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He reported a history of ischemic cardiomyopathy with coronary stent placement approximately 10 years prior, but could not recall the specific artery involved. Anecdotally, had there been symptoms unequivocally consistent with ACS then one could justifiably make the case for a potential D1 occlusion. Attached is the first ECG.
No wall motion abnormality This shows that significant ACS can have ZERO WMA!! I believe that I was the first to represent Wellens as a reperfusion syndrome, in my book , The ECG in Acute MI , pages 22-23 and 51, and in chapter 27 on Reperfusion and Reocclusion. The estimated pulmonary artery systolic pressure is 27 mmHg + RA pressure.
Note 2 other similar cases at the bottom that come from my book, The ECG in Acute MI. I remained unconvinced that this was due to ACS. With the added history, and the entirety of the presentation, it was determined by cardiology that the clinical presentation was not due to ACS. What do you think? This is very low.
Discussion: This case highlights many important points worthy of discussion, mainly because it represents very routine care for ACS but there are so many ways we could improve outcomes with tools we already have! Troponin was rising when last checked, 8928 ng/L.
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