed, full thickness (transmural) MI, which is what we have here. Patients with completed, transmural infarct are also at risk for post-infarction regional pericarditis and myocardial rupture.
Post-infarction Regional Pericarditis (PIRP) PIRP happens when MI is transmural, all the way from subendocardium to subepicardium, thus leading to inflammation of the subepicardium (next to the pericardium). MYOCARDIAL RUPTURE AND POSTINFARCTION REGIONAL PERICARDITIS KEY POINTS · Myocardial rupture occurs in 1 to 1.5% Re-occlusion 2.
Repeat CT angio chest (not CT coronary, unclear what protocol) showed possible LAD aneurysm and thrombus. Finally, coronary angiography was performed (at least 5 days after presentation) which confirmed LAD aneurysm with large thrombus burden, TIMI 0 flow, thrombectomy performed. Pericarditis? No further cath details available.
STE occurs primarily in viable ischemic myocardium; persistent STE after completed infarction is ominous and portends development of an aneurysm. This is the most important exception to the classic teaching of "diffuse STE without reciprocal depression is less likely ACS, more likely pericarditis". Our THANKS to Drs.
You do NOT see this in normal variant STE, nor in pericarditis. The only time you see this without ischemia is when there is an abnormal QRS, such as LVH, LBBB, LV aneurysm (old MI with persistent STE) or WPW." There is upsloping ST elevation in III, with reciprocal ST depression in aVL. Troponin I greater than 1.0
When there are QS-waves, one should always think about LV aneurysm, but ST to QRS ratio and T-wave to QRS ratio are far too large and not compatible with left ventricular aneurysm. These findings together are more commonly seen with pericarditis. There is some R wave in the lateral precordial leads.
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