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Cardiogenic shock (CS)is the most feared event following STEMI. We tend to perceive CS as an exclusive complication of STEMI. The incidence is half of that of STEMI, i.e., 2.5-5%. might show little elevation with considerable overlap of left main STEMI vs NSTEMI ) 2.Onset ACS pathophysiology is not that simple.
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. Obvious inferoposterior STEMI. It is posterior OMI until proven otherwise.
Clinical Course The paramedic activated a “Code STEMI” alert and transported the patient nearly 50 miles to the closest tertiary medical center. 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.
This suggests further severe ischemia. STEMI MINOCA versus NSTEMI MINOCA STEMI occurs in the presence of transmural ischaemia due to transient or persistent complete occlusion of the infarct-related coronary artery. This has resulted in an under-representation of STEMI MINOCA patients in the literature. From Gue at al.
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. His response: “subendocardial ischemia. Anything more on history? POCUS will be helpful.”
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?
STE limited to aVR is due to diffuse subendocardial ischemia, but what of STE in both aVR and V1? The last section is a detailed discussion of the research on aVR in both STEMI and NonSTEMI. Alternatively, it is a variant of diffuse subendocardial ischemia, with STE in V1 reciprocal to ST depression in inferior and lateral leads.
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?" All are, however, clearly massive STEMI. This is her ECG: An obvious STEMI, but which artery?
This ECG is diagnostic of diffuse subendocardial ischemia. Note that they finally have laid to rest the new or presumably new LBBB as a criteria for STEMI. Also note that they allow ST depression c/w posterior MI to be a STEMI equivalent. We studied this and published the abstract below in 2010. Kurkciyan et al.
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 ).
If it is STEMI, it would have to be RBBB with STEMI. 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.
Although this " Imbalance " of precordial T waves is not see n very often — in the “right” clinical setting, it has been associated with recent OMI ( O cclusion-based MI ) , most often from a LCx culprit artery ( See Manno et al: JACC 1:1213, 1983 — and the July 17, 2013 post by Salim Rezaie in ALiEM — and ECG Blog #350 ).
Code STEMI was activated by the ED physician based on the diagnostic ECG for LAD OMI in ventricular paced rhythm. This was several months after the 2022 ACC Guidelines adding modified Sgarbossa criteria as a STEMI equivalent in ventricular paced rhythm). LAFB, atrial flutter, anterolateral STEMI(+) OMI. Limkakeng AT.
The HEART and EDACS scores are helpful to risk stratify patients with chest pain, but they hinge on accurate ECG interpretation: a low score doesn’t apply if the ECG shows STEMI(+)OMI, and shouldn’t be used for STEMI(-)OMI or OMI reperfusion either 2. Int J Cardiol 2013 2. Backus BE, Six AJ, Kelder JC, et al.
While this ECG is negative for “posterior STEMI”, the resolution of anterior ST depression (accompanied by the troponin elevation) confirms posterior OMI with spontaneous reperfusion. The second opportunity to make the diagnosis and expedite angiography was missed because the ECG never met STEMI criteria and continued to be labeled ‘normal.’
The overall ST-T wave appearance in this lead looks more like LV “strain” than ischemia. This blog post reviews the basics for predicting the " C ulprit" A rtery — as well as the importance of the term, " O MI" ( = O cclusion-based MI ) as an improvement from the outdated STEMI paradigm.
A prior ECG from 1 month ago was available: The presentation ECG was interpreted as STEMI and the patient was transferred emergently to the nearest PCI center. BOTTOM Line: It can at times be extremely challenging to distinguish between anterior ST elevation from a benign Brugada Phenocopy pattern vs an acute anteroseptal STEMI.
2) The STE in V1 and V2 has an R'-wave and downsloping ST segments, very atypical for STEMI. Cardiology was consulted and they agreed that the EKG had an atypical morphology for STEMI and did not activate the cath lab. Smith comment: 1) Brugada ECG may have ST shifts in limb leads as well as precordial leads. Bicarb 20, Lactate 4.2,
Despite the clinical context, Cardiology was consulted due to concerns for a "STEMI". Hyperkalemia mimics STEMI and OMI in many distributions, but probably the most common is the Brugada morphology in V1-V2 which mimics anterior OMI for those who cannot recognize the Brugada pattern. Limb lead reversal can be easily recognized.
Figure 1-1 My colleague, a faithful student of ECG interpretation, handed me the tracing and said that it warranted STEMI activation because of apparent terminal QRS distortion (TQRSD) in V2. ASA 324mg was administered while a STEMI activation was simultaneously transmitted to the nearest PCI center. Attached is the first ECG.
PEARL # 3: Knowing there is an acute inferior STEMI I looked next to see if there is also acute posterior involvement ( which so often accompanies inferior MI ). But larger-than-expected Q waves in each of the inferior leads ( especially in lead III ) are probably the result of this patients ongoing acute inferior STEMI.
Smith : I recognize this as a STEMI mimic. Doesn't this necessarily mean that he was having ischemia? Although this is not a common phenomenon You will see it on occasion ( See the June 30, 2023 post the November 27, 2023 post and the July 24, 2013 post in Dr. Smith's ECG Blog ). I was not alarmed.
50% of LAD STEMI have Q-waves by one hour. Smith : In limb leads, the ST vector is towards lead II (STE lead II STE lead III, which is more likely with pericarditis than with STEMI). There were no other causes of dyspnea apparent and thus we can assume that myocardial ischemia started 6 days prior. See Raitt et al.:
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! There was indication of parasympathetic overdrive ( the acute inferior STEMI with profound bradycardia and junctional escape ).
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