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DISCUSSION: The 12-lead EKG EMS initially obtained for this patient showed severe ischemia, with profound "infero-lateral" ST depression and reciprocal ST elevation in lead aVR. The ECG cannot diagnose the etiology of ischemia; it only the presence of ischemia, from whatever etiology.
Post by Smith and Meyers Sam Ghali ( [link] ) just asked me (Smith): "Steve, do left main coronary artery *occlusions* (actual ones with transmural ischemia) have ST Depression or ST Elevation in aVR?" That said, complete LM occlusion would be expected to have subepicardial ischemia (STE) in these myocardial territories: STE vector 1.
Computer read: "Non-specific ST abnormality, consider anterior subendocardial ischemia" There are very poor R-waves in V1-V4 suggesting old anterior MI. Firstly, subendocardial ischemia does not localize on 12-Lead ECG. But the real question at hand is: Are these precordial ST-depressions a result of subendocardial ischemia?
Diagnosis of Acute MyocardialInfarction in the Presence of Left Bundle Branch Block using the ST Elevation to S-Wave Ratio in a Modified Sgarbossa Rule. Electrocardiographic Diagnosis of Acute Coronary Occlusion MyocardialInfarction in Ventricular Paced Rhythm Using the Modified Sgarbossa Criteria.
This suggests further severe ischemia. associated typical MyocardialInfarction therapies such as statins and ACE inhibitors with significantly decreased 1 year mortality in MINOCA patients, which suggests that they do indeed have a similar pathophysiology to MI patients with obstructive coronary disease. Downstream vasospasm?
This can be simply a equivalent of HT, with no true supply side ischemia with LVF with global ST depression ) Management *More or less similar to STEMI with aggressive opening of culprit lesions with few differences. 2013 Nov;6(6):708-15. Epub 2013 Nov 12. PMID: 35743628; PMCID: PMC9224589. Circ Cardiovasc Qual Outcomes.
His response: “subendocardial ischemia. Smith : It should be noted that, in subendocardial ischemia, in contrast to OMI, absence of wall motion abnormality is common. With the history of Afib, CTA abdomen was ordered to r/o mesenteric ischemia vs ischemic colitis vs small bowel obstruction. Anything more on history?
3 Patients with ASCVD are at a higher risk for major adverse cardiovascular events (MACE) including heart attack or myocardialinfarction (MI), stroke, and cardiovascular (CV) death.4 2013;368(21):2004-2013. Published 2013 Apr 4. Efficacy and Safety of Low-Dose Colchicine after MyocardialInfarction.
Int J Cardiol 2013 2. ST-elevation myocardialinfarction after pharmacologic persantine stress test in a patient with Wellens’ syndrome. Single High-Sensitivity Cardiac Troponin I to Rule Out Acute MyocardialInfarction. Was this objective evidence of inducible ischemia accompanied by chest pain?
Followup ECG: No Change Absence of evolution is the best evidence against ischemia as the etiology. I was taught that the tell-tale sign of ischemia vs an electrical abnormality was in the hx, i.e. chest pain for the ischemia and potential syncope for brugada. Ischemia/infarction. It helps a little bit.
This ECG is diagnostic of diffuse subendocardial ischemia. Door to balloon time (DBT) was 96 minutes for 7 patients with ST elevation myocardialinfarctions (STEMI) who had CT prior to PCI vs. 75 minutes for 11 patients who did not have CT, p=0.058. Conclusions: Head CT is common in NT-OHCA.
In the STEMI/NSTEMI dichotomy, NSTEMI is supposed to mean non-occlusive myocardialinfarction, but this patient had transient Occlusion MI that was at risk for re-occlusion (like ‘transient STEMI’). Arch Cardiovasc Dis 2013 Khan AR et al. JAHA 2022 Grosmaitre P et al. Eur Heart J 2017 Driver BE, Shroff GR, Smith SW.
There is no ST depression in V6, II, III, or aVF, and no significant ST elevation in aVR, all confirming that the ST vector is not consistent with diffuse subendocardial ischemia, but rather a focal ST vector pointed at the posterior wall. There is sinus rhythm with normal QRS complex and ST depression in V2-V5, maximal in V3-V4.
Chest pain with New LBBB: It helps to actually measure the ST/S ratio A Fascinating Demonstration of ST/S Ratio in LBBB and Resolving LAD Ischemia The cath lab was activated. This was formerly an indication for cath lab activation, but was abandoned in the 2013 guidelines because of poor specificity. is worrisome!
Here is his ECG: There is no clear evidence of OMI or ischemia. This " imbalance of precordial T waves" is not seen very often — and in the “right” clinical setting, has been associated with recent OMI from a LCx culprit artery ( See Manno et al: JACC 1:1213, 1983 — and the July 17, 2013 post by Salim Rezaie in ALiEM ).
He was found diaphoretic and uncomfortable, and verbalizing a prior history of myocardialinfarction and that, furthermore, the acute symptoms were identical to that which had been associated with RCA stent placement 4 years prior. Terminal QRS distortion is present in anterior myocardialinfarction but absent in early repolarization.
It could also, given a different clinical context be compatible with a subacute myocardialinfarction complicated by post infarct regional pericarditis. Due to the atypical and vague symptoms, the myocardialinfarct was not initially diagnosed. At presentation he had a history of dyspnea for 6 days.
It is possible there is microvascular dysfunction producing residual transmural ischemia. But this is most common when there is prolonged ischemia, and this patient had the fastest reperfusion imaginable! Acute myocardialinfarction: an uncommon complication of takotsubo cardiomyopathy. SanzRuiz, R., Solis, J., &
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