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This has been termed a “STEMI equivalent” and included in STEMI guidelines, suggesting this patient should receive dual anti-platelets, heparin and immediate cath lab activation–or thrombolysis in centres where cath lab is not available. aVR ST segment elevation: acute STEMI or not? aVR ST Segment Elevation: Acute STEMI or Not?
Prehospital Conventional algorithm interpretation: ANTERIOR INFARCT, STEMI Transformed ECG by PM Cardio: PM Cardio AI Bot interpretation: OMI with High Confidence What do you think? Mild Plaque no angiographically significant obstructive coronary artery disease. A 49 year old woman with h/o COPD only presented with sudden dyspnea.
During active chest pain an ECG was recorded: Meyers ECG interpretation: Sinus tachycardia, normal QRS complex, STD in V2-V6, I, II, III and aVF. A "STEMI alert" was called and soon cancelled. Shortly after receiving epinephrine, the patient developed new leg cramps and chest pain. Pain lasted for approximately 45 minutes.
LAD plaque with 0-25 percent stenosis. Later, she developed chest pain again, and had this ECG recorded: Obvious Anterior OMI that is also a STEMI Coronary angiogram- --Right dominant coronary artery system --The left main artery was normal in appearance and free of obstructive disease. --The A CT Coronary angiogram was ordered.
The axiom of "type 1 (ACS, plaque rupture) STEMIs are not tachycardic unless they are in cardiogenic shock" is not applicable outside of sinus rhythm. 2) Tachycardia to this degree can cause ST segment changes in several ways. Is that an obvious STEMI underneath that rhythm?
There is an obvious inferior STEMI, but what else? Besides the obvious inferior STEMI, there is across the precordial leads also, especially in V1. This STE is diagnostic of Right Ventricular STEMI (RV MI). In fact, the STE is widespread, mimicking an anterior STEMI. EKG is pictured below: What do you think?
As in all ischemia interpretations with OMI findings, the findings can be due to type 1 AMI (example: acute coronary plaque rupture and thrombosis) or type 2 AMI (with or without fixed CAD, with severe regional supply/demand mismatch essentially equaling zero blood flow). He had multiple cardiac arrests with ROSC regained each time.
She had this ECG recorded: Obvious massive anterior STEMI She was quickly brought to the critical care area and the cath lab was activated. Here is the ECG at 25 minutes: Terrible LAD STEMI (+) OMI So a CT scan was done which of course showed a normal aorta. This was ruptured plaque with thrombus. She was a walk-in at triage.
This ECG was recorded: It is difficult to appreciate P-waves, but I believe this is sinus tachycardia. This was attributed to a "Type 2 MI", which is acute MI that is not due to ruptured plaque, but rather due to "supply demand oxygen mismatch". This is extremely elevated for a type 2 MI and totally consistent with STEMI.
The fear comes built in with the diagnosis often amplified by young felllows on call (& often times by senior consultants as well) It may appear real, from a clinical angle, but trust, when we deal with the whole gamut of so-called ACS (other than STEMI), there is indeed a benign face in many of them.
In my review of the literature, there are many articles which purport to demonstrate an acutely increased risk of plaque rupture from emotional stress, but I could not find any credible case reports that were not at least as likely to be takotsubo. Mechanisms of plaque formation and rupture. Coronary plaque disruption.
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