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This is a value typical for a large subacute MI, n ormal value 48 hours after myocardial infarction is associated with Post-Infarction Regional Pericarditis ( PIRP ). As already mentioned, this patient could have post-infarction regional pericarditis from a large completed MI. Sinus tachycardia has many potential causes. Hammill SC.
Edited by Bracey, Meyers, Grauer, and Smith A 50-something-year-old female with a history of an unknown personality disorder and alcohol use disorder arrived via EMS following cardiac arrest with return of spontaneous circulation. Circulation. The described rhythm was an irregular, wide complex rhythm. JAMA Intern Med. 2017.3191.
More likely, the patient had crescendo angina, with REVERSIBLE ischemia for 48 hours that only became potentially irreversible (STEMI) at that point in time. During the 48 hours of angina, such reversible ischemia often leads to myocardial stunning with akinesis of the myocardial wall that puts it at risk for thrombus. Re-occlusion 2.
The ECG shows sinus tachycardia with RBBB and LAFB, without clear additional superimposed signs of ischemia. ECG of pneumopericardium and probable myocardial contusion shows typical pericarditis Male in 30's, 2 days after Motor Vehicle Collsion, complains of Chest Pain and Dyspnea Head On Motor Vehicle Collision. ST depression.
Pericarditis? For coronary anatomy, see here: [link] This is the post intervention ECG: All ST Elevation is gone (more proof that it was all a result of ischemia) Formal Echo: Normal estimated left ventricular ejection fraction - 55%. More likely, these T waves probably reflect ischemia of uncertain age. Is it normal variant?
Of course this depends on many factors: 1) duration of occlusion, 2) whether full or near occlusion with zero flow or some flow -- the flow in the artery is the critical factor, measured by "TIMI" flow, 3) presence of collateral circulation and others. Pericarditis would be even more unlikely in someone without chest pain.
The exception is with postinfarction pericarditis , in which a completed transmural infarct results in inflammation of the subepicardial myocardium and STE in the distribution of the infarct, and which results in increased STE and large upright T-waves. These findings together are more commonly seen with pericarditis.
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