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You've read in my previous posts that I have a lot of evidence that Wellens' represents spontaneously reperfused STEMI in which the STEMI went unrecorded. New ST elevation diagnostic of STEMI [equation value = 25.3 This T-wave inversion morphology is very specific for Wellens' waves. Computerized QTc = 417.
Here is the cath report: Echocardiogram: There is severe hypokinesis of entire LV apex and apical segment of all the walls. MINOCA may be due to: coronary spasm, coronary microvascular dysfunction, plaque disruption, spontaneous coronary thrombosis/emboli , and coronary dissection. ng/mL by 4th generation and older assays.)
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. See this case: what do you think the echocardiogram shows in this case?
The commonest causes of MINOCA include: atherosclerotic causes such as plaque rupture or erosion with spontaneous thrombolysis, and non-atherosclerotic causes such as coronary vasospasm (sometimes called variant angina or Prinzmetal's angina), coronary embolism or thrombosis, possibly microvascular dysfunction.
I think a good start would be a posterior EKG and a high quality contrast echocardiogram read by an expert. It was thought to be an in stent restenosis and thrombosis from a DES placed in the same region 6 months prior. His prior EF from an ECHO 6 months prior indicated 35% LVEF. What would you do in this scenario?
In this study of consecutive patients with LBBB who were hospitalized and had an echocardiogram, a QRS duration less than 170 ms (n = 262), vs. greater than 170 ms (n = 38), was associated with a significantly better ejection fraction (36% vs. 24%). This is extremely elevated for a type 2 MI and totally consistent with STEMI.
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