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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.
Furthermore, the term "STEMI equivalent" has no reliable or definable meaning except between two practitioners who both agree on the list of entities that they believe are STEMI equivalents and can agree on how to identify it. Obvious inferoposterior STEMI. J ACC 61(4):e78-140; page e83.
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. MINOCA I do not have the bandwidth here to write a review of MINOCA.
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.
The precordial ST-depression pattern on this ECG (and in this clinical setting) should immediately raise suspicion of Posterior STEMI! Posterior STEMI occurs in approximately 15-20% of acute MI, but the vast majority of the time it is seen in conjunction with inferior (Infero-Posterior) or lateral (Postero-Lateral) STEMI (1).
His ECG was repeated at this point: This shows a well developed anterior STEMI. To not see these findings is very common, and this patient would be given the diagnosis of NonSTEMI, with subsequent development of STEMI. It is not a missed STEMI, but it is a missed coronary occlusion. The peak troponin I was over 100.
When total LM occlusion does present with STE in aVR, there is ALWAYS ST Elevation elsewhere which makes STEMI obvious; in other words, STE is never limited to only aVR but instead it is part of a massive and usually obvious STEMI. All are, however, clearly massive STEMI. This is her ECG: An obvious STEMI, but which artery?
Notice on the right side of the image how the algorithm correctly measures STE sufficient in V1 and V2 to meet STEMI criteria in a man older than age 40. As most would agree, this ECG shows highly specific findings of anterolateral OMI, even with STEMI criteria in this case. Thus, this is obvious STEMI(+) OMI until proven otherwise.
One of our fine interns, Daniel Lee, who is also an ECG whiz, found this paper from 2013 and brought it to my attention: The delayed activation wave in non-ST-elevation myocardialinfarction. When present, the infarct artery is more likely to be the circumflex. Of all inferior STEMI, 85% are due to RCA.
They recorded a third ECG before intervention: No significant difference Angiogram : Impression and Recommendations: Culprit for the patient's non-ST elevation myocardialinfarction is a thrombotic occlusion of the mid circumflex Formal Echo Normal left ventricular cavity size, normal wall thickness and normal LV systolic function.
Note that they finally have laid to rest the new or presumably new LBBB as a criteria for STEMI. 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. Kurkciyan et al.
If it is STEMI, it would have to be RBBB with STEMI. Only 5-18% of ED patients with chest pain have a myocardialinfarction of any kind. The patient presented with chest pain. Here is the ECG: What do you think? I frankly did not know what to think. Is it Brugada pattern? But in a very unusual pattern. Only 1-5% have OMI.
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.’
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. aVR ST segment elevation: acute STEMI or not? aVR ST Segment Elevation: Acute STEMI or Not?
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. Lancet 2015 6.
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.
Clinical Course The paramedic activated a “Code STEMI” alert and transported the patient nearly 50 miles to the closest tertiary medical center. 2 The astute paramedic recognized this possibility and announced a CODE STEMI. myocardialinfarction), arrhythmias, valvular pathology, shunts, or outflow obstructions.
Background Since 2000, the definition of myocardialinfarction (MI) has evolved with reliance on cardiac troponin (cTn) tests. Methods We used linked hospitalisation data from all WA tertiary hospitals to identify patients with a principal diagnosis of STEMI, NSTEMI or UA between 2002 and 2016.
Smith: T waves are very hyperacute: these are a sign of ACUTE infarction, even if there are Q-waves. 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). See Raitt et al.:
The authors describe a case with some features in common with our patient -- a stressful event followed by a stress cardiomyopathy/acute myocardialinfarction overlap syndrome. Acute myocardialinfarction: an uncommon complication of takotsubo cardiomyopathy. Acute myocardialinfarction triggered by emotional stress.
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