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We discover that for STEMI/OMI vs subendocardial ischemia, we should look for STEMI(-)OMI, subacute OMI, and OMI in the presence of LBBB and RBBB, and consider the differential for diffuse ST depression with reciprocal ST elevation in aVR.
This ECG is diagnostic of anterior STEMI. The distal inferior apical LAD was cut off by distal embolization from LAD culprit. This is likely because 1) the ischemia to the inferior wall was only partial and 2) it reperfused quickly. The QRS is at least as important as the ST segment in diagnosing STEMI BP was 160.
This certainly looks like an anterior STEMI (proximal LAD occlusion), with STE and hyperacute T-waves (HATW) in V2-V6 and I and aVL. This rules out subendocardial ischemia and is diagnostic of posterior OMI. How do you explain the anterior STEMI(+)OMI immediately after ROSC evolving into posterior OMI 30 minutes later?
There is ST depression beyond the end of the wide QRS in I, II, aVF, and V4-V6, diagnostic of with subendocardial ischemia. It makes pulmonary embolism (PE) very likely. Although most cardiac arrest from MI is due to ventricular fibrillation, some is due to high grade AV block, and so this could indeed be due to large acute STEMI.
This suggests further severe ischemia. Transient and partial thrombosis at the site of a non-obstructive plaque with subsequent spontaneous fibrinolysis and distal embolization may be one of the mechanisms responsible for the occurrence of MINOCA. This has resulted in an under-representation of STEMI MINOCA patients in the literature.
Is this an anterior STEMI with LBBB? Explanation : The patient had a worrisome history: 59 yo with significant substernal chest pressure, so his pretest probability of MI (and even of STEMI) is reasonably high. Additionally, appropriate discordance is common in NonSTEMI, but very unusual in coronary occlusion (STEMI).
In terms of ischemia, there is both a signal of subendocardial ischemia (STD max in V5-V6 with reciprocal STE in aVR) AND a signal of transmural infarction of the inferior wall with Q wave and STE in lead III with reciprocal STD in I and aVL. The rhythm is atrial fibrillation. The QRS complex is within normal limits.
Normal RBBB, no evidence of ischemia. It is uncommon in the age of reperfusion therapy, as most STEMI get treated reasonably early, before transmural infarct. LV aneurysm puts them at risk for a mural thrombus, which puts them at risk for embolism, especially embolic stroke. R-waves of of normal height.
This meets "STEMI criteria" However, there is very high voltage, with a very deep S-wave in V2 and tall R-wave in V4. The morphology is not right for STEMI. My interpretation: LVH with secondary ST-T abnormalities, exaggerated by stress, not a STEMI. This is very good evidence that the ST elevation is not due to STEMI.
This is of course diagnostic of an acute coronary occlusion MI (OMI) that also meets STEMI criteria. However, by the time of the angiogram it had embolized distally, and had only done so after the right sided ECG was recorded. See P.S. below ) == P.S. : I believe I found another example of ischemia-induced J waves ( See Oct.
Both of these are very suggestive of " No-Reflow ," or poor microvascular reperfusion due to downstream embolization of microscopic platelet-fibrin aggregates. cm diameter in the apex The presence of thrombus led the clinicians to state that this was a "late presentation STEMI." LV Thrombus , 1.5 0 0 1 95 544 MMRF 4 1 638 14.0
Transient and partial thrombosis at the site of a non-obstructive plaque with subsequent spontaneous fibrinolysis and distal embolization may be one of the mechanisms responsible for the occurrence of MINOCA. This has resulted in an under-representation of STEMI MINOCA patients in the literature. From Gue at al.
50% of LAD STEMIs do not have reciprocal findings in inferior leads, and many LAD OMIs instead have STE and/or HATWs in inferior leads instead. The ECG easily meets STEMI criteria in all leads V2-V6, as well. CT angiogram chest: no aortic dissection or pulmonary embolism. 24 yo woman with chest pain: Is this STEMI?
In a series of 18 patients with COVID and ST elevation, 8 were diagnosed with STEMI, 6 of whom had an angiogram and it showed obstructive coronary disease. 12 All STEMI patients had very high cTn typical of STEMI (cTnT > 1.0 Available from: [link] 9. of Cardiology AC, Others. Troponin and BNP Use in COVID-19.
Third, a slow motion segment showing delayed, brisk filling of the PDA due to dislodgment of a thrombus from contrast injection and distal embolization. A distal RCA lesion ( blue arrow ), Delayed brisk filling of an initially occluded PDA due to a thrombus dislodged during injection which embolized distally.
His initial high sensitivity troponin I returned at 1300 ng/L and given that his cardiac workup was otherwise unremarkable, a CT was obtained to evaluate for pulmonary embolism and aortic aneurysm or dissection but this too was unrevealing. Another EKG was also obtained. ECG at time 82 minutes: What do you think?
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